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A 12-month-old female underwent both cochlear implantation under general anesthesia due to bilateral hearing loss. Her weight was 9 kg, her height was 73 cm, and she was on no regular medications. She was born at 38 weeks of gestation with a birthweight of 3.5 kg via cesarean section to a mother who had no underlying disease. She showed no congenital anomalies or developmental disorders. She received scheduled MMR vaccination 1 week before surgery and did not have any symptoms of upper respiratory infection or fever. All results of preoperative laboratory tests were within the respective normal ranges, including an electrocardiogram, chest X-ray, and blood and urine examinations. Brain magnetic resonance imaging showed no contraindications for cochlear implantation mapping. The patient entered the operating room without any premedication. After entering the operating room, monitoring was initiated, including noninvasive blood pressure, electrocardiogram activity, oxygen saturation, and pediatric bispectral index (BIS). Anesthesia was induced with 50 mg of thiopental sodium and 10 μg of fentanyl, and 5 mg of rocuronium was administered intravenously to facilitate intubation. Endotracheal intubation was performed using a tube (internal diameter, 3.5 mm) with a cuff, and both lungs sounded well. An esophageal thermometer and forced air blanket were applied to manage the patient's body temperature. Her initial core body temperature was 36.4°C, and it was maintained between 36.1°C and 36.5°C (Fig. ). Anesthesia was maintained with 1.5 to 2.0 vol% sevoflurane (with 50% oxygen and 50% nitrous oxide) at a target BIS range of 40 to 60; the end tidal carbon dioxide tension was in the range of 35 to 37 mmHg. The surgery proceeded normally without any adverse events; the total anesthesia time was 3 hours and 20 minutes. Fentanyl (10 μg) was administered intravenously 10 minutes before the end of surgery for pain control and to prevent emergence agitation. At the end of the operation, 2.5 mg of pyridostigmine and 0.1 mg of glycopyrrolate were added to restore neuromuscular blockade. The patient was transferred to the PACU after confirming full recovery of spontaneous eye opening and spontaneous respiration. The vital signs measured at the PACU were normal except for a temperature of 37.2°C measured at the axilla; a tympanic thermometer could not be used as both ears were covered after the operation, so the patient's body temperature was measured at the axilla. Due to the elevated body temperature, we decided to observe without further heating. Oxygen was supplied at a flow rate of 5 L/minute via a simple facial mask. The patient remained in the PACU for 40 minutes and recovered well from anesthesia. The patient had a Modified Aldrete Score of 9/10, and was scheduled to move to the general ward. However, she suddenly became lethargic and showed difficulty in breathing. The oxygen supplied to the mask was increased to 10 L/minute and a jaw-thrust maneuver was performed. The patient showed tonic-clonic movements. Thiopental sodium (50 mg) was administered intravenously and the seizures ceased. Endotracheal intubation and positive pressure ventilation were performed to prevent respiratory depression due to thiopental sodium. During intubation, the practitioner felt that the patient was abnormally warm. The body temperature measured at the axilla was 37.7°C, and the patient was immediately treated with tepid massage. An esophageal thermometer was inserted to allow continuous monitoring of her body temperature, which was shown to be 38.1°C. Despite tepid massage for 20 minutes, the patient's body temperature increased further to 39.0°C (Fig. ). Diclofenac β-dimethylaminoethanol (20 mg) was injected intramuscularly to prevent further body temperature elevation. Consciousness and spontaneous respiration were recovered 1 hour after the seizure. The patient's body temperature as measured with an esophageal thermometer had decreased to 37.5°C. In addition, her oxygen saturation was maintained at >97% after extubation. There was no evidence of atelectasis or pneumonia on a chest X-ray performed the following day. She had no additional seizures while in the general ward, and 60 mg of dexibuprofen was administered orally for 3 days to prevent any increase in body temperature. There was no epileptic wave on electroencephalography (EEG) performed on the fourth postoperative day, and she was discharged without convulsions or focal neurological symptoms on the fifth day. |
A 55-year-old incarcerated male presented to the emergency room with a two-week history of left-sided scrotal pain and swelling.\nThis patient had a history of prostate cancer and high-grade urothelial bladder cancer. His prostate cancer was diagnosed 15 years prior to the current presentation, managed with radiation, and had since remained stable. The patient's high-grade, high-risk bladder cancer was diagnosed two years prior to current presentation. At the time, the patient initially presented with hematuria. A CT urogram performed at the time revealed a nonspecific bladder mass. Biopsy of the mass confirmed urothelial carcinoma. The patient's therapy course included a transurethral resection of the bladder tumor (TURBT), intravesical mitomycin, interferon alfa-2b, and intravesical BCG therapy. He received a total of seven intravesical injections of 50 mg live BCG per injection (350 mg cumulative dose) over the course of 18 months.\nThe patient's other significant medical history included rheumatoid arthritis, for which the patient was on weekly methotrexate and daily tofacitinib treatment. Both medications were discontinued on admission.\nThe patient developed scrotal pain two weeks prior to admission. He initially presented to the emergency department with this pain. At that time, he was diagnosed with acute bacterial epididymitis and was prescribed a course of ciprofloxacin. He had no improvement in his symptoms despite this treatment. Over the subsequent days, he reported experiencing intermittent chills and night sweats. He denied any penile discharge or any history of a sexually transmitted disease.\nEvaluation of the testicle with ultrasound revealed multiple diffuse nodular areas of hypoechogenicity (Figure , ), as well as marked hypervascularity involving all of the left-sided structures (Figure , ). Routine blood and urine cultures were negative, and mycobacterial blood and urine cultures, as well as bladder biopsy, were pending as of this writing.\nAntituberculous therapy was started based on the following considerations regarding the patient's presentation. The lack of observed response to ciprofloxacin therapy decreased the likelihood of uncomplicated bacterial orchitis. We considered this patient's history of bladder cancer involving multiple BCG treatments and the increased likelihood of BCG orchitis. Possibly, his immunocompromised state secondary to the malignancy, in combination with mitomycin chemotherapy and immunomodulatory rheumatoid arthritis treatment, could have increased his susceptibility to a mycobacterial infection. Finally, as ultrasound findings were characteristic of BCG orchitis, the patient was promptly initiated on a combination therapy with levofloxacin, rifampin, isoniazid, and ethambutol. The patient showed marked improvement in pain control and testicular swelling over the following weeks. |
An asymptomatic 71-year-old woman was diagnosed with a left supratentorial and infratentorial dermoid cyst on screening magnetic resonance imaging (MRI) [] and admitted to our hospital. She had a past history of atrial fibrillation, tympanoplasty for tympanitis, and total ovariohysterectomy. Removal of the supratentorial and infratentorial cyst was performed via a left transzygomatic approach. The tumor was almost totally resected with no sequelae; the supratentorial and infratentorial compartments remained. Because the patient had a preoperative history of atrial fibrillation, postoperative warfarin therapy was administered to prevent embolism. The patient was followed-up by the outpatient service and developed no recurrence or any abnormal imaging signals in the residual cavity []. Although the patient had no history of head injury, a screening computed tomography (CT) scan performed 3.5 years postoperatively as part of annual follow-up revealed a density change within the supratentorial and infratentorial regions. At that point, we decided to perform periodic follow-ups once monthly because the patient was asymptomatic, and the hematoma did not appear to be compressing the brain stem. Four months after the start of follow-up, the patient was transferred to the emergency department because of cerebellar ataxia, vomiting, and deterioration of consciousness (Glasgow Coma Scale score: E3V4M6) with no paresis. A CT scan revealed enlargement of the hematoma in the posterior fossa and compression of the brain stem []. Two hematomas, one in the supratentorial region and one in the infratentorial region, were greatly compressing the brain, and seemed to be separate lesions. It was difficult to judge on CT whether there was communication between the two hematoma cavities. Because the patient's symptoms were considered to have resulted from compression of the brain stem and cerebellum, we urgently performed hematoma removal under general anesthesia via suboccipital craniotomy with a 6-cm linear incision behind the mastoid process along the hairline for the posterior fossa CSDH. Burr-hole irrigation was performed via a linear incision for the supratentorial CSDH. The tension in the posterior fossa was high, and the outer membrane was seen under the dura mater []. We resected the outer membrane of the CSDH as completely as possible and copiously irrigated the hematoma cavity. The fluid in both the supratentorial and infratentorial portions was the same reddish brown. After adequate irrigation of both fields, we confirmed communication between the supratentorial and infratentorial spaces. Closed-system subdural drainage catheters were inserted in both cavities until the day after the operation. Postoperative CT scans of the head revealed disappearance of the CSDH in both the supratentorial and infratentorial spaces [Figure and ]. Signal change was also confirmed on postoperative MRI []. The patient's symptoms gradually subsided, and she was discharged to her home with no neurological deficits on postoperative day 12. Apixaban was prescribed as anticoagulation therapy upon discharge. No recurrence was detected on CT scan 1 month postoperatively. At 1 year, CSDH had not recurred. |
A 47-year-old male presented with itchy and painful nodules of the head and neck (fig. ). The lesions had developed slowly over a period of 6 months and had gradually increased in number and size.\nThe patient had a 15-year-long history of diabetes mellitus II treated with insulin aspart as well as a history of allergic rhinitis and atopic dermatitis with recent flares. His filaggrin status was not known. Skin examination revealed multiple erythematous nodules on the scalp and the face that were painful on pressure. The lesions varied in size, with the biggest nodule measuring up to 2 cm (fig. ). A few scaly eczematous patches were detected on his arms and trunk. His skin was notably dry.\nA skin biopsy taken from one of the nodules showed blossom-like basophilic bacterial aggregations with a homogeneous eosinophilic rim surrounded by a dense mixed infiltrate with areas of abscess and granuloma (fig. ). Modified Gram stain (Brenn-Brown) revealed Gram-positive cocci in the center of the grains (fig. ). Microbiologic swabs from one of the lesions identified Staphylococcus aureus sensitive to methicillin. PCR on the same material was negative for mycobacteria of the tuberculosis complex. Throat, nasal and perianal swabs revealed physiologic flora. Mycological cultures yielded no growth. Blood values were largely within normal limits and showed no evidence for a severe immune dysfunction. Total serum levels of IgE and IgG were normal with only minor changes in the IgG3 and IgG4 subclass fractions, which were most likely due to a pronounced atopic predisposition and to chronic inflammation.\nAltogether, the clinical presentation and the diagnostic workup including a skin biopsy and microbiologic examinations confirmed the diagnosis of botryomycosis due to infection with S. aureus.\nWe initiated treatment with systemic rifampicin, flucloxacillin and fusidic acid, supported by topical disinfectant agents. No surgical intervention was performed.\nThe first follow-up 2 weeks later indicated a good response. However, the lesions relapsed on the scalp 4 weeks later. The further course of the disease was tenacious with rapid relapses and flares upon cessation of the treatment. |
A 52-year-old man presented to the emergency department with a 30-min history of chest pain. Prior to presentation, the patient had severe chest pain with transient loss of consciousness after intramuscular administration of 80 mg phloroglucinol to treat abdominal pain caused by right ureteral calculi. The patient's risk factors and past medical history included active tobacco use, diabetes mellitus for 6 years and treatment with insulin, and a known history of coronary artery disease. Two months earlier, the patient received stent implantation in the proximal right coronary artery (RCA), and the distal RCA showed 75% stenosis without percutaneous coronary intervention. He was taking aspirin, ticagrelor, and atorvastatin.\nVital signs on arrival showed a blood pressure of 82/46 mmHg. Notably, erythematous rash was found throughout the chest, abdomen and limbs of the patient (). The patient was first diagnosed with a systemic allergic reaction. We administered intravenous fluids and norepinephrine to maintain a blood pressure >90/60 mmHg. Dexamethasone (10 mg) and promethazine (25 mg) were administered to treat his allergic reaction. An initial twelve-lead electrocardiogram (ECG) immediately after admission showed ST-segment elevation in leads II, III and aVF (). Acute inferior myocardial infarction due to RCA occlusion was also considered. Emergency coronary angiography was performed (the right coronary angiography results after stent implantation 2 months earlier was shown in ), and the results revealed severe stenosis in the distal RCA (). Intravascular ultrasound showed plaque rupture and thrombosis (). The minimum lumen area at the stenosis was 3.0 mm2, and the plaque burden was 80.7%. Percutaneous coronary intervention was performed in the distal RCA with a 3.5 mm × 38 mm stent. Coronary angiography after stent implantation showed an acceptable angiographic result with a thrombolysis in myocardial infarction (TIMI) flow grade of 3 (). The procedure was successful, and the patient's symptoms were relieved completely. Postoperative ECG indicated ST-segment elevation in leads II, III and aVF disappeared (). Laboratory evaluation revealed a troponin I level of 0.448 ng/ml (normal range <0.03), an eosinophil count of 0.51 × 109/L (0.05–0.5), and an immunoglobulin E level of 405 IU/ml (0–100). Echocardiography revealed no obvious abnormality. The diagnosis of type II Kounis syndrome induced by phloroglucinol was made, and the condition manifested as acute ST-segment elevation myocardial infarction caused by allergic plaque rupture and thrombosis.\nThe patient received 100 mg/d aspirin, 180 mg/d ticagrelor, and 40 mg/d atorvastatin orally for myocardial infarction after percutaneous coronary intervention. The patient had an uneventful hospitalization and was discharged with a suggestion of avoiding phloroglucinol. During the 6-month follow-up, the patient did not experience chest pain. A detailed timeline from the onset of symptoms in the patient to his discharge is provided (). |
A 12-year-old female had consulted at the Department of Gynecology for pelvic pain for 22 days which was intense in the evening at lying. She had a polyuria for 10 days and occurred over the night where she woke up 7 times on average to urinate. There was no notion of traumatism. There was no medical and surgical history. There was no concept of sexually transmitted infections. The socio-economic level was considered average; she had never smoked and did not drink alcohol. She had normal pubertal development with chest changes and pubic hair.\nClinical examination displayed a temperature of temperature at 37 °C, a weight of 46 kg for a size of 1.34 m, BMI was 25,62Kg/m2. The blood pressure was 110/60mmhg. The general condition was good. The patient suffered from pain in the right pelvic region triggered by palpation, and thus, limiting the movement of the right hip. Palpable adenopathy was absent. The remaining physical examination was normal. The biological examination was normal. The abdominal ultrasound showed a solid mass that occupied the right ovary. The biological check-up was in normal. Alpha-fetoprotein and β-hCG were normal. Ultrasound of the abdomen showed a solid mass that occupied the right ovary.\nThe patient underwent an ovariectomy. The macroscopic analysis revealed that the ovariectomy was grayish, irregular and elastic and measured 17cmx14cmx9cm. The ovarian sections were heterogeneous, including red areas and hemorrhagic territories. The normal ovarian tissue was not identified. The Fallopian tube was normal. The contralateral adnexa and the uterine body were normal. The peritoneum was apparently normal and the peritoneal cavity contained approximately 1000 mL of blood ascetic fluid.\nThe sections of the ovarian tumor were made and ten blocks of paraffin were made. Conventional histology showed a malignant vascular tumor proliferation made of many very small vascular luminesces with endothelial cells exhibiting nuclear atypia and mitoses. The necrosis was present. As diagnostic hypotheses, we primarily reported angiosarcoma followed by hemangiopericytoma (Fig. ). Three blocks of paraffin embedded ovarian tissue were sent to a well-equipped laboratory in France for immunohistochemistry analysis to confirm the diagnosis.\nThe result of immunohistochemistry analysis was CD31+, CD34+, and Factor VIII+ (Figs. , and ). The tumor cells were SMA-, desmin-, melanin A-, and S-100-. The diagnosis of grade 2 angiosarcoma (FNCLCC) was confirmed after a multidisciplinary consultation. The patient was eligible for chemotherapy according to the CWS-2002P protocol. However, the patient’s family had a financial issue. |
A 5-year-old boy was referred to the Children’s heart centre at AUBMC after detecting a saturation of 92% while being screened by the anaesthesia team preceding a dental procedure. Patient was asymptomatic, denied any chest discomfort, dyspnoea, episodes of altered mental status, and other symptoms of hyperviscosity. His medical history, reported by the parents, revealed open-heart surgery for ASD closure in another country at the age of 2 years. Parents informed the medical staff that he had a smooth post-operative course and was discharged home after few days; however, no documentation was available. Follow-up after his surgical closure was done routinely showing good results and no abnormalities.\nHis assessment in our clinic revealed O2 saturation ranging from 90% to 94%, blood pressure 105/68, and respiratory rate 25. The patient had no dysmorphic features. His physical exam revealed minimal central cyanosis, normal apical impulse no right ventricular heaves or thrills, normal first and second heart sounds, and absence clubbing.\nThe electrocardiogram and chest X-ray were within normal limits. Echocardiogram showed a small fenestration through the ASD patch with a left to right shunt across it. Normal atrioventricular and normal ventriculoarterial concordance, left and right normal ventricular function and dimensions, no secondary signs of pulmonary hypertension. The superior vena cava (SVC) was draining into the right atrium. The pulmonary veins were draining normally into the LA, and the estimated pulmonary systolic and diastolic pressures were normal. However, the IVC flow was not directed into the right atrium (Figures and , , Video S1), and we suspected that the drainage was directed to LA. Pulmonary to systemic flow ratio was 0.6. A chest computed tomography was requested and the result confirmed our diagnosis (Figure ). A multidisciplinary meeting was held with the surgeon and a decision was taken to perform a surgical repair.\nTransoesophageal echocardiographies are performed routinely at our institution prior and after cardiothoracic surgeries looking for optimal surgical results. A transoesophageal study was done in the operating room immediately before surgery confirming our findings. A bicaval view was also taken showing the above mentioned findings (Figure ). Our patient had two central venous lines, one in his jugular vein and the second in the femoral vein. Central pressures were taken showing SVC pressure of 7 mmHg as compared to an IVC pressure of 13 mmHg. Saline was injected in the femoral venous line during the transthoracic echocardiography allowing the visualization of micro-bubbles in the LA and subsequently in the other chambers (Figures and , , Video S2). The intra-operative finding of aberrant IVC drainage to the LA was confirmed, and the IVC was re-implanted into the right atrium. The post-operative course was smooth, and the patient was discharged 5 days later having an SpO2 of 100%. One week later, during a routine follow-up, the patient was recovering well, fully saturated and had good surgical result confirmed by echocardiography. |
A 44-year-old previously fit and well Caucasian man presented with a one-day history of severe, unremitting, and diffuse colicky abdominal pain with absolute constipation. He had a four-month history of similar but less severe pain, preceded by loose stools with mucus and frequent PR bleeds on a background of poor appetite and 7 kg weight loss over six months. Family history was notable for colorectal cancer in his uncle at 71 years of age. Social history was significant for 10 cigarettes a day, 70 units of alcohol a week, and extensive travel history to Thailand. On examination, the lower abdomen was distended and diffusely tender with tinkling bowel sounds but no guarding or rigidity.\nA plain supine abdominal radiograph showed a hugely dilated caecum (maximum diameter: 15 cm) and transverse colon (maximum diameter: 10 cm) with paucity of gas in the descending colon (). A CT scan revealed apparent intussusception of a polypoid lead point into the distal descending colon () but no signs of bowel perforation as well as bilateral cavitating lesions in the lung apices ().\nAn urgent exploratory laparotomy revealed an irregular mass in the distal transverse colon and another adjacent mass in the splenic flexure with apparent spontaneous resolution of the intussusception seen on CT. Widespread lymphadenopathy was noted in the transverse colon mesentery. A left hemicolectomy was undertaken with excision of the left-sided omentum, followed by a side-to-side anastomosis with a defunctioning loop ileostomy.\nA Mantoux test yielded 16 mm induration, albeit in the context of prior BCG vaccination 30 years ago. However, alcohol and acid-fast bacilli (AAFB) were not detected in sputum samples. HIV test was negative.\nHistology sections from the colonic lesion showed an area of florid filiform polyposis () with no evidence of dysplasia but with adjacent ulceration of the colonic mucosa. The background colon showed areas of transmural chronic inflammation in the form of subserosal lymphoid aggregates arranged in a rosary pattern (). No AAFB, granulomas, features of colitis, or diverticular disease were identified. Multiple lymph nodes examined showed reactive-type changes only. The appearances were most in keeping with localised filiform polyposis.\nDespite the absence of AAFB on sputum microscopy and colonic histology, the Infectious Disease (ID) team treated the patient empirically for tuberculosis on a 6-month course of rifampicin (10 mg/kg/day up to 600 mg/day), isoniazid (5 mg/kg/day up to 300 mg/day), pyrazinamide (30 mg/kg/day up to 2 g/day), and ethambutol (15 mg/kg/day) on the basis of the cavitating lung lesions and positive Mantoux test. The patient recovered and was discharged from hospital a week later.\nSerial sputum cultures eventually grew fully sensitive Mycobacterium tuberculosis. A follow-up CT scan of the chest three months later showed mild improvement of his lung lesions. A water-soluble contrast enema four months after surgery showed the large bowel to have no abnormalities. At the time of last follow-up six months after surgery, the patient was well and awaiting the reversal of his ileostomy. The patient was under close follow-up from his General Practitioner in close liaison with the Infectious Diseases team. Contact tracing was difficult for this patient as he traveled overseas frequently and was likely to have contracted tuberculosis while being overseas. |
A 62-year-old woman with a history of cerebral palsy, dementia, dysphagia, cerebral vascular accident, and 18 months of percutaneous endoscopic gastrostomy (PEG) tube placement presented from a skilled nursing facility with multiple episodes of nonbloody, bilious emesis, fever, and hypotension. Gastric contents were aspirated from the PEG tube and abdominal distention was noted. Hemogram demonstrated an elevated white blood cell count of 31.5 K/mm3 with a left-band shift and a lactic acid level of 4.9 mmol/L. Abdominal computed tomography (CT) with contrast administered via PEG displayed the first and second portions of the duodenum to be thickened with evidence of retrograde jejunoduodenal intussusception due to tube migration into the left upper abdominal quadrant (Figure ). The PEG was initially evaluated and repositioned at bedside with deflation of the bumper and gentle retraction of the tube back toward the stomach. Repeat migration was of concern as the tube altered position over the following days. Later, the tube was replaced with a 20 French right-angle PEG with position confirmed via plain film. Repeat CT demonstrated resolution of intussusception with maintained thickening of the proximal duodenal wall (Figure ). Another CT scan performed 9 months later indicated continued proximal duodenal wall thickening likely due to scarring from the intussusception inflammatory process. Endoscopic evaluation was not performed to evaluate the duodenal wall thickening as multiple comorbidities, including severe dementia and mental retardation, precluded the patient to a change in management.\nRetrograde jejunoduodenal intussusception is a very rare complication of gastrostomy tube use. Bowel ischemia is of grave concern requiring a high level of suspicion in patients presenting with nausea and vomiting and a history of PEG tube. The mechanism of intussusception is not well understood, but several hypotheses have been previously discussed. Fundamentally, migration of the tube due to peristalsis, with subsequent fixation to the bowel wall, allows for retrograde jejunal invagination over the balloon. This may be further exacerbated by attempts to reposition the tube without balloon deflation causing retraction toward the pylorus. The use of external fixation devices seek to immobilize the balloon but has proven to be inadequate in some patients. Here, we recommend the use of a right-angle tube to further restrict movement. The right-angle tube was employed because the tube structure allows it to be less obtrusive, while the angulation anchors the tube against the external abdomen, thereby reducing inward migration. Low-profile tubes were not available in our facility as the demographic primarily attended to by our institution is nonpediatric and unconcerned with aesthetics. Additionally, carrying a full array of low-profile tubes is often costly for smaller facilities. Although rare, prevention of migration with resulting intussusception should be considered in patients with a history of recurrent malposition and may be reinforced by the advantages of utilizing a right-angle PEG. |
A 66-year-old man with a past medical history of uncontrolled hypertension (requiring three agents with persistent systolic blood pressure readings above 180 mmHg), coronary artery disease with three prior cardiac stents placed, and acid reflux (worsening in the presence of the mass) presented to his outside physician with dysphagia, chest pain, and shortness of breath. Workup revealed a 16.1 cm × 9.2 cm × 12.3-cm anterior mediastinal mass (Figure ) causing right ventricular outflow tract obstruction and displacement of the ascending aorta. This finding prompted a computed tomography-guided biopsy, which revealed a primary anterior mediastinal carcinoid tumor. Two-dimensional transthoracic echocardiography was performed, which corroborated findings of moderate to severe right ventricular outflow tract obstruction with a pressure gradient of 55 mmHg. Intraoperative transesophageal echocardiography highlighted this finding (Figure ). His transthoracic echocardiogram was otherwise unremarkable. The patient was discussed in the Thoracic Oncology Tumor Board, and the recommendation was for surgical excision of the mass. Anesthesia was consulted for anesthetic management of the surgical tumor resection.\nAnesthetic management proceeded with the placement of a thoracic epidural catheter at the T5-6 interspace via the institutionally preferred right paramedian approach in the preoperative holding area with no sedation required. A test dose of 3 mL lidocaine 1.5% with epinephrine 1:200,000 was administered with no hemodynamic changes. The patient was taken to the operating room, and procedural sedation was initiated with 1 mg of midazolam and a 0.8 mcg/kg/hr dexmedetomidine infusion. This medication regimen was chosen for anxiolysis and mild to moderate sedation while ensuring spontaneous ventilation. An additional benefit of this medication regimen is the minimal hemodynamic implications at this dose. The patient was positioned, prepared with antiseptic solution, and draped in the usual fashion. Radial arterial and femoral arterial and venous lines were placed under local anesthesia and conscious sedation. Following confirmation of adequate thoracic epidural anesthesia, a chest incision was made, and general anesthesia was induced with 2 mg of midazolam, 70 mg of ketamine, and 70 mg of propofol, maintaining spontaneous respiration while performing video laryngoscopy. Once a grade 1 view was obtained, muscle relaxant was administered, and a left-sided double-lumen endotracheal tube was placed and positioned appropriately with fiberoptic bronchoscopic guidance. Intermittent doses of phenylephrine were required to maintain hemodynamic stability throughout induction and surgical exposure and as such venoarterial extracorpeal membrane oxygenation cannulation and initiation were deemed unnecessary, although necessary equipment and staffing were on standby in the operating room.\nSurgical resection was performed via clamshell incision at the fourth intercostal space. The tumor had invaded the pericardium, necessitating a pericardiectomy, as well as the left brachiocephalic vein, requiring tangential resection and repair. Further cephalad, the tumor had encased the left phrenic nerve, requiring clipping of the nerve proximal and distal to the tumor. Along the right thoracic inlet, the tumor had invaded the right internal mammary vessels, requiring clipping and ligation. Ultimately, the tumor was freed and removed from the field. Bilateral chest tubes were placed, the incision was closed in layers, and the sternum was closed with two sternal wire sutures. The patient was extubated in the operating room and transported to the intensive care unit in stable condition for further care. There were no intraoperative complications.\nThe postoperative pathology report reflected atypical carcinoid with positive margins as well as a pleural implant, denoting stage IV disease. His postoperative course was complicated by angioedema and emergent reintubation on postoperative day 2, presumably due to anaphylaxis associated with tramadol administration due to temporal relation to previously naïve medication administration. The incidence of tramadol-related angioedema is reported to be 1:1000-1:10,000 []. The patient developed ST segment elevation following the episode of angioedema along with elevated troponins, likely attributed to significant hypertension following treatment of angioedema. No further cardiac intervention was performed as echocardiography did not reveal consistently elevated cardiac enzymes or EKG changes. The patient was extubated once the airway edema resolved on postoperative day 4. He was then downgraded from intensive care on postoperative day 7 and discharged home in stable condition without further complication on postoperative day 8. |
A 24-year-old man was admitted to our facility for IR. The patient had a history of percutaneous kidney biopsy under real-time ultrasound guidance using a cutting needle at 15 years of age. Macroscopic hematuria started shortly after biopsy, but ceased within a couple of days without development of significant anemia. The size of a subcapsular hematoma (up to 38 mm long by 7 mm wide), which occurs in most renal biopsies, also decreased over time. Thus, common complications such as gross hematuria and subcapsular hematoma occurred, but were settled within days of the biopsy. Based on our institutional protocol, the patient was discharged 7 days after biopsy. However, immediate rehospitalization was required on the day of discharge due to abrupt onset of severe left flank pain. Gross hematuria reemerged and was intermittently observed for several days, resulting in hypotension (94/58 mmHg), a significant decrease of blood hemoglobin (14.2 to 10.7 g/dl), and acute dysuria. Embolization via IR was considered as an emergency therapy to stop bleeding, but gross hematuria eventually disappeared within days with intravenous injection of hemostatic agents such as carbazochrome sodium sulfonate and tranexamic acid, in addition to bed rest. It was noteworthy that color-coded Doppler US detected AVF as a mosaic signal in the lower pole of the left kidney (Fig. ), which was the puncture site of the biopsy. However, in terms of size, this lesion was morphologically undetectable, even by dynamic contrast-enhanced computed tomography (CT) (Fig. ). After disappearance of gross hematuria, the patient was free from renal AVF-related manifestations, including abdominal pain, hypertension, and renal impairment. Thus, it was determined that IR was not required at this time.\nIgA nephropathy was diagnosed based on the findings of renal biopsy. The patient was hospitalized again six months later to receive steroid pulse therapy followed by tonsillectomy [] for this glomerulopathy. A striking improvement in urinary abnormalities was gradually achieved, with urinary protein reduced from 4.2 to 0.2 g/day and red blood cells decreased to a level of 5 cells per high-power field in sediment. Ultrasound examination was performed again, but growth of renal AVF was not evident in this period. Following the combination therapy, the patient regularly visited our hospital and took 300 mg dipyridamole and 6 mg candesartan orally each day. The angiotensin II receptor antagonist was prescribed as a renoprotective agent, rather than for a depressor effect. Blood pressure (125/75 mmHg), blood hemoglobin, and serum creatinine remained normal in this period and for over eight years.\nDespite the uneventful course, at the age of 24 the patient underwent abdominal ultrasound because of a slight elevation of serum alanine aminotransferase (up to 36 U/l), which had been noted approximately one year earlier. Unexpectedly, a mass lesion was found in the left kidney, whereas there were few morphological abnormalities in the liver. Dynamic contrast-enhanced CT subsequently delineated a gourd-shaped mass (26 × 22 and 12 × 11 mm) in the left kidney (Fig. ) and marked dilatation of the left renal vein (Fig. ). Three-dimensional CT (Fig. ) and maximum intensity projection CT (Fig. ) clearly revealed that this lesion directly led to the renal artery and vein, suggesting that the renal AVF had grown subclinically to a giant size over many years and had resulted in marked dilatation of the venous system. Therefore, IR was required to prevent further growth of the fistula and manifestation of symptoms.\nTranscatheter embolization of high-flow left renal AVF was performed using detachable coils by radiologists. The fistula was solidly packed with 7 Coil 400 Standard Complex® coils (Penumbra, Inc., Alameda, CA, USA) and 22 Presidio® coils (Codman, Inc., Raynham, MA, USA) under digital subtraction angiography. As shown in Fig. , the high-flow fistula was successfully blocked out, with conservation of renal blood flow. The patient was discharged on postoperative day 3 without adverse events. A follow-up test by contrast-enhanced MRI at about 3 months after IR showed maintained discontinuation of blood flow to the AVF (Fig. ), indicating the success of the treatment. |
A 1-year, 7-month-old boy was admitted to the hospital with high fever, vomiting, and diarrhea which have not improved for 2 days. According to the description of the patient's father, the patient started having nausea and vomiting after eating 2 days ago, and then, he got a high fever of 39.9°C. After receiving treatment in the clinic, the patient's vomiting improved, but his fever did not, and he started having frequent watery diarrhea, followed by blood-tinged mucus in stool. Later, the patient was admitted to the hospital because of dehydration.\nThe patient was given fluid supplement therapy through intravenous (IV) drip infusion after hospitalization. He was also provided with antibiotics (ceftriaxone 100 mg/kg/day IV Q12H) for 5 days due to blood test that showed leukocytosis and high C-reactive protein level []. As the patient was crying of intermittent periumbilical abdominal pain, an abdominal sonogram was performed on the 3rd day of hospitalization. The result showed intestinal dilation and bowel wall thickening caused by inflammation [] and also incidentally found a 1.3 cm × 0.6 cm gallbladder stone [Figures -]. However, the examination showed neither thickening of the gallbladder wall caused by inflammation nor any dilated bile duct.\nThe patient showed no clinical symptom of scleral jaundice and reported no right upper abdominal tenderness during his physical examination (murphy sign negative). His father had a family history of gallbladder stones, so he paid to have the patient to get an abdominal sonogram examination at birth, and the result showed no abnormality. After 5 days of hospitalization, the patient's fever was brought down. The stool culture confirmed that the patient had Salmonella enterocolitis (Salmonella Group D).\nAn abdominal sonogram was followed up 15 days after the patient discharged from the hospital. The test showed dissolution of gallstone with only some hyperechogenic lesions at the gallbladder orifice and main bile duct, believed to be residual biliary mud or sands [Figure and ]. |
A 90-year-old postmenopausal woman presented to the accident and emergency (A&E) department with acute pain of her right shoulder after turning the tap off in her kitchen. She reported hearing a “crack” whilst turning the tap off and noticed an obvious bump over her right shoulder, which prompted her to attend the A&E department. Patient denied any history of previous trauma to her right clavicle, and there was no prodromal symptom such as pain over the right shoulder or clavicle.\nRadiographs revealed an acute transverse right mid-clavicular fracture, with evidence of superior cortical thickening and a small superior spike (). Her only past medical history was osteoarthritis of her knees and bilateral varicose veins. She had been taking treatment dose of alendronic acid 70 mg once weekly for postmenopausal osteoporosis over the past seven years. Her other regular medication was Adcal-D3 tablets (1500 mg calcium carbonate and 400 iu colecalciferol) taken once daily and paracetamol 1 g tablets, taken four times a day. Her most recent serum 25 hydroxyvitamin D concentration was 140 nmol/L.\nThe patient was referred to our departmental fracture clinic a few days following her attendance in A&E. Apart from pain on movements of her right shoulder, patient's right upper limb was neurovascularly intact. There was no evidence of skin tenting or compromise on examination. She was therefore conservatively managed on a broad arm sling. Apart from the above-mentioned past medical history, she denied any signs and symptoms of systemic illnesses or malignancy. Blood tests including myeloma screen were all normal. Her initial radiographs () were suggestive of an atypical fracture associated with long-term bisphosphonate treatment; therefore, both patient and her general practitioner were advised to stop the regular alendronic acid prescription.\nFollow-up radiographs 4 weeks later () demonstrated some signs of callus formation. clearly demonstrates the transverse fracture and cortical thickening of the superior cortex and a small spike. At four weeks of followup, clinically, there was no gross deformity over her right shoulder. The patient's pain had reduced and she was beginning to improve her range of movement. Following discussion with the patient, a decision was made to continue treating this fracture conservatively as it would not impact her normal activities. |
A two-and-a-half-year-old girl was referred in to the ENT clinic with a tender fluctuant area involving the pre-auricular and inferior aspect of the pinna with mildly raised inflammatory markers (c-reactive protein: 45). The patient had no significant medical or prenatal related history. The patient was diagnosed with a peri-auricular abscess and underwent an incision and drainage of the lesion under general anaesthesia. Intraoperatively, the EAC and tympanic membrane were normal, however, a left-sided peri-auricular abscess was drained with pus sent to histology and microbiology for microscopy, culture and sensitivity, and to test for acid-fast Bacilli (AFB). The wound was washed out with 0.9% saline and betadine and a bismuth iodoform paraffin paste (BIPP) dressing applied. The patient was sent home to complete a seven-day course of oral antibiotics. The BIPP dressing was removed two days later and appeared to have healed well.\nThe patient was seen two weeks after the initial procedure. Full re-accumulation of the abscess had occurred. Previous histology showed inflammatory granulation tissue and no growth was seen on microbiology with AFB negative. The patient underwent a further incision and drainage under general anaesthesia. The wound was noted to be discharging from the previous scar and thus the wound was opened up with the granulation tissue debulked and sent for histology which again showed only inflammatory granulation tissue. Despite good early healing, the parents reported having to change the dressing daily owing to high wound output. The patient was unfortunately lost to follow up but represented eight months later and on this occasion, the lesion was solely inferior to the pinna and was noted to have a communication with the EAC with discharge noted with an intact tympanic membrane. The patient underwent a further incision and drainage, however, in postoperative follow-up, a possible diagnosis of a first branchial cleft abnormality was considered and a referral was made to a paediatric ENT specialist centre. The patient had an MRI which confirmed the diagnosis showing a left pre-auricular cystic swelling with a thick-walled and mildly enhancing tract extending to the floor of the lateral bony EAC suggestive of a first branchial cleft cyst (Figure ). The patient underwent an excision of the fistula via a parotidectomy approach. |
We describe the case of a 50-year-old man who had been diagnosed with Behçet’s disease (BD) 14 years previously and met the international criteria. He had first presented with recurrent oral aphthae at the age of 15 and presented 5 years later with simultaneous and recurrent genital ulcers with a clear positive pathergy test. The disease progressed with panniculitic lesions on the inferior limbs, bilateral auricular chondritis (MAGIC syndrome) and asymmetrical polyarthritis. Following the diagnosis of BD, he was initially treated for 3 years with corticosteroids and colchicine, but with only partial improvement. More exuberant oral and genital ulcers justified the initiation of thalidomide, initially at 50 mg per day but increasing to 100 mg per day 2 months later. Less than a month after beginning therapy, the patient showed complete remission of the genital ulcers and marked improvement of the oral aphthae, polyarthritis and auricular chondritis.\nHowever, 8 months later, the patient developed paraesthesia of the lower limbs. As these symptoms did not improve when thalidomide was reduced to 50 mg, an electromyogram was performed and revealed sensitive peripheral neuropathy. Thalidomide was suspended, and the patient was medicated with azathioprine together with corticosteroids and colchicine, but showed only a partial response. Later, due to worsening of BD symptoms and the development of abdominal pain and bloody diarrhoea (with colonoscopic evidence of colonic involvement), the patient was treated with adalimumab with an excellent response. However, 4 months later, he presented hilar and mediastinal adenopathy with pulmonary interstitial involvement; biopsy confirmed pulmonary sarcoidosis probably induced by adalimumab. Total reversal of the pulmonary lesions was observed when adalimumab was suspended. However, the BD worsened with erythema nodosum requiring high doses of corticosteroids, with the consequent development of iatrogenic diabetes and lumbar osteoporosis. The oral and genital ulcers persisted, causing a decrease in quality of life.\nLenalidomide was proposed and approved and the patient was started on 5 mg per day. There was immediate improvement, and the corticosteroid dose was reduced with no signs of peripheral neuropathy or haematological toxicity. Twenty months later there had been no new episodes of oral or genital ulcers and there was total remission of the bilateral auricular chondritis. The most recent electromyogram shows absence of motor or sensitive polyneuropathy of the lower limbs. |
A 44-year-old male with left-sided CBT excision a week prior presented to the emergency on day 8 following surgery with surgical site bleeding and pulsatile neck swelling. Preoperative computed tomography (CT) with angiogram () revealed an intensely enhancing lesion, 4.3 cm in maximum dimension, abutting and splaying the internal carotid artery (ICA) and external carotid artery (ECA) with an angle of contact of more than 180 degrees, suggesting a Shamblin type II tumor. Local examination showed a large pulsatile swelling at the surgical site on the left side of the neck. His blood pressure was 110/74 (84) mm of Hg and his pulse rate was 96 per minute. Blood investigations including hemoglobin and white blood cell count were within normal limits.\nA repeat CT scan of the neck with angiography demonstrated a pseudoaneurysm at the stump of ligated ECA with surrounding hematoma (). A diagnostic catheter angiogram showed narrowing of the distal common carotid artery (CCA) with small outpouching at ligated ECA origin with no active extravasation. He subsequently underwent neck exploration with excision of the pseudoaneurysm and primary repair of ECA rent.\nDuring this period, he was diagnosed with type II diabetes mellitus. The neck wound developed an infection with Pseudomonas aeruginosa, which was managed conservatively. At the time of discharge on day 14, he was having left marginal mandibular nerve palsy, deviation of the uvula to left, hoarseness of voice, and left-sided partial ptosis (Horner’s syndrome), which possibly were surgical complications.\nA week later on day 24, he again presented with surgical wound site swelling. Repeat CT angiography of the neck revealed mild arterial wall irregularity at the previous operative site with adjoining hematoma. No definite pseudoaneurysm sac was found on the CT angiogram.\nThe next day (day 25), early morning active bleeding started from the wound site with hypotension; hence the plan was for catheter angiography. A diagnostic catheter angiogram showed contrast outpouching at the left CCA-ICA junction (suggestive of ruptured carotid pseudoaneurysm) with active extravasation (). Since the patient had active bleeding with an infected wound and previously failed surgery, the decision for PAO was made. Balloon test occlusion (BTO) was done to look for cross flow and prognostication, though there was no other option to preserve the ICA. BTO showed good crossflow with a venous delay of less than 2 seconds with a small watershed perfusion defect in ACA-MCA territory. Multiple coils were deployed into the left ICA-CCA across the pseudoaneurysm with PAO leaving behind a small left CCA stump (). In the end, the check run showed no opacification or antegrade flow in the left ICA or ECA.\nThe patient was started on inotropes with the target to maintain the mean arterial pressure (MAP) in the range of 100–110 mmHg. Nevertheless, a couple of hours later, he developed right-sided upper and lower limb weakness, and a magnetic resonance imaging (MRI) scan showed left ACA-MCA watershed territory infarcts (). At that time, the patient’s MAP was in the range of 90–94 mmHg, despite a high dose of single inotrope. Double inotropes were started along with high-volume saline infusion to further increase the MAP. The right-sided weakness improved significantly in the next few hours.\nBut during the next morning (day 26), he suddenly became drowsy and confused. At that time, he was on a high-dose double inotrope with a MAP of 100–102 mmHg. An emergency MRI was done, which surprisingly revealed multiple new patchy foci of diffusion restriction involving the posterior circulation (bilateral cerebellar hemisphere, superior vermis, and occipital lobes) (). No new area of infarction was seen in the anterior circulation in comparison to the previous day’s MRI. He was managed with aspirin, anticoagulants (unfractionated heparin infusion), and maintenance of a high MAP.\nOver time, his neurological symptoms improved completely and ionotropic support was tapered, but we could not wean him off completely as he was having prolonged and persistent hypotension. He also developed another episode of hemodynamic stroke while trying to take him off ionotropic support. We managed this prolonged hypotension with high volume intravenous fluid, inotropes, and postural management. Ionotropic support was gradually tapered over the next 4 weeks and he was discharged in a stable condition on the 55th day following the first neck surgery. All events are summarized in . |
A 25-year-old man accidentally fell from a cliff and hit his right flank on the ground while camping. Initially, he was able to barely walk, but he ultimately became unable to walk at all due to severe flank pain. His colleague called an ambulance. He had no remarkable personal or family history and was a social drinker.\nInitially, he was transported to a local hospital, but computed tomography (CT) revealed right renal injury with massive retroperitoneal hematoma, so he was transported to our hospital by a physician-staffed helicopter 2 hours after the accident. Upon arrival, he showed clear consciousness but was in a hemorrhagic shock state. His vital signs were as follows: blood pressure, 84/50 mmHg; heart rate, 140 beats per minute; respiratory rate, 30 breaths per minute; percutaneous saturation; and 98% under 10 L/minute of oxygen via mask. He had marked right flank pain. A focused assessment with sonography in trauma was positive at Morrison's pouch. He urgently received 6 units of different-type blood transfusion, and his blood pressure temporarily increased. Enhanced CT revealed extravasation of contrast medium from the injured right kidney with massive retroperitoneal hematoma, which had pushed the visceral organs up into the ventral side (). Blood test findings on arrival are shown in . On returning to the emergency room, he suffered hemorrhagic shock again and subsequently underwent repeated massive blood transfusion, including red blood cells, cryoprecipitate, fresh-frozen plasma, and platelets, and also received tracheal intubation and an indwelling intra-aortic balloon occlusion catheter (IABP) at zone I as a prophylactic measure against cardiac arrest. He was moved to the angio suite for interventional radiology and underwent transarterial selective renal artery embolization, after which he was admitted to the intensive care unit. His vital signs stabilized on hospital day 2. The IABP was removed without inflation. He received 12 units of red blood cell and fresh-frozen plasma, 20 units of platelets, and 4 units of cryoprecipitate within 24 hours. He was extubated on day 3 after initiating diuresis. CT on the same day revealed renal partial infarction without pseudoaneurysmal formation or urinoma. On days 4 and 5, a blood examination revealed increased levels of amylase (360 and 904 IU/L, respectively) with new additional epigastralgia. Enhanced CT on day 5 did not show exudative inflammation around the pancreas, which was still shifted upward by the retroperitoneal hematoma (). Amylase isozyme patterns on day 5 identified the pancreas types, and the lipase level was 3061 IU/L. After receiving a diagnosis of mild-grade acute pancreatitis based on CT findings [], he abstained from food on days 5 and 6. As the severity of acute pancreatitis was mild, he began to eat again from day 7. The maximum amylase level was 1041 IU/L on day 6 and decreased day by day without deterioration of the severity of his acute pancreatitis (). Magnetic resonance cholangiopancreatography on day 12 showed no injury to the main pancreatic duct. As he was able to eat and walk, he was discharged on day 14. |
A 63 year-old man was transferred to our emergency department for significant gastrointestinal bleeding. Upon arrival, the patient was awake but not oriented. His vital signs included a respiratory rate of 40/min, a pulse of 121 beats/min, a blood pressure of 105/38 mmHg and 100% oxygen saturation at 2 L/min per nasal cannula. Physical examination showed a pale appearing male in severe distress but was otherwise unremarkable. A complete blood count revealed a hemoglobin concentration of 3 g/dL. His medical history included arterial hypertension, alcohol abuse and nicotine dependence. Treatment for hemorrhagic shock was initiated immediately by administering large intravenous volume infusions, transfusions and multiple vasopressors. A focused assessment with sonography for trauma scan was performed. However, the infrarenal part of aorta was not visible due to excessive bowel gas. The patient was intubated and a nasogastric tube was placed which revealed fresh red blood. An emergency esophagogastroduodenoscopy (EGD) was performed, which showed large blood clots in the stomach (). However, an active source of bleeding was not present, neither in the stomach nor the duodenum (). High-dose proton-pump inhibitors and erythromycin were infused intravenously. Despite rapid fluid replacement, the patient went into acute renal failure and required continuous hemofiltration. The next day, repeat EGD revealed a small gastric erosion which was supplied with a metal clip. Otherwise no source of bleeding could be identified. A few hours later, the patient suffered from repeat hypotension and hematochezia. A colonoscopy demonstrated blood clots in the colon but no source of bleeding. The following days, his condition improved. He had a nonbloody bowel movement and his renal function recovered. For three days, he did not exhibit any signs of bleeding. A scheduled computed tomography (CT) scan was postponed due to improved condition of the patient. However, after five days the patient suddenly developed hematemesis. During emergency EGD, the patient suffered cardiac arrest and required cardiopulmonary resuscitation (CPR). The distal part of the duodenum exhibited several ulcers and a pulsatile bleeding. Intraluminal exsanguination was massive and the exact localization of the bleeding could not be visualized. The patient was transferred to the operating room under continuous CPR for emergency laparotomy. The laparotomy disclosed a distended and partly ischemic small intestine. An abdominal aortic aneurysm of 5.5 cm diameter adherent to the third part of the duodenum was appreciated. The aortoduodenal fistula () was excised and an aortic 24 mm polyester graft was implanted in inlay technique (). The patient received intensive care treatment and numerous surgeries for several months. Diffuse bleeding was common and necessitated a total of 25 platelet transfusions, 118 units of fresh frozen plasma, and 173 units of packed red blood cells (PRBCs). Despite these efforts, multiple organ dysfunction evolved. Decision was made to limit treatment to palliative care in accordance with close family members and presumed will of the patient. After 122 days, the patient succumbed to his condition. |
A 38-year-old woman with a 3-month history of an anterior cervical mass located in the suprasternal region of her neck was referred to our hospital. Physical examination revealed that the 3-cm movable neck mass was firm and slightly tender on palpation and had a distinct margin from surrounding tissues. An ultrasound examination showed that the well-defined oval mass was 31 × 23 × 17 mm in size and exhibited heterogeneity. Furthermore, a non-enhanced computed tomography (CT) scan of the neck revealed that the distinct neck mass in the subcutaneous tissue had a mixture of soft tissue and fatty components (Fig. ). Based on these findings, the cervical tumor was clinically diagnosed to be an unusual lipoma with degeneration; however, we could not exclude the possibility of it being a malignant tumor such as liposarcoma. Thus, fine-needle aspiration cytology of the tumor was performed, but no diagnosis of malignant cells was obtained. Further examinations were conducted to address concerns related to her menstrual pain, and abdominal magnetic resonance imaging revealed bilateral ovarian cysts in the lower abdomen. Under general anesthesia, the patient underwent neck mass extirpation and bilateral ovarian cystectomy; pathological examination of the cysts resulted in a diagnosis of ovarian endometriotic cysts. During the surgery, the cervical mass was well demarcated and did not adhere to the surrounding tissues. The postoperative course was uneventful. The gross pathology report showed that the neck mass measured 3.0 × 2.5 × 2.0 cm. The cut surface of the specimen was heterogeneous, solid, whitish, and yellowish (Fig. ). Microscopically, the tumor was composed of spindle cells, epithelial nests, and mature adipose tissue (Fig. a, b). Immunohistochemical examination revealed that both spindle cells and epithelial nests were positive for cytokeratin (CK) AE1/AE3 (Fig. ). As these histopathological findings were consistent with the features of EHT, a diagnosis of EHT was confirmed. Over a follow-up period of 30 months, this patient exhibited no evidence of recurrence. |
The second patient is a 72-year-old woman with a past medical history including hypertension, type II diabetes, and obesity, who presented with weight loss and steatorrhea. As her symptoms were suggestive of pancreatic exocrine insufficiency, and with the associated weight loss, she underwent a CT scan for additional evaluation. This demonstrated a suspicious 2.5-cm complex cystic pancreatic head mass with associated pancreatic gland atrophy and a dilated pancreatic duct. She was also noted to have fatty infiltration of the liver (although not overt cirrhosis) and ascites.\nShe was then referred for further evaluation. Magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography demonstrated diffuse dilation of the pancreatic duct up to 7.5 mm with an associated cystic mass in the head of the pancreas, suggestive of main duct IPMN (). EUS was attempted, but was unable to be completed due to severe tortuosity of her esophagus. Positron emission tomography (PET) demonstrated heterogeneous metabolic activity within the pancreatic uncinate process and to a lesser degree within the body and tail. Additional workup included a paracentesis to evaluate the ascites, which was unremarkable and ultimately deemed secondary to poor nutritional status from her exocrine insufficiency. Laboratory results were within normal limits with the exception of tumor markers and a mildly low albumin (3.4 gm/dL). Carcinoembryonic antigen was elevated at 6.0 ng/mL, and CA 19-9 was elevated at 46.7 U/mL. She was placed on pancrelipase, which resolved her symptoms of exocrine insufficiency and helped improve her nutrition.\nDue to the concern for main duct IPMN, she was referred for surgical resection. Again, it was unclear if the diffuse dilation of the pancreatic duct was secondary to involvement by main duct IPMN or due to proximal pancreatic duct obstruction. The patient was planned for a Whipple procedure with possible total pancreatectomy if high-grade dysplasia was noted intraoperatively at the resection margin. Upon transection of the pancreatic neck, IPMN with focal high-grade dysplasia was indeed noted at the margin. Due to the abnormal preoperative PET scan, in addition to the high-grade dysplasia at the margin, a completion pancreatectomy was performed. Due to her poor nutritional status preoperatively, a gastrojejunal feeding tube was placed at the time of the operation. She had an unremarkable postoperative course and was discharged with feeding tube supplementation.\nHer final pathology demonstrated a 1.1 cm well-differentiated mucinous colloid carcinoma arising in a background of IPMN (intestinal type) with foci of high-grade dysplasia and intermediate grade dysplasia throughout the remaining pancreatic duct (). Staining of the tumor was positive for MUC1, MUC2, and MUC5. All margins were negative. Zero of 24 lymph nodes was involved with tumor. Her final pathologic staging was pT2N0Mx. She was referred to medical oncology for discussion of adjuvant therapy and will be initiating gemcitabine adjuvant chemotherapy in the near future. |
A 74-year-old female patient presented with a locally advanced tumor of the proximal pancreatic body. The patient showed no signs of obstructive jaundice and did not require biliary stenting. Initially, her tumor was noted to involve the major visceral vessels, including the celiac artery, portal vein, and splenic artery and vein (). The tumor was deemed unresectable and the patient underwent extensive chemotherapy with multiple cycles of gemcitabine, Abraxane, 5-fluorouracil, Alloxantin, Avastin, and Xeloda. After showing a favorable response, she was referred for surgical re-evaluation. The post neoadjuvant chemotherapy CT scan () showed a poorly defined infiltrative pancreatic neck and body mass measuring ∼25 × 15 mm with ill-defined soft tissue encasing the proximal splenic artery, common hepatic artery (CHA), distal celiac axis, and superior mesenteric artery (SMA). The mass also partially encased the portal vein and superior mesenteric vein (SMV). There was no radiologic evidence of hepatic metastasis and there was mild pancreatic duct dilatation. Pre-treatment and post-treatment serum CA 19–9 levels were 46 and 9, respectively. The patient did not receive any additional studies to assess GDA flow or the need for preoperative coiling/embolization. The absolute need for resection of the celiac axis was not determined until the time of the operation. The patient's functional status, perioperative risk, and likelihood of response were weighed and she was determined to be a candidate for an attempt at a modified Appleby procedure. After being properly informed of her various treatment options, she elected to undergo the operation.\nExploration of the duodenum and pancreas revealed a firm mass in the body of the pancreas with a soft pancreatic neck. No gross evidence of metastatic disease was present. There was a benign appearing lesion in the superior aspect of liver segment II, which was excised in its entirety and confirmed to be benign. Cholecystectomy was performed, followed by Kocherization of the duodenum and dissection of the pancreas and major vessels. We were fastidious in preserving the GDA. The splenic artery was controlled distal to the tumor, leaving a normal CHA pulse. The spleen and pancreatic body and tail were then serially elevated out of the retroperitoneum. The aorta was exposed, taking down the diaphragmatic crura. The celiac artery was identified at its origin, tied, divided, and oversewn with 5–0 polypropylene suture. Abnormal soft tissue was palpated along the proximal CHA. In light of this vessel involvement, we divided the distal CHA near the GDA. We then dissected the specimen off the SMA successfully and divided the pancreatic neck.\nThe inferior mesenteric vein was then clamped and tied. The inflamed pancreatic neck and proximal body were then dissected free from the right lateral aspect of the SMV and portal vein. The splenic vein was taken flush with the SMV, and its stump was oversewn, leaving good forward flow of the SMV to the portal vein. The proper hepatic artery (PHA) and the GDA were preserved throughout the resection. A Doppler ultrasound probe was used to test the GDA and PHA. Both arteries had adequate signal and in fact, the PHA had a faint palpable pulse. The liver parenchyma was also found to have a strong arterial signal. The specimen had two short stitches and purple dye placed at the neck margin and the rest of the specimen was inked per our Jefferson protocol.\nPathology of the resected specimen showed ductal adenocarcinoma with marked treatment effects with invasion of tumor into the peripancreatic soft tissue. The excision margins were free of neoplasia and the specimen had no regional lymph node metastasis (0/26). The tumor was within 2.0 cm from the pancreatic resection margin and within 0.1 cm of the circumferential margin in the posterior peripancreatic tissue. The maximum diameter of the tumor was 3.0 cm in size.\nIn the initial postoperative period, the patient had a transient transaminitis. A postoperative hepatic vascular ultrasound showed good hepatic arterial flow through the PHA and the transaminases normalized. The patient was discharged on postoperative day 9. She remains well without evidence of disease 7 months postoperatively, and has elected to receive no further chemotherapy. |
A 75-year-old woman with a past medical history of right breast lobular carcinoma in situ (LCIS) presented with a three-month history of right eye swelling and diplopia. On exam, she was noted to have periorbital edema and erythema, ptosis, and enophthalmos. She had limited ocular movements and small angle right hypotropia in primary gaze. There was no evidence of optic neuropathy. Neurologic exam was normal. Clinically, there was no evidence of recurrence in the breast, lymphadenopathy, or bone metastases. Biopsy revealed individual neoplastic cells infiltrating fibroadipose tissue in a linear pattern. Immunochemistry was positive for estrogen receptor (ER) expression and negative for progesterone (PR) receptor. Fluorescence in situ hybridization was negative for human epidural growth factor receptor 2 (HER2) gene amplification. Pathology was reported as invasive carcinoma, consistent with a mammary primary and suggestive of lobular carcinoma.\nPast medical history included a reported diagnosis of LCIS diagnosed 35 years ago after she presented with a right breast lump. She was treated with a bilateral nipple-sparing mastectomy with immediate implant reconstruction. Unfortunately, tissue from the initial LCIS tumor was not available for review. Since that time, she has had her implants replaced twice without any complications or suspicion of recurrence. She has had no symptoms or signs of breast cancer recurrence and has had negative surveillance mammograms.\nMagnetic resonance imaging (MRI) of the orbits demonstrated enhancement and edema of the extraocular muscles of the right eye and mild optic neuritis. Positron emission tomography and computed tomography (PET/CT) demonstrated generalized increased radiotracer uptake in the soft tissue of the right globe (Figure ). There was no other evidence of metastatic disease.\nThe patient was treated with anastrozole (one mg daily) for eight weeks with minimal improvement. She was then treated with proton radiotherapy to 45 cobalt gray equivalents (CGE) in 25 fractions delivered over 30 days. The radiation field is shown in Figure . The clinical and planning target volumes encompass the diffuse area of enhancement on MRI and hyperactivity on PET/CT. The dose was constrained to 45 CGE maximum for the right globe. The radiotherapy plan was designed to keep the dose to the left eye, optic nerves, and brain as low as possible, given her right vision changes and low volume, oligometastatic disease. The side effects of the treatment included tenderness, acute erythema, and skin desquamation at the end of treatment, which required antimicrobial therapy due to concern for cellulitis. There was no change in visual acuity.\nAn MRI four months after radiation treatment showed stable thickening but decreased contrast enhancement of the periorbital soft tissues, and a PET scan at 11 months after radiation treatment showed reduced radiotracer uptake in the right orbit compared to the exams prior to treatment (Figure ). She was last seen in follow-up 16 months following the completion of radiotherapy. Extraocular motility has improved, but she remains with a stable, small, angle right hypotropia that is well corrected with prism glasses. Ptosis and enophthalamos are stable. There are no signs of optic neuropathy or retinopathy. She continues anastrozole with no additional evidence of metastatic disease on surveillance exams and PET/CT. |
A 38-year-old white asymptomatic female without any significant past medical history or risk factors came to our clinic for cardiology consultation prior to cosmetic facial surgery. The patient, who recently returned from a mountain climbing trip in the Himalayas, was in good physical shape. On a physical examination a holosystolic murmur, best heard at the left lower sternal border, was noticed. The patient was sent for transthoracic echocardiography (TTE), which showed elliptical, mobile homogeneous hyperechoic mass, 28x24 mm, with smooth surface, located in the left atrium (Figure ).\nThe mass did not prolapse through the mitral orifice during diastole, did not obstruct diastolic filling of the left ventricle, was attached to the interatrial septum, although the peduncle was not clearly visualized (Video ). The left atrial diameter was on the upper limit of 3.8 cm. Color Doppler did not reveal increased velocity of blood flow across the mitral valve. Moderate tricuspid insufficiency was noticed. A diagnosis of a left atrial tumor was made. The findings were discussed with the patient and she was referred to a specialized Cardiac Surgery Center for surgical intervention. A minimally invasive approach was chosen.\nThe patient underwent a right lateral mini-thoracotomy under general anesthesia. Peripheral cardiopulmonary bypass using right femoral artery and vein and right internal jugular vein was established. Induced ventricular fibrillation was used. Left and right atria were opened. The tumor was excised with a part of an interatrial septum (Video ), which was closed using autopericardial patch. Heart chambers were closed, cardiopulmonary bypass was discontinued and the operation was finished in the usual manner. The total operation time was 220 minutes. The postoperative period was uncomplicated. The total hospital stay was four days.\nThe histopathological report confirmed a diagnosis of cardiac myxoma. Macroscopically, the specimen consisted of a small fragment of the left atrial wall and the oval-shaped tumor, presented by gelatinous tan-white tissue with the friable surface (Figure ).\nMicroscopically, hematoxylin and eosin-stained sections showed a neoplastic lesion with two components. The first, a cellular component, consisting of stellate and spindle cells with scant eosinophilic cytoplasm, round to oval nuclei (some multinucleated), and mild nuclear polymorphism (Figure ). No significant cytologic atypia, necrosis, or stromal desmoplasia was observed.\nThe second, extracellular component, was represented by an edematous eosinophilic stroma with foci of hyalinosis, numerous vessels, surrounded by accumulations of hemosiderin granules. Small vessels of the tumor had capillary type structure and resembled vascular slits and wide tubular formation. Large vessels consisted of only several layers of myxomal cells. The basement membrane, smooth muscle cells, and adventitia were absent (Figure ). It should be noted that the structural features of the vessels in the myxoma cause their slight vulnerability during traction in the turbulent blood-contracting chambers of the heart. This was confirmed by multiple hemorrhages in the tumor stroma of different ages.\nThe postoperative period was uncomplicated. The patient was followed up annually for three years with no signs of recurrence of the tumor. |
A 72-year-old Caucasian female patient was referred to the respiratory clinic with a 6-month history of exertional breathlessness. She gave a history of yearly chest infections, particularly in winter months. She, however, had no history of childhood respiratory problems or any significant respiratory symptoms during her adult life. She had a 30-pack-year smoking history but she quit 25 years prior to presentation. She worked as a nursing auxillary at a local hospital and had no prior asbestosis. She was on a 1 mg maintenance dose of prednisolone for polymyalgia rheumatica. Otherwise, she had no significant medical condition and was not on any regular medications. Her exercise tolerance was unlimited and she enjoyed a good health.\nHer O2 saturation was 95% on room air and her spirometry showed obstructive pattern with FEV1 1.14L (55%), FVC 2.09L (83%) and FEV1/FVC ratio 54%.\nAn initial chest radiograph 2 years prior to presentation suggested an increased radiolucency of the left lung but this was not investigated further (). Serial CXRs 2 years later showed a relatively unchanged appearance of the left hemithorax with progressively increased opacification in the periphery of the middle and lower zones, and accompanying reduction in lung volume, on the right side ().\nThe patient underwent a contrast-enhanced CT of the chest in view of the repeated chest infections and lack of complete resolution to rule out the possibility of an adenocarcinoma in situ or endobronchial lesion, respectively. Cross-sectional imaging was also carried out to assess the possibility of an underlying bronchiectasis in the presence of the recurrent chest infections and to further assess the interstitial changes seen on the CXR on the right side.\nHer CT showed hypoplastic left pulmonary artery (; arrow), attenuated peripheral pulmonary artery branches on the left (: arrows), hyperinflated left lung with air trapping and cystic bronchiectasis of the lingua and left lower lobe (). Features were in keeping with the diagnosis of Swyer-James-MacLeod syndrome (SJMS). Interestingly, the right lung was small in size with evidence of subpleural reticulation, traction bronchiectasis and ground-glass opacification suggesting an underlying pulmonary fibrosis (). The oligaemia of the left lung is shown as reduced FDG uptake () on PET CT, which was done to investigate a different pathology.\nSputum culture grew pseudomonas species and bronchoalveolar lavage from the right lung showed mixed cellularity with 22% eosinophils and a 36% neutrophils. |
We present a 57 year old gentleman with CKD 5 who had an autogenous brachiocephalic fistula 4 months prior to presentation to us. During their last surgical clinical visit, the fistula was noted to be poorly maturing and then referred to interventional radiology for fistulogram and possible endovascular intervention to assist with fistula maturation.\nThe patient had a fistulogram which demonstrated a high grade juxta-anastomotic stenosis which was successfully balloon dilated. After a 6 week follow up clinic visit the fistula was still immature and a duplex scan, a second fistulogram with possible intervention were requested.\nFistulogram was performed via an antegrade approach from an access just proximal to the swing point. There was an “apparent” stenosis (Fig. ) which was angioplastied then followed by severe spasm (Fig. ). which was perceived by the operator to be recalcitrant stenosis. In the light of this perceived recalcitrant stenosis, a decision to stent the area was taken. After measuring the vessel diameter based on the immediate post-plasty images a 6 mm diameter × 5 cm length Viabahn stent (Gore & Associates, Flagstaff, AZ) was selected and deployed in the standard fashion.\nFollowing stent deployment, the stent migrated and stopped at the confluence of the cephalic vein and the subclavian vein (Fig. ). At the time the operator thought the stent was stable and unlikely to cause harm to the patient in this position. However, after reviewing the images with colleagues including vascular surgeons a decision was made to attempt to retract the stent into the arm which would be easier for the surgeon to retrieve the stent surgically, if required. The patient was subsequently brought back 24 h later to the interventional radiology suite.\nInitial fluoroscopic image of the left shoulder region demonstrated the stent was absent from the final position documented the previous day indicating the stent had migrated further (Fig. ). Fluoroscopic scanning of the chest identified the stent to overlie the left lower lobe (Fig. ).\nSubsequent Pulmonary angiogram confirmed the stent to lie within a segmental pulmonary artery of the left lower lobe (Fig. ).\nAfter discussion of the options, risks and benefits with the patient and a multidisciplinary team, a decision to attempt stent retrieval was made versus leaving the stent in situ.\nAfter appropriate informed written consent, the right groin was prepped and in the standard fashion. Right common femoral vein access was then upsized to accept a 16 F sheath (Cook, Bloomington. IN USA). Main pulmonary access was then performed with an APC pulmonary catheter (Cook, Bloomington. IN USA). The APC catheter was then removed over a Storq wire (Cook, Bloomington. IN USA) wire and subsequently a 12 F 70 cm braided sheath was advanced into the main pulmonary artery and then left lower lobe pulmonary artery. Pulmonary angiograms performed identified the optimal projection to identify the vessel to access. After accessing the appropriate vessel the 12F sheath was advanced just to the origin of the branch above the stent. Subsequently a 15 mm Amplatz Gooseneck snare (ev3, Plymouth MN, USA) was manipulated until the stent was lassoed at about half way along the stent. Given the flexibility and potential collapsibility of the Viabahn stent it was over-sheathed carefully collapsing and gently retracting the captured stent to minimize potential vessel injury (Fig. , Additional file ). Once the stent had been totally ensheathed, the 12F sheath was retracted through the outer 16F sheath coaxially. The stent was retrieved intact (Fig. ).\nThe procedure was performed under moderate sedation using Fentanyl and midazolam with continuous monitoring of the patient’s vitals by a dedicated nurse. Throughout the procedure the patient remained hemodynamically stable with normal respiratory function. Post procedure the patient was observed for 6 h post procedure before being discharged home in a stable condition.\nThe patient has so far been followed up for 3.5 years and has not developed any adverse pulmonary or cardiac condition. Interval CTPA done at an outside facility showed normal pulmonary vasculature with no evidence of pulmonary vessel injury. |
A 69-year old male patient was admitted having gross painless hematuria for the last 2 months with no other comorbidities, apart from benign prostatic hyperplasia treated with a-blockers. Ultrasound of the kidneys, the bladder and the prostate showed an exophytic lesion of the bladder and dilatation of the left pelvicaliceal system. Intravenous urography (IVU) showed a radiolucent filling defect in the bladder and a non functioning left kidney (Fig. ). The next diagnostic step was to perform a cystoscopy, which confirmed the presence of a lesion, occupying the trigone of the bladder and the left ureteral orifice. The patient was subjected to a transurethral resection of the lesion. The histopathological assessment revealed an infiltrative mucinous adenocarcinoma. Computed tomography (CT) (Fig. ), colonoscopy and gastroscopy revealed no other primary malignant site. Based on the pathology report, the patient underwent a radical cystoprostatectomy with en block bilateral pelvic lymphadenectomy and urinary diversion with a Bricker ileostomy.\nThe specimen of radical cystoprostatectomy included the urinary bladder with pericystic fatty tissue and the prostate gland. On section, a tumour was identified, measuring in the greatest dimension 3 cm. The tumour was localized in the posterior bladder wall and had an exophytic growth pattern with solid (nodular) appearance. It seemed to invade the wall of the bladder, extending to the proximal urethral margin of the prostate.\nThe grossly described tumour is a primary mucinous adenocarcinoma of the urinary bladder, which invades the wall of the bladder, both lobes of the prostate gland and both seminal vesicles. We did not recognize normal urothelium with intestinal metaplasia. The carcinoma includes glandular configurations, having one cell layer of cuboidal or columnar epithelium with large, dark nuclei, signet-ring cells (Fig. ), nuclear atypia and several mitoses (Fig. ). The reactivity for PAS and PAS-diastase establishes the presence of intracellular and extracellular mucin (Fig. ). The primary nature of adenocarcinoma is confirmed by the immunoreactivity for keratins 7 and 20 (Fig. ). |
A 36-year-old Caucasian male presented to the emergency room complaining of a one-day history of abdominal pain. His main symptoms were that of nausea and vomiting, but he also reported periods of diarrhea. In the emergency room, his initial evaluation was significant for lab studies demonstrating a mild metabolic acidosis with a bicarb of 16.6 mEq/L, an elevation of his creatinine to 1.93 mg/dL, and a serum lactate level of 5.4 mmol/L. A computed tomography (CT) scan of the abdomen and pelvis was obtained and reviewed. The appendix was thought to be normal. There was no evidence of free intraperitoneal air, abscess, or volvulus. There did appear to be evidence of enterocolitis involving the ilium, cecum, and the proximal ascending colon. There was no evidence of pneumatosis or obstruction. Over the course of 12 hours the patient underwent conservative medical management, which included intravenous hydration, intravenous steroids, Toradol and Dilaudid for pain management, and the occasional dose of Ativan for agitation. Failure of conservative management along with medical decline lead to an exploratory laparotomy with a right hemicolectomy for an ileocolic intestinal infarction. Postoperative repeat CT scan of the abdomen incidentally showed pulmonary nodules in the lower lobe. A CT scan of the chest was then obtained, which revealed air in the left chest wall and axilla (Figure ). On physical exam there was very subtle mottling of the left shoulder. The patient was emergently taken back to the OR for further exploration of the shoulder with excisional debridement. Seropurulent fluid and extensive subcutaneous emphysema along the fascial planes of the left chest wall were consistent with necrotizing fasciitis. Both wounds were packed with a gauze bandage roll soaked in saline and then the patient was transferred back to the intensive care unit.\nOver the course of 15 days the patient underwent repeat trips to the OR for re-exploration, incision and drainage of the wounds, and dressing changes (Table ). On postoperative day 17, the wound, ostomy, continence nurse (WOCN) was consulted to evaluate the wound and make treatment recommendations.\nOn exam, there was still a significant amount of nonviable tissue in the base of the left chest and axilla wound. The left chest wound measured 8 x 19 x 8 cm and the left axilla wound measured 6.5 x 25 x 4 cm. NPWTi-d with ROCF-CC was applied to these wounds to aid in the removal of the nonviable tissue. Figures - show the presentation of the wounds prior to the application of the NPWTi-d with ROCF-CC.\nDuring the application of the NPWTi-d with ROCF-CC, care was taken to ensure that the contact layer of the dressing was in contact with the entire wound base. Barrier rings were applied to the skin creases along with any area that presented as a high risk for inadequate seal of the drape (Figure ). The therapy settings for the left axilla were 85 ml of hypochlorous acid solution (Vashe®, SteadMed, Fort Worth, TX), dwell time of 10 minutes with NPWT every hour at -125 mmHg. Therapy settings for the left chest wound were 50 ml of hypochlorous acid solution, dwell time of 10 minutes with NPWT every hour at -125 mmHg.\nDuring the first dressing change after the application of the NPWTi-d with ROCF-CC, there were notable improvements in the quality of the tissue in the wound bed (Figure ). The left chest wound bed was noted to have 100% red healthy tissue and the left axilla wound bed had a decrease in nonviable tissue. There was, however, seropurulent drainage noted deep within the intramuscular structures of the left axilla wound.\nNPWTi-d with ROCF-CC was reapplied to the axilla wound ensuring that the contact layer was placed deep into the wound bed to facilitate the removal of the seropurulent drainage. The left chest wound was transitioned to NPWTi-d to continue to promote granulation tissue (Figure ). The instillation solution was switched to normal saline due to blockage alarms we encountered with the hypochlorous acid solution without resolution.\nThe current treatment regimen was continued for two days until the next dressing change. At that time both wound bases were 100% red with granulation tissue present (Figure ). The seropurulent drainage deep in the intramuscular structures was no longer present. Since there was adequate removal of nonviable tissue and the quality of the tissue had significantly improved, the WOCN made the decision to transition both wounds to NPWTi-d instilling normal saline solution with a dwell time of 10 minutes and NPWT every two hours at -125 mmHg.\nFor the next two weeks the treatment regimen utilizing NPWTi-d to the wounds continued. The dressings were changed three times a week at the bedside by the WOCN. During initial assessment, the axilla wound measured in total volume 650 cm³ and the chest wound measured 1,216 cm³. After 17 days utilizing the combination of NPWTi-d with and without ROCF-CC, the axilla wound measured in total volume 342.25 cm³ and the chest wound measured 554.4 cm³. This presents a significant decrease in overall measurements. At this time, NPWTi-d was discontinued and standard NPWT with black granufoam was utilized to both wounds at -125 mmHg (Figures -).\nNPWT was utilized for approximately a month to promote granulation tissue and assist with wound contraction (Figures -). Once the wound had made vast improvements, NPWT was discontinued and a non-adherent antimicrobial alginate dressing (Silvercel™ Non-adherent, Acelity, San Antonio, TX) was lightly packed into the wound bed and covered with a dry sterile dressing. This dressing was then changed three times a week by a visiting nurse association. The wound measurements prior to discharge showed significant improvement in comparison to the wound measurement at presentation, with the left axilla wound measuring 1.5 x 10.5 x 0.3 cm and the left chest wound measuring 3.5 x 9 x 5 cm. |
A 59-year-old female (97 kg, 160 cm) was scheduled for left PCNL due to a 9 mm stone in the left renal pelvis.\nThe ESPC was performed using ultrasound at the level of T7. The T7 transverse process was located using the inferior angle of the scapula as a landmark. A curvilinear 5-2 MHz ultrasound probe was placed on the patient's back in a cephalad-to-caudal fashion at the level of T7. The trapezius and erector spinae muscle were visualized on the left side, and a 19G Tuohy needle was advanced (in-plane to the ultrasound probe) in a caudal direction toward the left-sided transverse process of T7. After confirming that the tip of the needle was below the erector spinae muscle with a small bolus of our local anesthetic solution (30 mL of 0.25% bupivacaine with dexamethasone 4 mg), we injected 20 mL of the solution into the space, noting the caudal spread of the injectate on ultrasound. Then, a 20-gauge epidural catheter was inserted through the Tuohy needle and advanced 5 cm into the space. Placement of the catheter under the erector spinae muscle was confirmed by injecting the final 10 mL of the local anesthetic through the catheter while visualizing the spread of the solution on ultrasound. The catheter was then secured using the LOCKIT Plus catheter securement device, which allows for mechanical securement of the catheter while maintaining its patency. Additionally, it provides easy access for visual inspection of the insertion site via a transparent window.\nThe PCNL was performed in the prone position using general anesthesia. The patient received acetaminophen 1 g in the preoperative area as part of a multimodal pain protocol (she refused the tramadol 50 mg which is also part of multimodal pain protocol). She underwent general anesthesia and received no opioid or other pain medications during the 118-min procedure; she was extubated without complication at the end of the case. Pain scores in the Post-Anesthesia Care Unit (PACU) were assessed by nursing using visual analogue scale (VAS) scores and recorded in the medication administration record (MAR). All medications given for pain and PONV were recorded in the MAR as well.\nThe patient remained in the PACU for 231 min and reported VAS scores of 0/0/0/0/0. She received ondansetron 4 mg intraoperatively and 4 mg prophylactically in PACU due to a patient-reported history of severe PONV. The patient was given an additional 10 mL bolus of 0.25% bupivacaine 1-h prior to discharge, and the catheter was removed with the tip intact. The patient was discharged home from the PACU without complications and reported no pain at all.\nThe patient returned to the hospital for a left-sided ureteral stent exchange 15 days later and reported that she had no residual pain in the days following her previous procedure. |
A two-month-old female patient, transferred from a tertiary healthcare center, was referred for autopsy with signs of developmental delay and respiratory failure. The patient had a medical history of being the fifth birth out of six overall pregnancies, with the parents being blood relatives (second cousins). The mother had suffered from an acute respiratory infection (unspecified) in the seventh gestational month and was a heavy smoker. The patient had been delivered 10 days prematurely per via naturalis with a weight of 2,250 g, height of 48 cm, and an Apgar score of 6 on the first minute and 8 on the fifth minute.\nOn the second day postpartum, decreased reflexes and generalized muscular hypotension had been noted. Following 24 days in the neonatal intensive care unit, the patient had been de-hospitalized. Two weeks later, the patient had been hospitalized again after rejecting food, with the presence of a severe dry cough and muscle hypotension. Upon admission, no fever had been noted; radiology had shown lung consolidation, and the patient had been treated with antibiotics for bilateral pneumonia. After two weeks of treatment, the condition of the patient had not improved, and she had been referred to our hospital for further diagnostic tests and treatment. However, upon admission, the patient's condition was extremely poor and a lethal exit was registered, following extensive reanimation. The patient was referred for an autopsy to identify the underlying condition.\nBefore autopsy, the patient weighed 3,140 g, was 50 cm in height, and head circumference was 33 cm (microcephaly). Furthermore, mild facial dysmorphism was noted, with retrognathia, gothic palate, and bulged zygomatic bones. On section of the thorax, the lungs were deformed and retracted towards the hilus with subpleural hemorrhages. The left lung weighed 30 g and the right one 38 g. A floating probe was performed with both lungs sinking. On a section floating probe, only the upper lobes of the lungs were semi-emergent in the liquid, with both inferior lobes and the middle lobe of the right lung sinking. On cross-section, the lungs were airless and consolidated. Histology revealed subtotal atelectasis and subpleural hemorrhages (Figure ).\nThe atria of the hearth were dilated, and the cardiac weight was 28 g. On section, a persistent and dilated foramen ovale was observed. Histology revealed a granular change in the cardiomyocytes, predominantly in the atria (Figure ).\nCranial section showed undisturbed dural duplicatures. Following the section of the tentorium cerebelli and the extraction of the cerebrum, cerebellum, brainstem, and spinal cord, the brainstem and cerebellum were noted to be severely hypoplastic, with a lack of basal foliation of the cerebellar cortex. The combined weight of the cerebrum, cerebellum, brainstem, and spinal cord was 270 g, with the cerebellum weighing only 5 g (Figure ). On section of the CNS, the lateral ventricles were noted to be dilated, especially the occipital horns. Histology of the cerebellum revealed subtotal lack of tertiary foliations, large sections of only secondary and primary foliations, abortive mushroom-like foliations, complete lack of foliations on the basal surface, tangential Purkinje branching, disarrangement of the Purkinje cells, and a severe variation of the cortical layer thickness and neuronal count (Figure ).\nThe medulla oblongata revealed a narrowed central canal, decreased neuronal count in the olivary nuclei as well as severely hypoplastic spinocerebellar tract (Figure ). The spinal cord also showed decreased neuronal count in the anterior horns and central canal stenosis (Figure ).\nThe clinical manifestation of hypoventilation respiratory failure with a right-to-left cardiac shunt and the gross and morphological changes in the cerebellum, brainstem, and spinal cord, with combined microcephaly and internal hydrocephalus, were in concordance with the morphological substrate of PCH type 1B. Therefore, the protocol was finalized as PCH type 1B to be the main condition. |
A 25-year-old male was brought to psychiatry outpatient Department of Tertiary Care Hospital in August 2013 by his mother. He was unmarried, illiterate and manual laborer in farm belonged to lower socioeconomic class. Mother reported that patient left home 9 days back early in the morning without telling anyone and then he was found wandering roadside in a village 26 km far from patient's home. His hygiene was poor and had unkempt appearance when found by local police. He failed to tell his name and residential address. He was conscious and alert but looked fatigued. On asking him, he couldn’t explain any reason to leave home. He told that 1-day early morning, he felt that his house looked different and changed. He felt vague uneasiness with a desire to move outside the home and started walking. He failed to recall properly what he did during this period, where he slept at night, how he got food and how he travelled. He admitted that he used to walk most of the time and didn’t travel in vehicle. He said that he occasionally begged for food. Patient said that his mind was blank and there was no thought since he left. Patient was hospitalized for detailed history and evaluation.\nPast history revealed that patient left home similar way without informing anyone 7 times in last 1½ year and was found wandering aimlessly away from home. He was traced thrice with help of police. Once he was found from a famous temple 80 km far from home begging outside. Once he was found in a fair doing religious rituals with a group of people 1-month after leaving home. Patient reported that he had twice experience that he found himself away from home at another place and he could not tell why and recall how he reached there. Patient said that he doesn’t know why he leaves home. There was no history suggestive of suspiciousness, unusual perceptual experiences, grossly disorganized behavior, high talk or increased goal-directed activity.\nNo history suggestive of alcohol, cannabis or any other substance use, episodes of fall, convulsion, sleep walking, head injury. No past history is suggestive of trance states or possession symptoms.\nIn first isolation interview patient did not revealed any stressor or recent stressful events preceding last fugue. Then patient's mother was interviewed in isolation, who reported that there was a conflict with patient's paternal uncle about the matter of property division 1½ years back. Mother reported that they are a farmer by occupation since many years but lost major part of land due to fraud made by his uncle in documents of property ownership.\nThe patient was probed about this issue during subsequent interviews, he opened up his concerns about loss of land. He told that their land was the only source of earning a livelihood for them. They suffer extreme financial crisis after the incidence. He also reported about poor social support from his other uncles. On asking, patient also reported that he didn’t like anything, low mood, lack of energy for last 6–8 months. He had occasional suicidal thoughts but avoids doing so, when he thinks about his elderly mother.\nHe lived with mother in nuclear family. Father passed away 7 years back by snake bite. He was the only child. Paternal grandfather had some psychiatric illness episodic nature having symptoms of headache, sleep disturbance and withdrawn behavior. No further details were recalled by patient's mother.\nHe left studies after fifth class and started labor work at their farm with his father because of the poor economical situation of family. According to mother, her son was quiet and responsible before the onset of illness. No unusual personality traits were reported.\nPhysical examination, neurological assessment, and blood investigation tests were normal. The head computed tomography scan could not be done because of non-affordability. The mental state examination revealed a young male with poor hygiene, unkempt appearance, and poor eye contact. His mood was depressed and effect was restricted which was appropriate to his mood. No thought or perceptual disturbance was found. He was oriented to time, place, and person, but had poor attention and concentration. No abnormality found in immediate, short-term, and remote memory, but the recall of events during fugue episode was patchy. Judgment and insight were intact.\nThe patient was diagnosed of dissociative fugue with major depressive disorder according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision. He was treated with fluoxetine supportive and insight-oriented psychotherapy. Psychoeducation was given both to patient and family. He responded well after 1-month and during subsequent visits after discharge, he was encouraged to find new work to earn. Efforts were made to enhance coping with stressors to prevent another fugue episode. He comes for regular follow-up since last 2 months and no fugue episode occurred. |
An 84-year-old man was referred to our tumour center with a large mass (8 × 5 cm) in the anteromedial side of tibial mid-diaphysis (Fig. ). The lesion was painless and the patient reported a rapid increase in its size during the last year. Before that time, he did not worry of its nature, as it was remained unchanged for many years. Plane X-Rays showed a radiolucent lesion adjacent to tibial bone without cortical disruption. Magnetic Resonance Imaging (MRI) revealed an ovular plurilobulated and inhomogeneous soft-tissue mass with a predominant semisolid matrix (Fig. ). Some necrotic as well as adipose tissue areas were also recognised. However, the tumour did not infiltrate the bone or the surrounding muscles (Fig. ). The patient had hypertension and diabetes but his general health was overall good.\nThe next step was fine needle aspiration biopsy of the mass. Histological examination revealed that the tumour was a malignant myxofibrosarcoma. Chest and abdominal Computed Tomography (CT) scans as well as radionuclide total bone scan excluded the presence of systemic lesions or metastasis. Therefore, the patient was scheduled to undergo surgical resection of the lesion with additional removal of the adjacent soft tissue structures.\nUnder general anaesthesia and after tourniquet inflation, en block wide excision of the mass was performed. As the tumour was in close proximity to mid-diaphyseal tibial bone, part of the tibial anterior-medial cortex was also removed to facilitate at least 2 cm tumour-free resection margins circumferentially. The tibial defect of 9 cm was filled with acrylic cement and fixed with a 4.5 mm locking plate and screws. Tumour removal was followed by coverage of the large remaining soft tissue and skin defect (25 cm) with a microvascular musculocutaneous flap from the contralateral thigh.\nHistological analysis of the excised tumour showed a high-grade myxofibrosarcoma with solid sheets and areas of necrosis. At higher magnification, multiple spindle cell cells of mesenchymal origin surrounded by many polygonal epithelioid cells with pleomorphism and elevated mitotic index were found. Surgical margins were disease free. In addition, immunohistochemical staining was negative for CD34, smooth muscular actin, for desmin, keratins, caldesmon, and S-100, which confirmed the high-grade character of the lesion.\nThe postoperative period was uneventful. Partial weight bearing for 6 weeks was advised. After wound healing, about 3 weeks, the patient was referred to the Oncology Department for local Radioterapy. At 2 years follow up evaluation, plain X-Rays and MRI of the operated site didn't reveal any signs of local recurrence (Fig. ). Furthermore, chest and abdominal CT scans were negative for metastasis. The flap looked intact and well vascularised. The patient could stand and walk without any restriction, he did not report any residual pain and he was able to perform his usual daily activities. |
The patient was a 35-year-old woman with no family history of neurofibromatosis. An inspection of her skin revealed extensive congenital plexiform neurofibroma in the outer quadrants of her right breast that extended to the nipple-areolar complex and to the homolateral axillary region and arm (Figure ). The lesion infiltrates the nerve itself and the surrounding tissues, which was leading to soft tissue overgrowth and causing dysfunction and disfigurement. Dermatological exploration also showed some smooth, margined, light-brown pigmented macules on her chest that varied in size and configuration. Moreover, a segmental vitiligo characterized by unilateral macules in dermatomal distribution was present on her left lower limb.\nMicroscopic findings of biopsy specimens of the lesions on the nipple-areolar complexes were obtained from all patients to confirm the diagnosis on histological grounds. Hematoxylin and eosin stained sections from sections that were fixed with formalin and embedded in paraffin were prepared. On histology, the nipple lesions of patients 1 to 8 were identified as neurofibromas. The neurofibromas contained interlacing bundles of elongated cells with dark staining nuclei. The cells were associated with strands of collagen, and small to moderate amounts of mucoid material separated the cells from the collagen. Occasional mast cells and lymphocytes were also present in the stroma. In particular, the 4th and 6th patients had neurofibromas that were composed of widely spaced cells devoid with elongated nuclei and scant cytoplasm and embedded in matrices that were rich in mucopolysaccharide and variably collagenous (Figures and ). The collagen fibres were typically delicate and lay within a matrix that was variable, abundant and rich in mucopolysaccharide.\nHistological finding showed plexiform neurofibroma in the 9th patient. The neurofibroma is located in both the dermal and subcutaneous tissues. The neurofibroma cells surround the adipose tissue. Tactile differentiation was apparent, and the pseudomeissnerian corpuscles were found to be spherical and aggregated (Figure ).\nIn all the patients we describe, clinical and histopathological examination at the time of their first presentation, as well as their subsequent examinations, did not show an association with breast carcinoma. |
An 80-year-old woman presented with a history of intermittent, severe epigastric pain. Over the preceding 5 months, she had less severe and self-resolving epigastric pain 15–30 min after every meal. The full blood count, serum biochemistry values, and C-reactive protein level were within normal ranges. Additionally, arterial gas analysis was normal. Abdominal plain radiography showed free air between the liver and diaphragm, and PI (Fig. ). Abdominal computed tomography showed severe calcification of the SMA origin; SMA peripheral flow was reserved (Fig. ). Computed tomography (CT) revealed bubble-like intramural gas of the small bowel with the contrasted wall pneumoperitoneum (Fig. ).\nSince the patient did not have peritonitis, a conservative approach was performed. She was managed in the condition of intensive care unit, due to fears of the potential for acute mesenteric ischemia due to mesenteric artery occlusion or non-occlusive mesenteric ischemia. She was managed for bowel obstruction, which included fasting and intravenous fluid administration. She received heparin infusion to prevent SMA occlusion and maintain collateral flow. During admission, she reported abdominal pain relief. Seven days after admission, abdominal plain radiography showed improvement in PI and pneumoperitoneum; therefore, she was permitted to begin drinking fluids. There was no evidence of recurrent abdominal pain after the fluid consumption, so she was allowed to eat solid food.\nAngiography was planned to relieve the postprandial abdominal pain. The findings showed severe stenosis of the SMA origin with calcification, and the SMA had replaced the common hepatic artery (Fig. , ). ET, namely stenting to the SMA and common hepatic artery, was performed. The SMA trunk was engaged with a 6F Parent Plus 60 guiding catheter (Medikit, Tokyo, Japan) from the left brachial artery. Initially, 8000 units of heparin was infused, and additional heparin was added to keep the activated whole blood clotting time over 200 s. The SMA occlusion was traversed using a 0.014” NEO EVT Guide Wire Cruise (ASAHI INTECC J-sales, Tokyo, Japan). The SMA trunk to the hepatic artery was traversed using a 0.014” NEO EVT Guide Wire Cruise, which was engaged with a 6F SheathLess PV (Cardian Health, Ohio, USA) from the right brachial artery. Intravascular ultrasonography (IVUS) (Navifocus WR, TERUMO, Tokyo, Japan) revealed severe stenosis of the SMA trunk with calcification. Balloon dilation was performed with the kissing ballon technique using a 4-mm Coyote ES (Boston Scientific, Marlborough, MA, USA) to the SMA and 5-mm SHIDEN RX (KANEKA MEDICAL, Osaka, Japan) to the common hepatic artery. After dilation, two balloon-expandable stents (5-mm PALMAZ Genesis (Cardian Health, Ohio, USA) to the SMA and 6-mm PALMAZ Genesis to the common hepatic artery) were implanted with the kissing stent technique from the common ostium (Fig. ). The sizes of the stents were based on the IVUS measurements. IVUS showed good orifice expansion. Final angiography showed satisfactory circulation to the terminal organ from the orifice (Fig. ).\nEndovascular therapy relieved the patient’s symptoms. She required dual anti-platelet therapy (DAPT) with aspirin and clopidogrel post-intervention. Follow-up computed tomography showed patency of the orifice of the common hepatic artery and SMA, and there was no evidence of PI or pneumoperitoneum. No recurrent postprandial abdominal pain occurred for two years after the ET. |
A 79-year-old male with a medical history of cholelithiasis, for which he underwent cholecystectomy 11 years ago, hyperlipidemia, essential hypertension, and paroxysmal atrial fibrillation was admitted for mild acute pancreatitis. His presentation included severe epigastric pain radiating to the back, lipase of 1840 u/L, and no organ failure. He denied fever, chills, or body aches. The patient denied alcohol consumption and reported to have quit smoking 41 years ago. Liver chemistries, serum bilirubin, serum triglycerides, and immunoglobulin subclasses were within normal limits (). Abdominal CT scan demonstrated peripancreatic haziness consistent with noncomplicated acute pancreatitis (). Home medications included atorvastatin for several years and the addition of 160 mg fenofibrate six months prior to admission. These medications were held upon admission but resumed at discharge. Full medication lists on admission and at discharge are shown in (). The patient was managed with fluid resuscitation and pain control. The patient recovered well and was able to tolerate regular diet without any pain or nausea. The patient was discharged in a stable condition after three hospital admission days, and lipase level at the day of discharge was 307 u/l.\nThree days later, the patient returned with similar symptoms. Lipase levels were >30,000 u/l (), and magnetic resonance cholangiopancreatography showed acute interstitial edematous pancreatitis (). The patient was treated conservatively with intravenous fluid resuscitation, pain control, and nothing per mouth until his symptoms resolved. Four days after his second admission, the patient recovered well and was discharged home in a stable condition. Fenofibrate and atorvastatin were discontinued ().\nTwo months later, the patient remained asymptomatic and returned for further workup to rule out an alternative cause to fenofibrate-induced pancreatitis. Endoscopic ultrasound (EUS) was done, which showed a 12 mm x 20 mm pancreatic head mass without pancreatic duct stenosis, strictures, or dilation. There were no common bile duct abnormalities. Fine needle aspiration was performed, and cytology was negative for malignant cells. Endoscopic retrograde cholangiopancreatography (ERCP) was performed to place a prophylactic pancreatic duct stent. Cholangiogram revealed a normal biliary system without dilation or strictures. The biliary tree was swept, and nothing was found. A prophylactic pancreatic duct stent was placed and a prophylactic sphincterotomy was performed. No recurrence of pancreatitis has occurred as of 6-month follow-up.\nGiven the course of the patient's illnesses in relation to fenofibrate usage, the timespan of drug initiation, and the fact that he had been taking atorvastatin for many years without previous signs or symptoms of acute pancreatitis, we hypothesize that his recurrent disease is probably due to the use of fenofibrate. |
A 58-year-old man presented to community hospital services with a 3-year history of bifrontal headache and associated neck pain. His symptoms usually worsened towards the evenings, when straining or exerting himself physically, and showed some degree of improvement overnight. There had been no response to analgesia prescribed by a general practitioner. A computed tomography and subsequent magnetic resonance imaging (MRI) scan performed 2 years earlier (in November 2012) were reported as normal.\nLeading up to his hospital presentation, the patient had begun to experience subtle blurring of vision, needing to give up driving as a result. A specialist ophthalmology assessment revealed impaired ocular motility featuring an upward gaze palsy and nystagmus, provoked by upgaze with exotropia in the right eye. Central vision was essentially preserved and there was no significant refractive error.\nIn September 2014, the patient was referred to quaternary neurology services suffering progressive difficulty in walking, loss of balance and poor concentration, in addition to headache and oculomotor symptoms. Examination of the cranial nerves confirmed bilateral upward gaze palsy, a constricted, unreactive left pupil and convergence-retraction nystagmus consistent with Parinaud's syndrome. Visual acuity and fundoscopy were normal in both eyes, trigeminal and facial nerves intact bilaterally. Peripheral nerve examination revealed mild, bilateral dysmetria, and an extensor plantar reflex on the right side.\nThe patient underwent a series of four MRI scans between 2012 and 2015. The first MRI performed in November 2012, which had erroneously been reported as normal, shows downward brainstem displacement (Fig. a). Of note, subdural collections and meningeal enhancement were absent. A second MRI performed in early September 2014 revealed a moderately expansile lesion occupying the posterior aspect of the midbrain (Fig. b).\nA third MRI performed in late September 2014 during an acute admission for worsening visual symptoms demonstrated interval enlargement of the midbrain mass (Fig. a and b) featuring acute petechial haemorrhage (Fig. c). There was no restricted diffusion or contrast enhancement at any time point. Sagging of the brainstem was evident on both studies in 2014, unchanged from the initial scan performed 2 years earlier.\nAlthough the possibility of intracranial hypotension was considered during clinicoradiological discussion, the growing lesion raised concern for a neoplasm and a consensus decision was made to perform a stereotactic biopsy.\nAfter biopsy, the specimen showed profuse haemorrhage, thought to be secondary to the procedure itself. The specimen showed no evidence of malignancy, but reactive features with a small volume of fresh haemorrhage and engorged vessels. A GFAP stain revealed severe gliosis, with spider-shaped reactive glia (Fig. ).\nFollowing a transient deterioration in balance following the biopsy, the patient clinically improved with subtotal resolution of his oculomotor symptoms. This was mirrored by a mild improvement in the degree of brainstem sagging on a follow-up MRI from 2015, further supporting a diagnosis of SIH (Fig. ). The patient declined a lumbar puncture and spinal imaging to assess for signs of a CSF leak. |
A 37-year-old man with complex heart disease and no history of prior procedures presented to Asan Medical Center with palpitations, dyspnea (New York Heart Association [NYHA] class IV), chest discomfort, and generalized edema. He was diagnosed at the age of 18 years as having left isomerism with azygos continuation and interruption of the inferior vena cava (IVC), direct drainage of the hepatic veins to the common atrium, complete atrioventricular septal defect, double outlet of right ventricle, pulmonary stenosis, bilateral superior vena cava, right aortic arch, and isolated dextrocardia (). At the time of his diagnosis at another institution, he was told that corrective surgery could be impossible because of Eisenmenger syndrome. He was subsequently hospitalized many times with worsening heart failure (NYHA functional class III–IV), repeated atrial fibrillations, and cyanosis (saturated arterial oxygen of 78%–80%).\nEchocardiography showed severe atrioventricular valvular regurgitation and a dilated atrioventricular valvular annulus of 55 mm with fair systemic ventricular function. Cardiac catheterization demonstrated a mean pulmonary artery pressure of 40 mmHg, a mean pulmonary wedge pressure of 34 mmHg, and an elevated left ventricular end diastolic pressure of 35 mmHg, but an otherwise normal pulmonary vascular resistance of 1.35 Wood units · m2.\nCardiac transplantation and atrioventricular valvular replacement were considered as treatment options. At first, we thought that he was a potential candidate for valvular replacement because of his fair ventricular function. However, this therapeutic option could not treat the patient’s ongoing heart failure due to his elevated left ventricular end diastolic pressure and the problematically large size of his atrioventricular valvular annulus (55 mm). Therefore, valvular replacement was not performed, and a decision was made to offer heart transplantation.\nA suitable donor heart became available from a 37-year-old male who died of suicide. The donor heart included the entire aortic arch, the main pulmonary artery and its branches, the superior vena cava (SVC) and the innominate vein, the IVC, and the pulmonary veins.\nThrough a median sternotomy, cardiopulmonary bypass (CPB) was instituted using an arterial cannula in the distal ascending aorta, and three venous cannulas were inserted into the bilateral SVCs and the hepatic vein. The recipient heart was excised from the thorax using the usual bicaval technique. The bilateral SVCs were dissected at the level of the SVC-atrium junction and a cuff was created from an isolated hepatic vein. The recipient main pulmonary artery was excised at the bifurcation level. An extended incision was then made toward the left pulmonary artery, because the recipient pulmonary artery was situated to the right and posterior to the ascending aorta (). The recipient aorta was dilated, so we performed V-shaped reduction plasty to decrease the size discrepancy between the donor and recipient aorta ().\nThe donor left atrium was anastomosed to the recipient anterior cuff of the left atrium. The donor pulmonary artery was transected at the distal part of the right pulmonary artery and was anastomosed to the recipient pulmonary artery (). After the aortic anastomosis, the donor IVC was connected to the recipient hepatic vein. The aortic cross-clamp was then released. Despite the reduction aortoplasty for the dilatation of the recipient ascending aorta, the recipient distal AAo still push out into the main PA. Due to the limited space between the two vessels, the newly reconstructed SVC was positioned anterior to the ascending aorta. The donor SVC and innominate vein were connected to the recipient right SVC and left SVC, and then augmented with the recipient resected right atrial wall ().\nThe patient was smoothly weaned from CPB without any difficulties. The CPB time was 322 minutes, and the aortic cross-clamp time was 161 minutes. The patient was extubated after 12 hours. Two weeks later, the patient complained of swelling in the left arm. Computed tomography was performed and thrombotic occlusion of the innominate vein was found. Collateral venous channels opened and the left arm swelling began to disappear gradually. Two weeks later, the patient was discharged without any complaints. Five months after the operation, chest radiography showed reduced cardiomegaly (). To date, the patient is in the NYHA functional class I without arrhythmic episodes, signs of transplant rejection, or left arm swelling. |
A 70-year-old white male with a previous history of NF1 was referred to our hospital in February 2003, where physical examination revealed the typical neurofibromas over the skin, the anterior and posterior chest and abdominal walls and café-au-lait spots () and in addition, an ulcerated subcutaneous lesion in his upper dorsum measuring 6 × 6 cm, that had been growing slowly over the past year (). A thoracic CT scan and Tc-99 m-depreotide scintigraphy (Neospect) were performed revealing a second lesion in the left axillary area, apparently representing an infiltrated lymph nodal block. The FNA from the dorsal lesion demonstrated malignant sarcomatous cells. The patient underwent a surgical excision of both lesions and biopsy confirmed the presence of a spindle cell sarcoma with features consistent with a malignant peripheral nerve sheath tumor. A year later, the patient was admitted to our department for his follow-up. CT and Neospect examination indicated a relapse in the area of both surgical excisions as well as a new mass in the right lateral body of the first thoracic vertebra. He started chemotherapy with carboplatin AUC6 on day one and etoposide 120 mg/m2/day on days 1-3, every three weeks. After the completion of eight courses with this regimen the patient achieved stable disease (SD). No grade 3 or 4 myelosuppression was noticed. The patient continued chemotherapy with ifosfamide 2 gr/m2/day over days 1-5, alternating every three weeks with cisplatin 100 mg/m2 and doxorubicin 60 mg/m2 both administered on day one and recycled every 3 weeks × 4 cycles. Grade 4 neutropenia was observed after cisplatin-doxorubicin administration, however no dose reduction was carried-out. A new radiographic evaluation performed in May 2005 showed complete eradication of the tumors in the dorsum and spine and a significant size reduction of the axillary nodal block. Thereafter, the patient received chemotherapy with carboplatin AUC2 and paclitaxel 40 mg/m2 administered once weekly concurrently with radiotherapy on all sites of residual disease for a total of four weeks. After the end of chemoradiation, complete remission (CR) was achieved. Eight months later, the patient developed multiple lung metastases and dyspnea. He was not subjected to further chemotherapy and died from progressive disease in the lung. |
A 36-year-old man with nephrotic syndrome treated with immunosuppressive therapy presented with acute urinary retention and a three-day history of lower abdominal discomfort. He was unable to void completely despite straining. These complaints were preceded by the eruption of a vesicular erythematous rash over the right side of his lower abdomen which extended to his right scrotum and thigh. The rash appeared approximately seven days before the voiding complaints and was not associated with pain or itching. He did not have similar symptoms previously. He had no fever and no other urinary symptoms such as dysuria, urgency, and increased frequency. He denied a history of lower back pain, abnormal sensation in the legs, and weakness and did not have constipation or loss of sexual ability. He had a history of childhood chickenpox.\nThe patient had a known history of nephrotic syndrome with stage III chronic kidney disease for two years. Although his renal biopsy was suggestive of minimal change disease with mesangial immune complex deposits, another biopsy performed five months prior confirmed a diagnosis of the tip lesion variant of focal segmental glomerulosclerosis. His medications were prednisolone (15 mg daily) and mycophenolate mofetil (1000 mg twice daily), both for approximately six months. These were not altered at admission.\nThe patient was vitally and clinically stable at admission. He had central obesity with corticosteroid-related cushingoid features such as a moon-like face, suprascapular fat pads, and abdominal striae. He had suprapubic tenderness, and his bladder was palpable above the symphysis pubis. There was a non-tender vesicular rash on a densely erythematous base with areas of purpura involving the L1 to L4 dermatomes (Figures -). The ruptured vesicles led to the development of ulcerations with crusted lesions of the same distribution. The rash also involved the S2 dermatome as evidenced by the right scrotal rash and erythema (Figures -). The patient’s respiratory and cardiovascular examinations were unremarkable, and a neurological examination showed no weaknesses in the lower limbs; sensation was intact. Deep tendon reflexes and anal sphincter tone were preserved.\nLaboratory tests showed that his white blood cell count was 6.08 x 109 per L, hemoglobin was 9.4 g/dL, platelet count was 198 x 109 per L, and random blood glucose was 6.5 mmol/L. His urea (19.1 mmol/L), creatinine (188 µmol /L), and electrolytes were within his baseline. Creatinine clearance was 40.88 mL/min, and his serum albumin was 24 g/L. Urinalysis showed 3+ proteinuria, no hematuria or pyuria, and no nitrates or glucose. Urine bacterial culture was negative as was urine cytology. His chest X-ray was normal with no interval changes.\nAn indwelling catheter was inserted to relieve the acute urinary retention, yielding a residual vesical volume of 800 mL. Postcatheterization, a kidney, ureter, and bladder ultrasound was performed, revealing a normal-sized prostate gland (20 mL) and no hydroureter or hydronephrosis. Cystoscopic findings were normal with no signs of urethral obstruction, strictures, or inflammatory changes. The bladder appeared normal with no evidence of cystitis. Urodynamic studies were not available at our facility.\nThe diagnosis was voiding dysfunction secondary to extensive lumbosacral herpes zoster infection. A 14-day renal dose of intravenous acyclovir was started. The improvement was remarkable after 10 days, reducing the rash to well-demarcated areas of scarring and hypopigmentation (Figures -) (Figures -).\nDuring the hospital stay, adequate urine output was maintained through an indwelling urinary catheter. A trial without a catheter was unsuccessful after the patient developed abdominal discomfort and could not empty his bladder completely despite straining and having an urge to void.\nThe patient was discharged with instructions for intermittent self-catheterization (two to three times daily) and close follow-up at the nephrology and urology outpatient clinics. Four weeks later, the voiding dysfunction resolved completely, and the patient was able to void spontaneously without the need for self-catheterization. On follow-up, he did not report abdominal discomfort, urgency, increased frequency, or post-void dribbling. |
A 71-year-old female presented to her primary care physician with complaints of lightheadedness. She had no other symptoms and her physical examination was unremarkable. A non-contrast head computed tomography scan was negative for any abnormalities. This prompted a cardiac work up for her symptoms. An electrocardiogram revealed premature ventricular contractions that led to a transthoracic echocardiogram (TTE). This showed a 1 cm mass within the left atrium, concerning for a thrombus. A transesophageal echocardiogram () with subsequent cardiac magnetic resonance imaging, was performed to better characterize the mass. This revealed a mass attached to the ridge between the left atrial appendage and superior pulmonary vein by a discrete stalk, measuring 1.4 x 1.1 x 1.0 cm. The mass appeared hypovascular on perfusion imaging, with no specific enhancement with delayed enhancement imaging (Figure 2). Her preoperative workup was completed with a left heart catheterization that did showed nonobstructive coronary anatomy. She was scheduled for elective resection of this mass.\nThe procedure was performed via median sternotomy with the aid of cardiopulmonary bypass. Central aortic arterial cannulation with bicaval venous cannulation was performed. The heart was arrested with aid of antegrade cardioplegia. For surgical exposure, Sondergaard’s groove was dissected and a left atriotomy performed. A 1 cm mobile, gelatinous mass on the left atrial wall was found (). This arose between the left atrial appendage and the left superior pulmonary vein. The lesion was resected en bloc, along with the stalk and a margin of the left atrial wall. The defect was closed using a 4-0 monofilament suture. The immediate post-operative course was uneventful and the patient was discharged home on post-operative day 4. On outpatient follow up she has been doing well and has remained asymptomatic. A repeat echocardiogram is scheduled to be performed at one year follow up.\nOn gross examination, the tumor was soft and grey-white, that appeared frond-like and translucent when submerged in liquid. Histologically, it was composed of branching avascular papillae with variable amount collagen and myxoid change consistent with papillary fibroelastoma, with no evidence of extension into the left atrial wall (). |
A 50-year-old male patient presented with a 2-year history of left-sided typical HFS. Painless irregular clonic contraction of the facial muscles began initially in the orbicularis oculi muscle of the lower lid. It gradually spread to other muscles innervated by the facial nerve on the left side of the face, including platysma. The paroxysm was induced or aggravated by emotional tension, stress, and voluntary and reflexive movements of the face. He had significant difficulty in his work and social life despite 2 times of botulinum toxin injection. Medical treatment with carbamazepine (up to 600 mg) and baclofen (30 mg) was not effective. He was referred for surgical treatment. His medical history was unremarkable. His physical and neurologic examinations were normal, including hearing. No tinnitus or discernible noise heard in his left ear was found. Only typical nature of clonic hemifacial spasm was evident. Abnormal synkinesis between the orbicularis oculi and orbicularis oris muscles was found by the electromyographic examination of the blink reflex. Despite typical HFS, there was no discernible vascular structure in the REZ of left facial nerve (). However, a meatal loop of AICA abutting to the cisternal portion of the facial nerve was found.\nUnder the impression of HFS caused by neurovascular compression of distal facial nerve, standard microsurgical procedure was performed as described previously [, , ]. In addition to intraoperative monitoring of BAEPs, LSR, which is an abnormal muscle response demonstrated by EMG recordings from mimic muscles that are innervated by a different branch of the facial nerve [], was also monitored throughout the operation. The entire course of the facial nerve and offending arteries were exposed under microscopic vision. Upon exposure of the REZ of the facial nerve, there was no offending vessel in the REZ as expected (). The distal, cisternal segment of the facial nerve was found to be bent by a meatal loop of the AICA (). A small piece of Teflon felt was interposed between the facial nerve and the meatal loop of the AICA with extreme care not to stretch the internal auditory artery and the distal facial nerve (). After interposition of Teflon felt, LSR immediately disappeared and BEAP was stable also (). The closure of the dura and wound was performed in routine manner. The HFS resolved completely following the surgery. The postoperative course was uneventful with no signs of facial weakness or hearing impairment by pure-tone audiometry. No recurrence of HFS or neurologic sequelae was evident at a 12-month follow-up. |
The patient is a 37 year old woman, born in Austria. She had two children (13 and 15 years) before her GBM diagnosis. She was diagnosed with GBM in the right frontal lobe in April 2008, and treated according to a current treatment standard consisting of a gross total resection of the tumor, fractionated confocal radiotherapy up to 60 Gy (2 Gy/fraction) and concomitant and adjuvant chemotherapy with temozolomide\n. Diagnosis and treatment were performed at the Medical University of Vienna (MUV). Following the concomitant therapy, she experienced amenorrhea for 6 months, followed by irregular menstrual cycles with oligomenorrhea. Two years later, a local recurrence of GBM was diagnosed. She underwent a second resection and followed 6 cycles of dose dense temozolomide, 100 mg/m\n2 orally for five days per week, with a drug holiday over every weekend. She became pregnant less than three weeks after the last intake of the sixth cycle of temozolomide, after a total dose of temozolomide of 20.9 g/m\n2 (\n).\nBoth parents wanted to carry the child to term. They were offered intensified pregnancy monitoring and genetic counselling, but no genetic tests were performed. During pregnancy the child developed normally as followed by close meshed ultrasound controls and the mother was doing well until week 27, when she developed signs of increased intracranial pressure as well as weakness of the left leg. She was admitted to the local general hospital for observance and anti edematous treatment. As the mother’s condition worsened, she received corticosteroids to induce lung maturation of the fetus, and the child was delivered after 32 weeks and 6 days of pregnancy by caesarean section using the Misgav Ladach method\n. The child showed Apgar scores of 8/9/9, one, five and ten minutes after birth, respectively, weighed 1876 g, cried spontaneously and was neurologically inconspicuous. The infant did not need further respiratory assistance after the third day of life, and was discharged from the neonatal intensive care unit after an uncomplicated stay without any signs of neurological or any other organ deficit, weighing 2.5 kg. The child has shown normal growth and development ever since.\nThe mother underwent her third neurosurgical procedure two weeks after delivery, followed by chemotherapy with fotemustine 100 mg/m\n2 every three weeks for six cycles combined with bevacizumab 10 mg/kg every two weeks 6 weeks later. Eight months after the caesarean section, distal progression in the brain was diagnosed on MRI and she was referred for radiotherapy of the distant recurrence. |
A 16-year old young man was transitioned to the Royal Brompton ILD service from the paediatric respiratory department with a diagnosis of IPH. He had the first episode of haemoptysis aged 7 and since then experienced recurrent episodes of haemoptysis, shortness of breath and cough. He was given a diagnosis of IPH based initially on symptoms, recurrent shadowing on imaging (Fig. a) and negative autoimmune screen. Interestingly, aged 6 he was diagnosed with Hashimoto thyroiditis. Exacerbations of his IPH were strongly associated with flare ups of his thyroiditis. Until the age of 10, his symptoms and imaging findings responded to intermittent courses of oral corticosteroids of various doses.\nAged 11 he was admitted to the local hospital with haemoptysis and severe respiratory failure. He was intubated and transferred to the paediatric intensive care unit at RBH. He underwent BAL and surgical lung biopsy. The BAL revealed large numbers of haemosiderin-laden macrophages on Perl’s stain. The biopsy showed DAH without supporting evidence of vasculitis (Fig. ). His HRCT at the time of the biopsy demonstrated diffuse ground glass opacity, perivascular emphysema and a small cavity in the right lower lobe (Fig. b) which raised suspicion for vasculitis but repeat ANCA testing was negative. He was treated with antibiotics and intravenous corticosteroids with good response and resolution of the cavity on subsequent imaging. His spirometry prior to this acute episode showed FEV1 41% and FVC 37%.\nUpon discharge, he was commenced on maintenance treatment with hydroxychloroquine, low dose prednisolone and azithromycin 250 mg three times weekly. Short term courses of increased doses of prednisolone were used for flare ups. A repeat HRCT 4 years after the biopsy showed extensive emphysema with a perivascular distribution, and superimposed diffuse ground glass opacities (Fig. c). The patient had never smoked nor had he ever been exposed to passive smoking.\nWhen he transitioned to the adult ILD clinic and 8 years after the biopsy, aged 19, the radiological picture had further progressed and was characterized by extensive emphysema and pleuroparenchymal fibroelastosis (PPFE) of both upper lobes (Fig. d). Lung function was severely impaired with FEV1 54%, FVC 46%, FEV1/FVC 99%, TLCO 33% and KCO 68% reflecting the combination of severe emphysema and PPFE. A repeat autoimmune screen revealed a p-ANCA with MPO positivity (4.6 u/mL). Following these results, he was started on low dose azathioprine, with ongoing hydroxycloroquine and azithromycin, with current symptomatic and functional stability. |
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 34 year-old woman previously operated for a solitary encapsulated papillary thyroid microcarcinoma in the right lobe of the gland, without familial history of breast or thyroid malignancy, was admitted to the Institute of Oncology and Radiology of Serbia, Belgrade, after feeling soreness at breast self-examination followed by a suspicious mammographic finding in the left breast. A lump measuring 30 × 30 × 20 mm in size was surgically removed. Grossly, the resected specimen featured a cyst (15 mm in diameter) with an intracystic proliferative lesion 10 × 10 × 8 mm in size. Histopatholological examination revealed an intracystic IDP without evidence of malignancy (Figure ). No axillary lymphadenopathy was found at the time of surgery. Whereas no changes were seen in the patient's breast on ultrasound or mammography during follow-up, an enlarged lymph node became palpable in the left axilla 10 years later. A metastatic carcinoma in ALN was suspected and the patient was subjected to excisional biopsy.\nA lymph node sized 15 mm in diameter was removed. Histology revealed a proliferative epithelial lesion measuring 11 mm in the largest dimension in the cystic space of the node. The proliferative lesion consisted of papillary and tubular structures lined by luminal cuboidal cells and a distinct outer layer of myoepithelial cells which were very similar to IDP of the breast (Figure and ). Apocrine metaplasia was found. No mitoses, necrosis or cells with atypical features were detected, suggesting the benign nature of the neoplasm. In addition, both the proliferative papillary lesion and small clusters of duct-like structures were also observed in the lymphoid tissue surrounding the cystic area (Figure and ). Immunostaining with a series of antibodies (all from Dako, Carpinteria, CA, USA) was used to confirm histogenetic origin of tumor cells in ALN. Staining for AE/AE3 was diffusely positive in tumor epithelium and staining for alpha-smooth muscle actin and p63 was focally positive in myoepithelial cells. Neoplastic and ectopic duct-like epithelial cells were estrogen (ER) and progesterone receptors (PR)-positive cumulatively confirming their origin from the breast. As a result, the presented case was diagnosed as IDP of ectopic breast tissue in ALN on the basis of histopathological and immunohistochemical findings. Eight years after ALN excision, the patient was in excellent condition without any signs of recurrence. |
A 13-year-old boy presented to us with pain in the left shoulder and chest, after allegedly being hit by a sport utility vehicle. The child was asleep, semi-prone with left shoulder up on a pavement when he was hit on his left shoulder by the vehicle.\nHe was brought awake, oriented to time, place and person to the emergency department 2 hours after injury. His blood pressure was 118/82 mm of mercury, and pulse was regular with a rate of 103 per minute. An ovoid, tender swelling was present over the left sternoclavicular joint []. There was tenderness over the lateral end of clavicle and difficulty in moving the ipsilateral shoulder. He complained of numbness over the medial aspect of upper forearm. There were no abrasions or tyre marks. A serendipity view radiograph of the Left side [] showed displacement of the medial fractured end of the clavicle with the proximal epiphyseal fragment in situ. The lateral epiphyseal end too remained in continuity with the joint while the fractured proximal fragment was displaced inferiorly and posteriorly. The serendipity view (40° cephalic tilt view) is considered the next best thing to a true cephalocaudal lateral view of the sternoclavicular joint. A Computed Tomography revealed a bipolar physeal injury of the left clavicle []. The middle floating shaft fragment had displaced anterosuperiorly at its medial end and posteroinferiorly at its lateral end. The Thurston Holland fragment was visualized at either ends [].\nAn initial attempt to reduce the medial physeal fracture failed, probably because of the floating intermediate segment which failed to transmit the reduction force. The position was accepted in view of the reported natural history of similar physeal injuries at either ends of the clavicle and the child was treated in a shoulder immobilizer. The parasthesia resolved over the next 2 days. The child was followed up at 2, 6, and 18 months. There was no sensory deficit at 2 months. At 18 months, the child had full range of movements at the shoulder and radiographs showed periosteal remodeling at either end with no joint incongruity []. |
A 71-year-old lady had undergone breast-conserving surgery (BCS) for invasive ductal carcinoma, no specific type (NST) of right breast nine years prior to current presentation in our unit. Her pathological stage at that time was T2N1M0 with negative estrogen and progesterone receptor status. She had received three cycles adjuvant chemotherapy with Epirubicin, 5-Fluorouracil and Cyclophosphamide 26 days post-operatively followed by adjuvant irradiation of the right breast with 50 Gray and again three cycles adjuvant chemotherapy with the same regimen.\nShe remained well after adjuvant therapy and was under regular follow up until this presentation. She presented this time with nodules in her lower inner quadrant of right breast for four months with discoloration, thickening and puckering of surrounding skin (Fig. ). There was no palpable mass in axilla or contralateral breast and no lymphedema of right upper limb. She had diabetes mellitus, hypertension and hypothyroidism. There was no history of headache, weight loss, jaundice or back pain.\nContrast enhanced computed tomography (CECT) of chest and abdomen showed two enhancing cutaneous nodules measuring 19 mm × 18 mm and 18 mm × 14 mm in medial aspect of right breast with minimal fat stranding noted in superficial subcutaneous plane (Fig. ). Surrounding skin was edematous. Other findings were lobulated outline of liver and few splenic cysts with no evidence of systemic metastasis. Fine needle aspiration cytology (FNAC) from the nodule revealed clusters and fragments and singly dispersed spindle shaped cells with elongated hyperchromatic nuclei with moderate cellular pleomorphism suggestive of malignant spindle cell neoplasm.\nThe patient underwent total mastectomy with negative margins. Intra-operatively there were two nodules (15 mm × 15 mm and 15 mm × 15 mm) arising from right breast skin without involving deeper tissues with thickening of surrounding skin and subcutaneous tissue (Fig. ).\nHistopathology report of the specimen showed intermediate grade angiosarcoma infiltrating into subcutaneous tissue (Fig. ).\nThree months after mastectomy, the patient presented again with a splotchy purplish nodule in the right breast below the scar line which on FNAC proved to be spindle cell neoplasm. The patient was advised for wide local excision, however the patient opted for chemotherapy. Patient succumbed to progressive disease six months after the local recurrence. |
A 71-year-old female patient was presented with an approximately 3 cm peri-areolar mass in the 12 o’clock position in her right breast on physical examination, with no nipple retraction, skin dimpling or palpable axillary lumps. Bilateral mammograms showed very dense breast tissue with a suggestion of an asymmetric density in the right retro-areolar area. It was however difficult to characterize the lesion due to increased breast density (Figures , ). Subsequent ultrasound examination of the whole right breast revealed a 26-mm ill-defined, somewhat heterogeneous, lobulated mass in the area of the palpable abnormality, mostly isoechoic to surrounding normal breast parenchyma. Ultrasound-guided core biopsy of the palpable mass was performed using a 14-gauge needle with three passes from the medio-lateral approach (Figures , ). Histopathology showed invasive mucinous carcinoma of the breast and the diagnosis was given to the patient 12 days after the biopsy. At the second visit, two separate masses were felt on physical examination, one mass in the 12 o’clock and a further adjacent hard nodule at 2 o’clock in the sub-areolar location. A second ultrasound scan was performed, which showed a new 12-mm heterogeneous, cone-shaped nodule contiguous with the main mass pointing medially and towards the skin (Figure ). Since the new palpable abnormality developed following the biopsy and aligned to the expected location of the biopsy needle tract, post biopsy organizing hematoma was suspected with a differential diagnosis of tumor displacement and growth in the biopsy tract. Dynamic contrast-enhanced MRI was performed to determine disease extent and to exclude additional lesions and tumor growth in the biopsy needle tract. The main tumor mass measured 25 mm which exhibited predominantly type 2 (plateau) time-signal intensity curves. Linear enhancement was demonstrated medial to the mass in keeping with the biopsy tract. Although this vague linear enhancement showed type 1 (steadily increasing) kinetics, there were two separate enhancing nodules along the tract measuring 10 mm and 8 mm with type 2 kinetics (Figures -). A diagnosis of tumor seeding and/or displacement within the biopsy needle tract was made prior to surgery. Central wide local excision with removal of the biopsy tract and sentinel lymph node biopsy was performed. Histopathological examination of the excision specimen showed a 32-mm pure type of invasive mucinous cancer with tumor deposits within the biopsy needle tract measuring up to 6 mm (Figures -). The whole size of tumor was 40 mm. One sentinel node was excised, which was involved by metastatic carcinoma. Due to involvement of sentinel lymph node, axillary dissection was done as second operation. |
The second case involves a 30-year-old Deaf, Hispanic male who presented to the Emergency Department after his mother reported that the he was behaving oddly and not taking his risperidone. Per reports, the patient was talking to his mother about going places in a UFO and exhibiting disorganized and illogical behaviors. He was subsequently placed under a Baker Act by the emergency room physician who documented that the patient was exhibiting auditory hallucinations. Initially an interpreter was brought to the hospital prior to his admission. Per the ASL-interpreter, the patient stated that he felt “fine and not crazy” and that all of these events are happening because his mother does not “understanding Deaf culture.” He also conveyed that he did not like to take his meds because they interfered with him being able to drink alcohol and caused drowsiness.\nUpon initial psychiatric interview an interpreter was not present as the hospital only agreed to set periods of time for the interpreter. As an effort to communicate, questions were prepared for the patient to answer via written responses. highlights a portion of the questions and answers that were constructed. From the responses he maintained bizarre delusions but denied current SI, HI, or AVH. When the ASL-interpreter arrived, the patient appeared jovial and yearned to express himself. The interpreter stated she had difficulties reading his rapid signing at first and had to have him slow down several times. However she did note that this was a common occurrence when addressing Deaf individuals.\nWith the interpreter's assistance, the patient was answering questions logically with a linear thought process. He reported that he had been diagnosed with schizophrenia as a teenager after having several interpersonal issues with his mother. She is Spanish speaking only and he stated that she has never fully understood how to communicate effectively with him. He had been taking risperidone for several years but was tired of continuing with the medication due to the side effects of drowsiness and weight gain, which he was never able to fully discuss with his psychiatrist. Patient reported he was in an ASL school and learning a career in massage therapy. After meeting a girlfriend there he began to develop a sense of independence that he reported his mother disapproved of. This caused an altercation that he reports his mother misinterpreted which precipitated his admission.\nThe patient continued to express that he was abducted by aliens as a child and could understand their language, but besides this he expressed no other psychotic processes. He was observed for two days without medications and remained calm/cooperative but was unable to participate in most activities due to limitations of the interpreter availability. After a family session was completed the patient was discharged home with plans to follow up with his community psychiatrist. The patients' diagnosis was changed to delusional disorder upon his discharge. |
A 25-year-old man, Middle Eastern origin, history of exposure to livestock was admitted to our unit complaining of a painful swelling of the right elbow. The swelling developed over 3 years and was associated with recent pain without fever or rigors, and pruritus. Anamnesis did not reveal any trauma to the elbow or prior medication.\nHe was afebrile on admission with good general conditions, and physical examination revealed a tender right lateral elbow mass with distension of overlying skin. Mass measured 4 cm by 6 cm and there were no signs of excoriations nor fistula (Fig. ).\nOn day 3, patient became febrile with a temperature of 38.8 °C. Lab test demonstrated a normal total WBC count of 5.0 × 109 cells/L, eosinophil level of 158 cells/L, and a normal erythrocyte sedimentation rate of 15 mm/h. Liver function tests were unremarkable. Hydatid serology was negative and there was no modification in the appearance of the mass.\nPlain elbow and chest radiographs were also unremarkable albeit diffuse soft tissue swelling of the elbow: there were no bone erosions nor calcifications. Ultrasound came back for a cystic lesion of the elbow with several floating membranes without color Doppler test. Magnetic resonance Imaging (MRI) depicted a unilocular cyst with multiple septations giving it a multivesicular or rosette appearance, confined to the soft tissues, adjacent to the medial elbow muscles without infiltrating bone nor surrounding neurovascular structures (Figs. and ).\nPatient was prepared for elective surgery with consent and antihelminthic therapy was initiated preoperatively for 5 days. En block surgical excision of the mass under general anesthesia was undertaken. Care was taken to remove the mass en block without perforating the cyst wall, through meticulous pericystectomy along surrounding muscle fibers (Fig. ). The cyst was multivesicular containing daughter cysts and were filled with muddy substance typical of hydatid disease (Fig. ). After excision, extensive washout of the surgical field was carried out. Wound could not be closed due to massive soft tissue loss (Fig. ).\nThe operating field was covered with adequate dressing. Cutaneous skin flap was done subsequently with favorable outcome and no signs of local recurrence 2 years after surgery. |
An 18-year-old nulliparous woman presented with abnormal vaginal bleeding. Ultrasound detected the presence of an endometrial polyp, which was confirmed on hysteroscopy and removed using a resectoscope. The polyp was approximately 2 cm in length. Histological analysis revealed benign endometrial glands with moderately cellular stromatolites showing some degree of periglandular condensation and mild pleomorphism. No SO or MI was noted. The histological diagnosis of low-grade adenosarcoma was made. Subsequently, the patient was advised to undergo hysterectomy, BSO and lymphadenectomy, but she declined to preserve her fertility. She was referred for a second opinion and following extensive counselling, opted for conservative management.\nOver the following 10 years, she was monitored with pelvic ultrasound, hysteroscopy and endometrial biopsy every 6 months, and with annual pelvic magnetic resonance imaging. Follow-up was largely uneventful, with normal imaging and histology. Nine years post-operatively an abnormal appearing area on the posterior aspect of the lower uterine segment was identified on hysteroscopy and subsequently resected. Histology was benign with no features of recurrence.\nEleven years post-operatively, she underwent in vitro fertilization (IVF) and successfully conceived following the first cycle. Unfortunately, she suffered a second trimester miscarriage at 16 weeks’ gestation, with a history suggestive of cervical incompetence after admission with a dilated cervix and bulging membranes. The following year she conceived twins following another IVF cycle. She underwent an uncomplicated elective trans-vaginal cervical suture. She delivered male twins at 28 weeks’ gestation following pre-term labour, which was attributed to placental abruption. Both children are alive and well. She was offered hysterectomy after delivery, and at each subsequent follow-up appointment, but declined as she was uncertain as to whether or not her family was complete. Following pregnancy, her follow-up intensity was reduced to annually with continued ultrasound scans along with hysteroscopy and endometrial biopsy. She continued to defer definitive treatment until, after a total of 20 years of follow-up, she finally underwent an uncomplicated laparoscopic hysterectomy with ovarian conservation. There was no histological evidence of disease recurrence. |
A 49-year-old Caucasian lady with history of polysubstance use disorder and related complications including, recurrent cutaneous abscesses, spinal diskitis and septic thrombophlebitis presented to the emergency room with complaints of intermittent fevers and right hip pain. A month prior to the presentation, she had left another hospital against medical advice after being diagnosed with Methicillin-resistant Staphylococcus aureus bacteremia and right hip septic arthritis. Post discharge, she was off antibiotics, but continued heroin and methamphetamine and was taking multiple dose of ibuprofen in addition for pain control. On admission, her physical exam was notable for severe tenderness in her right hip, marked bilateral lower extremity edema and multiple deep, circular, punched-out looking atrophic scars involving all extremities at prior skin popping (subcutaneous injection of illicit drugs) sites. Pertinent laboratory data included chronic anemia with a hemoglobin of 9.8 g/dL, WBC count of 10.23 k/uL and a platelet count of 395 k/uL. She had negative HIV, Hepatitis B antibodies and elevated Hepatitis C antibody with undetectable Hepatitis C viral load. Her basic metabolic profile noted a sodium of 140 mmol/L, potassium of 3.5 mmol/L and a creatinine of 2.9 mg/dL (estimated glomerular filtration rate of 17 ml/min) which was a significant rise from the normal creatinine levels a month earlier. Her urine analysis noted >500mg/dL proteinuria with a protein/creatinine ratio of 28.25. She had no monoclonal proteins on serum or urine electrophoresis. CT scan of her right hip noted marked degenerative changes in the right hip, with right acetabular protrusion and cortical disruption of the medial acetabular wall. She was diagnosed with right hip osteomyelitis and was in acute renal failure with evidence of nephrotic range proteinuria. She was placed on antibiotics (daptomycin) and underwent hip arthroscopy with irrigation and debridement along with lavage shortly after admission. Differential diagnoses considered for her renal disease included acute tubular necrosis due to sepsis, post infectious glomerulonephritis, focal segmental glomerulosclerosis associated with heroin use, acute interstitial nephritis from NSAIDs and membranoproliferative glomerulonephritis associated with Hepatitis C. She underwent a renal biopsy which revealed acute tubular necrosis and secondary (AA) amyloidosis with the classic apple green birefringence when stained with Congo red () and positive immunohistochemical stain for serum amyloid A protein (). Two weeks after admission she underwent Girdlestone arthroplasty. During the hospital stay, she developed intermittent hypotension, had evidence of primary adrenal insufficiency attributed to amyloidosis and was initiated on steroids. She was discharged home after completion of prolonged antibiotic therapy with daptomycin and was maintained on oral doxycycline. She was referred to outpatient opioid treatment program. Eight months after her admission, she remained committed to be off all illicit drugs and underwent right total hip replacement. Her creatine levels normalized (estimated GFR of 82 ml/min) but she continued to have proteinuria from renal amyloidosis (protein/creatinine ratio of 28.25) and required diuretic therapy for symptomatic management of her edema. |
A 26-year-old housewife presented in June 2010 with gradual progressive weakness in both lower limbs and back pain (at the operative site) since last 3 months. The patient was able to perform her routine activities without support prior to the onset of these symptoms. Weakness has gradually progressed to the extent that at the time of presentation patient was not able to move her limbs and was bedridden. Back pain was not associated with fever, and there were no aggravating and relieving factors. Sphincter incontinence was present.\nIn the past surgical history, the patient was admitted in June 2005 with a history of gradual progressive weakness in both the lower limbs of 1-month duration. There was no sensory and sphincter dysfunction. The onset of weakness was not associated with back pain, fever or trauma. According to the medical charts, bulk and nutrition of the muscles were normal and tone was reduced in the lower limbs. However, the power was reduced to 2/5 (Medical Research Council Scale) at the hip and to 3/5 at the knee and ankle on the right side. The power in the left lower limb was 2/5 at the hip, knee and the ankle. The power of the extensor halluces long us and the flexor halluces long us was 3/5 on both the sides. Rest of the neurological examination was normal at that time. Magnetic resonance imaging (MRI) dorsolumbar spine demonstrated an intramedullary mass measuring 3.3 cm ×7 cm ×2.1 cm in the spinal canal at D9-D10 causing severe compression and anterior displacement of the spinal cord []. The lesion was isointense on T1-weighted, intermediate to hyperintense on T2-weighted and showed diffuse enhancement on gadolinium contrast, and the provisional preoperative diagnosis was intramedullary astrocytoma or ependymoma. The patient was operated by D9-10 laminectomy and subtotal total excision of the tumor was achieved. The spinal cord was expanded. A midline durotomy and myelotomy was done. Intra-operatively, the lesion was intramedullary, grayish white in color, soft in consistency, suckable, and vascular. Histopathological examination was consistent with a diagnosis of astrocytoma (WHO grade 2). In the postoperative period, there was improvement in power to 4/5 at all the joints in both the lower limbs. The patient was gradually mobilized with the Taylor's brace, and physiotherapy was continued. The patient was planned for the MRI thoracic spine at 6 weeks. However the patient lost to follow-up.\nDuring the second admission in June 2010, neurological examination revealed that the tone was increased, and power was 0/5 in both the lower limbs. Deep tendon reflexes at all the joints in both the lower limbs were 3+ and planters were up going on both the sides. Sensory examination was normal. On local examination, operative scar was healthy, and there were no signs of inflammation.\nMagnetic resonance imaging dorsolumbar scan revealed recurrent intramedullary tumor involving the entire spinal cord extending from D8-D10 levels, measuring 1.46 cm × 5.92 cm × 1.57 cm with hydromyelia superior to the lesion at D6 and D7 levels. The lesion was isointense on T1-weighted, mildly hyperintense on T2-weighted and heterogeneously hyperintense on postcontrast study [Figures and ].\nThe patient was operated upon with an exploration of the previous incision and D8 laminectomy. Intra-operatively, thick calcified postlaminectomy membrane adherent to the dura over the tumor was present which was excised. The tumor was intramedullary in location, firm, grayish white, vascular and not easily suckable. There were dense adhesions between arachnoid membrane and piamater of the spinal cord at the level of tumor due to previous surgery. The tumor was firm in consistency, moderately vascular and diffusely infiltrated the spinal cord with ill-defined margins. In view of above findings, gross total excision of the tumor was achieved using ultrasonic aspirator.\nHistopathology (hematoxylin and eosin stain) showed highly cellular and fibrillary background. Cellular areas consist of small cells with highly pleomorphic and hyperchromatic nuclei. Numerous multinucleated giant cells and few xanthomatous cells with foamy cytoplasm were present with no evidence of mitosis or necrosis. These features were suggestive of PXA (WHO grade 2) [Figures and ].\nThe patient's low back pain had improved immediately following the surgery. However, the power in the lower limbs and sphincter incontinence did not improve at the time of discharge.\nAt the follow-up of 1-year, the power was 1/5 with flickering movement of toes in both lower limbs and no improvement in sphincter functions. |
A 45-year-old Haitian American female with no significant medical history presented with a six-month history of progressive solid food dysphagia and a one-month history of odynophagia. The patient had lost 15 pounds and was only able to tolerate pureed food or liquids. She had experienced no symptomatic relief on omeprazole 40 mg twice daily for the past two months and did not use tobacco, alcohol, or illicit substances. Her initial blood count and metabolic panel were unremarkable. An esophagogastroduodenoscopy (EGD) revealed erythematous and friable mucosa with ulcerations in the proximal esophagus (). There was a stricture encountered at 15 cm from the incisors through which the gastroscope could not be traversed. Biopsies were taken from the inflamed esophageal mucosa and the proximal lumen of the stricture. Brush cytology was collected through the stricture as there was a concern for malignancy. A subsequent barium esophagram and upper GI series demonstrated 2 cm irregular narrowing in the cervical esophagus, but no abnormalities in the rest of the esophagus, the gastroesophageal junction, stomach, duodenum, or proximal jejunum. Contrast-enhanced computed tomography (CT) of the chest showed no acute esophageal, mediastinal, pulmonary, or cardiac pathology. The esophageal biopsy indicated acute and chronic inflammation with filamentous sulfur granules consistent with Actinomyces; rare fungal hyphal elements were additionally identified (Figures , , and ). The cytology was negative for malignant cells and the acid-fast bacilli (AFB) stain was negative, ruling out Nocardia as a potential pathogen. The patient was started on intravenous (IV) Penicillin for a diagnosis of esophageal actinomycosis and oral Fluconazole for a presumed Candida coinfection given concurrent fungal elements. Her human immunodeficiency virus (HIV) status was negative and her fasting blood glucose was within the normal range. She was discharged on Fluconazole 200 mg daily for 2 weeks and IV Penicillin G 3 million units every 4 hours for 6 weeks followed by oral Penicillin to complete a total of 6 months of antibiotics. Her esophageal culture eventually grew normal oropharyngeal flora and rare Candida albicans. The patient returned to the hospital 6 weeks later due to an acute right upper extremity deep venous thrombosis (DVT) associated with her peripherally inserted central catheter (PICC). Her odynophagia had improved but she was still not able to advance her diet. Repeat EGD was performed, which showed resolution of her esophagitis, but a remaining stricture in the proximal esophagus (). During an attempt to dilate the stricture, a small mucosal tear was induced. The dilation had to be deferred at that point pending mucosal healing. A repeat barium esophagram illustrated the previously identified stricture with no perforation. The patient's PICC was removed and she was discharged on oral amoxicillin 875 mg twice daily to complete the 6-month course. The patient was given a follow-up appointment in our GI clinic where she would be reassessed for esophageal stricture dilation. Unfortunately, she was lost to follow-up. |
A 48-year-old woman presented to our hospital complaining of loss of vision in her right eye. Her VA at the time of initial examination was measured at RV = (0.03), LV = (1.5), RT = 12 mm Hg, LT = 11 mm Hg. No abnormalities were observed in the anterior segment, optic media, and fundus of her left eye. However, in the fundus of her right eye, a grayish-white choroidal tumor-like lesion, 7 disc diameters in size, was observed from the macular region to the temporal side (Fig. ). With the fundus findings in mind, we diagnosed CM in the right eye after examination by B-mode ultrasonic scan and MRI. We therefore performed GK therapy on the tumor with 3 shots from an 8-mm collimator using a marginal dose (the lowest tumor dose) of 30 Gy, and a maximum dose of 60 Gy (50% isodose). Although the tumor gradually shrank after GK treatment, hard exudates began to appear around the tumor at 6 months postoperatively (Fig. ). Fundus fluorescein angiography revealed a retinal nonperfusion area in the inferior quadrants, and laser photocoagulation was performed upon diagnosis of radiation retinopathy. Although the corrected VA of her right eye improved from (0.01) to (0.03) and stabilized after laser photocoagulation, further deterioration of vision in that eye began to occur at 8 years after the initial treatment.\nUpon examination, we found that a bullous retinal detachment with fixed folds had occurred in the superior-nasal quadrants of her right eye (Fig. ), and that the corrected VA was light perception. Scarring was found to have occurred around the tumor lesion, and laser scars from radiation retinopathy were also observed in the inferior quadrants. Optical coherence tomography (OCT) findings revealed a partial thinning of the macular retina, with the formation of a retinal inner break caused by traction resulting from the formation of preretinal membrane and posterior vitreous detachment (Fig. ). The outer retinal break was not clearly detectable. Serum levels of 5-S-cysteinyldopa (5-S-CD), a tumor marker for CM, were within the normal range of 2.1 nmol/L, MRI findings showed no increase in tumorous lesions (Fig. ), and 123I-IMP SPECT imaging showed no photon accumulation (Fig. ), thus indicating that there was no tumor activity. The patient's VA was extremely poor, so it was determined that there was no indication for vitreous surgery, and we decided to follow her progress. |
A 70-year-old African American male was seen in the emergency department for acute anxiety and paranoia. He reported that his son gave him melatonin to help him sleep, but he felt the medication was poisonous. He also reported that he was struggling with the death of his partner of 40 years and was feeling anxious. The patient was prescribed risperidone and lorazepam and was discharged shortly thereafter. Twenty-four hours later, he was seen again in the emergency department for worsening anxiety, psychosis, suicidal ideation, and command hallucinations. The patient's son reported that his father “had not slept in weeks.” The son reported progressive agitation, paranoia, and bizarre behavior. Due to the worsening psychosis, he was admitted to the medical floor for further work-up. He reported feeling as though people were watching him and that someone was going to harm him. When questioned about his reported suicidal ideation, he blamed that thought on his post-traumatic stress disorder; but would not elaborate on the event. The patient was given a one-to-one sitter due to his suicidal ideation.\nThis patient lives with his family of seven children. He has a history of prolonged incarceration. His past medical history is significant for hypertension and negative for seizure disorders. The patient had never been hospitalized for psychiatric issues prior to this visit. He denied past suicidal behavior and any history of physically or sexually aggressive behavior. The patient reported a history of excessive alcohol abuse for more than a year following the death of his partner. He reported that he stopped drinking “cold turkey” five months prior to this visit. The patient's family history is significant for a son with an anxiety disorder. He denied a history of physical or sexual abuse in the past.\nThe patient's mental status exam was significant for an anxious affect with referential and paranoid ideations. He denied any thought broadcasting, insertion, or withdrawal. He had some paranoid and persecutory delusions. Insight, judgment, and impulse control were poor.\nThe patient's initial physical exam revealed an inability to ambulate and overall weakness. Further neurological examination revealed mental disorientation with bilateral muscle wasting, sensory deficit, and hyporeflexive ankles. Additionally, the patient exhibited stance and gait abnormalities. A later eye exam revealed bilateral light-near dissociation with accommodation but no reaction to light. Otherwise, all other neurological components were intact and within normal limits.\nInitial routine testing was positive for the Treponema pallidum antibody, suggesting prior infection, but the distinction between treated and untreated syphilis cannot be made as the Treponemal-specific immunoglobulin G (IgG) may remain elevated throughout life. An RPR was then ordered to help distinguish between acute or chronic infection and a Treponema pallidum particle agglutination test was ordered to distinguish between syphilis infection and a false positive screening test. The RPR returned nonreactive but the Treponema pallidum particle agglutination returned reactive, indicating a prior infection of Treponema pallidum. The initial differential diagnosis workup included testing to exclude thiamine, folate and B12 deficiency, insomnia, hypocalcemia, hypothyroidism/hyperthyroidism, HIV encephalopathy, dementia, stroke, drug or alcohol intoxication, and normal pressure hydrocephalus.\nFurther labs showed white blood cell count, sodium, potassium, calcium, anion gap, creatinine, glomerular filtration rate, glucose, mean corpuscular volume, and thyroid stimulating hormone within normal limits. Urinalysis, toxicology screening, alcohol levels, and HIV antibody were also negative. Imaging included a head computed tomography (CT), which showed no abnormalities, a brain magnetic resonance imaging (MRI) that showed cortical atrophy, and an electroencephalogram within normal limits. |
A 34-year-old Sudanese male was admitted to Prince Saud Bin Jalawi Hospital, Al Ahsa, Saudi Arabia as a case of Malaria. As the patient complained of fever with no clear cause by routine investigations, he was admitted as a case of fever of unknown origin. During admission, the patient was diagnosed with typhoid using the Widal test. However, over two to three days, the pattern of fever was not characteristic of typhoid as the patient had recently arrived from Sudan. Hence, a malaria test was performed which was positive. For malaria, the patient was started on ciprofloxacin, quinine sulfate, and doxycycline. After initiating the treatment, his fever improved and he was ready for discharge.\nOn the third day of the admission, the patient developed generalized abdominal pain associated with nausea, inability to pass flatus or stool for 24 hours, and high-grade fever. On examination, he looked pale, severely ill, his temperature was 39°C, his pulse rate was 120 beats per minute, his respiratory rate was 34 breaths per minute, and his blood pressure was 80/65 mmHg. An abdominal examination revealed a rigid abdomen with tenderness all over but more pronounced in the left hypochondriac region and the right iliac fossa with absent bowel sounds.\nResuscitation was started immediately as he was deemed critically ill and a candidate for immediate surgical intervention. A sepsis survival campaign was initiated with an oxygen mask. Additionally, two wide bore cannulas were placed and a blood sample was obtained for laboratory investigations. Four units of packed red blood cells were prepared, and broad-spectrum antibiotics along with a bolus of pre-warmed crystalloid solution were administered.\nAfter stabilizing the patient, an abdominopelvic CT scan was performed which showed a grade IV ruptured spleen and acute appendicitis (Figure ). The findings were explained to the patient and his consent was obtained for splenectomy and an appendectomy.\nUnder general anesthesia, the patient underwent a midline laparotomy. Four-quadrant abdominal packing was done after the removal of clots and suction of blood. An emergency splenectomy was performed by dividing the splenic ligament and delivering the spleen to the surgical field where short gastric vessels followed by splenic artery and vein were ligated and divided. Following the splenectomy, an appendectomy was also performed. The appendix was inflamed and contained fecalith. The abdominal cavity was washed out with a copious amount of pre-warmed crystalloid solution. Two drains were placed: one at the splenic bed and another at the pelvis. PDS 0 was used for mass closure of the abdomen.\nHistological analysis of the spleen specimen and appendix showed malaria merozoite-like bodies in addition to the foci of infarcted necrosis, which confirmed malaria and acute suppurative appendicitis and serositis.\nThe patient was then transferred to the intensive care unit where he was kept under strict monitoring of vital signs, blood chemistries, and input-output chart of the nasogastric tube, drains, and Foley catheter. After two days, the nasogastric tube and Foley catheter were removed, where both the splenectomy drain and appendectomy drain were removed on the fourth day. He had a good recovery, and, on the fifth day, he was shifted to the general floor where anti-malaria medications were restarted.\nTable lists the results of the laboratory investigations done at the time of discharge. The patient received pneumococcal vaccination, Haemophilus influenzae type b vaccination, meningococcal vaccination, and was prescribed amoxicillin 250 mg per oral twice daily for one year. |
An anatomical variation in the coeliac trunk, renal and testicular vasculature was observed during routine dissection of the abdominal region of a 27-year-old male cadaver from the Western Cape, South Africa. The formalin embalmed cadaver formed part of a cohort of ten (3 female, 7 male), kindly donated to the Department of Anatomy, School of Medicine, University of Namibia, Namibia.\nThe cause of death was documented as pulmonary tuberculosis with no abdominal pathologies of note. Upon dissection it was found that the mesenteric artery originated from the coeliac artery at T12 (). The coeliacomesenteric trunk presents with a hepato-gastric trunk (circa 2.3 cm in length), splenic artery on the left, and a stand-alone right gastric artery (). The latter supplied not only the lesser curvature of the stomach but also the head of the pancreas and superior part of the duodenum; forming a secondary pancreatico-duodenal supply. Of interest was the hepatogastric trunk further divided into a common hepatic artery (). This in turn divided into a left and right hepatic (with cystic artery) arteries at the porta hepatis (). The gastro-duodenal artery originated from the right hepatic and then descended to the duodenum and pancreas; forming a primary superior pancreatico-duodenal supply (). The inferior pancreatico-duodenal arteries followed its traditional origin form the superior mesenteric arty ().\nAdditional findings in the same cadaver included a bifurcation of the abdominal aorta at L3 and a bilateral double renal arterial supply (). The right pair of renal arteries originated at L1 compared to the left sided pair (L1 and L2) (). The left kidney was slightly enlarged and more inferior, circa 2.5 cm, compared to the right kidney. The left testicular artery originated from the inferior renal artery and this pattern repeated itself on the right (). Of interest was that the right testicular artery passed posterior of the inferior vena cava (). The left renal vein was found to be retro-aortic and received venous blood from the left lumbar veins, posterior of the aorta. The left and right testicular veins drained into the left renal vein and inferior vena cava respectively (). The inferior mesenteric artery when observed, was normal and no other variations were observed. |
We report the case of a 56-years-old Caucasian male a histoty of clear cell renal carcinoma status post right nephrectomy 2 years prior, and who subsequently developed lung metastasis. The patient had progression of disease after several lines of treatment including to sutent, pazopanib and temsirolimus, and he was ultimately started on axitinib 5 mg by mouth twice a day with good initial clinical and radiological response after 1 one month of treatment.He presented to the emergency department of our institution complaining of 3-day-progressive dyspnea on minimal exertion, associated to dry cough and difficulty to speak. Vital signs on admission revealed a blood pressure of 93/59 mmHg, tachycardia, tachypnea, and hypoxemia with oxygen saturation of 90% on room air. Chest examination showed absent breath sounds in the left side of his chest. Chest X-ray (CXR) revealed a left-sided tension pneumothorax, which required thoracostomy by cardiothoracic surgery in an emergent fashion; a new CXR showed complete resolution of left pneumothorax, and for that reason after 3 days the chest tube was removed and the patient was discharged home. Unfortunately the next day he returned to the emergency department with a new onset of shortness of breath and left-sided chest pain; a new CXR showed left recurrent pneumothorax; thus chest tube was inserted again. High resolution CT scan showed biapical bullae and blebs, a small left pneumothorax, subcutaneous emphysema, and a 4.3 × 2.6 cm pneumatocele within the anterior segment of the left upper lobe.\nCardiothoracic surgery decided to perform a left video assisted thoracoscopy with apical blebs resection as a definitive treatment. In the operation room, and after performing a left upper lobe wedge resection of the blebs, reexpansion of the left lung was achieved and it revealed a large left upper lobe air leaking caused by 4 × 3 cm cavitated necrotic tumor at the level of the main pulmonary artery, so the decision was made to proceed with a left thoracotomy. During the procedure it was found that the necrotic mass was not resectable, and for that reason the lesion was covered and repaired via pericardial fat flap placement. Multiple biopsies were taken from this mass, with a final pathology report of a lesion consistent with mRCC with extensive associated necrosis (Figures and ). Postoperative course was also complicated with a left side empyema and new onset atrial fibrillation that were successfully treated and the patient eventually was discharged home. A comparative review of interval imaging studies before- and afteraxitinib use showed an initial 4 × 3 cm mass seen in the same location of this large cavitated necrotic tumor (Figures and ). Apparently this mass transformed into a cavitated tumor after one month of axitinib treatment and caused the recurrent pneumothorax. |
In a 44-year-old female Caucasian patient, adenocarcinoma of the oesophagus located in the gastro-oesophageal junction (33 to 39 cm) was diagnosed in August 2007. The disease was Stage III (T3 N1) because of adventitial involvement and proof of suspectly enhanced mediastinal and paraoesophageal lymph nodes. The patient underwent preoperative (neoadjuvant) chemotherapy using ECF (intravenous epirubicin 50 mg/m2 and cisplatin 60 mg/m2 every 3 weeks at day one respectively, with continuous infusion of 5-FU 200 mg/m2 per day). Three cycles of the intravenous chemotherapy were administered after implantation of a central venous access (,). The tip of the catheter was advanced to the distal part of the superior vena cava (SVC) from the left subclavian vein that was approached by percutaneous implantation using Seldinger technique in local anaesthesia. Following subcutaneous tunnelling the infusion port was embedded in front of the left pectoral muscle fascia.\nThree month following the beginning of the neoadjuvant chemotherapy the patient proceeded to surgery. A proximal gastric resection and transhiatal subtotal oesophagectomy without thoracotomy through median laparotomy and left sided cervical incision was performed. Proximal gastric resection, oesophageal resection and reconstruction were performed in a single operation. The oesophageal substitute was positioned in the posterior mediastinum in the original oesophageal bed (gastric pull-up). Following the gastric pull-up a feeding nasogastric tube was positioned in the substitute and bilateral chest drains were performed. The patient was monitored up to the third postoperative day on the intensive care unit. All drains were gradually removed until the seventh postoperative day. The postoperative course was uneventful, except for a cervical wound healing complication due to a slight leakage of the gastro-oesophageal anastomosis. Temporarily feeding was conducted by nasogastric tube, and the leakage was successively occluded by fibrin sealant via endoscopy. The patient was hospitalised up to the 28th postoperative day. One month following the operation endoscopy confirmed a healed cervical anastomosis. Therefore, the postoperative chemotherapy using ECF was resumed two month after the operation. Because of persistent vomiting and progressive loss of weight the intravenous chemotherapy was terminated after 2 cycles. Three and six months after termination of the oncological treatment, radiologically no recurrence was observed. Endoscopy did also not find any residual disease, anastomotic stenosis or signs of wound healing complications.\nEleven month after termination of the oncological treatment the patient was admitted to our outpatient clinic because of a left sided painful neck mass. The C-reactive protein was elevated up to 155 mg/l (reference range < 5), all other laboratory markers revealed no pathological results. An ultrasonic testing was performed and revealed a thrombosis of the left internal jugular vein due to a bar-shaped intravascular foreign body. Therefore, a computer tomography of the neck and upper thorax was arranged (). CT scan confirmed thrombosis and demonstrated an extension of the thrombus up to the left subclavian vein, which showed proper perfusion. The bar-shaped intravascular foreign body could be revealed as ipsilateral dislocated Port-A-Cath catheter in continuity, whereas a catheter rupture could be excepted. Following preparation of the patient the Port-a-Cath catheter was removed surgically. Preoperatively a bolus of 5000 I.U. of an unfractionated heparin was administered intravenously; subsequently 25.000 I.U. of an unfractionated heparin per day were administered continuously intravenously. From the first postoperative day up to the third postoperative month the anticoagulation was performed orally (Phenprocoumon). The hospitalisation was terminated at the third postoperative day. |
A 57-year-old male patient was diagnosed with malignant melanoma of the right upper arm and treated with wide local excision and sentinel lymph node biopsy. PET/CT performed at the time of surgery did not reveal lymph nodal [] or distant metastatic disease (not shown). Sentinel lymph node biopsy was also negative for metastasis. During the postoperative period, the patient developed wound infection in the right axilla which was successfully treated with debridement and antibiotics. Follow-up FDG-PET/CT scan done after 5 months revealed a new 4.1-cm right axillary mass with moderate FDG uptake (SUVmax = 4.4). Multiple linear radiopaque foci in the surgical bed which were presumed to be surgical clips were seen within the central portion of the mass []. Due to negative sentinel node biopsy at the time of surgery as well as prior history of postoperative wound infection, the increased FDG uptake was attributed to postoperative granulation tissue and less likely due to the development of metastatic disease and a short-interval follow-up examination was suggested. Follow-up scans performed after 2 months did not show significant interval change. As the patient continued to remain asymptomatic and the lesion showed stability over consecutive scans, no intervention was performed and the biopsy was deferred. The patient was then lost to follow-up.\nHowever, 2 years following the initial surgery, the patient returned with discomfort in the axilla and repeat PET/CT was performed. On repeat FDG-PET/CT, the lesion showed minimal increase in size to 4.6 cm and intense FDG activity with SUVmax of 14.4 []. On careful review of the images from the CT portion of the PET/CT, suspicion of retained surgical sponge was raised []. X-rays obtained for confirmation revealed a foreign body with wavy radiopaque hyperdense borders in the right axilla [], consistent with the retained surgical sponge. The diagnosis of gossypiboma was strongly considered and surgical resection was performed. Surgical pathology confirmed the presence of retained surgical sponge with foreign body reaction in the surrounding soft tissues, consistent with gossypiboma. |
A 4-year-old girl was admitted with a 3-year history of a cardiac murmur, and the admission weight was 17 kg. A 3/6 degree of systolic murmur at the third left intercostal space was detected by physical examination, and a perimembranous VSD of 6 mm was revealed by echocardiogram. The girl underwent VSD closure with inferior partial median sternotomy under cardiopulmonary bypass (CPB) at day 4 of hospitalization, and the VSD was closed with three interrupted horizontal mattress sutures. The operation was successful, and she was discharged at postoperative day 10.\nShe was readmitted at 20 days after the first surgery due to a high fever of 40°C at postoperative day 18 with no obvious causative factors and without characteristics of coughing, wheezing, retching, vomiting, or cardiac murmur. The girl showed a slight poor physical development and with no family history of genetic diseases and dysmorphism. She had received antibiotic therapy for 1 day before readmission at the local hospital. Laboratory examination showed that the white blood cell (WBC) count was 5.94 × 109/L, and the percentage of neutrophils was 81.8%. Blood culture showed positive for Staphylococcus aureus. The electrocardiograph showed frequently occurring ventricular premature beat, and ultrasonic cardiogram (UCG) showed a spherical cystic echo (82 × 76 mm) at the anterolateral aspect of the ascending aorta (). Then an emergent computed tomography angiography (CTA) was done which revealed an abnormal 86 × 78 mm echo located at the anterolateral aspect of the ascending aorta with a direct communication to the aorta, and the communicating hole was 8.9 mm in diameter (, ).\nAn emergency operation was performed under deep hypothermia (20°C) with CPB. In detail, the right femoral artery and vein were cannulated using 14# arterial cannula and 19# venous cannula, respectively. Then median sternotomy was immediately performed after the CPB started. We found the pseudo-aneurysm at the anterior mediastinum wrapped with amounts of inflammatory scar and thymus tissue. Because of the giant pseudo-aneurysm and severe surrounding tissue adhesions, there was no sufficient space to place the aortic cross-clamp and cardioplegic cannula needle. Then the patient was rapidly cooled to 20°C, and the heart was arrested, induced by hypothermia, while an ice hat was used to implement brain local mild hypothermia therapy. After the patient was placed in a head-down position, we incised the pseudo-aneurysm rapidly and found an ostium (8 × 9 mm in diameter) in the anterior wall of ascending aorta where the purse-string suture was made during the previous surgery. Cardioplegia solution (St. Thomas solution, 30 ml/kg) was infused directly via the coronary ostia to achieve cardiac arrest. A piece of appropriate size of aneurysmal wall was harvested and soaked in iodophor for 2 min then overlaid with Dacron patch for closing the ostium with continuous suture of 4–0 prolene (). After de-airing, the ostium was closed thoroughly, CPB was resumed, and the patient was warmed. After recovery to normal sinus rhythm, CPB was terminated, and the femoral cannulae were removed. The CPB time was 173 min, and circulatory arrest time was 15 min. After being weaned from CPB, the girl was closed up and returned to pediatric ICU for further therapy. Vancomycin and penicillin were administered intravenously for 10 days according to the results of drug sensitivity test, and then the oral antibiotics were administered until the day of discharge. The girl gradually recovered to asymptomatic condition and was discharged at 47 days after the secondary surgery. We followed up the girl for 2 years; the girl had a weight gain of 5 kg and good appetite that showed she is in good nutritional and well-developmental status. She received UCG and chest radiography examinations during the periodic outpatient reexaminations, and no abnormality was detected. The timeline of the overall therapeutic process is shown as a flow diagram in . |
A 62-year-old Caucasian man, service engineer presented to accident and emergency with sudden onset of low back pain whilst lifting a washing machine at work. Pain radiated to groins and was associated with progressive bilateral weakness with numbness in the legs, with more marked symptoms on the left side. There were no cardiovascular symptoms, and the patient had normal observations. He was previously fit and well. He had no medications. He was a smoker for around 40 years and smoked twenty cigarettes a day. He was referred to the orthopedic team as a possible case of cauda equina syndrome secondary to a prolapsed intervertebral disc.\nNeurological examination revealed profound motor deficit in the legs with Medical Research Council (MRC) grade 2/5 muscle power in the hip flexors and complete paralysis in all other groups distally. All reflexes including the plantar reflexes were absent, and sensation was altered throughout both legs. Sensory and motor functions at level T12 were preserved. Perianal tone and sensation were both markedly reduced and he was unable to feel the passage of a bladder catheter. His vital signs were stable with normal pulse and blood pressure. Complete cardiorespiratory examination was normal and all peripheral pulses were palpable. However, abdominal examination revealed a nontender pulsatile mass.\nBaseline laboratory investigations including Erythrocyte Sedimentation Rate were normal with the exception of a white cell count of 14.4 × 109/Lt. Lumbar puncture was unremarkable. His other blood parameters including LFT, Renal functions and bone profile were normal apart from slight raised cholesterol 6.2(5.3 mmol/lt). Plain radiographs revealed mild degenerative changes in the spine. An urgent MRI scan was requested to rule out caudaequina due to disc prolapse. An MRI revealed () multiple disc protrusions in the lumbar spine, in particular at the L5/S1 level, but there was no evidence of acute cord or caudal compression. The scan also revealed the presence of an abdominal aortic aneurysm eroding the L3 vertebral body. An Ultra sound scan and a subsequent CT scan confirmed the presence of a 6.6 × 5.8 cm infra-renal aneurysm (). Approximately, one third of the aortic lumen was filled by thrombus, but no leak or dissection was noted. A spinal arteriography was done early morning due to nonavailability of the investigation in out of hour's period. A diagnosis of spinal cord infarction secondary to emboli from an infra renal abdominal aortic aneurysm was made on the basis of all the above clinical, diagnostic and radiological tests.\nDecision to repair the aneurysm wad made after multidisciplinary meeting to prevent further neurological deterioration secondary to further embolisation and to avert possible aneurysm rupture. Following the successful repair and an uneventful recovery, the patient was transferred to the regional spinal injuries unit for rehabilitation. At the point of transfer, he had MRC grade 3/5 muscle power in hip flexors, and grade 0/5 power in all muscle groups beyond this. He had a motor and sensory level of T12 and continued to have fecal and urinary incontinence, requiring bladder catheterization.\nFollow up at 6 months showed an improvement in proximal motor function, with normal hip flexion bilaterally and normal knee extension on the right and MRC grade 3 on the left side. MRC grade remained 0/5 distal to the level of L3 bilaterally. Sensory level remained at T12, and whilst perianal sensation recovered, though he remained doubly incontinent. He was classed as having a neurological level of T12 ASIA “C”. |
A 58-year-old male with history of weakness and malaise for 18 months was referred to Shariati hospital. In the initial work up, frequent episodes of hypoglycemia and elevated erythrocyte sedimentation rate were detected (Table ). Chest CT scan showed 2 huge masses located in right hemi-thorax and multiple smaller masses located in the left hemi-thorax (Fig. , ). The histopathological result of core needle biopsy before surgery was in favor of a solitary fibrous tumor. Right posterolateral thoracotomy and resection of 2 huge masses were performed and Permanent pathologic examination confirmed the diagnosis. After surgery, symptoms of hypoglycemia resolved.\nIn spite of recommendations, the patient did not come back for resection of the left hemithorax masses. However, the patient visited our clinic due to hypoglycemic symptoms and dyspnea 2 years later. Imaging study revealed multiple bilateral parenchymal and pleural-based nodules (Fig. , ). He underwent left posterolateral thoracotomy again and 45 masses were excised. Permanent pathology report revealed a pulmonary blastoma (Figs. , ). His symptoms partially resolved and he was referred to an oncologist for adjuvant therapy after 32 days stay in ICU and surgical ward.\nAfterwards the patient’s history and laboratory profiles were reviewed and histology of the right sided tumor was reassessed. It was determined that the correct diagnosis for the right hemi-thorax tumor was PB, similar to the diagnosis for the left hemi thorax tumor.\nTumors causing hypoglycemia can be classified according to their mechanism of action. The first group acts by secreting insulin, Insulinoma is the most prevalent example of this group. The second group acts through secreting insulin-like growth factor. The third group consists of multiple myeloma, lymphoma, and leukemia. The fourth group consists of metastatic neoplasms [].\nTumors secreting insulin-like growth factor are also known as non-islet cell tumor hypoglycemia (NICTH); they can cause hypoglycemia through multiple mechanisms []. They mostly originate in lungs, the digestive system, adrenal gland, the pancreas, or the ovaries []. These groups of tumors frequently appear in the fifth or sixth decade of life. The average length of symptoms can range from a few weeks to a few months []. This patient was in sixth decade of life, when experienced an increase in insulin-like growth factor. Patient’s tumor was relatively large in all stages.\nHypoglycemia in these patients is mostly episodic. Each episode happens as a result of hunger, rather than eating food. Hypoglycemia in this patient was episodic and a result of hunger as well [].\nThe possible pathophysiological causes of hypoglycemia include increases in secretion of IGF, invasion of the liver by a tumor, disruption of counter regulatory mechanisms as a result of adrenal blockage, increase on consumption of glucose by the tumor, and antibodies against insulin and insulin receptors [, ]. In this patient, higher secretions of IGF and an increase in glucose consumption due to the tumor were the causes of hypoglycemia.\nTumors that emit IGF2 (NICTHs) are diagnosed when the following are observed: low serum glucose levels during acute attacks, low levels of insulin and C-peptide in the serum, low levels of growth hormone and the insulin-like growth factor-1, normal or high levels of the insulin-like growth factor-2, and higher relative levels of insulin-like growth factor 2 compared to its counterpart similar to insulin-like growth factor 1 [, , ].\nFrom a biochemical point of view, TIH is widely accompanied by hyperketonemia (<300 micromole/L). In 53 % of cases with NICTH hypokalemia is observed []. This patient had hypokalemia as well. Hypokalemia is caused by the insulin like activities of the insulin-like growth factor 2 (IGF2).\nIn all patients with epithelial or mesenchymal tumors that exhibit neuro psychiatric symptoms, NICTH should be considered []. Our patient reported weakness, tiredness, and excessive sweating. Furthermore, hypoglycemia was observed in the lab report.\nNICTHs have a large domain. 40 % of them have mesenchymal origin; these include mesothelioma, hemangiopericytoma, and sarcomas. Another 40 % have epithelial origin; these include hepatocellular and lung sarcomas. The origins of the remaining 20 % of tumors are unknown [].\nPB is a distinct form of carcinosarcoma which was defined by Adluri []. It can appear as a parenchymal tumor or sub pleural nodules with pulmonary effusion []. In this report, the patient had multiple bilateral parenchymal and subpleural tumors.\nPBs are divided into 3 groups according to their tissue make up. The first group is the monophasic group (good differentiation) which has an epithelial composition. The second group is the classic biphasic group, which consists of both epithelial and mesenchymal components (CBPB). The third group is the pleuropulmonary blastoma; they are tumors specific to childhood and only have mesenchymal tissue [, ]. This patient’s tumor was a CBPB.\nSymptoms of CBPB are similar to symptoms of lower respiratory system infection []. In second visit, the patient’s chief complaint was dyspnea. However, episodic hypoglycemia was a secondary complaint as well. PB can invade the heart, the diaphragm, and the liver []. CX Ray and CT scan can assist in diagnosis. Functional imaging methods are inefficient at recognizing relapse and metastasis in NICTH []. Immunohistochemistry has a vital role in recognizing CBPB [, ]. Despite the new techniques for diagnosis, correct recognition before surgery is still difficult [, , , , ]. In this patient, accurate diagnosis was reached after the second surgery.\nIn both surgeries, the majority of the tumor was removed during the operation, resulting in the disappearance of hypoglycemia. Approximately 2 years after the first operation, the symptoms returned. However, the removal of the tumor during the second surgery resulted in the disappearance of symptoms again. The hypoglycemia was accompanied by low serum insulin, IGF-1, and C-peptide levels; Therefore, it may have been caused by increased glucose consumption of the large tumor and excretion of IGF-2 by the tumor. However, it is not possible to confirm this hypothesis at this time, as there were no methods available to measure blood IGF-2 levels.\nMedical treatments for NICTH include diazoxide, octreotide, glucagon infusion, steroids, and recombinant growth hormone. Glucose tablets can be prescribed as well []. However, the definitive treatment is surgery [, , ].\nSurgical treatments for NICTH include complete removal of the tumor, or debulking accompanied with radiotherapy and chemotherapy [, , ].\nGlucocorticoids are the most effective method of long term management [, ]. The hypoglycemia can be controlled through chemotherapy, radiotherapy, and embolization with various success rates []. PBs are fast growing tumors with poor prognosis [, ]. Factors that illustrate the poor prognosis in adult PBs include relapse, metastatic illness, larger than 5 cm tumor, and lymphatic system involvement [, , ].\nThe effectiveness of chemotherapy and radiotherapy is unknown. However, due to the metastatic nature of this patient’s illness, he was referred for adjuvant treatment. In previous reports chemotherapy has been recommended in cases of metastasis [, ]. Overall, studies regarding the effects of chemotherapy and radiotherapy are scarce, but some researchers have reported the effectiveness of using platinum [].\nIn locally advanced tumors, mediastinal lymph node involvement, or metastatic cases chemotherapy / radiotherapy can be used. Chemotherapy’s effect on treatment is limited [, ].\nIn our patient, 40 months have passed since the beginning of illness. After 2 surgeries the tumor is currently under control with the help of chemotherapy. |
A 40 -year-old male patient, nondiabetic, nonsmoker and normotensive was presented with the history of persistent pain along the dorsal surface of right foot, which was aggravated with the activities. Conservative management was tried for 8 months without much relief. Diagnosis of ATTS was made on clinical examination. Nerve Conduction velocity (NCV) showed decreased conduction in deep peroneal nerve and stress test was positive. Patient was planned for operation. Under spinal anesthesia, the body part was prepared and tourniquet inflated. Intraoperatively, thrombosed dorsalis pedis artery was found along with two adjacent collateral vessels (, , and ). Retinaculum was released and nerve was mobilized. No adherence with the surrounding structures was found. Tight compartment got released. Upon deflating the tourniquet blood flow in the collaterals was checked, which was adequate. Dorsal pulsation was felt too. No excision was done. Wound was closed and the patient was followed up in outpatient department. Over 9 months of follow up, no recurrence of any symptoms was noted.\nTarsal tunnel corresponds to the carpel tunnel in the limb counterpart. Tight compartments exert pressure over the nerves resulting in the compressive neuropathies. Tarsal tunnel syndrome as the name suggests relates to the tightening of the inferior extensor retinaculum of the foot. It causes compression over the deep peroneal nerve resulting in the spectrum of symptoms. Numerous factors have been described to cause this compression. Intrinsic factors mentioned in the literature are due to osteophytes, ganglionic cysts or lipomas. These factors cause compensatory forefoot valgus leading to subtalar supination and midtarsal inversion leading to the pressure over the nerve.\nDistally the nerve is vulnerable to injury due to lack of protective sheath. Extrinsic factors like tight shoe laces or the external trauma can cause injury to the nerve. Edema or fibrosis causes pressure over the nerve and neural ischemia. The relation of nerve with the tendons and the vascular structures is depicted in . The little space in the tunnel formed by the inferior extensor retinaculum and the close proximity of the structures make the nerve vulnerable to compressive neuropathy. In an already small space, any addition to the structure can cause pressure over the nearby structures. The final brunt is to be burnt by the nerve, as happened in our case.\nThe patient had trivial trauma at the ankle, which can cause thrombosis at the dorsalis pedis artery. Over time, the collaterals had developed to compensate for the dysfunctional arterial segment and to bypass it. Addition of new vessels in the already tight tunnel had resulted in the pressure over the nearby structures, including the nerve. The mixed sensorimotor nature of the deep peroneal nerve leads to both sensory and motor symptoms as in our case. |
An otherwise healthy 45-year-old man sought orthopedic evaluation in December 2014 after experiencing 2 years of worsening right thigh pain. MRI at that time displayed a large, heterogeneous, contrast-enhancing lesion involving the distal right femoral metadiaphysis extending through the cortex into the anterior compartment without skip lesions. The patient was referred to a comprehensive cancer center for evaluation by a dedicated, multidisciplinary sarcoma service. An open biopsy was then performed, providing a tissue diagnosis of fibroblastic osteosarcoma. A CT of the chest and a whole-body bone scan completed the staging. The chest CT revealed two 2-mm, indeterminate nodules in the lungs, and the bone scan demonstrated radionuclide absorption at the site of the distal femoral lesion alone. Two weeks after presentation to the cancer center, the patient began neoadjuvant chemotherapy with doxorubicin, cisplatin, and high-dose methotrexate. He completed the neoadjuvant chemotherapy regimen according to the AOST 0331 protocol and had restaging studies prior to planned local control with wide surgical resection and limb salvage. No new sites of disease were noted and the lung nodules were stable. Surgical resection and endoprosthetic reconstruction with a compressive osteo-integrative device (Compress, Biomet) occurred 4 months after initial presentation. Pathologic assessment of the resected specimen revealed high-grade fibroblastic osteosarcoma with 60% necrosis. Unfortunately, malignancy-positive surgical margins were identified, and the patient underwent revision resection 1 month later; the re-resected specimen was reported to be negative for residual tumor.\nOn the first postoperative surveillance scans, 3 months after local control, chest CT revealed multiple new lesions throughout the lungs bilaterally, consistent with metastatic osteosarcoma. These nodules were <6 mm in dimension and were therefore not amenable to biopsy. In light of the poor necrosis rate and the patient's poor tolerance of neoadjuvant chemotherapy but the development of pulmonary nodules, the potential benefit of continuing the AOST 0331 treatment was discussed. Alternatives were explored, including gemcitabine/doxetaxol, ifosfamide/etoposide, or pazopanib. Despite the presence of concerning pulmonary nodules, the patient opted to hold on to additional medical treatments until demonstration of further progressive disease. At this same time, the patient experienced a twisting mechanism of injury to the operative extremity, resulting in failure of the connection between the compress endoprosthesis device and the host bone. This was addressed surgically with revision of the orthopedic construct, changing the Compress device to a cemented, stemmed prosthesis.\nEight months later, 15 months after initial presentation, the CT demonstrated enlarging nodules, now numbering 12 lesions measuring 1–2 cm, and new interstitial edema. Concurrently, a mass was noted at the distal femur surgical site, concerning for local recurrence. Both the thigh mass and the pulmonary masses were biopsied, and were histologically consistent with osteosarcoma. The patient began pazopanib treatment, having refused more aggressive medical regimens due to prior intolerance of the AOST 0331 protocol. He tolerated pazopanib well and, after 6 months of pazopanib therapy, patient underwent LLL and LUL pulmonary wedge resections without complication. Pulmonary metastatic disease continued to progress, and the patient underwent RLL and RUL wedge resections 5 months after the left. Amputation of the lower extremity had been discussed with the patient, but was delayed until the end of medical treatment in order to assess disease response. During consultation for the above knee amputation, now 27 months after presentation, the patient complained of abdominal pain. On detailed history and physical exam, it was noted that he had been having fever for 3 days to 39°C, sharp abdominal pain, nausea, loose stools, decreased appetite, and insomnia. He was admitted to the hospital and a CT of the abdomen was obtained. It revealed peritoneal thickening, ascites, small bowel obstruction, omental stippling, hepatic lesions, and bilateral adrenal nodules (Fig. ). A biopsy of the colon at the hepatic flexure showed malignant cells within the lamina propria with similar morphology to the original osteosarcoma specimen. There was no overlying epithelial dysplasia or keratin expression within the cells, arguing against a new colorectal primary tumor. Biopsy of an omental nodule demonstrated similar histologic features, confirming metastatic osteosarcoma. Abdominal symptoms were addressed with colonic stenting and palliative paracentesis, but the patient declined precipitously and ultimately developed tachycardia, lactic acidosis, and leukocytosis, succumbing to sepsis 4 weeks after onset of abdominal pain, 28 months after initially presenting with thigh pain. |
A 42-year-old male presented to our care in April 2018 for evaluation of excessive daytime sleepiness experiencing since childhood. In addition to EDS, the patient described falling asleep at a moment's notice especially after entering a state of extreme relaxation. According to the patient, he has experienced sleepiness while driving typically when stopped at a traffic light. Over the years, sleepiness while driving led to multiple motor vehicle accidents and latest accident occurred in early April 2018 requiring a visit to the emergency room. During this visit, his history of multiple motor vehicle accidents due to excessive sleepiness were documented resulting in his driving privileges being suspended until an appropriate evaluation with a sleep specialist. In addition to feeling sleepy, he reported experiencing probable episodes of cataplexy triggered by laughter mostly at comedy clubs. In light of these complaints, the patient was sent for a further workup including the STOP-BANG test (snoring, tiredness, observed apnea, blood pressure, body mass index, age, neck circumference and gender) and the Epworth Sleepiness Scale (ESS). In addition, a nocturnal polysomnogram (NPSG) and a multiple sleep latency test (MSLT) were also completed.\nThe STOP-Bang questionnaire is the best validated tool for screening obstructive sleep apnea (OSA) patients for preoperative risk and includes eight questions which are answered with a Yes or No. Scores of 3 to 4 are classified as an intermediate risk whereas score of ≥5 represents high risk of postoperative complications including extended hospital stay. Clinical evidence suggests that a score of ≥3 out of 8 is highly sensitive for diagnosing OSA []. Our patient scored 6 out of 8.\nThe ESS is a subjective test utilized to measure patient’s sleepiness. It includes eight scenarios in which the patient rates their tendency to become sleepy on a scale of 0 (no chance of dozing), 1 (slight chance of dozing), 2 (moderate chance of dozing), and 3 (high chance of dozing) []. These eight scenarios are sitting and reading, watching television, sitting inactive in a public place, as a passenger in a car for an hour without a break, in a car while stopped for a few minutes in traffic, lying down to rest in the afternoon, sitting and talking to someone, and sitting quietly after a lunch without alcohol. Our patient scored 22 which is highly associated with pathologic sleepiness because a score of greater than 15 suggests that the patient is excessively sleepy and should be treated [,].\nNocturnal polysomnogram (NPSG) is a sleep study which records brain waves, oxygen levels, heart rate and breathing patterns along with eye and extremity movement as the patient sleeps [,]. According to the results of NPSG, the patient slept 380.5 minutes out of 435.0 minutes in bed for a sleep efficiency of 87.47%. His sleep latency was recorded at 21.0 minutes with persistent sleep of 21.0 minutes. In addition, REM sleep and latency were logged at 16% and 98 minutes, respectively. Furthermore, the sleep study illustrated that the patient experienced 33 obstructive apneas, zero central and mixed apneas, 201 hypopneas, and apnea-hypopnea index of 36.9 events/hour; consistent with severe OSA. It is important to note that the patient's body mass index (BMI) was recorded as 40 (kg/m2) which is associated with morbid obesity.\nAn MSLT is the primary diagnostic tool for narcolepsy and is typically performed following an NPSG to measure sleep latency []. Sleep latency can be described as amount of time it takes to go from wakefulness to entering sleep. In addition, it also measures sleep onset REM periods (SOREMPs) which illustrates how quickly the patient enters REM sleep. This test typically includes four or five naps lasting for 20 minutes each. Results of the MSLT consisted of four nap trials with a sleep latency of 0, 3, 0 and 6.5 minutes, respectively and a mean sleep latency of 2.4 minutes. Furthermore, results indicated one SOREMPs by our patient which was achieved in the second nap. The diagnostic criterion requires an MSL of ≤8 minutes and ≥2 SOREMPs on an MSLT for an objective diagnosis of narcolepsy [].\nBased on the workup, the patient was diagnosed with narcolepsy which has been successfully managed with 4.5 g of sodium oxybate taken at bedtime and repeated 3 to 4 hours later. Furthermore, addition of 10 mg dextroamphetamine taken twice a day has worked well for this gentleman. In addition to narcolepsy, the patient was treated for obstructive sleep apnea with continuous positive airway pressure (CPAP) which has provided tremendous additional clinical benefit to the patient allowing him to obtain more refreshing sleep. On a follow-up visit, data from the patient’s CPAP download, set at 5-15 cm of water (cmH2O), proved patient’s compliance of 93.3% of the nights with more than 4 hours of usage. Moreover, the patient’s Apnea Hypopnea Index (AHI) dropped to 2.2 events per hour sleep, which is within the normal limits []. |
A 15-year-old girl was referred to a pediatrician due to repeated episodes of palpitations, dizziness, and presyncope (Table ). Seven months prior, she experienced chest discomfort and palpitations followed by syncope while walking. She had a history of post-traumatic stress syndrome but was free from pharmacological therapy. Family history with regard to cardiac disease was unremarkable. Twelve-lead ECG was normal except for frequent monomorphic PVCs (Figure ). Echocardiography ruled out structural heart disease. A 24-hour ambulatory ECG showed sinus rhythm with more than 20,000 monomorphic PVCs with left bundle branch block morphology in V1-V2 and electrical inferior frontal axis between 90° and 120°. During a bicycle exercise testing, the number of PVCs decreased when heart rate elevated. A Holter recording four months later revealed 86 episodes of monomorphic nonsustained VT (NSVT) with the same morphology as the PVCs in the initial Holter recording were detected. There were no late potentials in a signal-averaged ECG. The patient had no further syncope but continued to experience palpitations and metoprolol 100 mg once daily was started to alleviate symptoms. After this, she was lost to follow-up for four years due to social factors.\nShe was mainly asymptomatic during these years but at an age of 18 she experienced a single episode of palpitations during pregnancy. Her heart rate was irregular but no ECG was taken. A cesarean section was performed without complications. Two years later during her second pregnancy, she was referred to the cardiology clinic due to frequent palpitations. During a 24-hour ambulatory ECG monitoring, the longest NSVT was 12 beats at a rate of 200 beats per minute. After childbirth, she was assessed at a tertiary center with cardiac magnetic resonance that was normal except for an area that was 2 mm in diameter in the right ventricle with increased adipose tissue. This was deemed not diagnostic for arrhythmogenic right ventricular cardiomyopathy, and no arrhythmias were inducible in an electrophysiological study (EPS).\nPalpitations continued despite beta-blocker therapy, and three years later, the patient received an insertable cardiac monitor. A few months later, she had recurrent syncope and several episodes of rapid NSVT up to 33 beats were revealed. EPS was repeated and a short run of VT arising from the RVOT was induced. This was not reproducible and ablation could not be performed. Instead, flecainide 100 mg twice daily and sertraline 50 mg once daily was initiated due to palpitations and anxiety, respectively. Arrhythmia symptoms were ameliorated by flecainide, but the medication had to be stopped due to visual adverse effects. Thereafter, the patient was referred to another tertiary center for a third EPS and ablation. However, 5 days later recurring NSVT returned. Intravenous amiodarone decreased the frequency and duration of the VTs, but the patients remained highly symptomatic, and she was transported with airborne ambulance back to the tertiary center for reablation. Despite several ablations in the RVOT, the arrhythmia did not stop and antiarrhythmic medication was reinitiated. Four months later, she presented to the emergency department with electrical storm due to repeated episodes of sustained monomorphic VT (Figure ), which terminated following intravenous amiodarone.\nAfter washout of antiarrhythmic medications, a fifth EPS was performed with ablation in the RVOT but arrhythmia remained after the procedure. It was decided to refer the patient to a tertiary arrhythmia center in Finland. In the initial EPS in Tampere University Hospital, neither PVCs nor any VT was detected and no ablation was performed. However, during the following night the patients had frequent PVCs and multiple VTs. She was taken back for EPS in the next morning. Electroanatomical mapping using remote magnetic navigation revealed slightly earlier activation in the aortic root between the right and noncoronary cusp than in the RVOT area. Pace map in this site was excellent. Following ablation in this site, VT stopped but the PVCs did not disappear despite multiple ablations. Mapping of the distal coronary sinus and left ventricular outflow tract was not successful, whereas remapping of the RVOT revealed early activation and good pace map. Upon ablation in the RVOT (Figure ), PVCs disappeared and no VT was inducible at programmed ventricular stimulation. The patient was discharged two days later with no symptoms. During the seven-year follow-up period after the last ablation, she has had sporadic PVCs from another focus but no sustained or nonsustained VT has been detected by the insertable cardiac monitor or by ECG. |
A 57-year-old female presented with multiple skin colored asymptomatic lesions developing over face since the age of 3 years. The lesions gradually increased in size and number and by the age of 25 year involved entire face including bilateral ears along with the loss of eye brows. The lesions also involved the bilateral upper limbs and upper chest since 2-3 years. About 6 months previously, two lesions, one on forehead and other on the nose, had shown rapid growth. The female had no significant history of any drug intake or radiation exposure. There was a family history with her father having similar lesions.\nOn local examination, patient's skin showed multiple skin colored to yellowish nodules varying in size from 0.5 × 0.5 to 1.5 × 1.5 cm coalescing with each other involving the entire face including bilateral ears and upper eyelids []. Few lesions over forehead, nose and cheek were crusted and surrounded by zone of telangiectasia along with loss of eyebrows. Similar lesions of size 0.5-0.8 cm were present over bilateral upper limbs, chest, back and scalp. General examination was normal with no lymphadenopathy. Radiographic studies were unremarkable. Subsequently, biopsies were performed from the lesions over forehead, nose and left cheek.\nMicroscopic examination of lesions from forehead and left cheek revealed similar appearance which showed basaloid tumor islands, horn cysts filled with keratin and papillary mesenchymal bodies, with diagnosis consistent with trichoepithelioma []. However, the lesion from nose revealed a different microscopic appearance and represented by cells similar to those described earlier, although with irregular and voluminous nuclei with frequent mitotic figures. The tumor islands showed retraction pockets and peripheral palisading in some areas along with areas of follicular differentiation represented by tumor islands with keratinous material in the centre. We considered the differential diagnosis of malignant transformation of trichoepithelioma and basal cell carcinoma.\nImmunohistochemical stains including BCL-2, CD34 and Ki-67 were applied on these malignant tissue sections. The basaloid tumor islands showed diffuse positivity for BCL-2 whereas the peritumoral stromal cells were negative for CD34, positive in the endothelial lining of the blood vessels []. Ki-67 proliferative index was high being more than 10% []. Based on the light microscopic and immunohistochemical study, a final diagnosis of basal cell carcinoma was made. The malignant lesion was excised with wide margins and there was no evidence of distant metastasis. The patient is on regular follow-up every 6 months. |
The patient was a 65-year-old woman who presented with a 1-month history of bloody stool. A digital colonoscopy with biopsies revealed adenocarcinoma in the sigmoid colon. The patient elected to undergo primary laparoscopic colon resection, and the procedure was reported to be uneventful. However, on the 6th postoperative day, the patient noticed a large amount of yellow fluid coming out of a left side abdominal drain. The fluid appeared to be urine. An abdominal ultrasonography showed a collection of fluid in the patient's pelvis. A contrasted computed tomography (CT) scan showed contrast extravasation in the pelvis and around the descending colon (). The patient had decreased serum protein and albumin; however, complete blood count, creatinine, liver functions, and urine analysis were normal. On the 8th postoperative day, the patient was taken to the operating room for a ureteroscopy. The ureteroscopy revealed that the left ureter was completely severed about 4 to 5 cm from the ureteral orifice (, transected distal end of the ureter). The bowels could be seen through the ureteroscope (, intraabdominal cavity with bowels seen through the distal end of the transected ureter). No other obvious injury was identified. With patience, persistence, and some difficulty, the severed upper end of the ureter was identified and entered (, the proximal end of the transected ureter). We estimated that there was a 3- to 4-cm gap between the two ends of the ureter. Two 0.035″ guidewires were first passed, followed by the placement of two 4.5F Double-J ureteral stents. After placing the Double-J stents, the abdominal drainage quickly subsided. An abdominal ultrasonography 6 days after tube placement showed complete resolution of the abdominal fluid collection. The abdominal drain was removed and the patient was discharged. At the 3-month follow-up, a repeat CT scan showed no hydronephrosis, no abdominal fluid collection, and no contrast extravasation. The patient, however, had an asymptomatic urinary tract infection from Klebsiella pneumoniae, which was treated and resolved. A follow-up ureteroscopy over a guidewire showed excellent healing and realignment of the disrupted ureter. The only obvious sign of the transacted ureter was that the mucosa was paler than normal. Because of this unconventional treatment, we decided to continue stenting the ureter with two fresh 4.5F Double-J stents for an additional 4 weeks. Stents were removed 4 months after the injury. Follow-up contrast-enhanced CT scans taken 8 and 14 months after the initial endoscopic treatment showed mild but unchanged residual dilation of the renal pelvis and ureter with good drainage. There were no other abnormalities. |
A 70-year-old male patient presented to our institute with a midline abdominal swelling of ~6 month’s duration, clinically palpable over his epigastric region. He had no abdominal pain and the mass appeared to be increasing in size causing him discomfort. There was no history of trauma and the swelling appeared to be an incisional hernia, clinically replete with a positive cough impulse. He had a previous open mesh herniorrhaphy in the same area over a decade earlier. He had no other herniae clinically on his abdominal wall or his groin.\nHis medical history was significant for hypertension and alchoholism and both were well controlled. Radiological imaging included a computerized tomography (CT) scan which reported an internal hernia in the epigastrium (Figs and ). There were no radiological signs of bowel strangulation.\nAfter an extensive discussion with the patient and his wife he agreed to a diagnostic laparoscopy with a view to reducing the hernia and repairing the mesenteric defect. Intra-operatively there was no internal hernia. A mass was seen in the epigastrium on the anterior abdominal wall (Fig. ). The lesion could not be mobilized laparoscopically so the decision was made to convert to a laparotomy (Fig. ). The lesion in the anterior abdominal wall was then mobilized and excised.\nClinically it appeared to be a lipoma (Figs and ). The patient’s post-operative course was stormy with an iatrogenic small bowel perforation which necessitated a repeat laparotomy and bowel repair. He subsequently developed an aspiration pneumonia, requiring an intensive care unit (ICU) admission and total parenteral nutrition (TPN). Five days after his relaparotomy he developed a wound dehiscence that was managed with a vacuum assisted closure (VAC) device (Fig. ).\nFour weeks later he was discharged home and his VAC dressing was managed via homecare nursing.\nHe eventually made a complete recovery and his wound dehiscence closed 3 months later (Fig. ). The pathology report confirmed the lesion as a myelolipoma with adipocytes and trilineage haematopoeitic cell lines (Fig. ). |
A 49-year-old Caucasian lady with history of polysubstance use disorder and related complications including, recurrent cutaneous abscesses, spinal diskitis and septic thrombophlebitis presented to the emergency room with complaints of intermittent fevers and right hip pain. A month prior to the presentation, she had left another hospital against medical advice after being diagnosed with Methicillin-resistant Staphylococcus aureus bacteremia and right hip septic arthritis. Post discharge, she was off antibiotics, but continued heroin and methamphetamine and was taking multiple dose of ibuprofen in addition for pain control. On admission, her physical exam was notable for severe tenderness in her right hip, marked bilateral lower extremity edema and multiple deep, circular, punched-out looking atrophic scars involving all extremities at prior skin popping (subcutaneous injection of illicit drugs) sites. Pertinent laboratory data included chronic anemia with a hemoglobin of 9.8 g/dL, WBC count of 10.23 k/uL and a platelet count of 395 k/uL. She had negative HIV, Hepatitis B antibodies and elevated Hepatitis C antibody with undetectable Hepatitis C viral load. Her basic metabolic profile noted a sodium of 140 mmol/L, potassium of 3.5 mmol/L and a creatinine of 2.9 mg/dL (estimated glomerular filtration rate of 17 ml/min) which was a significant rise from the normal creatinine levels a month earlier. Her urine analysis noted >500mg/dL proteinuria with a protein/creatinine ratio of 28.25. She had no monoclonal proteins on serum or urine electrophoresis. CT scan of her right hip noted marked degenerative changes in the right hip, with right acetabular protrusion and cortical disruption of the medial acetabular wall. She was diagnosed with right hip osteomyelitis and was in acute renal failure with evidence of nephrotic range proteinuria. She was placed on antibiotics (daptomycin) and underwent hip arthroscopy with irrigation and debridement along with lavage shortly after admission. Differential diagnoses considered for her renal disease included acute tubular necrosis due to sepsis, post infectious glomerulonephritis, focal segmental glomerulosclerosis associated with heroin use, acute interstitial nephritis from NSAIDs and membranoproliferative glomerulonephritis associated with Hepatitis C. She underwent a renal biopsy which revealed acute tubular necrosis and secondary (AA) amyloidosis with the classic apple green birefringence when stained with Congo red () and positive immunohistochemical stain for serum amyloid A protein (). Two weeks after admission she underwent Girdlestone arthroplasty. During the hospital stay, she developed intermittent hypotension, had evidence of primary adrenal insufficiency attributed to amyloidosis and was initiated on steroids. She was discharged home after completion of prolonged antibiotic therapy with daptomycin and was maintained on oral doxycycline. She was referred to outpatient opioid treatment program. Eight months after her admission, she remained committed to be off all illicit drugs and underwent right total hip replacement. Her creatine levels normalized (estimated GFR of 82 ml/min) but she continued to have proteinuria from renal amyloidosis (protein/creatinine ratio of 28.25) and required diuretic therapy for symptomatic management of her edema. |
In December 2006, a 31-year-old woman was referred to a neurologist because of consciousness disorder and fainting. Her main problems were obesity, snoring and waking up with a feeling of suffocation in the middle of sleep. The intraoral examination showed a large soft palate (). The soft palate was scored as class III according to the Mallampati classification (visualization of the soft palate and the base of the uvula) []. The electroencephalogram (EEG) showed focal dysrhythmia during hyperventilation with scattered sharp waves (). The patient was depressed and had sleep disorders such as sleep apnea and myoclonus, especially at the onset of sleep. She had experienced several occurrences of complete loss of consciousness during swimming and at work. The patient was on anticonvulsants and antidepressants (at first, she had been prescribed with Lamotrigine for 5 months, but later she was given 500mg Sodium valproate per day).\nOne of the best treatments for snoring during sleep is UUUP. The success rate of this type of surgery is reported to be between 16% and 83% [].\nWe chose a minimally invasive surgical procedure for the present case since the patient had a proper facial profile and a large soft palate (class III according to the Mallampati classification) [].\nIn May 2007, after analyzing the lateral cephalogram, we evaluated the craniofacial and pharyngeal airway morphology before the surgery. Under general anesthesia, 1cm of the soft palatal mucosa, from the right tonsil to the left tonsil, was removed. The patient’s tonsils were also removed during the surgery, and the anterior and posterior tonsillar pillars were sutured together ().\nThe symptoms were significantly decreased after the recovery. The patient no longer had sleep apnea, and antidepressants and antiepileptic drugs were discontinued. After the surgery, sharp waves were detected on the EEG at the level of the trachea (), but the patient was clinically asymptomatic. The 10-year follow-up showed no symptoms of sleep apnea or seizure. The patient did not lose any weight during the follow-up period. |
The patient was a 65-year-old woman who presented with a 1-month history of bloody stool. A digital colonoscopy with biopsies revealed adenocarcinoma in the sigmoid colon. The patient elected to undergo primary laparoscopic colon resection, and the procedure was reported to be uneventful. However, on the 6th postoperative day, the patient noticed a large amount of yellow fluid coming out of a left side abdominal drain. The fluid appeared to be urine. An abdominal ultrasonography showed a collection of fluid in the patient's pelvis. A contrasted computed tomography (CT) scan showed contrast extravasation in the pelvis and around the descending colon (). The patient had decreased serum protein and albumin; however, complete blood count, creatinine, liver functions, and urine analysis were normal. On the 8th postoperative day, the patient was taken to the operating room for a ureteroscopy. The ureteroscopy revealed that the left ureter was completely severed about 4 to 5 cm from the ureteral orifice (, transected distal end of the ureter). The bowels could be seen through the ureteroscope (, intraabdominal cavity with bowels seen through the distal end of the transected ureter). No other obvious injury was identified. With patience, persistence, and some difficulty, the severed upper end of the ureter was identified and entered (, the proximal end of the transected ureter). We estimated that there was a 3- to 4-cm gap between the two ends of the ureter. Two 0.035″ guidewires were first passed, followed by the placement of two 4.5F Double-J ureteral stents. After placing the Double-J stents, the abdominal drainage quickly subsided. An abdominal ultrasonography 6 days after tube placement showed complete resolution of the abdominal fluid collection. The abdominal drain was removed and the patient was discharged. At the 3-month follow-up, a repeat CT scan showed no hydronephrosis, no abdominal fluid collection, and no contrast extravasation. The patient, however, had an asymptomatic urinary tract infection from Klebsiella pneumoniae, which was treated and resolved. A follow-up ureteroscopy over a guidewire showed excellent healing and realignment of the disrupted ureter. The only obvious sign of the transacted ureter was that the mucosa was paler than normal. Because of this unconventional treatment, we decided to continue stenting the ureter with two fresh 4.5F Double-J stents for an additional 4 weeks. Stents were removed 4 months after the injury. Follow-up contrast-enhanced CT scans taken 8 and 14 months after the initial endoscopic treatment showed mild but unchanged residual dilation of the renal pelvis and ureter with good drainage. There were no other abnormalities. |
A 6-year-old boy had a history of gingival overgrowth, which had been present since the boy’s first tooth erupted at 6 months of age. The painless overgrowth of the gingiva progressed slowly causing no discomfort up to the age of 6 years, when the esthetic appearance also became intolerable. No other complaints were noted. The child was systemically healthy and was the only child of two healthy non-consanguineous parents. Similar findings or a history of such findings were not identified in either the parents or their relatives.\nOral cavity examination showed severe gingival enlargement involving both the mandibular and maxillary arches and was particularly prominent over the anterior regions (Fig. ). The patient’s gingivae seemed to have slight redness and mild edema, with absence of normal stippling. The oral hygiene was poor due to the formation of pseudopockets containing large amounts of dental plaque and a small amount of calculus. As a result, the marginal gingiva was slightly inflamed. Apart from gingival enlargement, other mucosal lesions such as submucosal deposits or thickening, were not observed. Radiographical examination revealed no periodontal bone destruction.\nThe routine hematological and biochemical test results were unremarkable and initial phase therapy was administered. The gingival enlargement was not alleviated after the gingival inflammation was controlled. Gingivectomy was performed, and the wound healing was uneventful. Tissue specimens obtained during gingivectomy were sent for histopathologic examination. Hematoxylin–eosin (HE) staining revealed a hyperplastic epithelium, mild inflammatory cell infiltration, proliferation of the capillary layer, and an increase in the amount of fibrous tissue (Fig. A, B). This result did not indicate a definitive diagnosis. Meanwhile, recurrence of gingival enlargement occurred 1 week after the gingivectomy. Since this child presented with gingival enlargement as the only clinical manifestation and showed no other systemic involvement, the diagnosis proved difficult. Hence, genetic tests were performed.\nTrio whole exome sequencing (WES) of DNA isolated from peripheral blood was performed at the Chigene Translational Medicine Research Center Co. Ltd. (Beijing, China). Detailed methods of genetic tests are provided in the supplementary information (Additional file ). Genetic analysis revealed compound heterozygous mutations of ANTXR2 in this patient: c.524G > A (p.Cys175Tyr) in exon 6 and loss of exons 1 and 2. The patient’s father had a heterozygous ANTXR2 mutation, loss of exons 1 and 2, and his mother had a heterozygous ANTXR2 mutation, c.524G > A (Fig. ). The mutation in exon 6 of ANTXR2 was further verified via Sanger sequencing, and the loss of exons 1 and 2 in ANTXR2 was further verified by quantifying the copies of exons 1 and 2 via quantitative real-time polymerase chain reaction assays (Fig. ).\nGenetic analysis confirmed the diagnosis of HFS. Therefore, further physical, radiographic, and histopathologic examinations were performed after a literature review. No skin lesions or joint contractures were observed. Skeletal radiography showed no abnormalities of the bilateral distal humeri, radii, ulnae, carpal bones, metacarpals, distal femurs, tibiae, fibulae, metatarsi, and phalanges. The gingival-specimen sections were stained with periodic acid Schiff (PAS) and Congo red. Deposits of an amorphous, homogeneous, and PAS-positive hyaline substance were found in the lamina propria and perivascular spaces (Fig. C, D). The hyaline substance could not be stained with Congo red.\nBased on the clinical presentation and genetic analysis results, the child was diagnosed with HFS of grade 1. A treatment plan, including regular periodontal debridement, oral hygiene motivation, and gingivectomy when necessary was proposed. As HFS is a progressive disease, and manifestations tend to be additive over time, the child was referred to a pediatrician for regular follow-up considering the possibility of systemic involvement in the future. |
On June 16, 2020, a 39-year-old male patient was admitted to our hospital following 2 days of seizures that were preceded by 15 days of fever and headache. The patient denied having any prior psychiatric or other diseases. His neck was slightly stiff, and there were suspiciously positive bilateral Kernig's signs. On day 2 of hospitalization, the initial MRI examination showed FLAIR hyperintensities in the cortex and meninges of the bilateral frontal, temporal, and parietal lobes; the abnormalities were also clearly visualized on T1-weighted post-gadolinium-enhanced images (). The patient was considered to have developed a central nervous system (CNS) infection and was given empiric antibiotic and antiviral therapy, but his condition steadily worsened, suggesting that there may be other underlying etiologies (e.g., autoimmune encephalitis or tuberculous meningoencephalitis). After considering the pros and cons, we administered high-dose immunoglobulin treatment, and the patient's symptoms rapidly improved. The second MRI examination on day 8 demonstrated mildly regressed meningo-cortical lesions, but abnormalities were still observed (). No other test results (listed in ) supported the existence of autoimmune encephalitis or a CNS infection. We did not prescribe corticosteroid therapy due to concern about unknown infections. After further observation, the third MRI examination conducted on day 24 showed that the meningo-cortical lesions had decreased but were still clearly observable (). At that time, the patient exhibited good recovery except for mild palpitations and insomnia, and he was discharged on day 30 of hospitalization without a definite diagnosis.\nOn August 9, 2020, he was followed-up at our outpatient clinic and reported that the vision in his left eye was severely impaired. This symptom first manifested ~1 month earlier, but it was mild and he did not seek medical help. A fourth MRI examination was immediately conducted and showed that the meningo-cortical lesions were reduced compared, but new lesions were present in the right parietal lobe, right cerebellar dentate nucleus, and left optic nerve (). At this point, we realized that a demyelinating CNS disease was responsible for the symptoms. The patient refused hospital re-admission, further examinations, or further high-dose immunoglobulin therapy due to economic reasons, so we prescribed low-dose corticosteroid therapy. The patient's visual acuity was considerably improved after treatment, which he decided to discontinue after ~1 month. On December 19, 2020, the patient complained that his left visual acuity had again deteriorated, and he was re-admitted to the hospital. A fifth MRI examination showed that the original lesions were diminished, but new lesions had developed around the deep white matter (). A cell-based assay for serum anti-MOG-IgG was positive, and the final diagnosis was MOGAD. The patient accepted high-dose corticosteroid treatment, and his left visual acuity gradually improved. The sixth and final MRI examination was conducted on January 8, 2021 and showed substantial reductions in the original lesions without new lesion formation (). The patient was discharged on January 13, 2021. At the time of writing, he had remained in generally good condition.\nIn addition to the above MRI examinations, the patient also underwent a series of other tests at different time points that were crucial for diagnosis. The relevant details are listed in the timeline in . |
A 29-year-old man, a former semiprofessional handball player, had a traumatic rupture of the proximal side of the patellar tendon of the left knee in 2016 during a match. No associated disease was reported. Primary surgery was performed in another health facility through a median approach using 2 anchors for tendon repair protected by an additional ipsilateral semitendinosus graft (patellar and tibial tunnels). The patient came to our health facility following severe functional deficits after an iterative rupture without having experienced any new trauma 13 months after the initial surgery. The iterative rupture of the knee extensor mechanism was also an iatrogenic fracture of the transverse patellar tunnel (). Clinically, walking was not possible, there was a lack of active extension and hemarthrosis with pain. There were no scar problems, no signs of deep or superficial infection, and no cutaneous wound. A huge gap was clinically observed between the patella and the patellar tendon. Considering the patient's age, his preinjury sports level, and lack of active extension, the decision was made to perform a revision procedure. An artificial ligament (LARS®) and two adjustable loops, free ends of the PULLUP® BTB (SBM SAS, France), were used to enhance the patellar tendon repair.\nA preoperative lateral standard X-ray was taken of the contralateral knee at 30° of flexion to measure the Caton-Deschamps index and patellar height (). The patient was placed in a supine position under general anesthesia with a tourniquet at the proximal part of the thigh. The previous median approach was used. The patellar fracture and the site of the previous rupture were cleaned to remove fibrous tissue and hematoma. Previous anchors were left in place.\nThe first step was to place the ligament advanced reinforcement system (LARS® polyethylene terephthalate fibers 6 mm ref. L030307 ACFAR 32 CK). A new transverse tunnel was drilled in the tibia, distally to the tibial tunnel of the initial surgery, with a 5.5 mm drill, and the LARS® was inserted in the tibial tunnel. The artificial ligament was then passed through the lateral retinaculum and above the patella at the junction with the quadriceps tendon in a Pulvertaft manner and through the medial retinaculum to return to its origin (). Two longitudinal tunnels were drilled in the patella using a 2.4 mm drill. The loops of a PULLUP® BTB (the plate was removed from the device) were first passed into the patellar tendon and then into the patella through the two longitudinal tunnels using a shuttle relay. Next, the free ends were pulled down in the opposite patellar tunnels. At the proximal side of the reconstruction, the two free ends of the PULLUP® BTB were inserted into each braid to close the system (Figures and ). The distal and medial ends of the LARS® were tightened with a clamp in order to restore normal patellar height and secured with 2 staples. Then, the 2 PULLUP® BTB loops were tightened (). The previous tendon rupture was closed and reinforced with separate X-knots using absorbable sutures. The skin was closed. The knee was placed in an articulated brace with compressive ice therapy for 24 hours, and a postoperative X-ray was taken ().\nFor postoperative care, weight bearing was not allowed for 6 weeks and mobilization of the knee was immediately started between 0 and 45° for 3 weeks then from 0 to 90° from 3 to 6 weeks. No complication was reported during the postoperative period. At 3 months, the patient was pain free and could walk without the aid of crutches. He was able to resume handball practice at 6 months after a control MRI. At one-year follow-up, he was able to play handball with complete knee extension strength (compared with the contralateral side) and was able to return to a semiprofessional level. The range of motion of the knee was 0-0-130°. The MRI at 1 year showed complete healing of the patellar tendon and the bone (). |
In 2002, a 35-year-old male patient presented with multiple discharging sinuses on face for three years. Three years back, the patient had met with a vehicular accident which leads to lacerated wound on right side of face. Few weeks after the accident, the patient noticed pimple-like lesion at the site of wound. These lesions did not respond to local medications, rather went on increasing in number and size, and he went to a surgeon who excised the wound but the lesions recurred. Six months back, he was seen by a dermatologist and was diagnosed to have actinomycosis and was put on injection procaine penicillin for one month without any significant improvement. When the patient approached us, there were multiple tender fluctuant abscesses and discharging sinuses involving the frontal, temporal and small part of maxillary region with swelling of eyelids of right side []. However, there was no induration which is so characteristic of actinomycetoma. There were no grains.\nLooking at this picture, the differential diagnosis considered were actinomycosis, tuberculosis and osteomyelitis and the patient was further investigated. Blood count, blood sugar, urine analysis were within normal limits. ELISA for HIV was negative and X-ray of skull showed no bony involvement ruling out the possibility of osteomyelitis. Gram staining of the pus showed Gram positive branching filaments which on modified Zeil-Nelsons staining (decoloring with 1% H2SO4) showed partial acid fastness indicating Nocardia []. The diagnosis was confirmed when culture on L- J media grew dry granular pigmented colonies characteristic of Nocardia species. So the patient was put on tab septran (trimethoprim 160 mg + sulfamethoxazole 800mg) - 2 tablets BD. and Incision and drainage of some abscesses was also done. After one and a half month, the patient showed good improvement but lost to follow up. When he came again in 2007 for unrelated problem (T.Cruris), the face showed healed deep scars []. On enquiring, the patient reported to continue the same treatment for further two months and as all the lesions were healed, he did not turn up for follow up. |
An 84-year-old Caucasian female with a past medical history of hypertension, hypothyroidism, and chronic low back pain presented for an exacerbation of her low back pain. Before her hospitalization, she had been managing her low back pain with opioid analgesics and physical therapy at a skilled nursing facility for the prior four weeks. She was scheduled to see Neurosurgery in the outpatient setting, but her back pain became more severe. It progressed to the point that she could no longer sit nor ambulate without being in severe pain. Her back pain worsened with any movement, particularly while flexing forward, and radiated down the posterior aspect of the right leg in the S1 dermatome. She denied any numbness or tingling, and no saddle anesthesia or any acute bowel or bladder changes were noted. The extent of pain was truly debilitating, requiring hospitalization. She underwent a workup that included a magnetic resonance imaging (MRI) scan of the lumbar spine, which did not reveal any significant finding, and an MRI of the abdomen and pelvis, which revealed a severe bilateral SIF with grade 2 anterolisthesis of S1-S2 (Figure -). A subsequent computed tomography (CT) scan revealed bilateral L5 transverse process fractures, diffuse bone demineralization, and comminuted SIFs through the bilateral sacral ala with malalignment at the S1-S2 level (Figure -). Bone scintigraphy (Figure ) was obtained of the bony pelvis, which demonstrated an H-shaped increased uptake in the bilateral sacral ala and the anterior aspects of the sacrum. This situation would typically disable a patient and, in this age group, likely contribute to mortality. Surgical intervention was recommended to prevent further debilitation and aid in a return to former ambulatory status. Following the surgical intervention, she could ambulate on postoperative Day 1, with only mild discomfort. She returned to the skilled nursing facility to finish her rehabilitation and regained most of her preinjury level of function. She was ambulating independently and with no pain at her six-week postoperative follow-up. She experienced no complications from the surgery, nor did she experience the common complications of prolonged immobility associated with SIFs.\nThe surgical decision-making was complex, and several factors had to be considered. First, the author did not feel a sacroplasty was sufficient to fixate the sacral alar fractures and address the S1-S2 unstable anterolisthesis. Additionally, although commonly performed, sacroplasties are not FDA-approved and are considered “investigational.” Iliosacral screw fixation is another surgical technique to treat sacral fractures. The author was concerned about the patient’s bone quality and about the fact that a simple screw fixation would not be strong enough to stabilize the fractures adequately. With bilateral alar fractures in the sagittal plane and a dislocation of S1-S2 in the horizontal plane, the surgeon was looking for the strongest construct possible; yet, he wanted a less-invasive option to minimize surgical time and morbidity.\nThe lead author decided to perform a bilateral iliosacral fixation using the triangular titanium implants (iFuse implants from Si-BONE, San Jose, CA) commonly used for minimally invasive sacroiliac (SI) joint fusions. The shape of these implants is felt to be superior to standard threaded screws. The design of these implants also allows for the passage of a kyphoplasty needle (Kyphon Express from Medtronic, Dublin, Ireland) through the central cannulation. This permits the direct injection of polymethylmethacrylate (PMMA) through the iFuse implant into the sacral ala, providing additional fracture augmentation and implant strength.\nThe patient was positioned in the standard prone position on a Jackson operating table. She was prepped from hip to hip. A C-arm was used to mark the one-inch skin incision bilaterally, following the posterior sacral line on lateral fluoroscopy. After the skin had been incised, Steinmann pins were placed through the lateral ilium across the SI joint and into the sacral ala. After each pin had been placed, a three-dimensional image was obtained using the O-arm (Medtronic, Dublin, Ireland) to assess the pin position and make sure it crossed the alar fracture line. Next, the drill-guide was placed over the pin, resting on the lateral ilium. The implant length was then measured, and the implant trajectory was drilled over the pin. After the drilling, a triangular channel was created using the implant broach. The iFuse implant (Si-BONE, San Jose, CA) was then inserted and tapped into position. Three implants were placed on each side. Two implants were intentionally placed above the S1-S2 interspace, and the third inferior implant was placed below the transverse fracture line. After the implants were placed, a Kyphon Express needle (Medtronic, Dublin, Ireland) was placed through the central cannulation of each implant. Approximately 2 ml of PMMA was injected into the medial ala through each implant under live fluoroscopy. Several times during the cement delivery, a C-arm radiograph was obtained to make sure the cement did not undergo extravasation nor violate the S1 neuroforamen. This created a solid construct, fixating the sacrum securely to the ilium. The intraoperative C-arm fluoroscopic radiograph is shown in Figure . |
A 75-year-old male was admitted to the Thoracic Surgery Department in order to undergo an elective left lung upper lobe resection for a moderately differentiated lung adenocarcinoma. Patient medical history included diabetes mellitus, hypertension and dyslipidemia under medication. Moreover, the patient was a heavy smoker (140 Pack/Years). One year ago, he presented to his general practitioner (GP) suffering from cough, anemia, fatigue and weight loss of 12 kg during 3 months. The patient eventually underwent computed tomography (CT) scan, bronchoscopy and tumor biopsy, and he was diagnosed with a moderately differentiated lung cancer, stage IIIa, T3N2M0 according to seventh edition of the TNM staging system. T3 was attributed to tumor size (maximum diameter 10.8 cm) and N2 to metastasis to inferior mediastinal (subcarinal) lymph node according to the initial CT scan. The patient subsequently underwent six cycles of chemotherapy with pemetrexed and carboplatin. After that, a new CT scan, a fluorodeoxyglucose (FDG) uptake positron emission tomography (PET)-CT scan and a transthoracic echocardiogram were performed in order to evaluate tumor stage following chemotherapy. The tumor at that time was staged T3N1M0. Size was decreased (maximum diameter 9 cm) but remained T3, while only ipsilateral hilar lymph nodal metastases but no mediastinal nodes were found (downgrade to N1). Additionally, there was close proximity of the tumor to the aortic arch, but vessel wall invasion was not evident according to the radiology report (). Therefore, the patient was scheduled for left upper lung lobe resection.\nUnder general and thoracic epidural anesthesia, a left anterolateral thoracotomy was performed. In the left lung apex, the tumor was strongly adhered to the thoracic wall and the aortic arch and it seemed to invade the superior pulmonary vein, although this was not evident on the CT scan. Ligation of pulmonary vein and complete resection of tumor due to aortic arch invasion were not possible, so the tumor was considered nonresectable and thus resection was not attempted. A specimen of tumor adjacent to aortic arch and lymph nodes were resected for histopathological examination.\nWhile still in recovery, the patient complained of sudden onset of lower back pain and paralysis of the lower limbs. Initially, symptoms were attributed to epidural anesthesia, but subsequently the lower limbs became pale and cold and vascular consultation was requested. On clinical examination, arterial pulses of bilateral femoral, popliteal, dorsalis pedis and posterior tibial arteries were absent and there was no blood flow on handheld Doppler examination at the ankle level. The patient immediately underwent a CT angiography that revealed thrombosis of the infrarenal aorta in the presence of atherosclerotic lesions of the iliac arteries bilaterally ().\nThe patient was emergently taken back to the operating theater where bilateral femoral artery thromboembolectomies were performed. Although thrombus was removed after multiple embolectomies, blood flow was not adequately restored. Since arterial inflow was inadequate while the patient had just undergone a thoracotomy, it was decided to proceed to revascularization of the lower limbs with a subclavian-bifemoral bypass, in order to avoid a second major abdominal procedure. The bypass was performed with a Dacron 8-mm ringed graft. Femoral pulses were restored and postoperative ankle-brachial index was 0.6 on the right side and 0.85 on the left side which were similar to preoperative recordings.\nPostoperatively, the patient was transferred to intensive care unit (ICU), hemodynamically unstable with metabolic acidosis due to prolonged ischemia. The postoperative course was unfavorable and patient died on the fifth postoperative day due to multi-organ failure caused by reperfusion syndrome.\nHistopathological characteristics of thrombus obtained during embolectomy (–) were consistent with the histopathology of the biopsy of the primary lung tumor (–). The histopathology of the fraction of tumor adjacent to aortic arch revealed invasion of aortic adventitia (–). |
A 60-year-old woman was referred to the Department of Oral and Maxillofacial Surgery of the University of Ribeirão Preto (UNAERP) because she had displacement of three dental implants into the maxillary sinus, two of which were in the right sinus and one was in the left sinus. According to the report, the patient underwent surgery for implant placement in the maxilla 8 months ago. Three months after the surgery, she began to report pain and felt pressure in the premolar region, particularly on the right side. The patient also had pain on palpation of the anterior wall of the right maxillary sinus, with no sign of oroantral fistula ().\nAfter examination of panoramic radiography, two similar images of dental implants were noted in the right maxillary sinus with evidence of sinusitis, including opacification of the maxillary sinus. On the left sinus, the same image pattern, corresponding to a dental implant, was found; however, no sign of sinusitis was found. Computed tomography (CT) showed implants displaced into the maxillary sinus cavity with a significant opacification of the right maxillary sinus; however, the left sinus did not present the opacification; only the implant did (Figures and ).\nSurgical Procedure. The patient was operated under local anesthesia (Figures and ). An oral antibiotic prophylaxis (amoxicillin + clavulanate, 2.0 g) was administered 1 h prior to start of the procedure. The surgical intervention began with the Caldwell-Luc access bilaterally and the elevation of a trapezoidal full-thickness mucoperiosteal flap. The buccal aspect of the flap was raised to access the maxillary sinus bony wall. A low-speed straight hand piece with a circular diamond bur was used to perform spherical osteotomy. The Schneiderian membrane was perforated and removed through the bone window to gain full access into the sinus cavity (Figures and ). Immediately thereafter, the implants were identified and removed with a surgical aspirator and a Kelly clamp (Figures and ). In the right maxillary sinus, the inflammatory tissue was removed and the surgical field was irrigated with sterile saline in both maxillary sinuses. After irrigation, a porcine collagen membrane (Geistlich Bio-Gide, Switzerland) was installed in the lateral bone window to protect the sinus cavity (Figures and ). After irrigation of the surgical field with sterile saline, the surgical flap was sutured (Figures and ), and an antibiotic therapy with amoxicillin and clavulanate (1.0 g) was prescribed in association with a nonsteroidal anti-inflammatory drug every 8 h for 7 days. Chlorhexidine mouthwashes were used along with usual oral hygiene for 7 days. The patient was instructed to avoid using a mucosupported prosthesis for 15 days to prevent suture dehiscence. The postoperative recovery was uneventful. After 7 days, the patient returned to the university for suture removal and clinical examination. Twelve months after the procedure, a CT scan showed the maxillary sinus without the opacification, with no sign of sinusitis (Figures –). The patient is being regularly monitored for future rehabilitation of the edentulous area. The Helsinki declaration was followed in this case report. |
A 40-year-old male with a 20-year history of schizophrenia presented to the emergency department with long history of pharyngeal foreign body sensation which had progressed over one month to include sore throat, odynophagia, and dyspnea. Physical exam revealed asymmetric prominence of the right posterior oropharyngeal wall and trismus with maximal interincisural distance of two centimeters. There were tenderness, edema, and erythema of the right submandibular triangle without palpable mass.\nFlexible laryngoscopy showed fullness of the right posterior pharyngeal wall without mucosal abnormality, resulting in anterior displacement of the right aryepiglottic fold. This was encroaching on the airway but not causing critical airway stenosis. A computed tomography (CT) scan of the neck with contrast was obtained. This demonstrated a linear opacity extending from the oropharynx to the right thyroid ala. Reconstructed 3D images showed a uniform mass consistent with a foreign body (). Further psychiatric history was obtained and revealed a history of auditory hallucinations that had on several occasions led to suicide attempts, including one attempt two years ago in which the patient stabbed himself in the pharynx with a broken toothbrush handle. Prompt removal was recommended given risk for infection and airway compromise.\nThe patient was transorally intubated over a flexible bronchoscope and then underwent direct laryngoscopy. Swelling of the right posterior oropharynx and hypopharynx was noted (). An anterolateral neck incision was made and subplatysmal flaps were raised. The mass was easily palpated overlying the right thyroid ala, and blunt dissection allowed entry into the fibrous capsule surrounding the foreign body (). The capsule was opened, and the foreign body was removed. The length corresponded exactly to the length of the foreign body on the CT (). A sample was obtained for bacterial culture, the wound was irrigated, and a drain was placed. The patient was extubated and given a soft diet.\nVisual inspection and pathologic analysis confirmed that the foreign body was indeed a toothbrush handle. Cultures from the area grew heavy mixed bacteria including anaerobes. After an uneventful postoperative stay, the patient was discharged without complications. Discharge planning included psychiatry follow-up. |
A 42-year-old female presented to the ENT department with a short history of severe breathlessness and stridor for 7 days with no history of hemoptysis, chest pain, or change in voice. She gave a history of being operated for uterine fibroids 2 months ago following which she had developed disseminated intravascular coagulation and septicaemia, for which she remained intubated and ventilated for 20 days. Indirect laryngoscopy showed normal vocal cords. Fibreoptic bronchoscopic examination under local anesthesia (performed in a reclining position) preoperatively revealed a tracheal stenosis and computerized tomographic scan (CT) confirmed it to be at the level of lower border of T3. The length of the narrowed segment was 8 mm with an anteroposterior diameter of 0.53 cm []. A diagnosis of tracheal stenosis following prolonged endotracheal intubation was made and anticipating the need for CPB during surgery, the patient was referred to the CTVS department for tracheal resection and end-to-end anastomosis.\nPhysical examination revealed severe respiratory distress. The respiratory rate was 35--40/min, patient had stridor, and was unable to lie supine. She was somewhat comfortable at a reclining position of 60--70°. There was no swelling in the neck, she had an adequate mouth opening with a Mallampati grade I. All routine hematological and biochemical laboratory tests were within normal limits. Arterial blood gas analysis (ABG) was also acceptable with oxygen saturation of 90% and respiratory alkalosis when breathing room air. Institution of CPB via femoral route under local anesthesia was considered necessary, but was not executed due to technical difficulty posed by the patient not being able to lie supine. Hence, as in the first patient, it was planned to perform sternotomy in the reclining position using inhalational anesthetics. A thoracic epidural catheter was inserted before anesthetic induction in the sitting position at the level of T3--T4 (0.2% of ropivacaine with fentanyl was administered epidurally). The patient was managed similar to the first patient using inhalational anesthetics (oxygen, nitrous oxide, sevoflurane) supplemented with fentanyl (1 μg/kg), ketamine (0.5 mg/kg), and midazolam (1 mg). Intermittently, ventilation was assisted using bag-mask ensuring adequate ventilation parameters of EtCO2 (from 35 to 40 mm Hg) and oxygen saturation (>92%). After the swift establishment of CPB (around 10 min) via mid-sternotomy, a cuffed endotracheal tube (7.5 mm) was negotiated up to the stenosed portion and secured. Fiberoptic bronchoscopy was performed through the endotracheal tube to visualize the position of the tube and the site of stenosis. Resection of the stenosed area with end-to-end anastomosis was performed under CPB and endotracheal tube was repositioned beyond the anastomosis before separation from the CPB. Total duration of surgery was 200 min with CPB time of 140 min. The patient was electively ventilated and weaned off after 72 h. |
A 69-year-old Japanese woman with a right cementless THA undertaken 44 months previously had a right femoral shaft fracture. She recalled that she experienced acute pain in her right thigh while standing. She believed that the fracture occurred at that point in time, after which she fell down. Thus, it was not a result of trauma.\nRadiographs (Figure ) showed a noncomminuted transverse fracture located at the tip of the stem as well as localized periosteal thickening of the lateral cortex in the distal fragment. The fracture was complete, extending through both cortices, and was associated with a medial spike in the proximal fragment. There was no apparent loosening of the THA components. A radiograph taken at the 3-year follow-up of THA (8 months before the fracture) shows no abnormal findings (Figure ).\nAt 15 years prior to this episode she had been diagnosed with dermatomyositis and subsequently developed interstitial pneumonia. Prednisolone and immunosuppressants (azathioprine, cyclosporine, tacrolimus) were used to treat her dermatomyositis and interstitial pneumonia. She had been on home oxygen therapy for the past 3 years. THA of her right hip had been performed to treat hip joint destruction caused by avascular necrosis of the femoral head induced by steroid use.\nAt admission, her height was 153.5cm, and she weighed 41kg. Her body mass index was 17.4kg/m2. She was a prior smoker, having stopped 21 years ago. She did not drink alcohol. She had other past medical histories. Hemi-thyroidectomy was performed for a thyroid tumor 23 years ago, and she took thyroid hormone preparation. She also had necrotizing fasciitis of the anterior cervical region that had spread from a gingival abscess 7 months ago. In addition, she underwent total hysterectomy, although she did not remember exactly when it took place. She had been taking an anti-hypertension drug and an H2 blocker for some time.\nShe had been on alendronate for at least 7 years. Her oral surgeon discontinued it 7 months prior to this fracture. It was replaced by activated vitamin D and vitamin K to treat her osteoporosis. The bone mineral density examined after the fracture of the left femoral neck was 0.644g/cm2, which is 82% of the young adult mean. Radiographs and magnetic resonance imaging revealed no abnormalities in her contralateral femur.\nWe performed open reduction and internal fixation using a locking plate. We chose a reversed locking compression plate for the distal femur (LCP-DF; Synthes, Tokyo, Japan) for the contralateral side and an LCP cable system (Synthes). We judged that some fracture gap remained after the reduction and fixation, and so placed a small amount of β-tricalcium phosphate bone substitute to fill the gap. Autologous bone grafting was not performed. Bone healing progressed with time, and bony union was obtained 6 months after the surgery (Figure ).\nShe regained the ability to walk, although her activity was limited by her comorbidities, especially interstitial pneumonia. The latest follow-up was performed 2 years after the fracture surgery. She had no pain in her right hip joint or thigh. She could walk with a cane at home and used a wheelchair outside the home. A radiographic examination revealed no displacement or loosening of the implants, and the fracture site had remodeled well (Figure ). |
A former healthy 19-year-old male began suffering from 1 to 2-week long episodes (with regular 4–5 week intervals) where he was without any energy and could not attend school or do his daily routines. During the episodes he had difficulty in concentrating, slowness of thought, decreased short time memory, reduced physical energy, and feeling of derealization. He described himself being like a zombie or in an unreal state. The patient was examined by a psychiatrist both during and between the episodes, which did not reveal any psychiatric disorder. There was no history of drug abuse.\nBesides sleeping during the episodes he could at best watch a simple television program. He became extremely irritable when his parents pressed him to do anything. He spent most of his time in his bedroom and slept for 14–20 h/day for 1–2 weeks. During the episodes, he preferred to be in the dark and avoided communication with other people, even his best friends. Interestingly, he had almost no memory of the episodes. Between the episodes, he was perfectly normal, attending school without difficulty, and playing golf at a high level. During the episodes, his parents had to wake him up to give him food. He went self to the bathroom, but otherwise he stayed in bed. The attacks started relatively quickly, under a few hours and resided under a few hours. During the attacks he did not eat excessively and there were no signs of hypersexuality. No relative has suffered from a similar condition. Extensive psychiatric examination did not reveal any signs of psychiatric disease or depression. There were no signs of epilepsy. Somatic and neurologic examination was normal. Magnetic resonance imaging was normal. Extensive blood tests were normal. EEG showed some hypoactivity in the frontal-lobes, but no signs of epilepsy. At first, lamotrigine was titrated up to 100 mg twice daily and maintained for a few months without any effect. After 2 years his treatment was changed to lithium and serum levels kept between 0.6 and 0.9 mmol/l. Since then he has not had an attack for 3 years. He tolerates the medication well and has not wanted to stop the treatment. |
A 68-year-old asthmatic male patient presented to our center with 12 days history of melena. He denied any previous episode of melena or hematochezia or bleeding from another site. The patient did not have any other associated symptom, and had no other co-morbidities, or medication use. Upon referral, he was uncomfortable and looked pale. He was vitally unstable, with a blood pressure of 90/60 mmHg and a pulse rate of 120 beats/min. The examination revealed the presence of clotted blood on the anal verge, and some tarry stool on digital rectal examination. The hemoglobin level was 7.7 g/dl, the hematocrit was 22.8, and the blood urea nitrogen was 8 mg/dl. The prothrombin time and the partial thromboplastin time were normal.\nResuscitation was performed with transfusion of 2 units of packed red blood cells and intravenous fluids. He was admitted to the ICU for intensive monitoring. After admission and stabilization, upper and lower endoscopies were performed without demonstrating the bleeding site. They only revealed clotted and red blood throughout the colon.\nTechnetium-labeled red blood cell bleeding scan was done to localize the site of bleeding. This scan showed no evidence of early focal increased uptake in the abdomen to indicate active gastrointestinal bleeding during early images, but in the delayed images, it revealed that there was a focal uptake in the right and transverse colon. After that, capsule endoscopy was also performed without findings. As the angiography became available, the patient underwent selective angiography without findings noted at that time. These tests were inconclusive because they were performed while the episodes of bleeding ceased.\nAfter 8 days of conservative management and negative investigations to define the cause of the bleeding, a sudden drop in hemoglobin level from 10.8 mg/dl to 6.9 mg/dl occurred over 12 h, which mandated operative management. Exploratory laparotomy was performed. Extensive jejunal saccular pouches were found 10 cm distal to duodenojejunal junction extending 1.6 m distally Fig. . The bleeding was difficult to control and the decision to clamp the major branched was performed. Division of the small bowel proximal and distal to the diseased part using gastrointestinal stapler was performed with side to side primary anastomosis Fig. . The specimen was a part of small bowel, 117 cm in length, with congested wall and multiple pouches at the mesenteric site. Opening of the specimen showed normally looking mucosa with active bleeding that stopped after awhile. No polyps or masses were detected. We reviewed the angiography achieve after that and a suspicious shadow reflecting the diverticular outpouching was detected.\nMicroscopic examination of the specimen revealed many diverticula; some of which being true diverticula, while the others are devoid of muscularis propria (false diverticulae). Within the diverticula and in the intervening portions of the bowel wall, there were numerous dilated thick- and thin-walled small blood vessels in the submucosa. Additionally, submucosal intermediate-sized vascular clusters and feeder vessels in the muscularis propria and serosa were present. The overall features were those of small intestinal diverticulosis and arteriovenous malformations. The latter involves the diverticula and intervening portions of the bowel wall Fig. .\nPostoperatively, the patient was doing well, discharged home on day 5 postoperatively, with an uneventful postoperative course. He was followed up 2 years after that without complications. |
A 17-year-old Motswana boy of the Tswana ethnic group with a primary school education was brought to our psychiatric hospital with a 5-year history of tobacco smoking and delinquent behaviors. He is the first in a family of three children; both his parents are alive but separated. He lives with his mother who is of low socioeconomic status; she has a busy schedule and works full time. There is no history of mental illness or substance abuse in the family. He was observed at the age of 11 years to exhibit conduct disorder behaviors such as disobedience, stealing, truancy, and hanging out with “street kids.” He was first introduced to tobacco smoking by his friends at age 12 years. He started with a Peter Stuyvesant (nicotine content of 1.3 mg/cigarette) brand of cigarette which was initially unpleasant; however, he continued with persuasion from his friends. He gradually stepped up his use from one cigarette/day over the next 2 to 3 years to approximately 20 to 30 cigarettes per day to sustain the relaxing and stimulating effect which improved his daily performance. He admitted to craving for this substance to the extent of doing dirty jobs for people to sustain the habit and neglecting other previous forms of enjoyment, such as watching television with family members. He has had several unsuccessful attempts at controlling the amount he took in a day despite the knowledge of its harmful consequences. His longest period of abstinence was 3 months in a rehabilitation center which was approximately 3.5 years ago. He had once experimented with cannabis and alcohol, but he never enjoyed these substances and so did not continue.\nTwo months prior to his index presentation at our hospital, he progressively neglected his personal hygiene and food, became emaciated, and spent more time cigarette smoking (that is, smoking continuously); he decided to seek medical attention at this time.\nThere were no psychotic symptoms on admission, but he was very restless, irritable, and had intense craving for this substance. In addition he complained of headache and insomnia.\nHe has had no previous treatment or admission for any psychological disorder and was never on any psychotropic medication before his index presentation at our hospital. A year after he started smoking cigarettes, his mother decided to seek spiritual help when he was observed to be smoking cigarettes at the expense of other activities, pilfering, and playing truant, but there was no significant improvement. His cigarette smoking subsequently became excessive over the next 6 months and he consequently started neglecting his personal hygiene, withdrawing from family activities, and preferring to smoke cigarettes rather than eat; thus, he was becoming emaciated. As a result, his mother was advised to try a rehabilitation center. He spent 3 months in a rehabilitation center 3 years prior to his presenting at our hospital. He went through drug education, counselling, and was abstinent for only this period. He had neither psychotic nor mood symptoms before or during the period of rehabilitation, and did not experience any abnormal movement. He only complained of restlessness and tension; nevertheless, he was not placed on any medication other than multivitamins. While he was in the rehabilitation center, he was completely abstinent and his appetite and weight improved considerably. On leaving the rehabilitation center, he attended follow-up only once before he defaulted. Afterwards, he went back to smoking cigarettes and has had no period of abstinence until his index admission to our mental health facility.\nBefore he started smoking cigarettes, he was described as an easy child, quite cheerful, and an outgoing person who enjoyed the company of other children.\nA mental state examination at his index admission to our hospital revealed agitation, but there was no abnormality of speech, thought, or perception. He described his mood as fine, but objectively it was anxious.\nA physical examination revealed no significant abnormality. His blood pressure was 110/70 mmHg, pulse rate was 90 beats/minute, and his temperature was 37 °C. Investigations such as full blood count, liver function test, thyroid function test, as well as computed tomography (CT) scanning of his brain revealed no significant abnormality. Urine drug screening was negative for substances which included cannabis, cocaine, and phencyclidine, except for benzodiazepines, which was given to reduce restlessness and to improve sleep.\nThe working diagnosis made was mental and behavioral disorder due to psychoactive substance use; nicotine dependence with comorbid conduct disorder.\nThree days postadmission, he was observed to be having some abnormal involuntary movement such as occasional chewing movements, trunk twisting, and truncal tremor. During an interview he tried to conceal the involuntary movements of his hands by holding his chair with a firm grip. According to the nurses’ reports, these movements often disappeared during sleep and briefly whenever his attention was called to them. He admitted to the fact that he first experienced these movements approximately 2 years ago and has also observed their disappearance whenever he smokes. This claim was supported following some relief which he experienced with nicotine gum (Nicorette); an offer which he previously refused.\nHe was on admission for 4 weeks with scheduled sessions with a psychologist on drug counselling and education. In addition he was placed on diazepam 10 mg on the first night and twice daily for 5 days in addition to nicotine gum which was made available to him on demand.\nHis level of hygiene as well as his appetite improved approximately 2 weeks after admission in response to therapy. In addition, his abnormal movements reduced after 3 weeks on nicotine gum after which he was discharged home with the gum. He was to continue with monthly psychological sessions on an out-patient basis since there was no formal rehabilitation program in the facility. He was seen only once on follow-up during which it was noted that he did well on nicotine gum without any adverse effect. His appetite, level of hygiene, and weight were also well maintained but he then defaulted. |
A 62-year-old woman presented with intermittent generalized abdominal pain without radiation for 10 days. The pain was aggravated by movement and associated with 2 episodes of nonbloody, nonbilious emesis, and 2 episodes of watery nonbloody diarrhea after which she stopped passing both stool and gas. She denied any constitutional symptoms. There was no personal history of recurrent infections or family history of primary immunodeficiency diseases.\nThe laboratory evaluation revealed a leukocytosis of 17.0 × 109/L. Her chest radiograph was unremarkable. A computed tomography scan of the abdomen and pelvis with contrast showed diffuse small bowel enhancement and bowel thickening sparing the large bowel, and fluid was also noted in Morison’s pouch with small loculated fluid collections within the pelvis. A diagnosis of spontaneous bacterial peritonitis (SBP) was concluded, and the patient was started on ciprofloxacin and metronidazole. Her blood cultures grew Gram-positive cocci in pairs and chains and a Streptococcus pneumoniae urine antigen was positive. The patient was switched to ceftriaxone, but a repeat CT scan of the abdomen revealed increased multiloculated fluid collections prompting the placement of 3 image-guided peritoneal drains. The cytology of the collected fluid was exudative in nature, but the fluid was negative for abnormal cells or organism growth. S. pneumoniae DNA was detected with 16s rRNA primer set within the peritoneal fluid confirming the diagnosis of S. pneumoniae-induced peritonitis.\nDue to the presence of S. pneumoniae SBP, further evaluation for immunodeficiency was explored. HIV antigen/antibody screen was negative. The serum immunoglobulin studies were within normal limits with IgG 1190 mg/dL, IgM 197 mg/dL, and IgA 197 mg/dL. Her B cell phenotype and IgG subclasses are reported in . There was no decrease in IgG subclasses 1 to 4. Her B cell phenotype showed a relative decrease in non-switched memory B cells and relative increase of transitional B cells and plasmablasts. The impaired antibody response to 23-valent pneumococcal polysaccharide vaccine (PPV23) is shown in , suggesting the diagnosis of a specific antibody immunodeficiency (SAD). In addition, the patient did not respond to subsequent vaccination with streptococcus pneumoniae conjugate vaccine (PCV13). |
A 68-year old man complained about swallowing difficulties in December 2011 and visited a nearby clinic in February 2012. He was referred to our department in March 2012 because of a suspected hypopharyngeal tumor. According to the patient's previous medical history, he suffered from hypertension, had smoked 15 cigarettes per day for 50 years, and consumed alcohol at the rate of 3 L of beer per day. During the initial examination, a tumor lesion was found on the posterior wall of the hypopharynx (). Enlargement of bilateral retropharyngeal lymph nodes was seen on computed tomography (CT), whereas on magnetic resonance imaging (MRI), lesion infiltration from the posterior wall of hypopharynx to the prevertebral muscles was observed (). Squamous cell carcinoma was identified on the basis of biopsy findings, and stage IVb, T4bN2cM0 posterior hypopharyngeal wall carcinoma was diagnosed.\nRadical CCRT was performed from April to June 2012. The total radiation therapy dose was 70 Gy, which included a dose of 40 Gy to the whole neck field, followed by an additional 30 Gy to the primary tumor and involved lymph nodes. Cisplatin (70 mg/m2) plus 5-fluorouracil (700 mg/m2 per day for 5 days) was administered in 2 courses. The lesion disappeared after treatment completion, but the dysphagia did not improve. The patient was discharged after a jejunostomy was established.\nAfter discharge, the patient was followed up and TS-1 was administered as maintenance therapy; however, he experienced a sore throat in November 2012 (5 months after completing CCRT). A recurrence was suspected because visual examination had revealed necrosis of the hypopharyngeal mucosa and incompetence of the vocal cord opening, and thus, the patient was admitted for the second time. Tracheotomy and hypopharyngoscopy revealed extensive necrosis on the posterior wall of the hypopharynx. Pathological examination of the same area did not show the presence of any malignant cells. Because a gas pattern was observed in the prevertebral area on CT images, an infection was suspected. The patient was treated with meropenem (1.5 g/day) for 1 week. He was discharged following improvement in local findings and the sore throat.\nIn January 2013 (7 months after completing CCRT), the patient experienced pain in both shoulders and the anterior chest, as well as reduced muscle strength in his 4 limbs. He was admitted for the third time for the purpose of close examination. A large mucosal defect was observed on the posterior wall of the hypopharynx. A blood examination revealed a leukocyte count of 10,900/μL and a CRP level of 17.7 mg/dL, suggesting a strong inflammatory reaction; however, no accumulation was observed on bone scintigraphy. Cervical spine osteomyelitis and an epidural abscess on C4-C7 were observed on MRI (). The causative bacteria were not identified in a pharyngeal culture. Because the reduced muscle strength worsened despite the administration of meropenem, we discussed treatment for this case with the Orthopedic Surgery Department. We concluded that surgical treatment carried a high risk, and therefore, the patient underwent 25 rounds of hyperbaric oxygen therapy (HBO). The abscess gradually reduced and muscle strength improved, and the patient was subsequently discharged (). A defect of the posterior hypopharyngeal wall was also gradually improved. No recurrence has been noted and the patient is followed in outpatient. |
The current case report investigates the cognitive profile of a 35-year-old Caucasian woman with extremely severe and enduring AN who was diagnosed at the age of 10 years. The patient’s weight loss is accomplished through fasting. According to the DSM-5 [], the patient’s symptoms are in accordance with the restricting type and the severity of AN for the patient is categorized as extreme. The patient has had low body weight since the onset of the disease 25 years ago. Consequently, she is still prepubescent.\nThe patient’s extreme malnutrition, the medical complications, and the refeeding treatment has previously been described in a case report []. Since the previous report [], she has survived another 5 years, living in her own residence with several stabilizing hospitalizations. Her nadir BMI, defined as the lowest registered BMI, has decreased further to 7.2 kg/m2. To our knowledge, this is the lowest BMI reported in AN in the literature. During her long and severe illness course, she has participated in psychotherapy for years. However, during the past few years, she has refused to participate in psychotherapy, while she has continued the harm-reducing treatment in the nutrition department. No cognitive profile has been assessed before the current report.\nShe has continuously been provided supplementation with vitamins and minerals. At the present admission, she weighed 20.2 kg, including edema corresponding to at least 2 kg, and her height was 1.55 m, corresponding to a BMI of 8.41 kg/m2. After life-saving and stabilizing fluid and electrolyte correction, and refeeding according to guidelines [] during 2 weeks of hospitalization, we tested her with a neuropsychological test battery (2 weeks after admission: T0). After an additional 2 months of hospitalization, she could not be motivated to continue the treatment any longer. Due to years of history with rapid relapse after prolonged forced treatment, she was allowed to be discharged to outpatient follow-up. She was re-tested in the outpatient clinic 6 days following dropout from inpatient treatment and approximately 3 months after admission, (re-test: T1) with a weight of 22.4 kg (BMI: 9.3 kg/m2), and again at 12 months from T0, during a re-hospitalization, 7 days after admission (follow-up: T2), with BMI 7.7 kg/m2. Thus, T0 and T2 were done at the hospital after initial stabilizing glycemic, fluid- and electrolyte correction, whereas T1 was done in an outpatient setting, where she was in a clinically stable condition, but without the initial stabilizing treatment.\nThe patient scored 21 on the Beck Depression Inventory II (BDI-II [];) indicating moderate depression at 2 weeks after admission (T0). Her scores on the Eating Disorder Inventory 3 (EDI-3 [];) at T0 are presented in Table below. Compared to the Danish validation of EDI-3 for patients with AN ( []; Table ), her low scores on the Drive for Thinness, the Interoceptive Deficits, the Perfectionism, and the Asceticism subscales are of interest.\nDuring the first 2 weeks after admission, the patient was unable to participate in the neuropsychological assessment due to fatigue. Two weeks after admission, when the baseline assessment took place (T0), the patient was lying down during the assessment and was noticeably tired. This was neither the case at retest (T1) nor at follow-up (T2) where the patient was sitting at a table. Her alertness and energy level at follow-up (T2) were notable in light of her low BMI. The patient was calm during all three assessments (divided into six sessions) and expressed that the tests were fun. The aim of the study was explained to the patient before the first administration. However, only information written in the test manuals was given during each assessment.\nThe following validated neuropsychological tests were selected in cooperation with an experienced neuropsychologist to examine a wide range of cognitive functions: the Wechsler Memory Scale III (WMS-III) []; the d2-R Test of Attention – Revised [, ]; the Processing Speed Index (PSI) of the Wechsler Adult Intelligence Scale IV (WAIS-IV) []; the Delis-Kaplan Executive Function System (D-KEFS) [], Verbal Fluency Test, Design Fluency Test and Trail Making Test; and the Wisconsin Card Sorting Test Revised and Expanded (WCST) [] (only administered at T0). Information on each test variable, including internal consistency and test-retest reliability, are presented in Table . The test battery can be administered in approximately 2 h. For all three administrations, the test battery was divided into two sessions (1 h per session) 1 day apart.\nTable gives an overview of the timeline of the patient’s raw scores and scaled scores on the test battery. Table presents the patient’s norm scores and percentiles on the WMS-III, the WAIS-IV PSI, and the d2-R. Table presents the patient’s WCST scores at 2 weeks after admission (T0). Information on scoring are presented below each of the tables.\nThe patient’s scores on WMS-III indicate average to very superior auditory, visual, immediate and general memory performance (108 to 142; Mean: 100), and low average to average working memory (Table ). The technical manual for WMS-III reports adequate test – retest reliability for all indexes in the age group 16–54 years, except for the Auditory Recognition Delayed Index ( []; Table ). Estimated standard error of difference (SDiff) scores were calculated based on Iverson and Grant ( []; Table ). Differences between the three assessments are outlined here. Her scores on the Auditory Delayed Index decreased more than Sdiff: 6.70 from 132 (very superior) at 2 weeks after admission (T0) to 108 (average) at re-test (T1) and increased again to 132 (very superior) at follow-up (T2). Her scores on the Visual Immediate Index increased slightly more than Sdiff: 6.70 from 118 (high average) at re-test (T1) to 127 (superior) at follow-up (T2). Her scores on the Visual Delayed Index decreased more than Sdiff: 7.65 from 125 (superior) at re-test (T1) to 109 (average) at follow-up (T2). Her scores on the Immediate Memory Index increased more than Sdiff: 3.17 from 134 (very superior) at re-test (T1) to 142 (very superior) at follow-up (T2). Her scores on the Working Memory Index decreased more than Sdiff: 8.22 from 102 (average) at 2 weeks after admission (T0) to 88 (low average) at re-test (T1). The scores on the rest of the indexes did not change more than the estimated Sdiff scores between time points.\nOverall, she performed above average on the Verbal Fluency Test (Table ) at all three test times compared to the normative population for age, except for her performance at re-test (T1) on the switching condition, which was decreased more than Sdiff: 2.42 to average, and the high number of repetition errors (7; below average) at re-test (T1) and (3; average) at follow-up (T2).\nShe performed average to above average on the Design Fluency Test at all three test sessions (Table ). However, the switching condition score was lower [] at follow-up (T2) compared to 8 at 2 weeks after admission (T0) and re-test (T1), though still average.\nDuring follow-up (T2) on the Trail Making Test (Table ), her performance on the Number-Letter Sequencing test, measuring cognitive flexibility, was below average (111 s), in spite of being average at 2 weeks after admission (T0; 90 s) and re-test (T1; 79 s). The numbers condition was very low at T0 (55 s; below average), improving somewhat at re-test (T1; 46 s; below average) and follow-up (T3; 41 s; below average). We have no explanation for this result. On the other conditions, her performance was average at all three test times on the Trail Making Test.\nHer scores on the WCST (Table ) 2 weeks after admission (T0) place her in the mild to moderately-to-severely range of impairment on cognitive flexibility according to this task. She completed one out of six categories (< 1st percentile). She made 52 perseverative responses (< 1st percentile; standard score 55; moderately-to-severely impaired range). She committed 50 errors (8th percentile; standard score 79: mildly impaired range), of which 36 were perseverative errors (1st percentile; standard score 55: moderately impaired range).\nThe scores on the Processing Speed Index (Table ) were average compared to the normative population for age at all three test times. There were no relevant differences between time points. She scored 93 at admission (T0) and re-test (T1) and 98 at follow-up (T2).\nAt 2 weeks after admission (T0) and re-test (T1), she had a small number of processed targets (426 and 420), 18th to 21st percentile (Tables and ), her concentration performance was 175 and 176 corresponding to the 42nd percentile and she committed three and no errors respectively (> 90th percentile). At follow-up (T2), her concentration performance was above the mean (185; 54th percentile) but not increased more than Sdiff: 24.89. The total processed targets score was still low (451; 34th percentile), and she committed few errors (four; 90th percentile). |
A 76-year-old woman visited our clinic for severe low back pain recently aggravated without any predisposing factor. The patient had a medical history of type II diabetes mellitus and hypertension. Simple radiographs of the lumbar spine showed a compression fracture of L1. Mag- netic resonance imaging (MRI) scan revealed a benign compression fracture of L1. The patient was admitted to our department for kyphoplasty of L1. Blood pressure was maintained within the normal range and blood sugar level was well regulated. T-score for bone densitometry was calculated to be -4.3. Chest radiographs did not show any signs of pulmonary disease. Percutaneous kyphoplasty was performed under local anesthesia without any complications. The severe low back pain disappeared immediately after kyphoplasty. Three years later, the patient presented to the pain clinic complaining of recurrent low back pain. The patient underwent lumbar epidural block and facet joint block. Several days later, the patient returned to our department due to aggravation of low back pain and development of fever. Laboratory tests revealed elevated inflammatory markers, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and procalcitonin levels. Empirical broad-spectrum antibiotics were administered. MRI scan was conducted and showed new compression fracture at T12, paravertebral abscess, and spondylitis of T12 and L1 (). We suspected bacterial spondylitis, as there was no typical evidence of tuberculous spondylitis including commencement of infection at the anterior aspect of the vertebral body adjacent to the endplate. The patient did not respond to antibiotic treatment and there was no decrease in inflammatory markers. The patient complained of intolerable lower back pain and radiating leg pain. We performed surgery for tissue biopsy, pathogen identification and spinal decompression. Total corpectomy of T12 and L1 was performed using a transdiaphragmatic retropleural-retroperitoneal approach. Then anterior reinforcement with a titanium mesh cage filled with autologous rib graft was performed. The necrotic tissue was biopsied and cultured. However, the bacterial culture was negative. Histologic examination of the resected specimen revealed a granulomatous inflammation with caseous necrosis (). Therefore, specific polymerase chain reaction and acid-fast bacilli stain were subsequently carried out and they confirmed the diagnosis of a tuberculous infection. Subsequent tuberculosis culture showed evidence for mycobacterium tuberculosis. Antibiotics were promptly changed to anti-tuberculous medications including isoniazid, rifampicin, pyrazinamide, and ethambutol. Approximately three months after the surgery and anti-tuberculous medications, inflammatory markers decreased to subclinical levels. The anti-tuberculous medications were administered for 10 months, and the patient recovered without any sequelae. |
An 82-year-old man, presented to the emergency department, on February 2018, after sudden onset of left hemiparesis and vertigo. Symptoms started during a period of greater physical effort, upon participation in a zumba class. His past medical history included transient episodes of vertigo during exercise in the previous months, an anterior circulation right hemispheric stroke in 2015, that left no sequels, and hypertension controlled with a combination of 10 mg lisinopril and 2.5 mg amlodipine. The neurologic examination revealed mild left hemiparesis with facial involvement and crural predominance, vertical nystagmus, right internuclear ophthalmoplegia, dysarthria and dysmetria on the left arm. The total National Institutes of Health Stroke Scale (NIHSS) score was 6.\nThe plain brain CT scan was normal and a CT angiography showed hypoplasia of both vertebral arteries, the left terminating as the PICA, while the right gave origin to the BA. The BA had a filiform aspect in its proximal two thirds, having a normal caliber in the distal remaining third, after receiving a communicating artery from the cavernous segment of the left internal carotid artery, a PTA (Fig. ). No abrupt stop of flow was identified. Echocardiogram showed severe dilation of the left auricle, as well as mild dilation of the right auricle and a 35 mm dilation of the proximal portion of the ascending aorta. Electrocardiogram was normal and a 48 h cardiac telemetry monitoring didn’t show any periods of arrhythmia. Lipid profile showed borderline high low density lipoprotein level, at 139 mg/dL.\nThe patient underwent treatment with recombinant tissue plasminogen activator (rt-PA) at two hours of symptom onset, this decision was based on the clinical presentation and in the absence of hemorrhage in the CT scan. Shortly after treatment the NIHSS score was 2, maintaining a slight paresis of the left leg and dysmetria on the left arm. Months later, the patient showed no neurologic sequelae. |
The patient is a 29-year-old African American female, G1P1A0, with a history of stroke in multiple areas in the brain approximately two months ago; she was eight months postpartum following an uneventful pregnancy and normal vaginal delivery. At this time, the patient presented with confusion, unusual behavior pattern, headache, involuntary movements, and forgetfulness for the last three days. Patient reported that she had difficulty in performing easy tasks such as putting a bottle together, getting out of the car, and changing her baby. She also reported that, at times, she got lost in her home. She denied having weakness, numbness, seizures, chest pain, shortness of breath, fever, or chills. The patient had a previous ischemic stroke affecting her left side but no residual weakness at this time; however, she did report urinary incontinence since then. Multiple members in her family had a stroke when they were young. The patient was awake, alert, and oriented with no focal neurologic deficits. National Institutes of Health Stroke Scale (NIHSS) score was zero. The first stroke was two months ago, and at that time, she presented with left-sided weakness and cognitive deficits. She was found to have acute cerebral ischemic infarcts primarily noted in the right cerebral hemisphere (Figures –). Subsequently, she underwent a CT angiogram (CTA), which showed questionable stenosis of the bilateral middle cerebral artery (MCA) and distal right vertebral artery. On this admission, she had further progression of intracranial stenosis and ischemic infarcts noted bilaterally (Figures –). CTA of the head revealed moderate to severe narrowing of the supraclinoid segment of both internal carotid arteries (ICA) and extensive narrowing of both M1 segments of the MCAs and both A1 segments of anterior cerebral arteries (ACA). Cerebral perfusion imaging revealed diminished cerebral blood flow in the ACA, MCA, and watershed territories, compatible with ischemia. A diagnostic digital subtraction cerebral angiography showed progressive arteriopathy in both ICA terminals, M1, and A1 with prominent lateral lenticulostriate branches, indicating early collateralization of flow (Figures and ). Based on these clinical and radiological findings, our diagnostic considerations were MMD, primary CNS vasculitis, hypertensive disorder preceding multiple strokes, or hypercoagulability disorders. During this admission, her blood pressure was well controlled. There were no skipped lesions found to support vasculitidies. She denied the previous history of photosensitivity and rash on the face or limbs. There was no history of oral or nasal ulcers, hemoptysis, hematemesis, and recurrent urine infections. She denied a history of Raynaud phenomenon, and there was no history of blood clots that she is aware of. Detailed history and review of systems did not elicit any suspicion of rheumatologic disease. Basic blood work was within normal limits. Specific tests for hypercoagulability, antiphospholipid syndrome, and rheumatologic disorders were negative. CSF analysis was also unremarkable. In following with diagnostic criteria, we diagnosed our patient with MMD. We discharged patients with antihypertensive medications, high-dose statin, and dual antiplatelet therapy. |
A 70-year-old woman was referred to our institution in July 2012 for treatment of left ocular pain. She complained of ocular discomfort and decreased visual acuity (12/20) at the first visit. She underwent nasal pterygium excision with topical MMC in the left eye six years previously at another facility. A few years after surgery, symptoms of intermittent ocular discomfort and mild ocular pain developed, so she went for treatment to a local medical center. She had neither medical history or family history of ophthalmic disease.\nOn slit-lamp examination, the underlying sclera at the site of the prior pterygium excision was necrotic and avascular, and showed marked thinning in the nasal portion of the left eye (Fig. ). The scleral bed appeared conjunctivalization over the exposed ciliary body with no evidence of scleral perforation sign by Seidel test. The adjacent corneal epithelium was intact and there was no anterior chamber inflammatory reaction. We thought that the scleral thinning was a possible MMC-associated thinning. Microbial smears and cultures of the scleral bed were obtained at the first visit, but were negative.\nThe patient was started on topical 0.1 % fluorometholone and 0.5 % levofloxacin eye drops. Two weeks later, the patient’s ocular pain and discomfort was gone. After informed consent, the patient underwent an OCM graft with CAU at the scleral thinning area. The surgical technique is described in Fig. . Proparacaine hydrochloride eye drop (0.5 %, Alcaine; Alcon, Fort Worth, TX) was used as topical anesthesia before surgery. First, the necrotic soft tissues and devitalized sclera were surgically debrided with a diamond burr, taking care not to damage the exposed ciliary body and the unaffected adjacent conjunctiva. Gentle polishing with a diamond burr instead of a knife can produce a flat, regular surface without damaging the already much thinned scleral bed. All necrotic scleral tissue was dissected away until the scleral surface was clean, smooth, and even. Conjunctival hemorrhage during debridement was controlled by ocular bovie and cotton swab compression. To determine the boundary for the conjunctivectomy, the size of the scleral defect was measured and its margin was marked with a 3-mm diameter biopsy punch (Fig. ). The margin of scleral thinning area was trimmed by Vannas scissors and the OCM was cut with a circular-shaped biopsy punch of the same size (3-mm diameter). The OCM was trimmed and fitted to cover the scleral defect (Fig. ). The OCM was sutured with a recipient scleral wall using six stitches of 10–0 nylon interrupted sutures. The color of the OCM changed from white to red due to blood accumulation (Fig. ). Once the scleral defect was repaired, a 4-mm diameter, circular, free CAU was harvested from the superonasal bulbar conjunctiva with a punch biopsy 1 mm larger in diameter than that of the piece of OCM. A conjunctival graft that is larger than the scleral defect can achieve a stable, tension-free graft to avoid a wound dehiscence (Fig. ). The CAU was carefully positioned over the previously sutured OCM bed and anchored to the scleral wall and the healthy conjunctival margin through the OCM bed with 11 stitches of interrupted sutures of 10–0 nylon (Fig. ).\nAfter surgery, the patient was given a patch dressing with a topical antibiotic ointment (Erythromycin, Ecolicin®, Taejoon Pharm., Seoul, Korea) and a steroid ointment (Dexamethasone, Maxitrol®, Alcon Laboratories Inc., Fort Worth, TX, USA) to be taken four times daily. The patient was examined daily for the first five postoperative days. After five days, the ointment patch dressing was replaced by topical antibiotics (0.5 % levofloxacin, Cravit®, Taejoon Pharm, Seoul, Korea) and steroid eye drops (0.1 % fluorometholone, Flarex®, Alcon Laboratories Inc., Fort Worth, TX, USA) to be taken four times a day. Inflammation of the scleral bed subsided and the patient was comfortable. The ocular surface was re-epithelialized six days after surgery. The conjunctival sutures were removed at intervals of one week to one month over the postoperative course. Starting about one month after surgery, the topical 0.1 % fluorometholone and 0.5 % levofloxacin eye drops were tapered off over three months. Artificial tear substitutes were used continuously after surgery. The patient was examined weekly for the first two months and at three, four, six, nine, 12, 16, 20, and 24 months postoperative.\nOver the first postoperative month, the graft site vascularized and was taken up well (Fig. ). The conjunctival surface was stable at six months and 12 months postoperative. When reviewed 24 months later, the conjunctival surface was still stable with no recurrence of scleral thinning and scleromalacia (Fig. ). |
During medical examination, we detected an abnormal shadow in the chest of a 66-year-old man who was admitted to our hospital. Chest computed tomography (CT) revealed a mass lesion in the truncus intermedius of the right lung and swelling of the inferior tracheobronchial lymph nodes (A). Furthermore, CT scanning showed pulmonary infiltration shadows of the right lower lobe (B). Based on the findings of transbronchial lung biopsy, we gave the diagnosis of squamous cell carcinoma. Although we diagnosed the lung cancer as clinical stage IIIA (cT1cN2M0), we decided that chemoradiotherapy should not be performed due to the presence of obstructive pneumonia in the right lower lobe occurred by lung cancer. Instead, we planned to perform primary surgery.\nWe performed the operation via an anterolateral incision made with the patient in the lateral position. Although we did try to perform right middle and lower sleeve lobectomy, right pneumonectomy was ultimately chosen since the cancer had already spread to the right upper bronchus. We assessed the blood flow in the bronchial stump using an ICG injection under fluorescence navigation (VISERA ELITE II; Olympus, Tokyo, Japan) (C), which we then covered with a stemless pericardial fat pad (D).\nThe air-fluid level of the right pleural cavity suddenly dropped on the 19th postoperative day (A, B), and the air was detected around the bronchial stump using chest CT (C). Although we were unable to detect the fistula of the bronchial stump using bronchoscopy (D), we performed re-operation, as microscopic BPF could not be ruled out. Although a pressure of 30 cmH2O was applied into the airway, air leakage from the bronchial stump was not detected. However, we covered the bronchial stump with the omentum (A). The blood flow in the omentum was assessed using an ICG injection under fluorescence navigation (B).\nThe air-fluid level of the right pleural cavity decreased 9 days after the 2nd operation (C). Since the air-fluid level of the right pleural cavity declined further on the 14th day after the 2nd operation (D), we diagnosed the condition as BEPS. The patient was discharged on postoperative day 18 without any symptoms. |
A 41-year old male patient awoke to find sudden onset of left ptosis, right side numbness without identifiable history of trauma or physical stress. He first visited local medical center and had brain magnetic resonance imaging (MRI) taken, however, no specific findings were found. When he was referred to our neurosurgery department via emergent department, neurological examination presented left side ptosis, miosis and anhidrosis of left half of face which are typical symptoms of HS, and there was numbness below right side of the T8 dermatome. We consulted department of ophthalmology and confirmed left ptosis and miosis (). In darkness, pupils measured 5 mm on the right eye and 3 mm on the left eye, and the left pupil showed dilatation lag. There was 2 mm of left ptosis. Sweat test showed only right side starch powder on the face changed to dark brown color, which means left side anhidrosis (). The cervical spine MRI demonstrated an upward migrated and large left paramedian disc herniation with severe unilateral spinal cord compression at the C4-C5 level which is high signal intensity with internal low signal intensity on T2WI and intermediate signal intensity on T1WI. And extruded disc revealed some high density in cervical spine computed tomography (). As large disc herniation with cartilaginous endplate fragments was doubted, we conducted a standard microsurgical anterior approach to the C4-C5 interspace on 2 days after admission. Posterior longitudinal ligament had been ruptured and spinal cord was severely compressed especially at left side. The extruded disc material was migrated to upward including part of the cartilaginous endplate. After complete decompression of neural structures, anterior cervical fusion was performed with a cage filled with an allograft bone chip. Postoperatively, right side numbness was improved but left miosis and ptosis remained until discharge. However, after two months from the operation, miosis, ptosis and anhidrosis were completely recovered, too. |
We report a case of a 24-year-old Japanese woman, gravida 0, who had no relevant past medical history or family history when she became ill. She complained of prolonged menstruation and was examined with Cusco’s speculum. The patient presented with a uterine cervical tumor and was diagnosed with uterine leiomyoma. She underwent her first transvaginal resection of the tumor with a myomectomy and endometrial curettage. The pathological diagnosis was leiomyoma and endometrium, no malignancy, as a benign tumor. She underwent four additional tumor resections: polypectomy, two myoma resections, and a submucosal leiomyoma resection via hysteroscopy. The resections were performed at intervals of 10 months, 9 months, 9 months, and 6 months, respectively. After these resections, she gave birth to a 3396g boy via cesarean section at age 28 years. During her pregnancy, she was diagnosed with oligoamnios. The birth took place at the 39th week of pregnancy. At age 30 years, the patient developed a sixth tumor (a fibroid in statu nascendi), which was removed by exeresis at age 30 years. Four subsequent tumor resections were performed, at intervals of 23 months, 4 months, 12 months, and 3 months, respectively. When the seventh tumor was resected by polypectomy at age 32 years, the pathology report revealed for the first time the high density of the stroma and the necessity of careful follow-up. At the time these ten tumor resections were performed (five before and five after childbirth), the tumors were not diagnosed as malignant. The correct diagnosis was obtained by analysis of advanced-stage surgical specimens. The discovery of minimal elements of LGESS by a retrospective study of the transvaginally resected tumors led to a correct diagnosis of early-stage LGESS.\nThe patient visited our hospital, complaining of lower abdominal pain at age 34 years and was found to have a tumor 10cm in diameter behind the uterus (Fig. ), which was diagnosed as an advanced malignant ovarian tumor before surgery. Total abdominal hysterectomy, bilateral salpingo-oophorectomy, and resection of peritoneal dissemination were performed. The tumor was classified as International Federation of Gynecology and Obstetrics 1982 stage VIb for uterine corpus cancer and Union for International Cancer Control 1990 tumor, node, metastasis stage pT4NxM1 on the basis of the finding of tumor spreading in the peritoneal cavity. The histological result revealed LGESS of the uterine corpus. A great amount of bulky, disseminated tumor lingered in the abdominal cavity, particularly on the serosa of the rectum and descending colon. After the operation, gemcitabine (800mg/body surface area, Day 1 and 8) and docetaxel (60mg/body surface area, Day 8) combination chemotherapy (GD) was started with informed consent. A subcommittee of our institutional review board reviewed the case and gave approval to treat this patient with GD chemotherapy. Six cycles of GD were administered every 3 weeks, followed by six cycles every 3 months (age 36 years). After nine cycles of chemotherapy, the patient developed ileus and underwent surgery. She had a complete response to chemotherapy, and no visible tumor remained in the abdominal cavity. No recurrent tumor was detected for the next 4 years, and the patient did not undergo any treatment during that time.\nWhen the patient reached the age of 40 years, a new tumor was detected in the pelvic cavity. She underwent surgery to remove the recurrent tumor. The tumor, 2.5cm in diameter disseminated on the ileum, was resected. Numerous small disseminations remained. Five cycles of GD every 3 weeks were administered after surgery. The sixth cycle of GD was discontinued because the patient’s neutropenia worsened to a grade 4 adverse event as defined by Common Terminology Criteria for Adverse Events (CTCAE) version 3, even after granulocyte colony-stimulating factor was administered. No recurrent tumor was detected for the next 18 months.\nA small accumulation of fluid was detected in the pouch of Douglas when the patient was age 42 years. Computed tomography (CT) revealed recurrence of the tumor in the form of many disseminations in the right pleura, peritoneum, right diaphragm pleural and peritoneal surface, and liver surface (Fig. ). Although three cycles of GD at the initial dose were administered, the disease progressed and shock was induced by abdominal cavity bleeding (Fig. ). Infusion and blood transfusion were started with hospitalization to treat bleeding shock. Medroxyprogesterone acetate (MPA) was administered at a daily dose of 600mg. Although the bleeding in the patient’s abdominal cavity stopped, her pleural effusion and ascites did not decrease. Because the effect of MPA was not enough, a gonadotropin-releasing hormone analogue (leuprorelin acetate) at a dose of 3.75mg/body surface area once every 28 days was administered in addition to MPA. The increase in both the pleural effusion and ascites accelerated, and thoracic bleeding induced shock and dyspnea on the 18th day after leuprorelin acetate was first administered (Fig. ). The pleural effusion began to decrease at 1 month after leuprorelin acetate was first administered. Because the patient’s ascites were not decreasing, an aromatase inhibitor (anastrozole) 1mg/day was administered in addition to MPA and leuprorelin acetate. After beginning treatment with anastrozole, the patient’s ascites decreased. She was discharged from the hospital after 116 days.\nThree months later, the tumor had enlarged between the liver and diaphragm and had spread to the right pleura (Fig. ). Paclitaxel at a dose of 170mg/m2 and carboplatin (area under the curve =4) combination chemotherapy (TC) was started with MPA, leuprorelin acetate, and anastrozole. The dose of TC was reduced because during the time five cycles of GD were administered after the recurrent tumor on the ileum was resected the patient’s neutropenia gradually worsened to CTCAE grade 4. The tumor size and state were confirmed by CT after every three cycles of chemotherapy. The tumor gradually reduced, and the liver returned to the normal position. Chemotherapy was stopped after 18 cycles (Fig. ). The patient is currently alive and being treated with MPA, leuprorelin acetate, and anastrozole (age 45 years at the time of this report).\nThe first, sixth, and ninth tumors transvaginally resected in the early stage showed similar histopathological findings. The tumors had a polypoid appearance with various degrees of surface erosion (Fig. ). The surfaces were covered by non-atypical columnar epithelium of endocervical or endometrial type. The stroma was edematous, loosely fibrous, and paucicellular, often containing capillaries and small vessels recapitulating inflammatory granulation tissue (Fig. ). There were a few foci of mild stromal hypercellularity, where small, short spindle stromal cells surrounded the blood vessels (Fig. ). The seventh, eighth, and tenth transvaginally resected tumors were clinically diagnosed as endocervical or endometrial polyps, and they had wide areas of stromal hypercellularity, which is unusual for conventional endocervical or endometrial polyps (Fig. ). Although several suspicious findings were present, it was difficult to diagnose LGESS on the basis of only transvaginal resection of the tumors.\nThe surgically resected uterus in the advanced stage had multiple polypoid excrescences in the lower uterine segment. Examination of cut sections revealed multiple nodular lesions in the muscular layer of the uterine corpus and paraovarian connective tissue. The cut surfaces of these tumors were whitish yellow and had a monotonous solid appearance. Multiple peritoneal tumors ranging from 20mm to 60mm in diameter had similar macroscopic findings.\nHistologically, the polypoid endometrial lesions invaded the muscle layer with pushing margins and multiple tongue-like projections (Fig. ). Prominent intralymphatic tumor extensions were noted, especially in the paraovarian connective tissue (Fig. ). The tumor consisted of a monotonous proliferation of oval to short spindle cells with indistinct cytoplasm (Fig. ). The spindle cells often surrounded small arterioles in a concentric pattern. Some cells had abundant clear cytoplasm (Fig. ). In some areas, the stroma was edematous and cellularity was low (Fig. ). Such areas were similar to the pathological findings of the first, sixth, and ninth transvaginal polypectomy specimens.\nImmunohistochemically, the tumor cells of the surgically resected specimens were diffusely positive for estrogen receptor, progesterone receptor, and cluster of differentiation 10 (CD10) (Fig. ). The staining intensity of progesterone receptor and CD10 was strong, and that of estrogen receptor was weak to moderate. CD10 was also positive in the spindle cell of the pre-operative specimens of the transvaginal resections (Fig. ). The series of lesions, including those from the ten transvaginal resections and hysterectomy, were finally diagnosed as LGESS. Focal stromal hypercellularity surrounding small blood vessels seen in the first ten resected tumors was retrospectively considered the characteristic finding of LGESS. The recurrent intestinal serosal, peritoneal, and hepatic lesions showed essentially the same histological findings. |
A 27-year-old man (height, 181 cm; weight, 76 kg) visited the outpatient orthopedic department with a chief complaint of low back pain. He had received medication treatment 8 years previously due to the same symptoms. Since then, he had experienced pain rated as 3-4 on an 0-10 numeric rating scale (NRS) when bending and straightening at the waist, but had not received any other treatment. Without any specific inciting event, the pain had begun to worsen 2 years ago. In the past 4 months, the severity of the pain had increased, with the patient reporting severe low back pain reaching 8 on the 0-10 NRS, and numbness extending to the right leg. On lumbar spine magnetic resonance imaging (MRI), indications of HIVD and cauda equina compression were found at the 4th and 5th lumbar intervertebral disc levels (). Consequently, an emergency open discectomy was performed. There was no pattern of disc sequestration, but a huge mass compressing the right 5th lumbar vertebral (L5) nerve root was revealed. The surgery was completed with excision of the mass only. On postoperative day 2, the 0-10 NRS severity of the low back pain had decreased to 4. Although the right leg numbness persisted, the patient was discharged with plans for outpatient follow-up. At postoperative week 2, a physical examination performed at the orthopedics department showed no abnormalities of motor function, and the patient reported improvement in his symptoms, with only mild numbness remaining in the right leg. However, two days after that outpatient visit, the patient's low back pain began to gradually worsen. After one week, the patient was admitted to our emergency room with a chief complaint of pain severe enough to prevent ambulation. At that time, the extent intensity of his low back pain was 9-10 on the NRS. Physical examination in the emergency room revealed numbness along the L5 dermatome; the motor examination revealed only a slightly reduced extensor proprius hallucis muscle strength reduced slightly to 4/5, with an abnormal finding of 1-2 seconds of right ankle clonus.\nThe emergency lumbar spine MRI showed L5 nerve root compression by a 1.2 × 2 cm sized cystic lesion appearing in the area where the surgery had been performed, with concurrent cauda equina compression (, ). This lesion was radiologically diagnosed as a discal cyst with a connecting channel to the 4th lumbar and 5th lumbar intervertebral disc observed on the MRI. Because the patient refused re-operation, the case was referred to the department of anesthesiology for non-surgical intervention therapy.\nThe emergency MRI showed that the discal cyst was located just anterior to the right L4-5 facet joint, so the decision was made to perform a C-arm guided needle aspiration and steroid injection through the facet joint. Informed consent was obtained from the patient and his guardian. The procedure was performed on postoperative day 22. The patient was placed in the prone position and lumbar lordosis was reduced with a pillow placed under the lower abdomen. The cyst was approached through the superior aspect of the right L4-5 facet joint using a 25G spinal needle with a C-arm guide. However, because the patient complained of paresthesia in the right L5 dermatome, the needle was moved backward, rotated 180 degrees, and then re-advanced. Because the patient complained of paresthesia again, the needle was removed. Another approach was attempted inferiorly using a 22G spinal needle. After placement in the patient's right L4-5 facet joint space, the needle was advanced through the right L4-5 facet joint until the achievement of the "pop" sensation while the lateral image of the C-arm and the patient's symptoms were monitored. After injection of 0.5 ml contrast medium to confirm that the needle was inside the cyst, 1.2 ml of cystic fluid () was aspirated. The procedure was completed with the injection of 10 mg of triamcinolone (). After the procedure, the patient remained in the supine position under observation in the pain clinic. After 1 hour, the patient's pain improved to NRS 0-1. There were no other neurological abnormalities, and the patient was transferred to the general ward. Following 2 days of monitoring in the general ward, the patient was discharged, since the symptoms had not recurred and improvement had been maintained. The cystic fluid showed a red blood cell count of 512,000/µl and white blood cell count of 1,500/µl (differential count: polymorphonuclear cells 85%, and mononuclear cells 15%), while a culture showed no abnormal findings (no bacteria and no growth).\nDuring outpatient physical examinations 1 week, 1 month, and 3 months later, no abnormal neurological symptoms were present, and the pain did not persist. Thus, follow-up observation was terminated. |
A 33-year-old male patient was admitted to Aracatuba Dental School-UNESP, complaining about tooth sensitivity to temperature variations caused by the ingestion of different foods and acidic substances.\nWear on the lingual surface of the maxillary anterior teeth and the shortening of the cusps of upper and lower posterior teeth were observed. This change was just not observed in the lower anterior teeth. Slight reduction of occlusal vertical dimension of the patient was observed without the need of its restoration (Figures , , , , and ). Thus, the anamnesis was performed to check the presence of parafunctional habits—which was discarded—and to identify the possible cause of tooth wear. The patient was unaware of the presence of systemic disorders and reported a feeling of heartburn. This symptom was probably caused by an exaggerated intake of sports supplements (isotonics) which might have caused the gastroesophageal changes since the patient practiced physical activity regularly.\nThe patient was referred to a gastroenterologist and the presence of hiatal hernia and gastroesophageal reflux disease was diagnosed after performing some specific tests. The medical treatment was based on the use of 40 mg of Omeprazol, twice a day for 30 days, and also change in eating habits such as the reduction of isotonic drinks and other foods that could exacerbate the symptoms. There was a decreased sensation of heartburn after medication treatment and only a regular medical followup was required.\nThe dental treatment could be performed once the symptoms were controlled and the patient was treating the disease with medicines. Initial photographs were taken and impressions of both arches were performed with stock trays and alginate (Hydrogum, Zhermack SpA Rovigo, Italy) to obtain the study models. The models were positioned on semiadjustable articulator for drafting and proposing the treatment plan.\nAmong the proposed treatment options, the patient chose to restore the dental anatomy with metal-free crowns and porcelain veneers. Initially, the affected teeth were prepared (). Subsequently, impressions of the prepared teeth were made using silicone condensation in putty consistency and light body (Speedex, Vigodent SA Industria e Comercio, Bonsucesso, Rio de Janeiro, Brazil) and cervical margins of the preparations were exposed with gingival retractor cord number 000 (Ultrapack, Ultradent Products, Inc., South Jordan, Utah, USA) (Figures and ). Then, provisional restorations fabricated with indirect composite resin (Resilab, Wilcos do Brazil Industria e Comercio Ltda, Petropolis, Rio de Janeiro, Brazil) were cemented.\nThe zirconia (IPS e.max ZirPress, Ivoclar Vivadent AG, Schaan, Liechtenstein) cores were confectioned and lithium disilicate ceramic was used as veneering ceramic for posterior crowns and laminate veneers (IPS e.max Ceram, Ivoclar Vivadent AG, Schaan, Liechtenstein) (). The inner face of the laminate veneers was etched with 10% hydrofluoric acid (FGM Produtos Odontológicos, Joinville, Rio Grande do Sul, Brazil) for 20 seconds, rinsed with water, and dried with air and then a layer of silane was applied (Prosil, FGM Produtos Odontológicos, Joinville, Rio Grande do Sul, Brazil). The teeth were etched with 37% phosphoric acid (Dentsply, Petropolis, Rio de Janeiro, Brazil) for 30 seconds, rinsed with water, and dried and then a layer of adhesive was applied (Prime & Bond 2.1, Dentsply, Petrópolis, Rio de Janeiro, Brazil) (Figures and ).\nThe porcelain veneers were cemented only with base paste of resin cement (Variolink Veneer, Ivoclar Vivadent AG, Schaan, Liechtenstein), whereas the crowns were cemented with both pastes (base and catalyst) of dual resin cement (Variolink II, Ivoclar Vivadent AG, Schaan, Liechtenstein) ().\nThe patient reported no sensitivity after dental treatment and a homemade topical application of sodium fluoride gel 2% was recommended (Nupro Gel, Denstply, Petropolis, Rio de Janeiro, Brazil) every 15 days. After 4 years of followup the restorations showed no visible deterioration and the periodontal tissue was free of gingival inflammation (Figures , , and ). The patient was satisfied with the treatment. |
A 76-year-old man with a medical history of hypertension, atrial fibrillation, type 2 diabetes mellitus, and mild chronic renal impairment with a single functional kidney was referred to our hospital because of a Crawford type 3 thoracoabdominal aneurysm with a diameter of 6.4 cm. There was a preexisting occlusion of the left renal artery. Baseline serum creatinine was 1.81 mg/dL. The estimated glomerular filtration rate (eGFR) using the modified diet and renal disease study equation (MDRD) was 37 mL/min/1.73 m2.\nEndovascular repair was performed with an aortic branch graft including side branches for the celiac trunk, superior mesenteric artery (SMA), and the right renal artery. Covered stents were placed through the side branches in the target vessels and these were relined with nitinol self-expanding stents. The procedure was complicated by diplopia caused by occipital infarction, despite intraoperative heparinisation and immediate postoperative readministration of anticoagulant therapy (coumarin and clopidogrel). Postoperative serum creatinine remained unchanged. Three weeks after surgery, clopidogrel was discontinued because of side effects. Follow-up CT-angiography 6 weeks after discharge showed adequate position of the aortic branch graft (), patency of the visceral side branches, and target vessels without kinking of the (covered) stents. However, a mass in the left mamma was found. Additional diagnostic tests showed an invasive ductal carcinoma. Subsequently the patient was planned for mastectomy with sentinel node procedure. Anticoagulant therapy was discontinued 3 days before surgery. Upon admission for the planned surgery, the patient reported anuria for approximately 12 hours and right flank pain that had started early that morning. Blood test showed an increase in serum creatinine to 5.37 mg/dL. Ultrasound investigation showed an occlusion of the stents in the right renal artery side branch and minimal venous flow suggesting acute ischemic kidney injury. The side branches to the celiac trunk and SMA were patent without presence of thrombus. Systemic heparinisation was started immediately and the mastectomy was cancelled. Angiography was performed via left brachial access and occlusion of the right renal artery side branch was confirmed (). Via direct transcatheter injection, a single bolus of 250.000 IE urokinase was administered into the right renal side branch and an EKOS thrombolysis catheter (EKOS Endowave system; EKOS Corporation, Bothell, WA, USA) with a working length of 6 cm was placed in the occluded renal side branch (). Intra-arterial infusion with 100.000 IU/h of urokinase was started together with 10.000 IU/24 h of heparin via the side port of the sheath. Thrombolysis was started 19 hours after the beginning of anuria. Angiographic control 4 hours later showed some dissolution of the thrombus and thrombolysis was continued. Approximately 8 hours after the start of thrombolysis, diuresis recovered and right flank pain diminished. Second angiographic control 18 hours after beginning of therapy demonstrated complete lysis of the thrombus with a patent side branch of the aortic stent graft and adequate flow through the renal artery (), after which thrombolysis was stopped. Subsequently, anticoagulation with low molecular weight heparin was started. The serum creatinine increased to a maximum of 10.44 mg/dL on day 3 after procedure, requiring dialysis on days 3 and 5. Hereafter, there was partial renal function recovery (eGFR (MDRD) of 10 mL/min/1.73 m2), after which mastectomy was performed without cessation of anticoagulant therapy. Postoperative coumarin was started and the patient was discharged on day 9, after an uneventful postoperative course. Renal function continued to improve, and one month after thrombolysis, renal function approached baseline function (creatinine 2.33 mg/dL; eGFR (MDRD) 27 mL/min/1.73 m2). One year after surgery, the patient was doing well and renal function was stable and the same as before the aneurysm repair. All side branches of the aortic branch graft were patent and the aneurysm was shrinking. |
A 40-year-old para 0+2 woman presented at the Outpatient Department of a public tertiary hospital in Lagos with a five-month history of a mass in the vagina and four-month history of bleeding per vaginam. The mass was initially the size of a pebble, but progressively increased in size until it was visible at the introitus. There was associated pain in the vagina which was described as sharp with a severity of 7 on a scale of 10. The pain was said to be aggravated by sitting or walking around and relieved by the ingestion of analgesics. There was also occasional vaginal bleeding which started a one month after the onset of the vaginal mass; bleeding was described as bright red, foul smelling, and not associated with her menstrual cycle. She had no history of chronic irritation or previous surgical instrumentation of the vagina. Physical examination findings were essentially normal; however, her vulva inspection revealed a cauliflower growth at the introitus. Digital examination showed no abdominopelvic mass and the cervix was deviated to the left but appeared normal to palpation. The adnexa was free bilaterally. Sterile speculum examination showed a cervix that was deviated towards the left lateral aspect of the vagina and appeared grossly normal. There was a friable, non-tender mass measuring about 6cmx3cm at the posterior wall of the lower-third of the vagina and extending to the introitus. The patient was counselled on the findings and the need for examination under anaesthesia (EUA) and biopsy of the vaginal mass which she consented to. Her abdominopelvic ultrasound and computerised tomography (CT) scans revealed normal sized uterus and adnexa and chest X-ray showed no abnormality. Her full blood count and serum electrolyte, urea and creatinine were all within normal limits. Retroviral screening, hepatitis B and C virus screenings were all negative. Her Pap smear was negative for intraepithelial lesion or malignancy. She subsequently had EUA and punch biopsy of the vaginal mass in theatre and the histological examination of the tissue revealed glands with widespread atypical pseudostratified cuboidal to columnar cells and goblet cells floating in a mucinous background and with the cells lining containing pleomorphic, hyperchromatic nuclei and vacuolated cytoplasm in areas with an intestinal-type appearance [Figs and ]. A diagnosis of invasive adenocarcinoma (intestinal-type mucinous carcinoma) was made. Patient was managed as FIGO clinical stage 1 disease and she was subsequently referred to the Radiation Oncology unit for chemoradiation therapy which comprised of intracavitary/external beam radiation therapy combined with weekly dose of intravenous Cisplatin. Patient responded optimally to the treatment and she was still on follow-up as at the time of writing this report. |
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