Three-month-old female infant was admitted for the management of fever, cough and dyspnea. She was born at 35 weeks gestation by Cesarian section with birth weight of 2.46 kg. After birth, she was diagnosed as Down syndrome due to a characteristic morphology and chromosomal anomaly. At that time, a small ventricular septal defect was discovered by echocardiogram. Her height was 60 cm (50 percentile) and body weight was 4.05 kg (<3 percentile). Physical examinations of chest revealed crackles and moderate grade of subcostal retraction. Laboratory findings were nonspecific with normal C-reactive protein and mild elevation of liver enzymes (aspartate aminotransferase/alanine aminotransferase 50/81 mg/dL). No virus was detected in the respiraotory virus polymerase chain reaction (PCR) assay in nasopharyngeal aspirates. Her chest x-rays showed bilateral peribronchial infiltrations. She was managed under the diagnosis of viral pneumonia and improved with treatment.
On day 8, high-grade fever, vomiting, and watery diarrhea developed. After 2 days of gastroenteritis symptoms, laboratory findings revealed metabolic acidosis and prerenal failure features due to a dehydration by frequent (20 times a day) diarrhea (pH, 6.90; HCO3-, 7.2 mmol/L; blood urea nitrogen (BUN)/Cr, 49.4/2.3 mg/dL; Na+/K+/Cl-, 138/5.1/117 mmol/L; anion gap, 18.9). At that time, her pulse rate was 210/min, body temperature was 39.9℃ and body weight was 4.0 kg. Her volume status was underestimated and total intake of volume (maintenance fluid volume by 5% dextrose sodium potassium (Na 34, K 20 meq/L, 20 mL/hr) and oral intake) was not adequate for her sudden volume loss over the short period. She was transferred to the intensive care unit for close monitoring and aggressive volume therapy. After delivering a bolus of normal saline (40 mL/kg) and bicarbonate infusion, 5% dextrose in 0.9% normal saline was infused (20 mL/hr). Laboratory findings were normalized (pH, 7.31; HCO3-, 21.0; BUN/Cr, 16.5/0.5 mg/dL) on day 10 and maintenance fluid was changed to 5% Dextrose sodium potassium (Na 34, K 20 meq/L, 20 mL/hr). However, her abdomen was severely distended and plain radiograms of abdomen showed dilatation of the small intestine. We performed abdominal ultrasonography and it showed dilatation and wall thickening of small bowel loops indicating small bowel obstruction. We closely observed her for the possibility of development of acute surgical abdomen. On day 11, plain abdominal radiogram showed suspicious free gas on upper abdomen (). We performed the crosstable abdominal radiogram and it showed free bowel gas (). She underwent an emergent laparotomy. Multiple necroses with 1 cm perforation were observed in terminal ileum 10 cm away from the ileocecal valve (). Distension of the whole small bowel and peritonitis were also found. Segmental resection of terminal ileum was performed. Histopathology of the resected bowel revealed a transmural coagulative necrosis, submucosal congestion, and focal lymphoid hyperplasia. Fecal specimen culture was negative but reverse transcriptase-PCR (RT-PCR) for NoV was positive. It was reported as GII and genotype 4 (GII. 4). The antigen test and enzyme immunoassay for adenovirus and rotavirus were negative, respectively. RT-PCR for astrovirus was also negative. Cytomegalovirus workup was not performed. After the operation, her abdominal distension improved and oral feeding was started on the day 9 after operation. However, bacterial pneumonia developed and she was intubated on day 21. We performed laboratory tests for the evaluation of her immune functions. She had a normal B, T lymphocytes and Natural-Killer cell counts. Immunoglobulin G/A/M levels were also within the normal range. She was discharged on day 48 in good general condition.


The first patient was a 62-year-old woman. She underwent a routine check-up due to a minor injury to her foot. Elevated liver enzyme levels were noted, and subsequent abdomen ultrasonography revealed a submucosal mass in the stomach. She had neither signs of tuberous sclerosis complex nor any family history of it. An abdomen computed tomography image showed a 4.2-cm subepithelial mass with broad base in the prepyloric antrum (). Endoscopic ultrasound revealed a hypoechoic mass involving the proper muscle layer, and laparoscopic wedge resection of stomach was performed. Lymph node enlargement or peritoneal metastasis was not detected. The patient was discharged after the surgery without any complication.
On gross examination, the subepithelial mass measured 4.2×3.2×2.0 cm and demonstrated fleshy cut surface with a well-defined border (). Microscopically, the tumor displayed a nested pattern of epithelioid tumor cells with abundant granular eosinophilic cytoplasm and round to oval nuclei (). The nests were surrounded by thin walled capillaries and a radial arrangement of tumor cells was found around the vascular lumens. The tumor cells showed mild pleomorphism, but coagulation necrosis was not observed. The mitotic count was 1 in 50 high power fields (HPF). Lymphovascular or perineural invasion was not found. The tumor was focally positive for human melanoma black 45 (HMB-45), smooth muscle actin (SMA), and desmin (), and negative for Melan A, vimentin, CD117, CD34, S100, pancytokeratin, and transcription factor E3 (TFE3). The Ki-67 labeling index was 1%.


The 7-month-old male child presented with an increased size of the head, vomiting, refusal to eat, fontanelle tension, respiratory failure.
The child was born at 33–34 weeks in critical clinical condition. His Apgar score was 7/7. The artificial lung ventilation was started from the 2nd day of life, the convulsions were observed. At the 15th day after delivery, the child was transferred from the hospital to the newborn pathology department with purulent meningoencephalitis, ventriculitis, intraventricular hemorrhage, stage II, complicated with obstructive hydrocephalus. During stay in the ward, he received prolonged antibiotic therapy, valproic acid, acetazolamide. The child was discharged at the age of 4 months. At the age of 5 months, the child was hospitalized to the local neurosurgery department where the VP-shunt was installed. One month after that the revision and removal of VP-shunt and installation of external drainage were made because of the shunt dysfunction. After removal of the drainage, the patient was discharged and referred to our clinic. The last 3 days before admission the child demonstrated severe deterioration: Reduction of motor activity, complete rejection of food and drink, vomiting, reducing the breath frequency. The child immediately was hospitalized in the children's department of our clinic with a serious condition. The child was asleep and adynamic. The neurological examination revealed bradypnea 12/min with periods of apnea lasting 10–15 s, exotropia, Graefe's sign, sluggish motor response on inspection and painful stimuli, pseudobulbar syndrome, central moderate tetraparesis. His head had hydrocephalic shape and circumference 53 cm. The anterior fontanelle had size 6 cm × 6 cm and was tense.
Magnetic resonance imaging showed multiloculated occlusive hydrocephalus with isolated cysts of III and IV ventricles [].
An urgent endoscopic intervention was performed using the neuronavigation, which resulted in the interconnected lateral ventricles and cysts of III and IV ventricles. Through the formed holes the silicone stent was placed into the III and IV ventricles and used as a ventricular catheter of VP-shunt [].
The clinical improvement including the regression of intracranial hypertension, improving of general condition, normalization of respiratory function, shifting from tube feeding to oral feeding, reduction of oculomotor disturbances, appearance of emotional reactions were seen postoperatively. The patient was discharged in good condition.


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.
In 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.
During 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.
Magnetic 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 ].
The 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.
Histopathology (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 ].
The 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.
At 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 77-year-old male visited our hospital to undergo follow-up examinations after treatment for FL. He had been suffering from advanced-stage FL, which was initially diagnosed 14 years previously. He had been treated with six cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone), ibritumomab tiuxetan, and two cycles of bendamustine, and achieved a durable complete remission for 4 years.
A laboratory test performed at the time of his visit showed pancytopenia. The patient’s peripheral white blood cell count was 1,200/µL (neutrophils, 46%; blastic cells, 2%), hemoglobin level was 7.9 g/dL, and platelet count was 9.8 × 104/µL. Bone marrow aspiration revealed a hypocellular bone marrow and dysplastic changes in three lineages. Blastic cells accounted for 8.8% of all nucleated cells. Complex karyotypic abnormalities, including del (7), were observed during G-banding. Based on these results, therapy-related MDS was diagnosed (refractory anemia with an excess of blasts type 2 (RAEB-2) with high-risk features of the International Prognostic Scoring System (IPSS)).
The patient was treated with azacitidine (75 mg/m2/day for 5 days) via subcutaneous injection. During the first cycle, he suffered from septic arthritis of the left hip and required hospitalization, whereby intravenous piperacillin/tazobactam and vancomycin were administered for 14 days. After the patient recovered from his septic arthritis, he commenced the second cycle of azacitidine combined with oral levofloxacin as a prophylaxis against infection.
On day 4 of cycle 2, he had a fever of up to 38.4℃ and exhibited oxygen desaturation. His peripheral white blood cell count was 1,300/µL (neutrophils, 17%; blastic cells, 13%). His CD4-positive T-cell count was low (119/µL). His other laboratory findings are shown in . Treatment for febrile neutropenia (intravenous cefepime and micafungin) was initiated, but his symptoms did not improve. The patient’s clinical course is summarized in .
A whole-body computed tomography (CT) scan revealed diffuse ground-glass opacities in both lungs, which were not observed on the baseline CT scan ( and ). These findings closely resembled those of Pneumocystis jirovecii pneumonia (PCP). However, blood and sputum cultures were negative, and the patient’s serum beta-D-glucan level was not elevated. Tests for cytomegalovirus antigen and galactomannan antigen were also negative. Bronchoscopy was considered, but could not be performed because of the patient’s low platelet count. Although PCP is relatively rare in patients with myeloid neoplasms, based on the patient’s CT findings and low CD4-positive T cell count, atovaquone was administered as an empiric therapy for PCP.
The patient’s symptoms spontaneously improved, but the intermittent elevation of his body temperature continued. To ameliorate his symptoms, 0.5 mg/kg prednisolone was initiated on day 18 of cycle 2, and the patient’s fever and oxygen desaturation gradually improved within a week. His CT findings were also improved on day 25 of cycle 2 (). Based on the patient’s clinical course, it was suspected that the lung injury had an immunological pathophysiology, e.g., it was tumor-related or drug-induced rather than an infectious pathophysiology.
Although azacitidine did not produce any hematological improvement, a bone marrow examination performed on day 28 of cycle 2 did not reveal any evidence of disease progression or transformation to AML. Considering these clinical benefits, a third cycle of azacitidine was started. However, the fever occurred again on day 3, and the patient’s chest CT findings worsened (). The exacerbation of the lung injury followed the course of azacitidine treatment, and there was no evidence of other infectious causes, such as bacterial, fungal, or viral infections. Thus, the patient was clinically diagnosed with azacitidine-induced ALI. The azacitidine treatment was suspended, and 1 mg/kg prednisolone was administered for 2 weeks. After the initiation of prednisolone treatment, the patient’s fever and oxygen desaturation improved markedly.


We report the case of a 23-year-old male referred to us with a 10-year history of left temporofrontal scalp swelling. The swelling was manifested by a headache and tinnitus in the left ear. The swelling had been gradually increasing in size to attain a giant size and was pulsatile nature there was the previous history of blunt head trauma when he was 12-year-old. First, he found an irregular small mass in his left forehead that became gradually spread. No visual disturbances or seizure was seen.
On examination, he was found to have a pulsatile soft tissue swelling over the left temporofrontal scalp which was slightly mobile over the underlying bone.
The mass was 12 cm horizontally and 6 cm vertically in diameter. A bruit was also demonstrated over the swelling [].
Examination of cardiovascular system was essentially within normal limits. Hematological and biochemical parameters were also normal. Chest X-ray and electrocardiography showed no abnormality.
A preliminary ultrasound and color Doppler of scalp was done which suggested features of pseudoaneurysm over the same region with no intracranial extension and with high velocity blood flow from superficial temporal artery. Computed tomography (CT) scan with intravenous (IV) contrast of head showed evidence of abnormal filled vessels involving the scalp on the left side in temporofrontal region. There was no intracranial extension of the lesion and intracranial AVM. In ventricles, too, was not seen any significant abnormality [].
The patients went to many clinics and were told him that because of congenital origin, surgery is not effective. However, we advised him to surgery after explaining calculated risks. En bloc resection of involved scalp was performed, and primary closure with split thickness skin graft was done. Excised soft tissue was sent to the department of pathology for histopathological examination, Alzahra Hospital, Isfahan. Histopathological data confirmed the diagnosis as AVM of superficial temporal artery postoperatively [Figures –].
The patient was followed for 6 months. Clinically, the patient was relived of symptoms with minimal scars [Figures and ].


A 71-year-old lady presented with an abnormal ECG finding during a scheduled primary care appointment. She was asymptomic and had a history of type 2 diabetes mellitus, essential hypertension, and dyslipidemia. During the consultation, the ECG reading showed premature ventricular contraction at a 1:1 ratio (ventricular bigeminy) with a heart rate of 46/min (). Her ECG from the previous year () showed non-specific changes, possibly related to early left ventricular hypertrophy. The recorded vital signs were as follows: blood pressure, 159/74 mm Hg; heart rate, 62/min; and respiratory rate, 18 breaths/min. On physical examination, heart murmurs were not audible and other findings were unremarkable. The laboratory findings were: glycated hemoglobin, 7.1%; urea, 10.0 mg/dL; creatinine 1.0 mg/dL; Na+, 137 mEq/L; and K+, 3.6 mEq/L. In order to rule out secondary causes that could have led to the changes in the ECG, various blood investigations were ordered. An urgent appointment was scheduled a week later to review these results. The patient was also advised to seek urgent medical attention if she felt palpitations or giddiness. During the second consultation, a week later, the repeat ECG showed atrial flutter with a 3:1 atrioventricular block (). All the results of the blood investigations were normal (thyroid stimulating hormone, 4.26 µIU/mL; Na+, 135 mEq/L; K+, 4.4 mEq/L; corrected Ca2+, 8.9 mg/dL; PO4-, 0.32 mg/dL; hemoglobin, 12.9 g/dL; and white blood cell count, 7.4×103/µL), except for an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels (88 mm/h and 9.8 mg/L).
Urgent transthoracic echocardiography revealed a dilated left atrium and ventricle without any myocardial hypokinetic changes. A large echogenic mass measuring 3.1×4.1 cm was identified at the left atrium (). The mass was solid and appeared pedunculated, arising from a stalk at the endocardium. The patient had a left ventricular ejection fraction of 54%. The patient was immediately referred to a tertiary care cardiology clinic where a second transthoracic echocardiography was performed. An imaging diagnosis of left atrial myxoma was confirmed. The tumor measured approximately 2.9×3.1 cm. A paroxysmal atrial fibrillation pattern was observed on the ECG. Warfarin treatment was initiated while aiming for a target international normalized ratio between 2 and 3. Currently, the patient is jointly cared for by the primary care physician and a multidisciplinary team that is helping to manage the anticoagulation therapy. The patient is unwilling to undergo surgery to remove the tumor.


A 25-year-old woman, with hypertension, presented to the emergency department at our medical centre with a markedly elevated blood pressure. This was the second emergency room visit within four days of a prior visit for the same complaint. During her previous visit, she was discharged on bisoprolol 5 mg twice daily, telmisartan 80 mg daily, hydrochlorothiazide 25 mg daily, spironolactone 25 mg once daily and nifedipine 20 mg twice daily. Her uncle, who brought her to the hospital, reported severe hypotension (80/50 mmHg) with telmisartan so she has stopped taking it.
Her blood pressure upon presentation was 218/150 mmHg, heart rate: 90 bpm, temperature 36.7℃, O2 saturation 100% and a BMI of 29.7 kg/m2. She reported dizziness, sudden onset headache, tinnitus, blurry vision, vertigo, nausea, fatigue and diffuse numbness. She reported compliance with a low sodium diet. She denied any chest pain, dyspnoea, haematuria, decreased urine output, seizures or muscle weakness. Review of systems revealed constipation, hirsutism, menstrual irregularities and intentional weight loss (37 kg over the past year). Her physical exam (including fundoscopy) was otherwise normal. Her laboratory tests including a complete blood count, chemistry profile, troponin and urinalysis were normal as well as an ECG and a computed brain tomography. Urine toxicology screen was negative for amphetamines and cocaine.
She was diagnosed with hypertension at the age of 23. Earlier in her disease course, her blood pressure was relatively controlled. However in the past year, she has had recurrent emergency room visits for elevated blood pressure. She suffers from major depressive disorder which started after she lost her mother secondary to ruptured brain aneurysm three years prior to her current presentation. She was also diagnosed with anxiety and was recently started on escitalopram 10 mg once daily with weekly psychotherapy sessions.
She has a positive family history of hypertension, chronic kidney disease, ruptured brain aneurysm in her mother and cardiovascular disease in her father.
Her psychosocial history is complex. She lives with her father whom she describes as being abusive to her mother. She is close to her mother’s family, but she describes them as overprotective and they can be in total charge of her life. She doesn’t smoke, drink alcohol or use illicit drugs.


A 71-year-old man was referred for evaluation of a palpable mass on his anterior chest wall. He had no dysphagia or chest symptoms. Based on findings from chest computed tomography (CT), the mass was suspected to be a malignant tumor, such as a sarcoma, plasmacytoma, or metastatic cancer (). Positron emission tomography (PET)-CT was performed as part of a metastatic cancer work-up. PET-CT revealed that the mass was probably a plasmacytoma or sarcoma and revealed focal hypermetabolic activity in the rectum suspicious of a rectal polyp or malignant tumor. A surgical biopsy of the tumor on the anterior chest wall was performed through a subxiphoid vertical incision. C-KIT (3+) and CD34 (3+) immunohistochemistry suggested that the tumor was an extra-gastrointestinal stromal tumor (EGIST). Resection of the tumor was performed through an anterior midline incision from the level of the fourth rib to 2 cm below the xiphoid process. The tumor had invaded the lower sternum, the fourth to the eighth costal cartilages on both sides, the pericardium, the diaphragm, and the peritoneum. There was no invasion of the lung or the liver. En bloc resection of the tumor, including partial resection of the sternum, costal cartilage, pericardium, diaphragm, and peritoneum, was performed (). To achieve a negative resection margin, the tumor was resected radically, maintaining a 3- to 5-cm margin grossly. The partially resected diaphragm and peritoneum were reconstructed with a bovine pericardial patch. The anterior chest wall was reconstructed with a 2-mm Gore-Tex patch. On postoperative day 2, the patient was transferred to the general ward. On postoperative day 6, his chest tube was removed. Because a rectal polyp was revealed on PET-CT imaging, a colonoscopy was performed preoperatively. A biopsy of the rectal polyp was performed during the colonoscopy, and the pathologic report indicated a well-differentiated adenocarcinoma. On postoperative day 11, the rectal polyp was resected through endoscopic submucosal dissection. Pathologic evaluation after the en bloc resection of the tumor revealed a negative resection margin, and the tumor was definitively confirmed to be an EGIST. On postoperative day 17, the patient was discharged without any complications.
At the 2 -week follow-up, the patient was doing well and exhibited no symptoms. The patient was referred to an oncologist for further follow-up and adjuvant therapy. Although further surgery for rectal cancer was required, the patient refused to undergo it. The oncologist recommended follow-up visits every 3 months thereafter.


A 45-year-old male presents to our clinic for an asymptomatic skin eruption of the upper and lower limbs that has been evolving for 2 months followed by bilateral eyebrow thinning. He was diagnosed with chronic myeloid leukemia with a Bcr-Abl kinase mutation 6 months ago then started, for the first time, on nilotinib 300 mg twice daily. The patient had been taking the same dose of nilotinib for 4 months before the onset of the eruption. A relevant episode of sudden hair loss occurred in a circular area of 4 cm on his right wrist; it appeared 2 months after he had started on nilotinib and spontaneously resolved 2 months later. Furthermore, 3 months after this event, there has been a rapidly progressing hair loss of his eyebrows and thinning of his chest hair. He was not treated with any other medication during this period and did not have any personal or family history of any similar rash nor alopecia.
On examination, the patient has extensive keratotic, red-brown, follicular papules over upper and lower limbs [Figures and ]. The rash was predominant over the extensor surfaces of the upper limbs, but the face and scalp remain intact. In addition, the patient presents diffuse thinning of his eyebrows without perifollicular erythema, hyperkeratosis, or any other evidence of scarring []. The disease does not affect scalp hair, eyelashes, or nails. The normal hair density on his right wrist is noted again. The remainder of the exam is normal and the patient declines any skin biopsy.
The follicular eruption is diagnosed as nilotinib-induced KP and the patient is given a topical 2% salicylic acid cream. For eyebrow thinning, clobetasol propionate 0.05% cream and minoxidil 5% spray are prescribed. Nilotinib cannot be discontinued due to its substantial role in the treatment of his chronic myeloid leukemia.


A 10-year-old girl presented with an approximately 70×35×20 mm reddish, verrucous, protruded lesion on the tongue (). The lesion was detected 4 years ago and showed occasional bleeding. Mild swelling first appeared on the right side and gradually progressed to involve the left also. No specific treatment was administered. Examination revealed a yellowish and dark brownish thickening of the tongue. Multiple hemorrhagic, translucent vesicles were observed. Regional lymphadenopathy was absent. On palpation, the swelling was compressible and soft. Head/neck magnetic resonance imaging revealed a 50×35×25 mm ill-defined lesion in the right two-thirds of the tongue, posterior sublingual space, and genioglossus (). Incisional biopsy confirmed lymphangioma circumscriptum ().
Combination triamcinolone and bleomycin was directly injected in the tongue at monthly intervals. shows the detailed injection ratios. Prophylactic intravenous antibiotics were administered before each intralesional injection. The initial triamcinolone concentration was greater than the bleomycin concentration to prevent post-injection swelling and airway obstruction because steroids inhibit the synthesis of multiple inflammatory proteins []. After the first treatment, the lymphangioma decreased in size substantially (). Each month, as the lymphangioma and tongue size decreased, the triamcinolone concentration was reduced and the bleomycin concentration was increased. Eight months after the first treatment, the lesion size stabilized (). The lymphatic malformation had decreased substantially, but complete remission was not achieved. Intralesional bevacizumab was subsequently included with the triamcinolone/bleomycin combination. The lesion began to regress again. The bevacizumab and bleomycin levels were increased and the steroid concentration was decreased in the monthly injection. Four further intralesional injections were administered. After 1 year of treatment, almost complete regression was achieved, but multiple small vesicles on the tongue surface had not resolved. Tangential excision of the vesicles was performed, resulting in a nearly even tongue surface. Thereafter, a minimum dose of combination injection was administered every 3 months for another year (). After finishing the 1-year treatment, 3 years after the initial treatment, neither recurrence nor complications were noted ().


A 51-year-old male patient presented to the outpatient clinic with a painless nodule near the right lower eyelid. The mass had grown slowly over the past 3 years, and measured 0.9×0.7 cm during examination (). The lesion appeared benign in clinical examination, and under local anesthesia, the patient underwent a 3-mm-margin elliptical excision and primary closure. Histologic study of this first specimen revealed epithelial cell islands floating in a mucin lake, with the final diagnosis being mucinous carcinoma. The epithelial component showed a solid and cribriform growth pattern and the tumor cells revealed moderate nuclear atypia and a mitotic aspect. Additional immunostaining study revealed that the tumor cells were immunopositive for cytokeratins (CK)-7 and negative for CK-20 with 10% Ki-67 positivity in the active area (). We performed re-excision of the surgical site with an additional 3-mm margin, which was free of malignant histology. The possibility of a metastatic primary mucinous carcinoma (e.g., breast or gastrointestinal tract) could not be completely ruled out, but a systemic evaluation by positron emission tomography-computed tomography revealed no other suspected site of malignancy. During a close follow-up over 2 years, the patient did not experience any postoperative complication or recurrence ().


An 8-year-old boy was referred to Endodontic Clinic Department of Islamic Azad University of Tehran for management of an immature permanent anterior tooth with pulp necrosis secondary to trauma and severe pain on chewing. In his dental history, the root canal of tooth #9 had already been opened and instrumented. On clinical examination, tooth number #9 had complicated crown fracture and severe sensitivity to percussion and palpation but mobility and probing measurement were in normal limit. The pulp responses to cold, heat, and electronic pulp tester (EPT) tests were negative, whereas the contralateral and adjacent teeth were normally responded. No swelling or sinus tracts were detected. In periapical initial radiograph, incomplete root apical formation was observed, along with periapical radiolucency []. According to clinical and radiographic findings, a common diagnosis of pulp necrosis and acute apical periodontitis was determined. Based on wide-open apex, a modified regenerative treatment was planed.
An informed written consent was obtained from his parents after complete explanation of the risks and possible failures and the alternative treatment modalities.
A two-visit regenerative endodontic procedure was performed. On initial visit, the access cavity was reopened after administration of local anesthesia by 3% mepivacaine plain (Septodont, Cedex, France) without vasoconstrictor and rubber dam isolation. Following working length determination through an ISO #45 K-file and periapical radiograph, the root canal was gently irrigated with 20 ml of 2.5% sodium hypochlorite (NaOCl) without any mechanical instrumentation. To prevent the destruction of thin dentinal walls and progenitor cells which exist in the apical tissues, a passive decontamination was performed using NaOCl without conventional mechanical instrumentation.[]
Final rinse with 10 ml normal saline was performed to remove the remaining NaOCl. After irrigation, a double antibiotic paste (prepared from the precursors of ciprofloxacin 250 mg and metronidazole 250 mg in 1:1 ratio)[] was mixed with sterile distilled water in a 3:1 ratio as manufacturer's instruction. Then, the mixture was placed in the canal though lentulo spiral and taped down the root canal with a moist large paper cone. The access cavity was sealed with e-Temp (DiaDent Group International, Korea), and the patient was recalled 4 weeks later.
On second visit, the tooth was asymptomatic. The tooth was anesthetized with 3% mepivacaine plain (Septodont, Cedex, France) without vasoconstrictor, isolated by rubber dam, and reopened. The double antibiotic paste was removed with copious irrigation of 20 ml of 2.5% NaOCl and final rinse with 20 ml normal saline; thereafter, the root canal was irrigated by different dilutions of EDTA as a TDM protocol preparation (root canals were dried with paper points and filled with 1 ml of 17% EDTA for 5-min, 10% EDTA for 5-min and 5% EDTA for 10-min, respectively, and distilled water at regular intervals) and a final rinse with 10 ml sterile saline.[] Apical bleeding was induced by gentle apical patency into apical tissue with ISO#35 K-files, until an obvious blood hemorrhage was achieved approximately at 2-3 mm below the cementoenamel junction (CEJ). A sterile cotton pellet was inserted into the canal and held there for 10 min to allow blood clot formation. Next, calcium-enriched mixture (CEM) cement (CEM-Bionique Dent, Iran) was mixed on a glass-mixing pad according to the manufacturer's instructions and applied gently on the blood clot just below the CEJ at a 5–6 mm thickness using a micro spoon excavator and large paper points. Finally, a wet cotton pellet was placed over the CEM cement, and the access cavity was temporarily restored with resin-modified glass-ionomer cement (RMGIC) base material, Vitrabond (3M, ESPE, St. Paul, MN, USA). The tooth was restored with final resin bonded composite restoration 4 days later after removing cotton pellet and RMGIC. The patients' parent was instructed to refer to our dental clinic in case of any pain or discomfort, tenderness to chewing pressures, mobility, and swelling.


A 7-year-old boy was referred to Endodontic Department Clinic of Islamic Azad University of Tehran by a general practitioner for endodontic management of an immature permanent molar with pulp necrosis secondary to caries. The tooth #29 had been instrumented and dressed with Ca(OH)2 by his referral dentist 3 weeks ago. On clinical examination, the tooth was asymptomatic and no responses to percussion and palpation. Periodontal examination revealed no mobility and normal probing depth (<3 mm). Responses to cold, heat, and EPT tests were negative, whereas the contralateral teeth were normally responsive. No signs of swelling and sinus tract were observed.
Radiographic examination revealed incomplete root formation and periapical radiolucencies []. All clinical and radiographic findings indicated pulp necrosis along with chronic apical periodontitis. According to the immature root formation with wide-open apices, endodontic revascularization treatment was planned.
An informed written consent was obtained from his parents after complete explanation of the risks and possible failures and the alternative treatment modalities.
Since the patient and his parents lived overseas and could not attend again earlier than 6 months, the tooth was treated by one-visit endodontic revascularization protocol. The tooth was anesthetized with 3% mepivacaine plain (Septodont, Cedex, France) without vasoconstrictor, isolated with rubber dam, and reopened. Remnant of Ca(OH)2 paste was removed by gentle filing and copious normal saline irrigation. Then, the root canals were gently irrigated by 20 ml of full strength (5.25%) NaOCl followed by 10 ml sterile normal saline, then 10 ml 2% chlorhexidine (CHX) and a final rinse with sterile normal saline.
The chemically cleaned root canals were filled with different dilutions of EDTA based on a TDM protocol preparation (root canals dried with paper points and filled with 1 ml of 17% EDTA for 5-min, 10% EDTA for 5-min and 5% EDTA for 10-min, respectively, and distilled water at regular intervals) and final irrigation with 10 ml sterile saline and dried with paper points.[] Apical bleeding was induced by gentle apical patency with #35 K-file. Blood hemorrhage was established 1–2 mm below the orifice levels. After 5 min and formation of the blood clot, CEM cement (CEM-Bionique Dent, Iran) was mixed on a glass-mixing pad based on the manufacturer's instructions and was placed and back-filled over blood clot to the level of the CEJ with a 4–5 mm thickness using a micro spoon excavator and large paper points. Finally, a well-moistened cotton pellet was temporary placed over the CEM Cement for 15 min. After initial set of CEM cement, the access cavity was permanently restored with amalgam restoration over a RMGIC base material, Vitrebond (3M, ESPE, St. Paul, MN, USA) at the same visit.
After 6 months, the tooth was symptom-free and complete radiographic healing of periradicular radiolucencies was observed. At 12-month follow-up, radiographic examination showed visible increase in the roots canal wall thickness []. The roots showed complete apical closure. During 6- and 12-month recall examinations, the tooth was not responsive to EPT and cold tests.


A 4-year-old boy without significant medical history was admitted for limited neck motion for 3 wk. The physical examination showed an irreducible torticollis with analgesic attitude of cervical spine. The active and passive mobilization of the neck was painful and no motor or sensory deficit was detected. The general condition of the patient was good, the clinical examination did not show a tumoral syndrome and the neurological examination as well as skin examination and laboratory tests were normal.
The magnetic resonance imaging (MRI) of cerebro-spinal cord uncovered an infiltrative mass involving the dens of C2 which is hypointense on T1 sequence and hyperintense on T2 sequence, extending to the surrounding soft tissues leading to an increase in C1-C2 space, without compression of the spinal cervical cord. Complementary CT showed fragmented dens with important C1-C2 dislocation (Figure ).
The odontoïd and mass biopsy was performed by endoscopic guidance. Histological features were consistent with inflammatory EG. The positivity of the immunostain by the antibody anti Ps100 and the antibody anti CD1a confirms the diagnosis of LCH (Figure ).
Initial treatment was started prednisolone 40 mg/m2 per day orally, with weekly reduction starting from week 4 and intravenous Vinblastine 6 mg/m2 per week for six weeks. An external immobilization by a cervical collar was maintained during the entire period of chemotherapy.
The evolution was marked by a decrease in pain secondary to the active mobilization of the neck with a persistent passive analgesic position. The control radiologic MRI showed a displaced horizontal fracture of the dens responsible for a posterior wall recoil reducing cervical occipital hinge without intramedullary signal abnormality. The infiltrative process had regressed in size (Figure ).
A posterior cervical arthrodesis was performed and the spine was stabilized with a metal lacing associated with tricortical iliac crest graft interposed between the posterior arch of C1 and C2. No neuro-vascular complications have been detected.
The patient is still under treatment consisting of prednisolone 40 mg/m2 per day orally for five days in a week every four weeks and IV Vinblastine 6 mg/m2 bolus every four weeks for 12 mo. Repeated CT scans revealed at 5 mo a consolidation of C2 fracture with moderate stenosis of the occipital hinge (Figure )


A 25-year-old female patient (weight: 52 kg and height: 162 cm) with dentofacial anomalies having both anterior edge to edge bite relationship and facial asymmetry was scheduled to have Le Fort I osteotomy and bilateral sagittal split osteotomy (BSSRO) surgery under general anesthesia. The patient was also diagnosed with factor XI deficiency with an increased activated partial thromboplastin time (aPTT) of 87.5 seconds (normal: 26-35.3 seconds), and a factor XI activity of 5% (normal: 60-150%). Other laboratory values, including prothrombin time and international normalized ratio (PT INR) (1.06, normal: 0.8-1.2), and PT % (91.0%, normal: 80-120%) were within normal limits. The hemoglobin (Hb), hematocrit (Hct) and platelet counts were 12.8 g/dl (normal: 12-16 g/dl), 37.6 (normal: 36-48%), and 194,000/mm3, respectively. A chest radiograph, electrocardiogram (ECG), and other laboratory findings were unremarkable. The decision was made to operate on the patient using both the SpHb and rotation thromboelastometry for effective perioperative management.
During surgery, the patient's ECG, noninvasive blood pressure, percutaneous oxygen saturation, temperature, and arterial line were actively monitored. Intravenous thiopental 175.0 mg was used to induce anesthesia. The patient was intubated nasally after the administration of cisatracurium 12.0 mg. Anesthesia was maintained with 5-6% desflurane, 50% nitrous oxide and oxygen. The patient's vital signs were stable throughout the procedure (). The surgery time was total 250 minutes and the anesthesia time was 300 minutes. There was a total of 560 ml blood loss, and 500 ml of urine output. The patient's Hb levels were continuously checked through the SpHb values (). Four units of fresh frozen plasma (FFP) and two autologous units of blood (360 ml) were used during surgery based upon the continuously monitored blood levels of Hb. At the end of surgery, the patient's Hb was 8.1 g/dl and Hct was 27%. The patient was extubated with the removal of the endotracheal tube when she resumed spontaneous breathing but before she recovered consciousness. The patient was transferred to the recovery room. The ROTEM™ analysis showed normal variables in the extrinsically activated test (EXTEM) and intrinsically activated test (INTEM) ().
After surgery but before the patient's discharge, her bleeding tendency was investigated using coagulation tests including aPTT. Seven days after surgery, aPTT was slightly elevated at 48.4 seconds. The patient was discharged without any complications.


The patient was a 50-year-old man (height 159 cm, weight 69 kg) scheduled for extraction of impacted wisdom teeth (#18, 28, 38, and 48) and saucerization owing to chronic osteomyelitis in the right mandibular molar area. The patient had a history of heavy snoring, but was otherwise in good health. However, he had an extreme phobia of tooth extraction. The oral surgeon also determined that the procedure would be highly invasive; as a result, intravenous sedation was requested from the department of dental anesthesiology. We planned conscious sedation using dexmedetomidine to help secure the patient's airway during the extraction procedure. The authors also planned PCS for adequate titration of sedation levels. The patient received an explanation about the dental procedure under sedation, after which he provided written consents for the procedure and the case report.
The results of the pre-anesthesia examination performed the day before the surgery after the patient was admitted showed no specific findings, except eosinophil levels elevated to 13% in the blood test. He was given instruction for NPO for eight hours before the procedure and was sent to the operating room after securing an 18-gauge intravenous line in his left arm.
The PCS pump used was a Perfusor® Space PCA Infusion Pump System (B. Braun Medical Inc., Germany). Dexmedetomidine (Precedex 200 µg/2 ml) was diluted in normal saline to prepare a 50 ml solution at 4 µg/ml. Without setting a basal infusion dose in the PCS pump, the bolus dose, lock-out time, and injection speed were set to 0.1 µg/kg, 1 min, and 1,500 ml/h, respectively.
Electrocardiogram, noninvasive blood pressure, oxygen saturation, and bispectral index (BIS) monitors were attached to the patient. The patient held the PCS demand button in one hand and the patient was instructed to push the button if he felt any anxiety or pain. Oxygen was supplied through a nasal canula, while capnography measurements were obtained simultaneously ().
The sedation procedure took a total of 100 min, and the procedure included saucerization of the region around #37 and extraction of impacted wisdom teeth (#18, 28, 38, and 48). The single dose administered when the patient pushed the button was 1.73 ml, equivalent to 6.93 µg. The patient pushed the button a total of 13 times, but was pushed four times within the lock-out time; therefore, the drug was actually administered nine times, totaling 15.6 ml (62.4 µg).
The patient maintained his state of consciousness and was able to respond to commands. His respiratory rate and vital signs also remained within a normal range (). During the operation, the button was pushed several times during painful procedures. Afterwards, the BIS value dropped to around 60 once, but was maintained around 90 throughout. The serum dexmedetomidine concentrations calculated from the patient and the number of times the button was pushed are shown in . The patient was discharged the next day without any complications.


A 67-year-old female patient was hospitalized at the authors’ institution for left distal femur fracture that was treated with open reduction and internal fixation. During her postoperative stay, it was noted that food particles were draining from an anterior cervical wound. Patient had a history of two previous cervical spine surgeries, both performed at other institutions. The first was a C4-6 posterior laminectomy without fusion, performed eight years prior to this hospitalization. The second surgery was performed 4 mo prior to her admission to the authors’ institution. It consisted of C4 and C5 partial corpectomy with insertion of a polyetheretherketone (PEEK) cage and C3-6 anterior cervical instrumentation.
The spine service was consulted and plain radiograph demonstrated inferior screws pullout with plate migration (Figure ). Computed tomography (CT) scan showed subcutaneous air tracking along the neck soft tissues. General surgery and otolaryngology were consulted and an esophagram (Figure ) revealed ingested oral contrast tracking along the right subcutaneous tissues of the neck confirming perforation of the esophagus at the level of the inferior screws with fistulization through the anterior surgical wound. Blood work showed normal white cell count 8000 (normal 4500-10000), decreased prealbumin 6.1 mg/dL (normal 17-34) and serum iron level 15 mg/dL (normal 50-212) that confirmed malnutrition.
The patient’s oral intake was suspended and a nasogastric tube placed to facilitate feeding. The patient was taken to the operating room and underwent removal of the anterior hardware, drainage of cervical abscess, revision C4-5 corpectomy, C3-C6 fusion using tricortical iliac crest strut autograft and halo vest immobilization. The wound was left open and managed by the general surgery and otolaryngology services. One week after the revision cervical fusion, the patient was taken to the operating room by general surgery for irrigation and debridement, insertion of a 10 French gauge rubber tube for irrigation and Penrose drain. The wound was irrigated via the rubber tube two times daily with a dilute hydrogen peroxide solution. The patient was placed on ceftriaxone and flagyl for 6 wk as cultures grew polymicrobial mouth flora.
The halo vest removed at 3 mo. The fistulous tract healed at 3 mo and patient resumed oral feeding. Six months follow-up CT scan showed graft incorporation (Figure ). At two years follow up, patient denied any neck pain or dysphagia and plain radiograph showed maintenance of the cervical spine alignment (Figure ).


A 78-year-old male presented to a hospital with the chief complaints of dyspnea and ache in his left shoulder. Cardiomegaly was detected on chest X-ray scans, and the presence of pericardial effusion and moderate aortic regurgitation was observed by echocardiography. He was treated with diuretic agents, and his symptoms improved. Three months later, he presented to the hospital again with worsening dyspnea. Worsening cardiomegaly was detected on chest X-ray scans (Fig. ), and marked pericardial effusion was observed on echocardiography. Pericardiocentesis was performed, and 1,500 mL of hemorrhagic pericardial effusion fluid was drained. Chest examination by computed tomography revealed the presence of a mediastinal mass, pericardial thickening, and pericardial effusion (Fig. , ), and the patient was transferred to our hospital for treatment. He showed marked emaciation (he was 164.6 cm tall and weighed 43.6 kg) and a low blood pressure (81/47 mm Hg). He was assessed to have an Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 2. His laboratory findings from a complete blood cell count analysis were almost normal; his hepatic and renal functions were normal; his albumin levels were lower than normal (2.7 mg/dL), and his C-reactive protein levels were high (10.00 mg/dL). The levels of the soluble serum tumor marker CYFRA 21-1 (cytokeratin-19 fragment) were increased (36.0 ng/mL). After further examination, he was diagnosed with squamous cell carcinoma of the thymus. According to the tumor-node-metastasis staging system, the carcinoma stage was cT4N3M0 or stage IV.
Carboplatin was administered on day 1 at a dose of a targeted area under the concentration-time curve of 5, and nab-paclitaxel at a dose of 70 mg/m2 on days 1, 8, and 15 for every 4 weeks. Four cycles of this regimen were administered. During 3 of 4 cycles, grade 3 or 4 neutropenia occurred, and 3 doses of nab-paclitaxel on day 15 or 8 could not be administered. The patient did not experience any other severe adverse events. After the administration of 2 cycles of this regimen, chest computed tomography scans revealed a reduction of the tumor diameter (Fig. ); administration of 2 additional cycles led to further reductions (Fig. ). The ECOG PS of the patient improved to 0 (zero). The serum CYFRA 21-1 levels decreased to 2.3 ng/mL. After the interval of 1 month, these levels increased again to 4.3 ng/mL. Resultantly, maintenance nab-paclitaxel monotherapy at a dosage of 70 mg/m2 on days 1 and 8, for every 3 weeks was initiated. A total of 8 cycles of maintenance nab-paclitaxel monotherapy were administered in 4.8 months, after which the tumor showed regrowth. The patient experienced a total of 10.3 months of progression-free survival from the start of chemotherapy. After the regrowth of the tumor, the patient has received second-line treatment. Till date, the patient has been alive for a total of 22.0 months from the start of first-line chemotherapy.


A 20-year old male developed complex partial seizures by the age of 3 (April 1996). Magnetic resonance imaging (MRI) revealed a nonenhancing T2/FLAIR hyperintense, well-defined mass in the left frontal lobe. After a subtotal resection (STR) in 1997, histopathological analysis concluded that the tumor was a DNT of so-called simple form [ and ]. After surgery, the seizures diminished in intensity and frequency but did not cease. He remained on antiepileptic drug treatments (AEDs) with acceptable therapeutic effect. In 2001, the patient deteriorated with increased electroencephalography (EEG) verified complex partial seizures. A diagnostic MRI showed residual, nonenhancing tumor in the left frontal lobe, which led to a second STR in 2002 [Figure –].
Histopathological analysis confirmed the tumor to be a DNT of simple form without malignant transformation. After the second surgery, the patient developed a right-sided spastic palsy, and in later years, signs of cognitive dysfunction, especially with respect to learning skills. The seizures gradually diminished in frequency and intensity, reaching an ENGEL Epilepsy Surgery Outcome Scale (ES) of 2 in 2003, although the patient remained on AEDs. Follow-up MRI in January 2003 [Figure –] showed nonenhancing residual tumor, without radiological signs of malignant transformation. A 11C-methionine positron emission tomography (MET PET) performed in 2005 confirmed the absence of malignant transformation, with MET uptake lower than in the contralateral frontal cortex. A third surgical resection was deemed too high risk, while both fractionated radiotherapy with LINAC as well as chemotherapy were judged likely to be ineffective, with salvage radiosurgery by GKRS assessed to be the only viable treatment option. The patient was treated in 2005 with a peripheral prescription dose of 10 Gy at the 50% isodose line []. Follow-up MRI revealed tumor regression, with no signs of adverse radiation effect (ARE); nevertheless, his epileptic status remained unchanged. Follow-up MRI in 2009 showed a 7-mm contrast-enhancing lesion/presumed recurrence in the surgical margin, but without relation to the previous GKRS target and no suspected malignant transformation. A new GKRS treatment was performed with a prescription dose of 12 Gy to the 50% isodose line (2010). Serial follow-up MRIs between 2010 and 2015 have shown no progress of residual tumor and no signs of ARE. Seizures gradually decreased in frequency and intensity after the second GKRS. Remaining on AEDs, the patient has been seizure-free (ES 1) since early 2013. Major clinical impairment at present consists of a minor right foot palsy, while a neuropsychological assessment performed in April 2014 showed no major cognitive impairment. His overall quality of life remains good.


A 27-year-old male had developed intermittent numbness and right-sided neuralgia with upper limb predominance at the age of 11 (1999). A diagnostic MRI demonstrated a 3 cm mass with asymmetrical, nodular, and curvilinear contrast enhancement located in the left postcentral gyrus with an appearance deemed at the time consistent with a low-grade glial tumor. The EEG revealed an epileptic focus in the left frontal-temporal regions. AEDs proved ineffective for seizure control. A functional MRI located the hand motor cortex anterior to the tumor. The patient underwent gross total resection (GTR) in 1999. The initial microscopic evaluation could not differentiate between pilocytic astrocytoma and DNT. Further re-examination based on immunohistochemistry and molecular analyses (MA) proved the lesion to be a complicated type of DNT, displaying mosaic-like patterns composed of complex structures together with nonspecific elements (low-grade glioma-like structures, see and ).
The seizures ceased almost immediately after surgery (ES 1). Postsurgical MRI demonstrated a nonenhancing residual tumor. Two years after surgery, the sensory seizures recurred. A follow-up MRI showed a new contrast-enhancing lesion within the surgical margins. Open surgery was assessed to be highly hazardous due to the tumor's close relation to adjacent motor fibers. GKRS was deemed to be the best treatment alternative. The patient was treated in 2002 with a peripheral dose of 12 Gy at the 50% isodose line [Figure – and ]. The seizures ceased shortly after treatment (ES 1) and the patient remained free from AEDs and seizures thereafter. Serial follow-up MRIs between 2004 and 2006 showed a gradual decrease in tumor volume and contrast enhancement. There have been no signs of recurrence or radiation necrosis/edema on subsequent annual MRI from 2008 to 2013 [Figure and ]. With the last clinical follow-up in 2015, the patient remained AED and seizure-free (ES 1) and showed no neurological impairment.


A 28-year-old male had developed complex partial seizures at the age of 6. MRI (without IV contrast) revealed a T1 hypointense/T2 hyperintense, well-delineated, possibly multilobular mass located in the inferomedial aspect of the right temporal lobe including hippocampus [Figure and ]. Contrast-enhanced images were not available at the time of writing of this paper; as such it remains unclear whether or not the tumor was originally contrast-enhancing.
In this case, we could not find evidence of prior diagnostic EEG. The patient underwent STR in 1994 and, despite the subtotal nature of the resection, seizures ceased shortly after (ES 1) and AEDs were discontinued. The histopathological analysis revealed a DNT of complex form with specific glioneuronal elements and associated FCD [ and ].
The patient remained stable until 2001, when a follow-up MRI demonstrated a suspect nodular contrast enhancement in the region of the residual tumor located in the right hippocampus and posterior aspect of the medial temporal lobe [Figure –]. A follow-up MRI in 2003 showed clear signs of local contrast-enhancing tumor progression. The patient underwent STR in early 2004. No pathology report from the second operation is available to us. Because seizures recurred prior to surgery, AEDs were restarted. The seizures ceased after surgery, but the patient was kept on prophylactic AEDs. Follow-up MRI the same year (2004) and subsequent follow-up examination the year after showed gradual progression of the contrast-enhancing residual tumor. The lesion was located in the posteromedial aspect of the right temporal lobe, including the hippocampus and parahippocampal gyrus, bulging into the quadrigeminal plate cistern with subtle mass effect on the midbrain. Volumetric studies assessed the tumor to be 2 cm3 (18 × 16 × 15 mm). Despite the above, the patient was still seizure-free (ES 1). Because open surgery was not an option due to the tumor location, the patient underwent GKRS in 2005. The lesion was treated with a peripheral dose of 12 Gy at the 50% isodose [Figure – and ]. Serial MRI imaging between 2006 and 2013 showed a gradual decrease in tumor size, ultimately without any signs of ARE [Figure –]. No signs of neurocognitive dysfunction have been described. The patient remains seizure-free and leads a normal and active life. Mainly due to the patient's line of work, he has been kept on prophylactic AEDs.


A 75-year-old woman with a history of cholecystectomy and surgery for breast cancer was admitted in 2003 with a 10 cm large ruptured infrarenal abdominal aortic aneurism (AAA). Immediate surgery with implantation of a polyester tube graft was performed. Postoperatively, sepsis due to Staphylococcus aureus occurred. The source was not identified, and Penicillin and Ciprofloxacin were administered intravenously for 3 weeks until discharge.
Three months postoperatively, she was admitted with sepsis and pain in her right foot. Computer tomography (CT) confirmed a plantar abscess which was treated surgically. Intravenous Ciprofloxacin and Cloxacillin were administered for 10 days followed by oral antibiotics for 1 week. Supplementary CT angiography (CTA) was performed, revealing a 4.2 cm large pseudoaneurysm at the cranial graft anastomosis. Microbiological cultures grew negative. The patient responded following 3 weeks of intravenous Cloxacillin. The pseudoaneurysm was followed with ultrasound every 6 months until a diameter of 5.2 cm in December 2004. To exclude the pseudoaneurysm, a stentgraft (Endurant®, Medtronic) was implanted in March 2005. Early onset postoperative sepsis complicated the course, and CTA revealed abscess formation in the pseudoaneurysm. CT-guided puncture was performed (Fig. ). Cultures grew Streptococcus milleri, Eikenella corrodens and Bacterioides sp. Meropenem was administered with clinical response. Four weeks after stentgraft implantation, open revision of infected and necrotic tissue was performed. The graft implanted in 2003 and the stentgraft were partially exposed in a range from 2 to 5 cm distal from the renal arteries. A fistula from the last part of duodenum to the aneurysm sac was closed surgically. A decision was made not to explant the grafts due to impaired general condition and high age, and that graft excision would include suprarenal aortic clamping. Gentamycin (Gentacoll®) sponge was applied locally on the grafts and coverage with omentum was performed. Two weeks postoperatively, the patient was discharged with Ciprofloxacin and Clindamycin for 3 months. In June 2005, CTA revealed no sign of infection and antibiotics were continued for 6 months. In 2007, she presented with fever, and blood cultures grew Actinomyces. A decision was made to treat with antibiotics indefinitely. During the period 2008–13, the patient was admitted at several occasions with sepsis, successfully treated.
In December 2013, she was admitted with melena. Gastroscopy, CTA and sigmoidoscopy did not identify the bleeding source. The hemorrhage stopped spontaneously. Readmission occurred 2 weeks later due to hypovolemic shock. Endoscopic ultrasound revealed an aortoenteric fistula with a 3 × 2 cm2 opening with exposure of aortic graft material. Open surgery was considered too risky and a new stentgraft (Endurant®, Medtronic) was implanted in January 2014. For the next 2 years there were several admissions due to sepsis. In 2016, the patient was admitted due to hematemesis. Endoscopy visualized aortic graft material penetrating the duodenal wall (Fig. ). The patient was stabilized and was discharged to her home.


A 14-year-old castrated male Maine Coon cat presented for left hindlimb lameness of 1 day’s duration without known trauma. Physical examination revealed a non-weightbearing lameness on the left hindlimb, with sensitivity upon palpation of the stifle. The stifle joint was stable and there was no swelling. Following sedation, orthogonal radiographs were made of the pelvis and stifles. A complete transverse fracture of the left patella with mild proximal displacement of the base was documented. There was severe sclerosis of the patella with loss of corticomedullary demarcation (). There was no stifle effusion or soft tissue swelling. A focal region of the cranial and caudal cortex of the left tibia were thickened and the fibula did not have a distinct medullary canal (). The right patella was also sclerotic but had no evidence of a fracture. The cat was treated with oral buprenorphine (15 µg/kg transmucosally) for pain management, along with restricted activity, and it recovered well. Two months following the initial lameness, the cat was re-presented for acute right hindlimb lameness. Radiographs confirmed a complete transverse fracture of the right patella, sclerosis of the right patella and a non-union fracture of the left patella (,b). Pain management and rest were re-instituted and the cat was doing well approximately 1 month after the second patellar fracture.
Further review of the cat’s medical history revealed that this cat had received alendronate (5 mg PO once weekly) for the past 8 years. A veterinary dental specialist had initially prescribed alendronate to prevent further development of tooth resorption, following extraction of multiple teeth affected by this condition. At 13 years of age the cat’s serum creatinine was 2.1 mg/dl (reference interval [RI] 0.8–2.3 mg/dl) and blood urea nitrogen was also within the RI. A complete urinalysis revealed a urine specific gravity (USG) of 1.050 at this time. In the 8 years during which the cat was treated with alendronate, serum calcium and phosphorus were within the RIs on numerous serum biochemical panels; magnesium was not measured. Serum creatinine exceeded the RI three times during this time period but was most often in the upper-third of the RI. Paired USGs during this time frame were ⩾1.050.
Radiographs of this cat’s tibia were compared with those from a group of geriatric cats ⩾8 years old that presented to the orthopedic service for investigation of hindlimb lameness and had images of the whole tibia, including lateral and craniocaudal projections, allowing measurements to be taken. Thirty-five cats were identified from The Ohio State University – Veterinary Medical Center digital radiography archive from 2003–2013. Complete radiographic studies were not available for all cats. Age ranged from 8–20 years (median 12 years). Sex distribution included 20 castrated males, two intact males and 13 spayed females. The most common indications for imaging were stifle osteoarthritis and tibial fracture associated with trauma. These cats were normal based on history and physical examination, other than that related to the musculoskeletal system. Serum creatinine was measured in 27 of these cats. Serum creatinine was a median of 1.6 mg/dl (range 0.6–2.8 mg/dl) in 27 cats. Serum creatinine was within the RI in 20 cats and >2.0 in seven cats.
Measurements of the tibia were made using a digital caliper applied perpendicular to the tibial long axis at two locations in both the mediolateral and craniocaudal radiographic projections (). One set of measurements was made proximally at the junction of the proximal and middle thirds of the tibia (distal to the tibial crest), and the second set was taken distally at the junction of the middle and distal thirds of the tibia. The width of the cranial and caudal cortex was determined on the mediolateral projection, and the width of the medial and lateral cortex on the craniocaudal projection. The external diameter of the bone was measured at both proximal and distal sites on both radiographic projections. The diameter of the medullary canal was calculated by subtraction of the cortical measurement from the total diameter measurement. To compensate for variability in tibial size between cats and allow comparison with the cat of this report, measurements were expressed as percentages of external cortical diameter (). Compared with this population of control cats, the cat of this case report had greater cortical bone thickness and a narrower medullary canal. shows the comparison of all radiographic measurements taken. Measurements of the medullary canal diameter that were most likely to differentiate controls from the subject were taken from the distal craniocaudal (median was 59% in controls vs 33.5% in subject) and lateral projections (median was 52.5% in controls vs 31.5% in subject), and from the proximal craniocaudal projection (median was 54% in controls vs 34% in subject).


Our patient is a 59-year-old female with a significant past medical history of hypertension, iron deficiency anemia, and tobacco dependence amounting to a 40-pack-year smoking history. She initially presented to her primary care physician (PCP) with a 6-month history of generalized fatigue with associated symptoms of anorexia and a 20-pound unintended weight loss. Fearing the possibility of a lung cancer, her PCP obtained a computed tomography (CT) scan of the chest, which showed a 3-mm nodule in the right lower lobe of the lungs, multiple heterogeneous hepatic lesions, the largest of which measured 7.2 × 5.6 cm, and a hypoattenuating lesion measuring 4.8 × 3.1 cm at the tail of the pancreas (Fig. ). A follow-up CT scan of the abdomen and pelvis re-demonstrated these findings with multiple enlarged periaortic lymph nodes. At the same time, her laboratory test revealed elevated liver transaminases and cancer antigen 19-9 level. An ultrasound-guided core biopsy of the liver was performed and histology confirmed liver lesions to be small-cell carcinoma, poorly differentiated. Positron emission tomography (PET) scan showed uptake consistent with malignancy in the liver and pancreas, but no PET-avid lesions were seen anywhere else.
After discussing the diagnosis and treatment options with the patient, she elected to proceed with palliative chemotherapy. She was started on a standard regimen of carboplatin and etoposide. Restaging scans after two cycles showed great response with some reduction in the sizes of both the hepatic and pancreatic lesions. The subsequent imaging after 6 cycles showed a stable disease. She was at this time referred to a tertiary teaching hospital where she was evaluated for a clinical trial but was found ineligible to participate. Unfortunately, repeat CT scan of the abdomen and pelvis 2 months after completing 6 cycles of palliative chemotherapy showed disease progression with increase in the sizes of the previously seen hepatic lesion and new metastatic lesions. She was subsequently started on topotecan. A restaging scan performed after cycle 2 of second-line palliative chemotherapy showed further disease progression (Fig. ). She had a good ECOG performance status of 1. We reviewed the treatment goals and options with the patient once again. We introduced the idea of a trial of nivolumab based on preliminary results of CheckMate 32 studies showing favorable outcomes for the treatment of recurrent SCLC and she welcomed the idea. A repeat CT scan after 5 weeks and 4 doses of nivolumab treatment showed a reduction in size of the largest hepatic lesion from 7.2 × 6.6 cm to 4.8 × 3.7 cm and the number of hepatic metastases. Similarly, the pancreatic tail mass was decreased in size from 3.7 × 3.5 cm to 3.6 × 2.4 cm (Fig. ).


Patient 1 was a 41-year-old female with approximately 2.5 years of chart note data. Her history included multiple instances of bleeding and easy bruising throughout the first 2 years of data, with symptoms including “substantial” and “excessive” bleeding, spontaneous bleeding from the nose, rectum, and bright red blood in the stool. Her last 1.5 years of chart note data included multiple mentions of FVIII deficiency (“mild” and “moderately; decrease”) and hemophilia. Her records did not indicate any use of treatments for hemophilia. She received ICD-9-CM codes of 286.0 and 286.9. Overall, these data seem to indicate a case of symptomatic hemophilia A in a probably heterozygous female (carrier).


Patient 2 was a 33-year-old female with approximately 3 years of chart note data. She experienced at least 3 pregnancies during this period, of which 2 ended in miscarriage and 1 led to “delivery complications”. Recurrent symptoms of bleeding were noted throughout her medical history, which included “unusual” and “abnormal” bleeding, “frequent” nose bleeding, internal bleeding, hematuria, and hematochezia. On the day of her delivery, she experienced “excessive” bleeding and “significant” “intra-abdominal” hemorrhage, and “acquired” FVIII deficiency was noted. Her chart notes included numerous additional mentions of “acquired” FVIII deficiency or “acquired” hemophilia, as well as “rare” blood disorder and “pregnancy-induced” blood disorder. She received ICD-9-CM 286 codes of 286.0, 286.5, and 286.9. Together these data strongly suggest that this was a case of peri-partum acquired hemophilia rather than congenital hemophilia.


Patient 3 was a 78-year-old female with approximately 3.5 years of chart note data. Her history included multiple recurrent bruising and bleeding symptoms, including hematuria, hematochezia, mucosal bleeding, and gastrointestinal bleeding. She also experienced recurrent anemia and thrombocytopenia, potentially as a result of her chronic bleeding symptoms. Although her records did not indicate any use of hemophilia treatments, her chart notes included numerous mentions of “factor VIII inhibitor” associated with FVIII deficiency, coagulopathy, and bruising. She received ICD-9-CM 286 codes of 286.0, 286.5, 286.59, 286.7, and 286.9. Overall, these data seem to suggest that this is a case of acquired hemophilia rather than congenital hemophilia.


Patient 4 was a 69-year-old male with approximately 4 years of chart note data. His history included multiple instances of postoperative bleeding associated with hem-arthrosis and a medial meniscus tear, and again with a perforated appendix and acute appendicitis. His chart notes included 4 mentions each of hemophilia A and hemophilia C (an alternate name for factor XI deficiency); most often these diagnoses were mentioned on the same day. In most cases, hemophilia A was described as “mild”. His chart notes also included a single mention of FIX deficiency (hemophilia B) and 2 mentions of FVIII deficiency (hemophilia A). He received ICD-9-CM 286 codes of 286.0 and 286.1 and received treatment with FVIII but not FIX. Together, these data are most consistent with a case of congenital hemophilia A due to the specific treatment with FVIII, which would have been ineffective in hemophilia B or C.


Patient 5 was a 57-year-old male with approximately 4 years of chart note data. His history included multiple mentions of hemophilia and FVIII deficiency, as well as chronic hepatitis C, bleeding, “recurrent” and “chronic” hemarthrosis, joint pain, and degenerative joint disease. He received ICD-9-CM 286 codes of 286.0 and 286.2 but had no indications of having received hemophilia treatment. Together these data suggest a case of moderate or severe hemophilia A; however, based upon symptoms and the presence of hepatitis C (implying prior exposure to plasma-derived factor products before viral inactivation steps were added to purification in 1988), the lack of treatment over 4 years is unexpected for an individual with severe hemophilia.


Patient 6 was a 76-year-old male with approximately 6.5 years of chart note data. He had multiple recurrent bleeding symptoms throughout, including frequent mention of “gastro-intestinal” bleeding, hematuria, and hematochezia. His chart notes also included 21 mentions of hemophilia, 16 mentions of factor V deficiency, 5 mentions of factor V Leiden deficiency, and a single mention of factor IV defi-ciency. He received ICD-9-CM 286 codes of 286.0, 286.3, and 286.9 but had no indications of having received hemophilia treatment. Ten aPTT scores were reported ranging from 83.9 s to 150.01 s; however, no PT scores were reported. Together these data suggest a case of factor VIII deficiency (286.0), V deficiency (coded under 286.3), or a rare case of a FVIII and FV inhibitor, given that factor V Leiden mutation is associated with thrombotic risk (not bleeding).


A 70-year-old woman presented with shortness of breath and an increased production of purulent sputum over the previous 6 weeks. Her past medical history included several episodes of respiratory tract infections during childhood. The patient had no history of smoking or congenital heart disease. She had experienced a gradual decrease in exercise tolerance for 7 years. She was admitted to our clinic for an acute exacerbation of chronic obstructive lung disease. On admission, right-sided infiltrates and volume loss in the upper lobe were noted. A physical examination revealed the patient to be clinically septic and in moderate respiratory distress. Her blood pressure was 130/80 mm Hg, her pulse rate was 105 beats/min, her respiratory rate was 32 breaths/min and her temperature was 37.7°C. During the pulmonary examination, a visual inspection of the chest revealed intercostal indrawing. Auscultation revealed rales at the right apex. Her right hemithorax was dull to percussion and respiratory rates were diminished. The rest of the examination was unremarkable.
A coronal computed tomography (CT; fig. ) showed bronchiectatic consolidation with air bronchogram formation involving the anterior segment of the upper lobe of the right lung with a 70% loss of volume. The right deviation of the trachea was also demonstrated on the CT scan. Axial, sagittal and coronal oblique CT scans showed bronchiectasis in the right upper lobe (fig. , ) and a poststenotic dilatation of the right pulmonary artery with a diameter of 32 mm (fig. ). The CT scan also revealed compression of the superior vena cava between an ascending aortic aneurysm and the dilated right pulmonary artery (fig. , ). There was compression of the bronchus of the right upper lobe in the CT image. A volume-rendered three-dimensional (3D) CT angiography image showed an aneurysmal ascending aorta, right pulmonary artery kinking, poststenotic dilatation of the right pulmonary artery, and compression of the superior vena cava (fig. ). The 3D CT angiography also revealed a dilatation of the proximal superior vena cava. A conventional right upper lobectomy was recommended to the patient, but she refused surgical therapy. Therefore, she was treated medically and monitored.


A 72-year-old female with medical history of renal clear cell carcinoma, breast cancer (status post lumpectomy and radiotherapy), and papillary serous carcinoma of uterus (pT2N0Mx - status post total abdominal hysterectomy and bilateral salpingo-oophrectomy, and omentectomy status post chemotherapy completed 5 months prior) presented with a complaint of dysphagia. Our patient reported about 4 - 6 weeks duration of poor appetite and progressive weakness which rapidly deteriorated 4 days prior to admission. She experienced difficulty in swallowing both liquids and solid foods with an associated thirty pound unintentional weight loss over a 3-month duration. Physical examination revealed a chronically ill appearing woman with areas of hyperpigmentation on the head (), arms and legs without a periorbital heliotropic rash. The metacarpophalangeal joints and proximal interphalangeal joints were flexed bilaterally, without scaling or Gottron’s papules, and distal phalanges with periungual hyperemia (). Our patient had symmetric proximal muscle weakness, 4/5 power in the upper extremities, and 2/5 power in the lower extremities.
Laboratory findings were significant for an elevated serum creatinine phosphokinase (CPK) level of 3,222 U/L, creatine kinase isoform MB 369.7 ng/mL, aldolase 31.7 U/L, erythrocyte sedimentation rate 40 mm/h, C-reactive protein 8.41 mg/L, lactate dehydrogenase (LDH) 804 U/L, and antinuclear antibody positive > 1:640. Barium esophagram revealed significant difficulty in initiating swallow with laryngeal penetration and aspiration of contrast material.
Esophagogastroduodenoscopy showed pooling of saliva in the piriform fossa with a normal appearing esophagus (). Random esophageal biopsies returned with the final pathology of squamous esophageal mucosa with mild chronic non-specific esophagitis and hyperkeratosis. Subsequently, a left biceps muscle biopsy was performed and revealed inflammatory myositis with severe necrotizing component suggestive of DM (). Further staining with nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) stain identified frequent myofibers with targetoid-like changes consistent with DM (). Our patient was treated with intravenous corticosteroids; however, she did not respond to the treatment. Thus, a percutaneous gastrostomy tube was placed for enteral feeding.


A 70-year-old woman underwent pancreaticoduodenectomy with modified Child reconstruction for pancreatic head cancer in March 2016. After the operation, the patient suffered anastomotic leakage at the site of gastrojejunostomy, and percutaneous intraperitoneal drainage (PID) was performed. The hepato-cholangio parameters such as total bilirubin, alkaline phosphatase, aspartate transaminase, and alanine aminotransferase levels, and computed tomography (CT) revealed an obstructed choledochojejunostomy with no recurrent findings 4 months after the operation. Percutaneous transhepatic cholangiography (PTC) confirmed complete obstruction of the upper common bile duct (CBD), which was the anastomosis of choledochojejunostomy, and percutaneous transhepatic cholangiographic drainage (PTCD) was performed. However, it was not able to pass the guidewire through the anastomosis. Cytology of the drainage from both PID and PTCD was negative for cancer.
After the recovery of the leakage and reducing ascites, enteroscopy (PCF-Q260AZI; Olympus Medical Systems, Tokyo, Japan) was performed. Although it was possible to reach adjacent to the anastomosis of choledochojejunostomy, the scar of the anastomosis was not observed. The length of the obstruction was 7 mm, as measured by cholangiography and fluoroscopy (). IDUS (20 MHz, UM-3R, Olympus Medical Systems) through the PTCD tube dilated to 22 Fr demonstrated a fibrous heterogeneous hyperechoic appearance; however, no fluid collection, vessels or foreign bodies were observed between the CBD and jejunum (). We therefore performed choledochojejunostomy via the MCA technique. Written informed consent was obtained from the patient, and the institutional ethics review board at Kyoto Okamoto Memorial Hospital approved this treatment.
We prepared two cylindrical neodymium magnets (6 × 6 mm; Magfine, Sendai, Japan) each with a small hole 1 mm in diameter, to which a nylon thread was passed through each hole. One magnet was inserted into the obstruction of the hepatic side through the PTCD fistula. The other was delivered endoscopically to the obstruction of the jejunal side. The two magnets were immediately attracted towards each other transmurally (). Reanastomosis was confirmed 7 days after starting the compression by cholangiography through the PTCD tube (). The magnets were easily retrieved endoscopically. A 16-Fr indwelling drainage tube was placed in the jejunum through PTCD tube to maintain the patency of the anastomosis (). The internal tube is still in place 6 months after reanastomosis and no MCA-related complications have been observed.


A 71-year-old male visited our hospital by ambulance after he vomited a large amount of blood. Upon arrival, he was alert, blood pressure was 90/61 mm Hg, and heart rate was 73 bpm. Complete blood count (CBC) revealed mild anemia: red blood count (RBC) was 395 × 104/µL and hemoglobin level was 12.0 g/dL. Emergency upper gastrointestinal (UGI) endoscopy revealed massive coagulated blood over the stomach, with no visual field secured (). Active bleeding from the stomach was discovered. RBC dropped to 274 × 104/µL and hemoglobin level dropped to 8.1 g/dL; subsequently, administration of 6 units of red cell concentration (RCC) was required. Endoscopic hemostasis was abandoned and transcatheter arterial embolization (TAE) was planned. Before angiography, contrast-enhanced computed tomography (CT) was performed, and the results suggested extravasation from the posterior walls of the lower stomach body (). Celiac angiography revealed extravasation from the posterior gastric artery (). A microcatheter was advanced into the branch of the posterior gastric artery () and it was occluded by a gelatin sponge (). On the following day, UGI endoscopy revealed successful hemostasis and Bormann 3 type cancer at the posterior walls of the lower gastric body (). Biopsies taken from the gastric cancer revealed moderately-differentiated adenocarcinoma. His hemoglobin levels were elevated to 10.0 g/dL. However, on day 25, he fell into hemodynamic instability because of re-bleeding from exposed vessels of the cancerous lesion. Therefore, emergency surgery was performed with total gastrectomy. The postoperative course was uneventful.


A 66-year-old male presented with blood in stools and dizziness. His medical history included chronic hepatitis B, which was followed up regularly without medication. On arrival, he was drowsy, blood pressure was 131/61 mm Hg, and heart rate was 98 bpm. CBC revealed moderate anemia: RBC was 277 × 104/µL and hemoglobin level was 8.4 g/dL. Non-contrast CT suggested retention of coagulated clots in the stomach. Subsequently, he was referred for emergency UGI endoscopy. UGI endoscopy revealed moderately retained fresh bleeding, coagulated clots, and Bormann 2 type cancer with exposed vessels at the angle of the stomach (). On examination, there was no active bleeding. The exposed vessels were staunched by endoscopic clips (). Immediately after UGI treatment, his consciousness level dropped to Glasgow coma scale E1V1M1 with a systolic blood pressure of 60 mm Hg. CBC revealed severe anemia: RBC was 180 × 104/µL and hemoglobin level was 5.5 g/dL. Due to re-bleeding from the gastric cancer, he was referred for angiography. After left gastric artery (LGA) angiography, a microcatheter was advanced into the distal LGA, and the contrast injection revealed extravasation (). The responsible vessel was occluded using microcoils (). On day 3, UGI endoscopy confirmed successful hemostasis. Biopsies taken from the gastric cancer revealed poorly differentiated adenocarcinoma with signet-ring cells. On day 25, distal gastrectomy with Billroth-I reconstruction was performed. The postoperative course was uneventful.


A 75-year-old male presented with melena. He could not walk unassisted; therefore, he visited our hospital by ambulance. His medical history included type 2 diabetes mellitus and benign prostatic hyperplasia, which were treated by oral medication. On arrival, his consciousness was unclear, blood pressure was 85/56 mm Hg, and heart rate was 104 bpm. CBC revealed severe anemia: RBC was 229 × 104/µL and hemoglobin level was 7.1 g/dL. After administration of 4 units of RCC, his hemoglobin level was elevated to 8.4 g/dL. On the following day, UGI endoscopy was performed, revealing coagulated clots in the anterior walls of the duodenal bulb. He was treated conservatively with fasting and prescription of proton pump inhibitor (PPI). On day 7, he presented with dizziness, hematemesis, and melena. RBC and hemoglobin level dropped to 180 × 104/µL and 5.7 g/dL, respectively. UGI endoscopy revealed oozing at the duodenal bulb (). Endoscopic hemostasis was considered challenging because of the unsecured visual field; therefore, he was referred for angiography. After gastroduodenal artery (GDA) angiography (), a microcatheter was advanced into the distal right gastro-omental artery. Contrast injection revealed extravasation (); then, the main trunk of the right gastro-omental artery was occluded by microcoils (). On day 9, UGI endoscopy revealed successful homeostasis of the suspected exposed vessel (). Gastrography under endoscopy revealed the narrowed duodenal bulb (). He did not clinically present the symptoms of duodenal obstruction. Serum pylori antibody was positive; then, eradication treatment of Helicobacter pylori was provided. Thereafter, the clinical course was uneventful.


An 82-year-old male visited our hospital by ambulance, presenting with a low-grade fever, dyspnea, and melena. On arrival, he was drowsy, blood pressure was 150/68 mm Hg, and heart rate was 79 bpm. His medical history included cerebral infarction. He was provided with enteral nutrition via a percutaneous endoscopic gastrostomy feeding tube. Laboratory analysis revealed severe anemia (RBC 199 × 104/µL and hemoglobin level 6.7 g/dL), abnormal renal function (creatinine 3.25 mg/dL and blood urea nitrogen 175.6 mg/dL), and abnormal electrolytes (Na+ 156 mEq/L, K+ 7.4 mEq/L, and Cl- 122 mEq/L). Subsequently, transfusion and RCC were administered, and emergency hemodialysis for hyperkalemia was initiated. On day 3, UGI endoscopy was performed, revealing an exposed vessel at the posterior walls of the descending duodenum. An attempt to staunch the exposed vessel was made using endoscopic clips; however, oozing was uncontrollable (). Then, he was referred for angiography. GDA angiography revealed no evidence of extravasation (); subsequently, empiric embolization was planned. With endoscopic clips, the anterior superior pancreatico-duodenal artery (ASPDA) was considered the responsible vessel. Therefore, the ASPDA was occluded using microcoils (). UGI endoscopy on the same day revealed successful hemostasis (). Administration of PPI was continued. Re-bleeding did not occur during his hospital stay.


A 63-year-old male presented with blood in stools. His past medical history included coronary artery disease which was treated by coronary stenting and dual anti-platelet therapy, and hypertension and dyslipidemia that were treated by oral medicine. He also had a medical history of diverticular hemorrhage that was treated with endoscopic hemostasis. Upon arrival, he was alert, blood pressure was 158/74 mm Hg, and heart rate was 71 bpm with regular rhythm. CBC revealed no anemia: RBC was 434 × 104/µL and hemoglobin level was 13.7 g/dL. Emergency colonoscopy revealed multiple diverticulosis in the ascending colon with active bleeding (). Endoscopic hemostasis failed; then, he was referred for angiography. Before angiography, contrast-enhanced CT was performed, revealing extravasation at the distal superior mesenteric artery (SMA) (). After SMA angiography, a microcatheter was advanced into the distal SMA. Contrast injection from the microcatheter revealed extravasation (). Distal SMA was occluded by a microcoil ().


An 82-year-old female presented with blood in stools. Her past medical history included coronary artery disease which was treated by coronary stenting and dual anti-platelet therapy, and atrial fibrillation that was treated by anti-coagulant medicine. On arrival, she was alert, blood pressure was 112/72 mm Hg, and heart rate was 71 bpm with irregular rhythm. CBC revealed mild anemia: RBC was 400 × 104/µL and hemoglobin level was 10.9 g/dL. Emergency colonoscopy revealed multiple diverticulosis in the ascending colon without evidence of bleeding (). On the following day, 99m-labelled red blood cell scintigraphy was performed, suggesting the bleeding sites in the ascending colon (). Subsequently, contrast-enhanced CT was performed, suggesting extravasation at the middle of ascending colon (). Due to worsening anemia, administration of 6 units of RCC was required. The patient was referred for angiography. SMA angiography revealed extravasation from the middle colic artery (). A microcatheter was advanced into the distal middle colic artery and it was occluded by a gelatin sponge. On the following day, colonoscopy revealed successful hemostasis and mild colonic ischemia (). The colonic ischemia was observed by a conservative treatment.


A 93-year-old female presented with blood in stools during her hospitalization due to acute cholecystitis. Her medical history included chronic renal failure and colon polyps that were resected by endoscopy 3 years ago. Emergency colonoscopy revealed ulcerative scars with a suspected exposed vessel at sigmoid colon 40 cm from anal canal, but there was no evidence of active bleeding (). Therefore, she was observed by a conservative treatment. On the following day, she excreted 1,000 g of bloody stools and, subsequently, her blood pressure dropped to 74/50 mm Hg. Endoscopic hemostasis was considered challenging because of the possibly unsecured visual field; thereafter, he was referred for angiography. After the inferior mesenteric artery (IMA) angiography, a microcatheter was advanced into the distal IMA. Contrast injection revealed extravasation () and the distal IMA was occluded by a gelatin sponge (). On day 4, colonoscopy revealed successful homeostasis with mild ischemic changes at sigmoid colon () that were observed with a conservative treatment.


After obtaining the Ethical Committee approval and written informed consent from a 45-year-old female, American Society of Anesthesiologists physical status I scheduled for laparoscopic cholecystectomy. Preanesthetic checkup was done a day before surgery; relevant investigations were done and informed written consent was taken. The patient was asked to remain nil per oral 8 h before surgery. The patient was premedicated with tablet alprazolam 0.5 mg and tablet ranitidine 150 mg in the night before surgery. Patient was preloaded with 500 ml lactated Ringer's solution. In operation theater, a good intravenous (IV) access was secured for preloading and a monitor was attached for monitoring electrocardiogram, heart rate (HR), noninvasive blood pressure, oxygen saturation (SpO2), temperature, and respiratory rate. Patient was given injection ranitidine 50 mg and injection ondansetron 4 mg IV and was made to sit with their elbows resting on their thighs on operating table. Flexion of the spine was done and midline approach was used.
Segmental thoracic spinal anesthesia was given using 1 ml hyperbaric bupivacaine 5 mg/ml mixed with 0.5 ml of fentanyl 50 μg/ml injected at T10-11 interspace with a 26-gauge spinal needle after confirming its placement by free flow of clear cerebrospinal fluid []. Finally, the patient was turned to the supine horizontal position for the operation, and oxygen was started at 6 L/min by face mask. Onset of action and level of sensory block was judged by pin prick method every minute until the establishment of desired block. The overall quality of intraoperative muscle relaxation (poor, fair, good, or excellent) was evaluated by the surgeon at the end of the surgery. Hypotension was defined as systolic blood pressure <90 mmHg or >20% decrease in baseline values and was treated by fluids and vasopressors (mephentermine 6 mg). Bradycardia was defined as HR <50/min and was treated by 0.6 mg of atropine injection. HR, blood pressure, and SpO2 were recorded every 3 min. Intra- and post-operative complications such as nausea, vomiting, pain, pruritus, headache, or any other side effects were recorded.
The segmental thoracic spinal anesthesia was performed easily in the patient. Onset of sensory block T4-L2 required for minimally invasive laparoscopic cholecystectomy was achieved in 7 min and duration of block was 3 h. Surgery commenced using carbon dioxide insufflation and a pressure limit of 10–12 mmHg. Anxiety was treated with midazolam 1 mg and shoulder pain with 20 mg ketamine IV. There was no requirement of vasopressors and atropine during the surgery and the patient was hemodynamically stable during intraoperative and postoperative period. Furthermore, SpO2 was above 96% at all-time intervals. Specific enquiry was made about postdural puncture headache (PDPH) which was not experienced by our patient, and the patient passed urine after the effect of block was over. Muscle relaxation was judged fair by the surgeon. Patient was followed for 48 h postoperatively in the ward and no complications were reported. Patient was examined for any remnant neurological deficit postoperatively and was not present.


An 8-month-old female infant with a history of recurrent vomiting and regurgitation of feeds attributed to gastroesophageal reflux was referred for cardiac evaluation of a systolic murmur as well as fast breathing noticed particularly during feeding. Her weight gain was appropriate for age with no other concurrent illnesses.
She did not exhibit any pallor or cyanosis, and all her peripheral pulses were present and equal. She was mildly tachypneic (respiratory rate 50/min) with minimal subcostal and suprasternal retractions but no stridor. On cardiac evaluation, her first heart sound was normal with a wide and fixed splitting of the second heart sound and a grade 2/6 - ejection systolic murmur at the left second intercostal space.
Her echocardiogram revealed a large secundum atrial septal defect with moderate dilatation of the right heart structures. The intracardiac anatomy was otherwise normal. There was a suspicion of the double aortic arch, and hence, a cardiac computed tomogram was obtained to delineate the arch anatomy. This demonstrated a right-sided aortic arch with the first branch being the right common carotid artery, followed by the right subclavian artery. The left brachiocephalic artery arose from the proximal descending aorta and tracked a retroesophageal course before dividing into the left subclavian and common carotid arteries []. The left common carotid artery spanned a length of 9 mm before bifurcation. It measured 4.1 mm proximally before constricting to 1.7 mm just before the bifurcation []. This implied a high possibility of Kommerell's diverticulum with the left ligamentum and given her esophageal compression symptoms; the patient underwent surgery through a midline sternotomy. A left-sided ligamentum arteriosum was identified and divided during the surgery with concomitant closure of the atrial septal defect.
The postoperative recovery was uneventful, and at follow-up 8 months after surgery, she was asymptomatic with marked improvement in her gastroesophageal reflux.