The deceased was a 6-day-old premature female newborn who was born to an 18-year-old gravida one woman. The mother presented with fever and prolonged premature rupture of membranes (PPROM) for one week prior to admission at 27 weeks. On admission, she received two doses each of betamethasone, ampicillin, and gentamicin. Due to worsening maternal respiratory distress needing mechanical ventilation, failure to progress after induction, PPROM, and suspected chorioamnionitis, she underwent emergency cesarean section delivery. The infant was born at 28 weeks and 1 day gestation, weighing 1140 gm. At birth, the baby needed mechanical ventilation and was started on intravenous ampicillin and gentamicin, which were discontinued when the blood cultures were negative at 48 hours of age.
While in the neonatal intensive care unit, the patient was extubated successfully after one day and placed on noninvasive ventilation. On the fourth day, the baby was less active and had temperature instability with bradycardia, and she was started on vancomycin and cefotaxime. Later the same day, due to multiple episodes of apnea, deteriorating bradycardic spells, desaturation, and hypercarbia, she was re-intubated and placed on synchronized intermittent mandatory ventilation. The antibiotics were changed to cefepime, fluconazole, and acyclovir. After an additional 24 hours (then day 5), with increasing metabolic acidosis and worsening respiratory failure, she was placed on high frequency oscillating ventilation; however, her condition continued to deteriorate. She became hypotensive with poor perfusion despite vasopressors, and blood products. A bedside echocardiogram revealed a normal-appearing heart with a patent ductus arteriosus, a left-to-right shunt, pulmonary hypertension, a small pericardial effusion, and moderately decreased left ventricular function, with signs of low cardiac output. The patient was in sepsis with a severe metabolic acidosis and disseminated intravascular coagulation, despite antibiotic, antifungal, and antiviral therapy. After 40 hours since the onset of symptoms (on day 6), the patient went into cardiopulmonary arrest and passed away. Of note, the mucocutaneous culture sampled on the day of symptom onset returned positive for HSV, many days after the patient’s death.
The placental pathology report described a third-trimester placenta with moderate intervillous fibrosis, but did not show any evidence of chorioamnionitis or funisitis.
A complete autopsy performed within 24 hours revealed a normally developed premature female infant with no dysmorphic features or congenital anomalies.
The weight of the body was 1525 gm (actual birth weight of 1140 gm). Pertinent gross findings included serous fluid in the right pleural cavity (20 ml), left pleural cavity (25 ml), and pericardial sac (3 ml). There was 25 ml of serosanguineous ascites. The cardiovascular system revealed a normal-sized heart without any significant abnormalities, and microscopy revealed unremarkable immature myocardium. The ductus arteriosus and foramen ovale were open. The lungs revealed hemorrhagic right upper and middle lobes.
Sections through the right and left lung showed thickened septa. The lungs were in the saccular stage of development. The airway epithelium had disorganized large cells without cilia, and viral nuclear inclusions were present ().
An immunohistochemical stain for HSV-1 and HSV-2 was positive. There were diffuse fibrin plugs in bronchioles throughout the lungs, and diffuse alveolar hemorrhage was present primarily in the right middle lobe.
The stomach contained a small amount of bloody mucus with normal mucosa. The liver weighed 65 gm (reference range: 45.5 gm +/- 15 gm). The parenchyma was red-brown with centrilobular congestion, with hemorrhage around portal areas and under the capsule ().
Hepatocyte nuclei showed viral inclusions with chromatin displaced to the nuclear membrane (margination or wine red appearance) ( to ). Immunohistochemistry for HSV-1 and HSV-2 was positive in hepatocytes. ()
The kidneys had peripelvic hemorrhage, but no evidence of herpetic infection. The spleen showed karyorrhexis and perivascular cell fragments (). Central nervous system (CNS) examination was unremarkable except for sections through the midbrain and thalamus, which showed microglial nodules ().
HSV was isolated from postmortem lung cultures. The final pathologic diagnoses were a premature female infant with resolving hyaline membrane disease of lungs along with disseminated HSV infection of the liver, lung, and brain with microglial nodules in the midbrain and thalamus. In addition, ascites, pleural effusion, persistent ductus arteriosus, involution of thymus, and medullary congestion and pelvic hemorrhage of the kidneys.


We present the case of a 31-year-old Caucasian man with a history of recurrent mucosal ulcerations of the mouth and larynx for 11 years. The first presentation of his condition was to an Ear, Nose and Throat (ENT) department, aged 20, for severe odynophagia. Clinical examination and investigation at that time revealed a 1 cm ulceration of the oropharynx. A biopsy was performed, which showed a non-specific inflammatory infiltrate. The patient received conservative treatment and was discharged. Over the next 10 years, he was admitted twice to the ENT department for severe odynophagia, once with stridor due to supraglottic oedema with a partial response to corticotherapy.
The clinical history and examination revealed the presence of recurrent oral ulcerative lesions (Fig. a and b) that developed in crops and lasted up to several weeks, with ulcerative lesions on the epiglottis and the left aryepiglottic fold (Fig. ) and another lesion on the rectal mucosa. Biopsies taken from both lesions showed non-specific inflammatory infiltrates, with a predominance of neutrophils. The patient also reported papular skin lesions and pathergy following blood tests (Fig. c).
The differential diagnosis at that stage included multiple aetiologies. Infectious causes, were excluded by biopsy and negative tests for bacteria (e.g. tuberculosis) and viral infections (HIV, Herpesviridae viruses). The patient was screened for malignancy by blood tumour markers and imaging, which were negative. An autoimmune work-up, including ANA, dsDNA, p-ANCA, c-ANCA, Ro, La antibodies were all negative.
Considering the presence of recurrent oral ulcerations and excluding neoplastic and infectious causes, the possibility of BD was entertained, and the patient was referred to one of the UK Centres of Excellence for BD.
At that time, the patient did not meet the formal classification criteria for BD, but he was closely monitored and received treatment with colchicine and low dose corticosteroids, with symptomatic benefit. In time, he developed genital ulcers and several deep vein thromboses (despite appropriate anticoagulant treatment), thus fulfilling the requirements according to the International Criteria for Behçet’s Disease (ICBD).
Treatment included immunosuppression with azathioprine, colchicine and low dose cortisone therapy to minimize the recurrence of ulcerations, to which the patient responded well.


A 22-year-old male, university student presented with a history of sudden-onset abdominal pain of 1-day duration. The pain was colicky, constant and diffuse. It did not radiate and had no aggravating or relieving factor, but it was associated with vomiting. The patient also reported having no bowel movement for one day. He presented to emergency department 2 days ago complain of ataxia and slurred speech, due to a carbamazepine overdose, for which he admitted under neurology and received activated charcoal 150 g, through a nasogastric tube, over 24 h. He had charcoal-stained vomiting during admission; however, his clinical condition improved, and kept for observation then he was subsequently discharged.
The patient had no history of fever, weight loss, fatigue, night sweats or previous episodes of abdominal pain. His medical history was remarkable for dilated cardiomyopathy, for which he was receiving medications. He also had a history of sleeve gastrectomy, which had been performed four years earlier. His family history was unremarkable.
On examination, the patient was conscious, alert, and oriented, but he complained of mild pain. His vital signs were as follows: heart rate, 83 beats per minute; respiratory rate, 22 cycles per minute; blood pressure, 125/83 mmHg; temperature, 37.2°C; and oxygen saturation, 98%. A chest and lung examination was unremarkable. Similarly, a heart examination showed normal first and second heart sounds with no added sounds. His abdomen was soft and distended, with mild generalized tenderness; however, no sign of rigidity or guarding was observed. A digital rectal examination revealed an empty rectum with no blood or stool.
Blood was drawn for a complete blood count, urea and electrolytes, liver function test, coagulation profile, serum glucose level, carcinoembryonic antigen and cancer antigen, and the results were all within normal limits. An initial abdominal X-ray showed multiple air fluid levels and a dilated bowel (Fig. A and B). A computed tomography scan of the abdomen and pelvis showed small bowel obstruction to the level of the proximal ileal loops, with a transition point between the dilated proximal loops and the collapsed terminal ileal loops (Fig. A and B).
The patient was initially managed conservatively, but the abdominal pain and distention did not improve. Consequently, laparoscopic-assisted abdominal exploration was performed, and the charcoal plug was removed. Intra-operatively, ~40 cm from the ileocecal junction, was a transitional zone with intramural material causing small bowel obstruction (Fig. ). A 1.5 cm enterotomy was made, and it revealed a hard charcoal plug obstructing the small bowel (Fig. ).
The charcoal plug was removed, and the enterotomy site was closed transversely in two layers. The first layer was closed using full-thickness vicryl suture, and the second was closed using Lembert seromuscular sutures. Manual bowel decompression was performed up to the level of the duodenojejunal junction, and suctioning yielded ~1700 ml of charcoal-stained fluid (Fig. ).
The patient’s postoperative course was uneventful. He tolerated oral intake on postoperative Day 1 and was discharged on Day 2 with close follow-up care.


An 81-year-old male presented with complaints of right wrist pain. He had injured his wrist 6 months prior while changing a wheel bearing. Since that time, he complained of worsening right wrist pain that was located radially and exacerbated with activity. He had begun experiencing paresthesia of his right fingertips, but denied any constitutional symptoms.
His past medical history was significant for colon adenocarcinoma, for which he underwent total colectomy and ileostomy nearly one year prior to presentation. He had finished a chemotherapy regimen, and a recent PET scan was negative for thoracic and abdominal metastasis.
Physical exam revealed no palpable masses and no erythema or swelling. There was tenderness to palpation in the anatomic snuffbox. Radial deviation and extension of the wrist caused an increase in pain. Sensation was intact in the median, radial and ulnar nerve distributions. Anterior interosseous, posterior interosseous and ulnar nerve motor function was intact. Distal pulses were normal.
Radiographs of the right hand and wrist revealed a lytic lesion in the scaphoid with nearly complete destruction of the distal pole (Fig. a–c). The lateral radiograph also demonstrated some abnormal scalloping of the distal radius articular surface (Fig. c). Magnetic resonance imaging (MRI) showed destructive changes of the radial sided carpus (Fig. a and b), suggestive of neoplastic or infectious processes, but was inconclusive.
After a thorough discussion with the patient, we decided to perform a proximal row carpectomy (PRC) along with biopsy and culture of the lesion. The PRC was performed through a dorsal approach. Once the carpus was exposed, a gelatinous mass was seen emanating from the scaphoid (Fig. ). The mass was eroding into the lunate, trapezium and distal radius articular surface. The entirety of the gelatinous mass was excised and sent for biopsy (Fig. ). Culture was also taken at this time. The remainder of the scaphoid, as well as the lunate and triquetrum were excised, thus completing the PRC. Copious irrigation was then performed followed by a layered closure.
Pathology revealed glandular tissue consistent with metastatic adenocarcinoma of the colon. Cultures were negative.
During routine postoperative follow-up, his physical exam revealed improved pain with a decreased range of motion at the wrist. He was evaluated by his medical oncologist after surgery and another course of chemotherapy was given. Radiation treatment was discussed, but the patient declined secondary to the ongoing pain relief he experienced after surgery. The patient survived 1 year after his scaphoid metastases were discovered.


A 25-year-old man was involved in a cutting machine accident, resulting in complete amputation of his left middle and ring fingers at the base of the distal phalanx and at the shaft of the distal phalanx, respectively. The stumps of both affected fingers were severely crushed. Both fingers were replanted. At 3 weeks post-replantation, the middle finger had survived but the nail bed of the ring finger had necrotized. After removing the necrotic sterile matrix, we found the distal phalanx bone to be viable, so we covered it with a thenar fascial flap. In this particular case, skin and subcutaneous tissue were also carried over to cover a fingertip defect. Two weeks later, the flap was divided and nail bed grafting was performed. At the 9-month follow-up, one minor variation of the transverse groove was observed, and the new nail was graded as “very good” ().


A 50-year-old woman was involved in a press machine accident resulting in a crush injury to her left index finger. Almost the entire sterile matrix was lost. A thenar fascial flap was applied, and subsequent nail bed grafting was performed. At the 20-month follow-up, the new nail was graded as “excellent” ().


A 59-year-old man with a smoking history was admitted to our hospital for a conventional health checkup with a nodule in his upper-left lung. After pulmonary computed tomography () and magnetic resonance imaging (MRI) of the head in hospital, the patient was assessed as being acceptable for surgery, without distant metastasis. Left-lung resection and lymph node-dissection were then performed. Postoperative pathology showed a diagnosis of moderately differentiated lung adenocarcinoma in his upper-left lung ().
Genetic testing of common driver genes, such as EGFR, ALK, ROS1, was not performed in hospital. At 3 months after surgery, four cycles of standard chemotherapy (pemetrexed and carboplatin) was administered, and this patient did not come to hospital for regular routine follow-up visits until 28 months later, with a complain of chest congestion. Pulmonary CT and MRI screening showed multiple metastases in both lungs and brain metastasis, respectively ().
Second-line chemotherapy with docetaxel (120 mg according to the patient’s surface area, 75 mg/m2, once every 3 weeks) was performed without any benefit. To explore potential targeted therapies, next-generation sequencing was performed in tumor tissue and revealed a new type of ALK arrangement (NCOA1–ALK, ). Mutation profiling of this patient is summarized in , and expression of the ALK protein was confirmed by immunohistochemistry (). Oral crizotinib (250 mg twice a day) was administered immediately. After 2 months of crizotinib treatment, the multiple metastatic nodules in the right lung had decreased significantly () and the brain-lesion metastases were stable (). Several follow-up visits were recorded, and the patient was still alive without disease progression in lung lesions () or brain metastases (). The progression-free survival of this patient had exceeded 18 months.


We present the case of a 68-year-old Caucasian female who presented to our institution, having been referred by her GP, with a 6 week history of epigastric pain, nausea and multiple episodes of vomiting. Her medical history was significant for a left breast wide local excision for ductal carcinoma in situ as well as sero-negative rheumatoid arthritis. Her regular medications included methotrexate, folic acid and a proton pump inhibitor. Notably she had no history of foreign body ingestion, malignancy, radiotherapy or inflammatory bowel disease. She also had no history of previous gastrointestinal tract obstruction.
On examination she was haemodynamically stable and apyrexial. Her abdomen was soft except for some tenderness on superficial palpation of her right upper quadrant and she had a positive Murphy's sign. There was no organomegaly, scars, herniae or masses. On haematological testing she was found to have a normocytic anemia with a haemoglobin level of 10.9 g/dl with a mean corpuscular volume of 88.6 fl. Her white cell count was 4.4 and her platelet count was 409. Her renal function was normal and inflammatory markers were as follows: C-reactive protein = 33.4 mg/l, erythrocyte sedimentation rate = 52 mm/h. More importantly, results of her liver function tests, amylase and lactate dehydrogenase are as follows: bilirubin 5 μmol/l, alanine transferase 13 U/l, alkaline phosphatase 117 U/l, gamma glutamyltranspeptidase 68 U/l, albumin 37 g/dl, amylase 14 U/l and lactate dehyrogenase 167 U/l.
Radiological examinations performed included a chest/abdominal radiograph which were normal. The patient proceeded to have a computed tomography scan of the abdomen and pelvis with oral and intravenous contrast as shown in Fig. a and b. The CT scan shows a large gallstone as well as air within the gallbladder. The gallbladder is adherent to the distal gastric antrum and there is a slight deficiency of the wall of the gallbladder that appears to communicate with the antrum indicating a cholecystogastric fistula. There are some mild associated inflammatory changes around the gallbladder.
Ultrasound and gastroscopy was then recommended. The ultrasound of the biliary tree performed showed the gallbladder indenting on the gastric antrum with a fistula present between the two. There was also extensive thickening of the gallbladder wall. Air was seen to pass from the stomach around the gallstones in the gallbladder. The patient then proceeded to upper gastrointestinal tract endoscopy as shown in Fig. a and b.
The image shows a large visible gallstone and cholecystogastric fistula in the antrum of the stomach. Endoscopic retrieval of the stone failed and the patient proceeded to urgent open gastrostomy with removal of the stone. Intra-operative images are shown in Fig. a–c.
Once removed, the stone measured just <3 cm. Of note, the fistula was not repaired and the patient had an uneventful post-operative course. She was discharged home in the following week and has been seen since in the outpatient department and is very well. As the only visible stone was removed, the patient did not require interval cholecystectomy.


A 6-year and 2-month-old boy who was admitted to our institution 10 weeks after a rollover motor vehicle collision. The child was ejected and found transiently unconscious and hypotensive. At the local hospital, he was intubated and underwent immediate exploratory laparotomy where a splenectomy was performed. He also had a right tibia fracture that was treated with immobilisation. The cervical spine injury was detected while recovering from the laparotomy. His initial cervical radiographs and magnetic resonance imaging (MRI) were obtained after noticing right-sided weakness ( and ()). The family brought the child to our institution after his tibia fracture had healed. The neurological assessment at arrival revealed a Frankel grade D incomplete spinal cord injury. Right brown sequard hemiplegia was documented. There was more motor weakness in the right upper extremity, especially of the hand along with sensory loss in the left hand. A repeated MRI that was done under fiberoptic intubation with general anaesthesia on the way to the operating room showed improvement of the abnormal signal intensity and reduction of the impinging C4-5 disc ().
We did not perform skull traction as the CT scan did show at least partial healing of the dislocated facets (), and we started posteriorly because remodelled facets were felt to be restrictive to any anterior manipulation. Altering the natural facet articulation for the posterior release increases instability even after reduction and because of the small C4 lateral mass, we instrumented two vertebrae above and below the injured level.
The surgical procedure constituted three approaches, starting posteriorly for facets release, which did not result in reduction (), then anteriorly where we did a C5 corpectomy as well as discectomy of the adjacent discs. For the reduction, standard techniques were employed to realign the vertebrae. Despite the small size of the vertebrae, we were able to place divergent distraction pins and used them effectively (). After the reduction, a structural allograft was placed followed by an anterior plate. We then turned the patient prone again and placed lateral mass screws and rods. The fixation was extended between C3 and C6. Due to anatomical constraints, the C4 lateral masses were not instrumented. The transcranial motor evoked potentials deteriorated momentarily twice: first, after log-rolling to the prone position while adjusting the Mayfield frame before we started the procedure, which improved once we flexed the neck slightly and corrected translation; and second during an attempt at reduction anteriorly using a laminar spreader. The deterioration resolved immediately after the release of the distraction. Although the C4-5 facets were released posteriorly, the anterior lamina spreader did not lead to satisfactory realignment under fluoroscopic assessment. Postoperatively, he was kept intubated for 2 days in the intensive care unit. He was then admitted to the rehabilitation hospital for 4 weeks and used a semi-rigid cervical collar for 3 months.
During rehabilitation, the patient regained independent ambulation without walking aids or orthoses. At 2-year follow-up, the patient had no pain or functional limitations, and there was no notable restriction in neck range of motion or a limp. His neurological exam improved, but remained Frankel grade D. He was able to write clearly with his right hand. The final radiographs showed union ( and ()).


A 37-year-old man, diagnosed previously as a “chorioretinal scar” in the macula, came for follow-up examination at our retina clinic. He had no ocular symptoms. Systemic history was normal. Eye examination revealed a visual acuity of 6/6 in both eyes. Anterior segment examination was normal in both eyes. Dilated fundus examination revealed pink and healthy optic nerves with normal physiologic cupping in each eye. Right eye macular examination revealed a classical, torpedo-shaped, hypopigmented chorioretinal lesion. Left eye macula was unremarkable. Peripheral retina was normal in both eyes. CF, OCT, and MC imaging was done [Fig. and , ].


A 23-year-old girl was referred by a general ophthalmologist to the retina clinic as a macular lesion in the right eye. She was asymptomatic and her systemic history was insignificant. Visual acuity was 6/6 in both eyes. Anterior segment examination was normal in both eyes. On dilated fundus examination, optic nerves were normal. Right eye macular examination revealed a torpedo-shaped, hypopigmented chorioretinal lesion with pigmented area at the tail. Multimodal imaging of the torpedo lesion with CF, OCT, and MC imaging was done [Fig. and , ]. On OCT (Heidelberg Spectralis HRA-OCT), there was an excavation of the inner surface of the retina corresponding to the area with pigmentation. Along the whole lesion, there was increased transmission of the signal. The outer retina including the IZ, EZ, and the external limiting membrane was disturbed, and the outer nuclear and plexiform layers were thinner at the depigmented nasal part of the lesion. At the area of retinal excavation, the retina was thin and retinal layers external to inner nuclear layer were not appreciated. Inner retinal layers showed no retinal thinning. A conforming focal choroidal excavation was noted along with an outer retinal defect overlying it. The choroid was very thin at the location of choroidal excavation. Left eye macula was unremarkable. Peripheral retina was normal in both eyes.


A 58-year-old female presented with a chief complaint of left hip pain of 5 months’ duration. The patient had been seen approximately 10 months prior to presentation, shortly after experiencing a “clunk” in her right hip. She reported that her pain was stable and had not increased since that episode. Relevant history included a left primary THA approximately 25 years ago. The patient also reported a right primary THA at the age of 33 years, followed by a head and liner exchange 10 years later due to poly wear and broken tine. A right total knee arthroplasty procedure was performed approximately 1 year ago. Comorbid conditions reported included degenerative joint disease, thrombocytopenia, cirrhosis of the liver, lumbar spondylosis and anemia. The patient had been managing any ongoing hip pain with anti-inflammatories and routine monitoring of poly wear with annual radiographs.
On physical examination, a pain-free range of motion (ROM) of the affected hip was noted, although the patient demonstrated hesitation at the extremes of motion. Slightly reduced ROM was noted with internal and external rotation when compared with the right hip. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal. Radiographs were obtained and revealed severe polyethylene wear and asymmetry in the left hip (). Some acetabular and proximal femoral lysis was noted, although there was no change in the acetabulofemoral component interface.
The pre-operative plan for this patient was to exchange the polyethylene liner only; however, during surgery, it was observed that the locking mechanism on the poly component was incompetent. Furthermore, intraoperative measurement with the navigation system indicated anteversion of 5° (radiographic definition), revealing a cup component significantly more retroverted than the 18° indicated by the pre-operative radiograph (). A decision was made to exchange both the liner and the cup component ().
Surgery was successful, and post-operatively, the patient was prescribed standard posterior hip precautions with toe-touch weight-bearing for 6 weeks. At 2 weeks post-op, the patient was progressing well.


A 49-year-old woman presented to the emergency department with worsening dyspnea and generalized edema for 10 days. Her past, personal, and family histories were unremarkable. On physical examination, her temperature was 36.6°C, blood pressure was 194/112 mmHg, pulse was 120 beats/min, and respiratory rate was 24 breaths/min. Oxygen saturation was 100% under ambient air. Expiratory wheezes bilaterally and crackles at the left base were noted. A grade 2/6 systolic murmur was heard at the left upper sternal border and apex, radiating to the axilla. Generalized anasarca with pitting edema over the bilateral upper and lower extremities was noted.
An electrocardiogram showed sinus tachycardia and left ventricular hypertrophy with a strain pattern. A chest X-ray revealed cardiomegaly and patchy airspace consolidations with infiltrations in the right lung field []. A transthoracic echocardiogram showed a global left ventricular hypertrophy and hypokinesia with an ejection fraction of 22%. Pertinent laboratory results revealed normocytic anemia and elevated serum B-type natriuretic peptides levels of 2,440 pg/mL, with normal liver function, kidney function, and electrolyte status. Medications with intravenous nitrite, furosemide 20 mg twice daily, and oral anti-hypertensive heart failure medications including bisoprolol 0.625 mg once daily, perindopril 5 mg once daily, sustained-released nifedipine 30 mg twice daily, and spironolactone 25 mg twice daily were prescribed. An abdominal sonography was performed to evaluate the underlying causes of secondary hypertension, which demonstrated a huge lobulated heterogeneous mass (approximately 7.7 × 6.4 × 9.3 cm3) at the lower pole of the right kidney and a mass (approximately 4.2 × 3.2 cm) over the left suprarenal area. The masses were confirmed through magnetic resonance imaging []. Moreover, a urine catecholamine analysis revealed elevated levels of dopamine (991.7 μg/day, normal range 138–540 μg/day) and norepinephrine (104.1 μg/day, normal range 10–80 μg/day) with a normal epinephrine (7.6 μg/day, normal range 0–24 μg/day) level. The medication of bisoprolol was shifted to labetalol 200 mg twice daily. The patient underwent computed tomography-guided biopsy of the pulmonary nodule, left laparoscopic adrenalectomy, and right laparoscopic radical nephrectomy. Grossly, a renal tumor extended into major vein and invaded perirenal fat and peri-pelvic fat tissue. The adrenal gland was a brown tumor mass. Histopathological analysis confirmed the diagnoses of clear cell RCC of the right kidney (Fuhrman nuclear grade II) with metastasis to the lung. To exclude the possibility of neuroendocrine differentiation, which impacts the overall prognosis of RCC, immunohistochemical staining for the neuroendocrine feature, including chromogranin-A and synaptophysin, was performed and revealed negative results.[] Moreover, based on the WHO Pathology and Genetics of Tumors of Endocrine Organs, few foci revealed spindle cell change, nuclear hyperchromasia, and necrosis of tumor cells, indicating biologically aggressive behavior (atypical) pheochromocytoma of the left adrenal gland [].[] Genetic analysis of the patient revealed no mutation in the coding region of von Hippel-Lindau (VHL) gene. Target therapy with sunitinib was initiated. The blood pressure was 146/86 mmHg 1 month after surgery. One year later, a chest X-ray revealed a normal heart size without visible airspace consolidations [], and an echocardiography demonstrated normal left ventricular systolic function. Possibly due to the residual tumor, pre-existing hypertension, or sunitinib-related hypertension, the patient is presently under target therapy for her RCC and takes oral antihypertensive medications with stable disease.


A 40-year-old man was admitted to the department of emergency in August 2018 due to committing suicide by intentional ingestion of about 100 ml diquat (20 g/100 ml) and 400 ml glyphosate (41 g/100 ml). His wife provided a history of depression. Three hours before admission, his family found the patient unconscious and his vomit around. He was immediately sent to the emergency department of our hospital. Gastric lavage with montmorillonite and endotracheal intubation were performed immediately and then the patient was transferred into the intensive care unit (ICU). Examination on admission to the ICU revealed ventricular fibrillation. His heart rate returned to normal after 20 minutes cardiopulmonary resuscitation and defibrillation. Ventricular fibrillation recurred 40 minutes later and the same treatment was given until he recovered. Physical examination revealed comatose with Glasgow Coma Scale score of 7. His temperature was 38.6°C with a normal heart rate of 68beats/min (bpm), blood pressure of 116 /76 mm Hg (with norepinephrine 10 ug/min) and respiratory rate 44/min (bpm). Oxygen saturation was about 90% using tracheal intubation and assisted ventilation (BIPAP mode was set with PC 20cmH20, PEEP 10cmH20, and FiO2 100%). Physical examination also showed oral and tracheal hemorrhage, wet rales over both lungs on pulmonary auscultation and abdominal distension. Within a few hours, his oxygen saturation fell to 85% on ventilation and progressive oliguria developed. Laboratory tests suggested severe hypoxia and liver and kidney function damage (Table ). Bedside chest radiography suggested multiple exudations of both lungs (Fig. ).
After successful cardiopulmonary resuscitation, resuscitation fluid to maintain blood pressure, protective lung ventilation strategy to maintain oxygenation, removement of toxins, antioxidant and antifibrotic treatment were given. However, his oxygenation deteriorated on day 2 with the PO2/FiO2 being less than 100. Veno-venous ECMO program was initiated on day 2 and he was weaned off ECMO support successfully after 140 hours. On day 9 after admission, endotracheal intubation and mechanical ventilation were removed. Immediately after admission, the patient was treated with continuous veno-venous hemofiltration (CVVH), but his renal function recovered slowly. He was withdrawn from CVVH on the 41st day after admission. The patient was discharged from the Department of Nephrology on day 46 and was discharged on the 68th day after admission. No obvious lesions were found in the chest CT on the 5th day after discharge (Fig. 2).


A 61-year-old man was referred to Uijeongbu St. Mary’s Hospital with a pathologic diagnosis of suspected malignancy. He had undergone partial resection of a painful mass on the left chest wall at a different medical facility 10 days prior to the referral. The size of the preoperative mass was reported as approximately 5×4.5×4 cm in the transfer summary, and preoperative chest computed tomography (CT) had not been performed. The patient’s medical history was remarkable for hypertension. Laboratory findings were all within normal limits. Available imaging studies included chest radiography, chest CT, a whole-body bone scan, and positron emission tomography (PET)/CT utilizing fluorine-18 fluoro-2-deoxy-D-glucose (FDG). Chest CT revealed a residual mass on the left lower chest wall (). Mediastinal lymph node enlargement was not noted, and there was no evidence of hematogenous or lymphangitic metastasis in either lung.
Malignant fibrous histiocytoma (MFH) was confirmed by ultrasound-guided fine-needle aspiration biopsy of the chest wall mass (). A whole-body bone scan showed no bony involvement. PET/CT revealed a suspected metastatic lesion in the right upper arm (maximum standardized uptake value [SUVmax]=3.57) (), while the SUVmax of the chest wall mass was 3.53. Magnetic resonance imaging (MRI) of the right arm also suggested a solid tumor, such as MFH (). Ultrasound-guided fine-needle aspiration biopsy of the right upper arm mass was conducted and confirmed the diagnosis of schwannoma ().
The operation was performed on April 11, 2008. The tumor margin was inaccurate because of a previous partial resection. Thus, based on the operative scar, transfer summary, and chest CT findings, the entire chest wall was radically resected, including the sixth to eighth ribs, while securing a safety margin of approximately 4 cm. No pleural adhesion was observed. The chest wall defect was reconstructed using 2 sheets of Marlex mesh and a latissimus dorsi myocutaneous flap (). The schwannoma in the right arm was simultaneously excised. The postoperative course was uneventful and the resection margins were microscopically clear. The patient was treated with postoperative radiation (54 Gy) and was placed under observation as an outpatient for over 9 years, during which period no evidence of recurrence was observed.
This study was approved by the institutional review board (IRB approval no., UC13ZISE0103). Written informed consent was obtained from the patient for publication of this manuscript and any accompanying images.


An 82-year-old Japanese man was admitted to our hospital with gait disturbance. He had previously been diagnosed with angina, atrial fibrillation, hypertension and diabetes mellitus (DM). He had experienced pain and swelling of the left hand and right toe a few days before admission. These symptoms were progressive and made it difficult for him to walk. Similar symptoms had appeared on the right upper and lower extremities one year before, and he was treated with an antibiotic at another hospital. However, the pain and swelling had not improved, and joint deformation remained.
On admission, his blood pressure, heart rate and temperature were 150/100 mmHg, 92 beats per minute, and 37.0°C. His consciousness state was alert. Both upper eyelids, the salivary gland, the dorsum of the left hand and both legs were swollen (, ). He also reported joint pain and showed a limited range of motion. Scratches were also seen on both dorsa of the feet. Neurological examination showed motor weakness of distal limbs (manual muscle testing 3/5) and decreased touch, pain and vibration sensation of the dorsum of the left hand and both legs. Deep tendon reflex in both legs was also decreased. Laboratory examinations revealed high inflammatory responses (white blood cell count 13 200/μl (neutrophils 72.2%, lymphocytes 16.7%, eosinophils 0.1%), C-reactive protein 14.37 mg/dl, elevated sedimentation rate 34 mm/h) and hyperuricemia (9.7 mg/dl). Liver function (aspartate transaminase, alanine transaminase, γ-glutamyltransferase, lactate dehydrogenase), renal function (blood urea nitrogen, creatinine), and amylase were within normal ranges. Glycometabolism (HbA1c [5.7%]), thyroidal function (thyroid-stimulating hormone, free T4), creatine kinase, and gonadal hormones (testosterone [0.69 ng/ml])were also within normal ranges. High serum IgG (2417 mg/ml) and IgG4 (630 mg/dl, 26.1% of total IgG) were seen, although autoimmune antibodies were all negative (rheumatoid factor, anti-nuclear antibody, anti-cyclic citrullinated peptide antibody, anti-topoisomerase antibody, anti-centromere antibody, anti-SS-A antibody, anti-SS-B antibody, and anti-neutrophil cytoplasmic antibody). As for other serum laboratory examinations, immuno-electrophoresis showed a chronic inflammatory pattern and serum vascular endothelial growth factor was elevated (351 pg/ml). Cerebrospinal fluid (CSF) showed no elevation of protein or pleocytosis. Urinalysis was negative for protein, occult blood, glucose, and ketones. The cultivation test revealed Staphylococcus aureus in two blood cultures and no bacterium in CSF. No abnormal lesions were seen in brain and spine MRI. Wrist MRI revealed swelling of the synovium and myelin sheath with fluid accumulation on the left side. The electromyographic (EMG) study showed signs of mononeuritis multiplex (). In conduction studies, compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs) were absent in the left median and ulnar nerves. In the right median and left lower extremities, CMAP amplitudes were reduced. Needle EMG showed neurogenic changes with the voluntary movement of the upper and lower extremities, and no denervation potential at rest. Enhanced computed tomography and gallium scintigraphy showed no inflammatory lesions or malignant tumors. Lymph node echography showed only reactive swellings. Lacrimal and salivary gland echography showed low echoic mass lesions, suggesting swelling of the glandular tissue. Based on this finding, a lacrimal gland biopsy was performed and showed lymphoid follicles with a germinal center. Enzyme immunostaining with anti-IgG4 antibody revealed IgG-positive plasma cells, of which about a half were IgG4-positive, on the lymphoid follicles (). Based on these results, Mikulicz’s disease was diagnosed.


A 26-year-old man presented to us with pain in the right scapula. He had an injury by the car door hitting against his right shoulder 3 weeks ago. Since the pain had not subsided and there appeared a swelling in the lower part of the scapula, he reported to us.
On examination, there was a diffuse swelling with tenderness in the right inferior part of the scapula (). Overlying skin was normal.


A 42-year-old female patient, farmer by occupation, resident of Chamba district, presented to our outpatient department with chief complaints of fever for 2 months and right-sided chest pain for the same duration. The patient was apparently well before that when she presented with fever documented up to 102° Fahrenheit with evening rise in temperature and it was associated with night sweats but not associated with any chills and rigor or any rash or skin changes. Her right-sided chest pain was localized to infra-axillary region, nonradiating, sharp, nonexertional, and got aggravated on deep inspiration and coughing. There was no history of cough and shortness of breath. Ten years ago, she took treatment for lymph node (LN) TB but defaulted after 3 months of therapy. She never took any medication for diabetes and hypertension. There was no history suggestive of any contact with TB patient, or high-risk sexual behavior. Family history, menstrual history, and recent treatment history were unremarkable. On examination, the patient had pallor and mild dependent edema. Five LNs were palpable in the right cervical region superior and middle cervical region, the largest being 2.5 cm in diameter, matted, nontender, and not associated with any overlying skin changes not fixed to the underlying structure or skin. On respiratory system examination, the right infra-scapular and infra-axillary region were dull on percussion and breath sounds were decreased with shifting dullness suggestive of right-sided pleural effusion, which was confirmed by chest X-ray. About 5 mL of straw colored fluid was tapped and sent for investigation.
Investigations revealed the following: Hb 8.9 g/dL, total leukocyte count 4970 (neutrophils 76%, lymphocytes 15%, eosinophils 5%, basophils 3%, monocytes 1%), platelet 320,000, serum glutamic oxaloacetic transaminase 44, serum glutamic pyruvate transaminase 34, bilirubin total 0.8, albumin 3.9, alkaline phosphatase 128, urea 96, creatinine 1.9, Na 143, K 4.5, calcium 11.3 mg/dL, phosphorous 4.9, serum and urine electrophoresis was negative, intact parathyroid hormone 20 ng/L (8–51 pg/mL), arterial blood gas showed pH of 7.38, 25(OH) vitamin D 97 ng/mL (30–100 ng/mL), angiotensin converting enzyme level 10 U/L, urine routine and microscopy were normal, and urine for acid fast bacilli was negative. Urinary calcium level was higher than normal (U Ca/Cr = 32). Chloride level was 23 mmol/L. Ultrasonography KUB and noncontrast computed tomography KUB [] were suggestive of medullary macro-calcification without any evidences of renal TB. Renal biopsy [] was done showing interstitial deposition of calcium without any histological evidences for renal parenchymal TB. Intravenous pyelogram was done and it did not reveal any lesion suggestive of genitourinary TB. LN biopsy revealed caseating granulomatous change with Genexpert (CB-NAAT) positive. Pleural fluid was exudative, and lymphocyte was predominant (95%) with adenosine deaminase level of 67 ng/mL. Hence, a diagnosis of extrapulmonary TB was made.


A 51-year-old woman was admitted to the Gastroenterology Intensive Care Unit for hemorrhagic shock secondary to massive rectal bleeding.
The patient had lost about 15 kg over the past 5 mo, with recurrent episodes of diffuse abdominal pain that worsened following meals. Bloody diarrhea had started a few days before hospitalization, being intermittently mixed with stool first and progressing to massive rectal bleeding.
The patient had very limited medical history, comprised of very low visual acuity only. She reported having been abandoned at birth, and thus not knowing her family.
Initial physical examination demonstrated oculocutaneous albinism with whitish hair, pale skin, horizontal nystagmus and strabismus. Abdominal palpation elicited pain, and perineal examination did not show any anal fissure or fistula. The patient had a slight dyspnea, requiring low flow oxygen therapy, and pulmonary auscultation revealed bilateral crackles. She also had a severe undernutrition status, with a weight of 32 kg and a body mass index of 13.6 kg/m2.
Laboratory findings were: hemoglobin of 5.4 g/dL (normal range: 13-18 g/dL), C-reactive protein (commonly known as CRP) of 73 mg/L (normal: < 5 mg/L), and hypoalbuminemia (1.6 g/dL; normal range: 3.4-5.4 g/dL). The white blood cell count (8.66 × 103/μL) and platelet count (268 × 103/μL) were normal. Bleeding time, activated partial thromboplastin time, and prothrombin time were normal. Stool samples cultures were negative, including for Clostridium difficile.
A computed tomography scan revealed diffuse bilateral interstitial infiltrates consistent with a severe pulmonary fibrosis (Figure ), and thickening of the descending/sigmoid colon associated with a transverse and ascending colon mild dilatation. Sigmoidoscopy showed active bleeding colitis, with continuous deep ulcerations (Figure ).


A 39-year-old woman with history of hypercholesterolemia referred asthenia and heaviness in both legs. She had sedentary lifestyle, balanced diet and did not complain intestinal issues.
Her weight was 56 kg, height 170 cm, body mass index 19 kg/m2, waist circumference 73 cm and her blood pressure was tested at a value of 13/10 KPa.
She was born from healthy and non-consanguineous parents and her development was normal. She had not familiarity for early cardiovascular disease, and did not report personal history of hypertension, chronic kidney or liver diseases.
During her life she needed hospitalizations for a miscarriage (28 years old) and a delivery of a healthy male newborn by caesarean section (30 years old). The pedigree of her family is reported in Figure and shows the premature death of one of her brothers for unknown reasons at the age of 1 wk.
The patient’s lipid profile showed a significant elevation of the total (321 mg/dL), low-density lipoprotein (LDL) (161 mg/dL) and high-density lipoprotein (HDL) (118 mg/dL) cholesterol, whereas triglyceride levels were normal. Serum apolipoprotein-A and -B were 291 mg/dL (n.v. 115 mg/dL-210 mg/dL) and 145 mg/dL (n.v. 55 mg/dL-135 mg/dL) respectively.
Since the patient and her relatives had neither clinical history nor physical signs (xanthoma and xanthelasma) of a genetic hypercholesterolemia, we studied other possible causes of her dyslipidemia through further laboratory tests. Blood count, liver and kidney function, coagulation tests, autoimmunity assays, PCR and urine dipstick were normal. Thyroid function tests displayed a subclinical hypothyroidism. Albumin level, detected by nephelometric method, was critically reduced (0.2 g/dL, n.v. 3.4 g/dL-5 g/dL) and total bilirubin was undetectable. Calcium level was 7.5 mg/dL (n.v. 8.5 mg/dL-10.1 mg/dL), total protein 5.8 g/dL (n.v. 6.4 g/dL-8.2 g/dL), pre-albumin 0.46 g/L (n.v. 0.2 g/L-0.4 g/L). Finally, serum protein electrophoresis (Figure ) showed the presence of a minimal amount of serum albumin (1.6%, n.v.55.8%-66.1%), with a simultaneous increase of the other serum protein fractions (alpha-1, alpha-2, beta-1, beta-2 and gamma), including transferrin (607 mg/dL, n.v. 200 mg/dL-360 mg/dL), alpha 1-antitrypsin (2.56 g/L, n.v. 0.9 g/L-2.0 g/L) and complement C4 (0.46 g/L, n.v. 0.10 g/L-0.40 g/L). Those seemed to compensate the lack of albumin[] .
These findings led us to investigate on the patient’s hypoalbuminemia. Proteinuria was excluded by normal spot urine albumin/creatinine ratio and total protein/creatinine ratio. Other possible secondary causes of hypoalbuminemia, such as inflammatory state and insufficient hepatic synthesis, were ruled out by normal laboratory tests and abdominal ultrasonography. The latter was negative except for mild hepatic steatosis. All the other examined members of the family (her parents, her brother, and her son) showed albumin level close to the upper limit of the normal range, suggesting that they may be heterozygous for a variation in the ALB[] . For the above reasons, we tested the hypothesis of CAA by mutation analysis of the ALB[]. After we obtained informed consent, we collected blood samples from all the available members of the family and two unrelated healthy volunteers as a control, and extracted genomic DNA from whole blood. For a rapid identification of variations in the ALB, we used a gel-based mutation detection strategy, which we developed and applied to the identification of many other cases of CAA[]. Shortly, we PCR amplified the fourteen genomic fragments of the ALB encompassing the fourteen coding exons and their intron-exon junctions, using the specific primer pairs described by Watkins et al[] . The fragments were then examined by heteroduplex and SSCP analysis: The combination of these two techniques usually allowed us to identify the region of ALB containing the molecular defect, which was then submitted to direct DNA sequencing[]. In the present case heteroduplex analysis clearly indicated that the only detectable change in both homozygous and heterozygous samples occurred in the 386 bp long region amplified by using PCR primers A23A and A24A encompassing exon 12 and the intron 11-exon 12 and exon 12-intron 13 junctions (Figure ). All the other members of the family are heterozygous, since they show the presence of four bands corresponding to homoduplex and heteroduplex PCR products (Figure , lanes 2, 2′, 3, 3′, 4, 4’ 5, 5’). The homozygous sample (Figure , lanes 1 and 1′) revealed only one band but with a different mobility when compared with controls (Figure , lanes 6, 7, 6′, and 7′). No variation due to conformation polymorphism could be seen under these electrophoretic conditions (data not shown). The results of the DNA sequence analysis performed on the abnormal fragment showed that our patient is homozygous for a CA deletion near the 3′ end of exon 12, at nucleotide positions c. 1614-1615, according to the Human Genome Variation Society rules, i.e,. starting from the initiator codon (Figure ). The subsequent frame-shift should give rise to a predicted translation product of 516 amino acid residues instead of the 585 found in the mature protein (p.Leu540Phefs*2), in which the sequence Cys(538)-Thr-Leu-Ser has been changed to Cys(538)-Thr-Phe-Stop. Unfortunately, we could not perform a search for this truncated variant in the serum of our patient, but no evidence was found so far for the presence of the putative albumin molecule produced in all the cases of CAA studied at the molecular level[,]. The electropherograms from the parents confirmed that they are both heterozygous for the same mutation (data not shown). This result brought to the molecular diagnosis of CAA in our patient.


We report a case of a 60-year-old man with a smoking history of 25 pack years stopped in 2001, high blood pressure, hypercholesterolaemia and depression. In 2011, the patient underwent curative medium and lower right bilobectomy for a stage IB squamous cell lung carcinoma, followed by radiotherapy and chemotherapy.
In October 2017, cancer recurrence was diagnosed with bilateral pulmonary and tracheal metastasis. One month later, the patient developed dyspnoea with inspiratory and expiratory stridor in the context of a mixed tracheal mass (intrinsic and extrinsic) visualised by a computer tomography scan of the chest (). The patient was scheduled for rigid bronchoscopy under general anaesthesia and fasted 6 hours for solid food and 2 hours for clear liquids. The examination confirmed the presence of a mixed tumour of the proximal trachea located 40 mm from the vocal cords with a critical narrowing of its lumen over 40 mm in length (). After partial resection of the intrinsic component of the tracheal metastasis using a bronchoscope and YAP (Yttrium-Aluminum-Perovskite) laser (Lokki Lis Laser, Bryan, Woburn, USA), an 18×50 mm self-expanding, fully covered metal stent was placed to contain the residual extrinsic compression. The resection was only partial to maintain the stent in place. The procedure was performed without complications with immediate resolution of dyspnoea. Radiography of the thorax confirmed the correct placement of the tracheal stent ().
On postoperative day 1, the patient experienced severe acute dyspnoea (grade 4 of the modified Medical Research Council dyspnoea scale) at rest with chest discomfort after a period of intense coughing. Oxygen saturation was 94% at ambient air. Chest X-ray confirmed migration of the tracheal stent requiring emergent rigid bronchoscopy for its retrieval (). The dyspnoea was attributed to the extrinsic component of stenosis and the irritation caused by the displaced stent. As he had eaten a full meal in the previous hour, 250 mg (3 mg/kg) of intravenous erythromycin was administered to accelerate gastric emptying. One hour later, a senior gastroenterologist performed gastric nasofibroscopy under local anaesthesia using a nasofibroscope (Olympus Europa SE & Co, Hamburg, Germany) with an external diameter of 4.8 mm. The patient was positioned on the bronchoscopy table in the operating room with the head slightly up. Intranasal and oral local anaesthesia was administered using a 10% lidocaine spray. The procedure was of very short duration (50 s), very well tolerated and confirmed the complete emptying of the stomach (). This allowed the general anaesthesia for rigid bronchoscopy to be performed safely without any risk of bronchoaspiration. Bronchoscopy revealed a distal migration of the tracheal stent, which was removed with forceps. Additional resection of the tumorous mass was performed with the YAP laser, without the need to place a new stent as the tracheal calibre was satisfactory.
One month later, another emergency bronchoscopy was necessary due to an aggravation of dyspnoea in the context of tumour progression. As the patient was not fasting, he received intravenous erythromycin again followed by gastric nasofibroscopy under local anaesthetic, which showed complete gastric emptying. Bronchoscopy confirmed severe tracheal stenosis with a residual lumen of approximately 20% of the normal lumen, which required the implantation of a new 18×60 mm silicone tracheal stent with excellent immediate results. The procedure was uneventful.


A 19-year-old healthy female presented with complaint of seeing black spot in front of her left eye for 1 week. The left eye showed a faint yellowish brown-wedge-shaped depigmentation inferonasal to fovea []. Multicolor image showed a zone of pale-pink discoloration with loss of perifoveal greenish hue []. SDOCT line scan through the lesion showed focal thickening of OPL with thinning of underlying ONL and focal disruption of ELM []. Infrared channel of multicolor imaging aimed at picking the outer retinal lesions showed zone of hyperreflectance []. The pseudocolor encoding for this channel is red which explains the pinkish discoloration of lesion amidst the greenish perifoveal hue on multicolor image.[] Based on these findings, a diagnosis of AMN was made. Blue autofluorescence (BAF) image showed wedge-shaped hyperautofluorescence interspersed with hypoautofluorescent zones [].


A 68-year-old Caucasian female patient presented in our Department with abdominal pain and a concomitant 15 kg weight loss over the past 6 months that was unintentional. The pain was mainly located in the epigastrium. She also had symptoms of dehydration, due to persistent postprandial vomiting, during these months. Her medical history included hypertension and diabetes mellitus. Her physical examination was normal and her blood results and an abdominal ultrasound were within normal range.
On admission, a nasogastric tube was inserted and the fluid and electrolyte balance was corrected by parenteric infusion of crystalloid fluids. Two days later, the patient was subjected to gastroscopy which showed mild inflammation of the lower esophageal mucosa and gastritis. The instrument could not pass further from the third part of the duodenum, due to extraluminal pressure on the duodenal wall. Gastrografin swallow confirmed the obstruction of the third part of the duodenum with proximal dilation of the stomach and duodenum (Fig. ).
Computerized tomography (CT) scan of the upper and lower abdomen excluded the possibility of a tumor or an annular pancreas to be the cause of the compression of the duodenum. The subsequent CT scan showed an acute angle of 15° (Figs. and ) between the superior mesenteric artery and the aorta.
Thus, based on the history, the unintentional weight loss may have induced the compression of the third part of the duodenum. In this case, the clinical and the imaging findings of the patient concluded the diagnosis of SMA syndrome.
Following extensive discussion with the patient and her family, she opted for surgery rather than conservative management. She was unwilling to try nasojejunal feeds or total parenteral nutrition (TPN) in the interim.
Therefore, after obtaining informed and written concern, the patient was subjected to laparotomy. The first and second parts of the duodenum were not dilated and hypertrophied as expected, due to acute onset of the syndrome. The duodenum was obstructed at the point where the superior mesenteric artery crossed the third part of the duodenum (Fig. ). These findings confirmed the diagnosis of SMA syndrome.
Due to patient’s hemodynamic instability intraoperatively, Strong’s procedure was performed with lysis of the ligament of Treitz and mobilization of the duodenum (Fig. ).
The postoperative course was not uncomplicated. There was evidence of gastric outlet obstruction and persistent ileus. The patient had a nasogastric tube that drained about 1.5 l of bilious material per day. She was then subjected to upper gastrointestinal endoscopy to rule out other pathology that may demonstrate external pressure on the third portion of the duodenum.
In addition, repeated difficulties with intravenous line placement, electrolyte abnormalities and falling serum albumin levels indicated that Strong procedure had failed and the patient’s condition necessitated again surgical intervention.
A week after the first operation, she was subjected to new laparotomy where a side to side gastrojejunostomy was performed. The postoperative course was now uncomplicated and she was admitted after 2 weeks.
Afterwards, a barium meal a month later showed postoperatively unobstructed passage of the contents from the stomach to the jejunum.


A 4-year-old boy was referred because of a history of bloody stools for 8 months. Before referral, a stool culture had shown Campylobacter jejuni which was adequately treated with antibiotics (). Control culture was negative. There was no history of diarrhea or hard stools. However, the boy continued to complain of abdominal pain and the bloody stools persisted. Laboratory investigations showed no biological markers for anemia, a slightly elevated sedimentation rate (27 mm/h), normal C-reactive protein (CRP, 1 mg/L), and normal coagulation. Serology for celiac disease was negative. Colonoscopy revealed rectal irritation. Histology of rectal biopsies showed a few lymphocytes and signs of intestinal spirochetosis confirmed by Warthin-Starry staining (WSS). A 10-day course of amoxicillin-clavulanic acid (50 mg/kg/day) was administered. The blood in the stool disappeared as well as abdominal complaints.
However, 2 months later, he presented at the emergency ward with complaints of bloody diarrhea for 2 days without abdominal pain. A new diagnostic work-up with colonoscopy revealed the presence of a juvenile polyp (JP) at 3 cm from the anal margin and a second one at 20 cm. There were no longer signs of intestinal spirochetosis on biopsies. These polyps were removed. They showed an histology compatible with juvenile polyposis. His symptoms disappeared after removal of polyps. The patient remained asymptomatic during 3 months of follow-up.


An 8-year-old boy was presented because of a history of hyperphagia, abdominal pain, chronic diarrhea, and perianal irritation. His complaints started after a recent vacation in Egypt (). A blood sample showed no signs of anemia or inflammation. A colonoscopy seemed normal. However, biopsies revealed an intestinal spirochetosis.
A treatment with metronidazole was started for 2 weeks. The abdominal pain and hyperphagia disappeared almost immediately. However, diarrhea and perianal irritation resolved gradually in the following weeks. Fifteen months after the initial presentation, the patient had again complaints of hyperphagia, diarrhea, and perianal irritation for 3 weeks. A treatment with metronidazole was administered without performing an endoscopy. After this treatment, he had no longer complaints for 1 year. Afterward, he relapsed, suffering from chronic diarrhea and hyperphagia again without abdominal pain. Therefore, he was treated with metronidazole. This time, metronidazole was administered for 4 weeks. After 4 weeks of treatment with metronidazole, an endoscopy was performed. It showed no signs of intestinal spirochetosis.


A 7-year-old boy had non-bloody diarrhea, encopresis, abdominal pain, and peri-anal rash for 18 months. A stool culture was negative. An ultrasound of the abdomen showed no abnormalities (). Blood results revealed no signs of anemia or inflammation with normal tissue transglutaminase. A lower GI-tract endoscopy revealed mild rectal irritation. Histology of biopsies from the rectum and sigmoid showed signs of intestinal spirochetosis. A treatment with metronidazole at 30 mg/kg/day for 10 days was administered. At a follow-up visit 2 months later, the boy no longer suffered from diarrhea or abdominal pain. However, he still had some complaints of encopresis and anal rash. Control endoscopy showed disappearance of intestinal spirochetosis.


A 12-year old boy complained of episodes of abdominal pain, non-bloody diarrhea, and loss of appetite for the last year (). During initial presentation, a stool culture was negative. Blood sample showed some signs of mild inflammation (CRP, 16.6 mg/L; erythrocyte sedimentation rate, 16 mm/h) and discrete anemia (hemoglobin, 12.1 g/dL; normal range, 13–16.5 g/dL). Although the macroscopic aspect of colonic mucosa was normal, histology showed discrete signs of colitis. No spirochetes were found. His symptoms improved without treatment.
After 7 months, he was reevaluated because of relapsed symptoms. Blood results showed again a moderate elevation of inflammation parameters. Stool culture was positive for Salmonella. Ultrasound and abdominal computed tomography scan showed mesenteric adenitis and colitis. A new endoscopy was performed and the macroscopic aspect of the colon mucosa was normal However, histology showed colon mucosae with proximal and distal zones of mild inflammation and cryptitis. WSS was positive in the caecum and colon transversum. A treatment with amoxicillin and metronidazole was commenced for 10 days. His symptoms disappeared after this treatment.


A 42-year-old Saudi lady with known medical history of hypertension and hypothyroidism presented to emergency department with a complaint of right iliac fossa pain of 3 days duration. The pain was severe in nature, associated with nausea. She denied any history of fever, vomiting, anorexia and changes of bowel habits.
On physical examination, she appeared in pain. She was tachycardiac with 109 beats per minutes and elevated blood pressure of 170/110. Her other vital signs were within normal. Her abdominal examination revealed tenderness and rebound in the right lower quadrant. Chest and cardiovascular examinations were clear.
Upon reviewing her laboratory investigations, C-reactive protein was the only elevated parameter of 18.51 mg/l. All other routine laboratory were within normal range. She underwent a CT abdomen/pelvis, which showed an oval shaped well-defined fatty texture at right lower quadrant measuring 2.8 × 2.4 cm with fat stranding that was suggestive of an epiploic appendagitis (Fig. ). The CT also noted a large well-defined cyst with a single septum suggestive of left adnexal cyst. A pelvic ultrasound examination showed a cystic structure measuring 6 × 6 cm in left ovary with normal color flow doppler seen.
The patient was under the care of Obstetrics/Gynecology and due to persistent pain they elected to take her for emergency laparoscopy exploration. Intraoperative, general surgery team was consulted due to a gangrenous mass adherent to the right lower quadrant abdominal wall, originating from sigmoid colon. The small bowel was inspected from the duodenojejunal junction until the terminal ileum, which was healthy, the colon was inspected until reaching the gangrenous mass, adhesionlysis done and the mass separated from the abdominal wall (Fig. ). The decision was to proceed for excision of the gangrenous sigmoid appendagitis and deroofing of left ovarian cyst. The postoperative period was uneventful. The histopathology result of specimen reveled necrotic adipose tissue. The ovarian cyst showed a serous cystadenoma.


A16-year-old male patient was presented with headache and vomiting for 2 months. He developed left upper and lower limb weakness for 15 days. There was no history of immune suppression, family history of melanoma, or nevus or sunburns. His general examination did not reveal any nevus. Neurological examination revealed bilateral papilledema and Grade 4 power in the left upper and lower limb.
Computed tomography (CT) plain imaging showed cortical based hyperdense lesion measuring 26 mm × 26 mm in the right parietal region. It was associated with bleed measuring 48 mm × 38 mm. [] Magnetic resonance imaging (MRI) showed well-circumscribed, lobulated, cortical-based lesion with bleed in the right parietal region. It measured 26 mm × 26 mm × 18 mm in size. It was isointense to gray matter on both T1, T2W images and mildly hyperintense on fluid-attenuated inversion recovery images. Diffusion-weighted images (DWI) showed irregular peripheral restriction of the lesion and susceptibility on susceptibility-weighted images. Heterogeneous enhancement on contrast images was noted. The lesion was associated with varying ages of bleed measured 48 mm × 42 mm × 34 mm. The bleed showed intense hyperintensity on T1W images and iso- to hyper-intense on T2W images. There was perilesional edema with midline shift of 5 mm. Magnetic resonance (MR) angiography showed normal flow signals within the intracranial arteries. No other abnormality was seen [Figure –]. Based on imaging findings, we considered hemorrhagic mass lesions such as high-grade glioma or metastatic lesions as possibilities. He underwent a right parietal craniotomy and total excision of the lesion and evacuation of hematoma. Intraoperatively, hematoma was seen on the pia. The lesion was soft to firm, fleshy reddish dark brown, and vascular. Apart from the blood, there was no pigmentation of the meninges. There were no areas of pigmentation in the inner surface of the dura mater [Figure and ] Postoperative period was uneventful. Postoperative CT and MRI showed total excision of lesion with bleed [Figure –].
Histopathology from paraffin blocks showed interesting features. Sections examined from the tumor showed cellular neoplasm composed of large cells with abundant eosinophilic cytoplasm, arranged in perivascular papillary pattern and in sheets. Tumor cells had coarse chromatin with brisk mitotic activity (8–10/10 hpf). At places, the tumor cells exhibited nuclear atypia. Focally, the tumor cells had intracytoplasmic brownish pigment along with hemosiderin-laden macrophages. Necrosis and thrombosed vessels were noted. The differential diagnoses considered based on these histological features were a high-grade glioma and a papillary meningioma.
Immunohistochemistry for epithelial membrane antigen (EMA), glial fibrillary acidic protein (GFAP), IDH-1 (R132H), cytokeratin, CD34, chromogranin, and synaptophysin was negative and strongly positive for S-100 protein. INI-1 showed retained expression. MIB-1 labeling index was15%–20%. In view of diffuse and strong S-100 immunohistochemistry (IHC), further IHC with human melanin black-45 (HMB-45) antibody was performed. The tumor showed strong HMB-45 immunopositivity and the final diagnosis of MM was offered [Figure –]. BRAF mutations analysis could not be done in this patient as our laboratory was not equipped with the facilities for doing it.
The patient underwent screening to look for the primary site for melanoma. A thorough search was made for a primary lesion in the other probable sites such as skin, mucus membrane, eyes, and lower gastrointestinal tract, which yielded negative results. CT scans of the thorax and abdomen yielded normal findings with no evidence of primary lesion. We confirmed that the intracranial lesion was a PMM. He was referred to oncologist for further treatment. Four months following surgery, he completed intensity-modulated radiotherapy 60 Gy in 30 fractions. He did not receive any chemotherapy. He again developed headache and vomiting immediately after completion of the radiation therapy. CT brain showed right parietooccipital bleed [Figure and ]. MRI done showed a tentorial-based recurrent tumor in the right parietooccipital region. It was measuring 1.5 cm × 1.3 cm size. It was heterogenous intense in both T1 and T2W sequences with contrast enhancement. Gliotic area was seen in the previously operated cavity. Imaging confirmed a recurrent tumor remote from the previously operated site and away from the leptomeninges [Figure –]. He underwent a right parietooccipital craniotomy and total excision of the tumor. Tumor was soft and suckable mixed with blood clots [Figure and ]. Falx and tentorium were seen and brain was lax at the end. The patient had a normal postoperative course without any complications. Postoperative CT confirmed total excision [Figure and ] and histopathology confirmed HMB-45 strongly positive recurrent melanoma. Five months following second surgery, the patient eventually succumbed to recurrence and expired.


A 33-year-old male patient presented with a chief complaint of swelling in the right side of lower jaw for 6 months. Swelling was sudden in onset and gradually increased in size. Extraoral examination revealed that swelling was diffuse extending on the right side of mandible, superoinferiorly from ala-tragus line to the lower border of mandible and anterioposteriorly 1 inch behind corner of mouth to the angle of mandible []. Swelling was firm in consistency with no local rise in temperature. Right submandibular lymph nodes were palpable and were tender and mobile. Intraoral examination revealed obliteration of right lower buccal vestibule.
Radiographic examination revealed a well-defined unilocular radiolucency with sclerotic borders on the right side of posterior body and ramus of mandible, extending superiorly till the sigmoid notch with the involvement of coronoid process and inferiorly thinning of lower border of mandible. Root resorption was evident in 46 and 47 [].
Based on the patient history, clinical features and imaging findings a provisional diagnosis of ameloblastoma were considered. Odontogenic keratocyst, calcifying epithelial odontogenic tumor, primary intraosseous carcinoma and metastatic tumors were in the list of differentials.
Fine needle aspiration cytology was performed with no significant findings.
Patient underwent incisional biopsy procedure in a private clinic and presented with the histopathology report of Basaloid Squamous Cell Carcinoma (BSCC).
Considering the lesion as malignant, hemimandibulectomy was planned and Right submandibular gland along with lymphnodes were removed and the specimen was sent for histopathological examination [].
Microscopic examination revealed odontogenic epithelium arranged in variegated pattern predominantly plexiform and with few areas of follicular pattern. Sheets and nests of basoloid cells with peripheral palisading was evident. The cells showed hyperchromatic nucleoli and stippling with lack of cytoplasm. Few follicles exhibited stellate reticulum like areas along with squamous metaplasia and microcystic change. Marked cellular atypia with increased mitotic activity was seen. Stroma was minimal with moderate fibrous tissue component. Submandibular glands and lymphnodes were free of tumor infiltration. Reactive changes like prominent germinal center and sinus histocytosis were seen in the lymphnodes [Figure –].
Based on the histopathological features a working diagnosis of Ameloblastic carcinoma was considered.
Periodic Acid Schiff (PAS) special stain was performed, showed negative expression for mucin in the microcystic space [].
Immunohistochemistry showed an immunoreactivity for cytokeratin (CK) 19 [].
Thus, the histopathology and immunohistochemistry confirmed the diagnosis of AC of right mandible.
The patient was followed up and was free of recurrence for a period of 6 months.


A 61-year-old female presented with complaints of a neck swelling she noticed 4 years
ago. Initially, the swelling increased in size and reached a stable level. The
patient also reported that the swelling enlarged with coughing and straining. She
denied stridor, dysphagia, dysphonia, neck pain, and having other neck masses. On
examination, there was a mass located in the right lower region of the patient’s
neck with no overlying skin changes. The mass increased in size with Valsalva (). On palpation, the
mass was compressible with transmitted pulse. Auscultation showed no bruit. Flexible
nasolaryngoscopy showed unremarkable examination. Computerized tomography (CT) scan
of head and neck with contrast was done (–). No treatment was indicated. Thus, the patient was scheduled for
follow-up and observation. On patient follow-up after 1 year with US Doppler, the
internal jugular vein was patent within size compared to previous CT image and no
thrombus formation ().


A 60-year-old man with repaired tetralogy of Fallot (TOF) and mitral valve (MV) repair for endocarditis as well as an implantable cardioverter-defibrillator for secondary prevention in situ was admitted with haemodynamic compromising monomorphic VT despite Bisoprolol 5 mg. His cardiovascular examination showed a mid-sternotomy scar and when in sinus rhythm the auscultation showed normal heart sounds with no murmurs. His jugular venous pressure was not raised with a blood pressure measured at 110/60 mmHg. His respiratory examination was unremarkable. A 12-lead electrocardiography documentation of the monomorphic VT (Figure ) demonstrated a right bundle branch block QRS morphology, transition in lead V4 with south-west axis, suggesting a VT exit from the LV lateral wall. Patient underwent VT ablation with three-dimensional (3D) EAM under general anaesthesia. The initial 3D-EAM of the LV was performed using the Orion catheter. After completion of the initial mapping, an ablation catheter was used for further point-by-point mapping at sites of interest. An irrigated 4-mm tip bidirectional steerable catheter (IntellaNav OI, Boston Scientific, Natick, MA, USA) was positioned in the LV for EAM via a steerable bidirectional sheath (Agilis, St. Jude Medical Inc., St. Paul, MN, USA) following an anterograde approach via a transseptal puncture.
The catheter moved freely within the LV until it became stuck. Fluoroscope suggested an extracardiac position. Contrast injection via the irrigation port of the catheters confirmed pericardial staining (Figure ), but it only became apparent on further withdraw of the catheter that the catheter was inside a coronary vein (see Figure and see ). Transthoracic echocardiography confirmed the intubation of basal LV wall with the catheter tip which then exited into the epicardial space (Figure ). The catheter was removed without any further sequelae. Subsequently the patient’s Bisoprolol was increased and underwent a VT provocation test at 5-month follow-up with a negative result.


An 85-year-old woman was referred to our institution because of inferior ST-segment elevation myocardial infarction (STEMI) with a moderate troponin peak of 10.88 μg/L (N < 0.04 μg/L). Angiographic data showed a two-vessel coronary artery disease with a proximal occlusion of the right coronary artery (RCA) and a complex highly calcified bifurcation stenosis involving the left anterior descending artery (LAD segment 2) and the ostium of the second diagonal branch. The patient underwent angioplasty of the infarct-related RCA. Decision was made to refer the patient within a month to our cath lab for secondary treatment of the LAD bifurcation lesion. The discharge TTE disclosed inferior wall akinesia, small basal inferior aneurysm, and normal left ventricular ejection fraction (LVEF). The patient was readmitted 17 days after discharge due to recurrent acute anterior STEMI and cardiogenic shock (severe left ventricular (LV) dysfunction with LVEF of 25% at the time of admission in the cath lab).
Urgent coronary angiography was performed 4 h after symptoms onset and showed a complete occlusion of the proximal LAD, well above the bifurcation lesion. Percutaneous coronary intervention with stenting of the culprit lesion was performed, but revascularization of the bifurcation lesion was considered too high risk. Transthoracic echocardiography disclosed a large defect (8.5 mm) of the basal inferior wall (Figure ), with extension in to a pseudoaneurysm. A colour Doppler analysis (Figure ) showed shunt flows passing from the LV to the aneurysmal pouch.
2D and 3D maximum intensity projection (MIP) multiphasic cardiac CT images provided a non-invasive modality for the evaluation of the pseudoaneurysm. It helped to define the anatomy, size, course, relationship of the pseudoaneurysm and determine further therapeutic strategies. Cardiac CT revealed a giant pseudoaneurysm (31 × 47 mm) running the length of the right ventricle (Figure ). The final diagnosis was cardiogenic shock related to recurrent anterior STEMI and the fast growing development of an inferior pseudoaneurysm.


A 74-year-old woman, with controlled hypertension and dyslipidaemia, presented to the emergency department due to altered speech, left-sided facial droop and decreased muscle strength on the right side of her body with 12 hours of evolution. Physical examination showed aphasia, central facial nerve palsy on the left side, slight right-sided hemiparesis, Babinski’s sign on the left and fever. Computed tomography of the head (head-CT) showed bilateral nucleocapsular and subcortical fronto-parietal ischaemic infarctions of unknown date. The electrocardiogram (ECG) showed sinus rhythm and the thorax x-ray a small left pleural effusion. Blood analysis showed 14,400 leucocytes/μl, increased C-reactive protein (217.8 mg/l), LDH 459 U/l and INR 1.57. The patient was medicated with aspirin and hospitalized with ischaemic stroke. Blood cultures were collected. Doppler ultrasonography of the neck vessels and a trans-thoracic echocardiogram showed no alterations. Magnetic resonance imaging (MRI) revealed multiple acute ischaemic infarctions scattered over both cerebellar and cerebral hemispheres, reflecting strokes in the posterior and anterior circulations ().
Given the possibility of cardioembolic aetiology, enoxaparin was initiated (on the 7th day of hospitalization), however transoesophageal echocardiography showed no alterations. Neurological deficits deteriorated on the day anticoagulation was started, leading to prostration. Head-CT was repeated, revealing a massive parenchymal haematoma in the left frontal region which led to suspension of the enoxaparin.
After the most common stroke aetiologies were excluded, the following examinations were performed, but showed no alterations: lupus anticoagulant, anticardiolipin and anti-beta2-glycoprotein I antibodies, antithrombin III, proteins S and C, antineutrophil cytoplasmic autoantibodies, mutation of the prothrombin gene and factor V Leiden, and HIV, HBV, HCV and VDRL serologies. Antinuclear antibodies were positive (1:160) and D-dimers were high at 1,644 μg/l (normal <230 μg/l), while fibrinogen was low at 1.4 g/l (normal 2–4 g/l).
A whole-body CT scan revealed a solid lesion in the left lower lobe of the left lung, multiple mediastinal pathological lymph nodes, peripheral lung thromboembolism with greater expression on the right, right femoropopliteal venous thrombosis and splenic and renal infarctions (–).
Faced with the impossibility of resuming anticoagulation immediately, a filter was placed on the inferior vena cava. Cerebral angiography showed occlusion of the right internal carotid artery (recall previous normal Doppler ultrasonography of the neck vessels) and excluded vasculitis.
Endoscopic ultrasound-guided transoesophageal biopsy of a mediastinal lymph node revealed non-small cell lung cancer. Immunohistochemistry testing for the lung cancer subtype proved inconclusive.
Disseminated intravascular coagulation (DIC) with multiple brain and systemic thrombotic events was diagnosed as a manifestation of a paraneoplastic syndrome of the hidden lung neoplasia. With favourable evolution of the brain haemorrhage, enoxaparin was resumed 2 weeks after the event. However, as there were new thromboembolic events despite the reintroduction of anticoagulation, it was definitively suspended due to progressively worsening thrombocytopenia.
During hospitalization, the patient remained feverish, with high inflammatory parameters, but no infectious source was identified and microbiological cultures were negative. Such alterations were considered to be correlated with systemic thromboses.
At this stage, the patient was mute and tetraparetic, with a level 4 performance status (ECOG). It was decided in a multidisciplinary meeting not to start cytostatics as no benefit was anticipated in view of the advanced neoplasia (stage IIIB/IV) and a high degree of dependence. The patient was referred to palliative care and died a few days later.


A 72-year-old man was admitted to our hospital with intermittent claudication due to diffuse stenosis in the right superficial femoral artery (SFA). His medical history revealed that he had two Wallstents (Boston Scientific, Marlborough, MA, USA) implanted in his bilateral common iliac arteries 14 years ago. The patient’s risk factors of atherosclerosis included diabetes mellitus with insulin therapy, a smoking habit, and hypercholesterolemia. He took 100 mg of aspirin daily over the 14-year period and had statin therapy for several years. Aortography showed mobile translucency in the Wallstent in the right iliac artery (). We observed this mobile translucency using intravascular ultrasound (IVUS) and angioscopy (Visible, INTER-TEC MEDICALS, Tokyo, Japan). The IVUS revealed heterogeneous regions in the thrombus and angioscopy showed a mobile solid thrombus () with dendrite morphology () at the side of the vessel wall and rubbing yellow plaque on the stent struts.
We scheduled femoral–popliteal artery bypass surgery for dealing with the SFA stenosis. However, we did not schedule treatment for the thrombus, because it and its stalk could not be released and distally moved. Moreover, we deemed the thrombus to be too large to remove using an aspiration catheter. Therefore, no pathological information about the thrombus exists.


Ms A, 26-year-old, was brought by the family for sudden onset behavioral abnormalities, reduced sleep, restlessness, anxious and irritable mood, beliefs of being pregnant despite a negative urinary pregnancy test, and delusions of persecution. She refused to take her meals, was aggressive, and had a labile mood. We diagnosed her with acute polymorphic psychotic disorder without symptoms of schizophrenia (an International Classification of Diseases tenth revision/ICD-10 diagnosis). Her complete hemogram, serum biochemistries, and thyroid function were normal. In view of recent-onset amenorrhea, we ruled out pregnancy by the urine pregnancy test and pelvic ultrasonography. She was treated as an inpatient with olanzapine 10 mg/day and clonazepam 0.5 mg twice a day and had about 50% relief in 2 days and was discharged. However, she did not achieve remission, and her symptoms changed during the next 2–3 weeks. She started remaining sad, stopped participating in household activities, and repeatedly voiced her concern about conception. She would prefer to stay alone and had depressive cognitions in the form of bleak views of future, hopelessness, and suicidal ideations. She also had delusions which were mood congruent and revolved around her conception. However, her appetite was increased, and she gained nearly 3 kg of weight during this period. In view of the change of symptomatology, the diagnosis was revised to major depressive disorder current episode of severe depression with psychotic symptoms (F32.3) and she was re-admitted due to suicidal ideations. The rating of her psychopathology on the Brief Psychiatric Rating Scale (BPRS) revealed a score of 55, suggestive of a severe illness. After informed consent, she was administered modified bi-temporal electroconvulsive therapy (ECT) at a frequency of three treatments/week. In view of weight gain, olanzapine was replaced with lurasidone which was increased to up to 40 mg twice a day. The treatment and associated details are mentioned in . Olanzapine was cross-tapered with lurasidone over a period of 2 weeks to avoid a rebound of psychotic symptoms. Consultation with an obstetrician was done for amenorrhea. The levels of luteinizing hormone (11.78 mIU/mL), follicle stimulating hormone (7.76 mIU/mL), and estradiol (21.56 pg/mL) were normal; prolactin (41.20 ng/ml) was slightly raised and endometrial thickness was 3 mm. In view of the slightly raised prolactin levels, an endocrinology consultation was also sought, and additional investigations were suggested. These included serum cortisol levels and a brain magnetic resonance imaging (MRI), both of which turned out to be normal, and so no medications were advised. Her depressive symptoms improved significantly within 2 weeks of treatment, but she developed an expressionless mask-like face and had slow gait and reduced span of arm swing. The ratings on the Extrapyramidal Symptom Rating Scale (ESRS)[] were moderate (score on questionnaire – 3, bradykinesia – 4, gait and posture – 2, and expressive movements – 4). On clinical global impression (CGI), the severity of parkinsonism was rated as 4, i.e., moderate. A repeat serum prolactin showed very high levels (252.4 ng/ml) but she tested negative for urine alpha-fetoprotein. We attributed the extrapyramidal symptoms and hyperprolactinemia to lurasidone. It was tapered and replaced with low dose aripiprazole (5 mg/day) along with trihexyphenidyl 2 mg thrice a day. There was a significant decline in the DIP within the next week, and she was discharged. After 4 weeks of discharge, repeat serum prolactin level was 11.07 ng/ml and her menstruation had resumed.


In October 2015, a 40-year-old female patient with a history of sinus venous thrombosis and hypertension sought medical consultation. Her blood pressure was resistant despite treatment. She had a good NYHA Class I/IV and exercised frequently. She was adherent to dietary approach to stop hypertension (DASH) and regularly attended medical visits.
A review of systems was negative. She did not have toxic habits. On her physical exam she had normal respiratory sounds, her cardiac exam was normal without murmurs or rubs, the heart sounds were regular and rhythmic, and her point of maximal impulse (PMI) was non-displaced. No murmurs nor bruits were found on her anterior abdomen or on her lumbar regions. Her body mass index was measured at 20 kg/m2.
Her prior treatment plan included verapamil 160 mg po qd, losartan 100 mg po qd, hydrochlorothiazide 25 mg po qd, aspirin 100 mg po qd, and clopidogrel 75 mg po qd. Despite treatment, the patient was found with diastolic blood pressures >100 mmHg. In that visit, verapamil was increased to 240 mg po qd.
Her laboratory results included: creatinine 0.55 mg/dL (NV 0.4–1.1 mg/dL), BUN 11.4 mg/dL (NV 3–20 mg/dL), K 4.27 mEq/L (NV 3.5–5.1 mEq/L), glucose 86 mg/dL (NV 70–99 mg/dL), total cholesterol 191 mg/dL (NV < 200 mg/dL), HDL 65 mg/dL (NV 50–60 mg/dL), triglycerides 72 mg/dL (NV < 100 mg/dL), and uric acid 2 mg/dL (NV 1.9–7.5 mg/dL). She had a normal electrocardiogram and transthoracic echocardiogram.
Based on the results of the October 2015 visit, the treatment plan was changed to: verapamil/trandolapril 240/4 mg po qd, hydrochlorothiazide 25 mg po qd, and spironolactone 25 mg po qd. In addition, ambulatory blood pressure monitoring (ABPM) was ordered as a precautionary measure (Figure ).
She was seen again in December of 2015; the ABPM showed good blood pressure control, but the patient complained of intolerance to spironolactone, which was subsequently stopped (Figure ).
A renal artery Doppler was completed in March of 2016 with all results being normal.
In July 2016, the patient complained of frontal headaches that were resolved with conventional analgesics. Her systolic blood pressure was 170 mmHg, so her treatment plan was supplemented with prazosin 3 mg po qd and eplerenone 25 mg po qd.
Despite the pharmacological changes, her blood pressure remained greater than 160/100 mmHg.
In May 2017, an angio-CT of the renal arteries was performed (Figures and ), and it showed bilateral renal fibromuscular dysplasia. The right renal artery was 100% abnormal, and the left renal artery was affected on its distal third.
A subsequent Doppler of renal arteries was completed in June 2017 (Figure ) and showed abnormal findings. The right renal/aortic index was 3.9; a high suspicion of FMD exists when the renal/aortic index is greater than 3.5. The peak-systolic velocity at the right renal artery was measured at 267 cm/s with a stenosis of 60%. The left renal artery was normal; a possible explanation for this normal finding could be the distal FMD at the left renal artery found in the angio-CT. The intra-renal blood flow had a spectrum type tardus et parvus, prolonged acceleration times, and normal resistance indexes.
The patient underwent renal arteriography (Figure ) and balloon angioplasty in June 2017. The most critical stenosis had a 5 mm diameter on the left side and 6 mm on the right side. 5 × 40 mm and 6 × 20 mm balloons were used on the left side, inflated to 8 atmospheres for two and a half minutes. The right side (more severely affected by FMD) was treated with a 6 × 20 mm balloon starting on the distal part of the vessel, inflated to 8 atmospheres for two and a half minutes. The medium and proximal thirds of the vessel were treated with a 6 × 20 mm balloon, inflated to 10 atmospheres.
There was a good angiographic result after the procedure, the stenosis improved significantly and there were no spasms or dissections observed. There were no complications. The patient remained in the clinic for a short period to monitor for possible complications and variations in her blood pressure.
After discharge, the patient has displayed good control of blood pressure; she is under treatment with only losartan/amlodipine 50/2.5 mg po qd. She has been asymptomatic and in good overall clinical condition.


A 58-year old man presented to our emergency center with a 2-day history of abdominal pain in the left hypochondrium, general malaise and pyrexia. The physical examination of the abdomen was normal. On both lower legs, the patient had yellow-brown skin lesions with indurated borders (Fig. ). On the right leg this lesion was located on the pretibial area (Fig. ), while on the left leg the lesion was located in the medial part of crural region.
At the admission, erythrocyte sedimentation was 80 mm/h (normal value 3 mm/h), C-reactive protein was 137.7 mg/l (normal value 0.0–6.0 mg/l), leukocytes were 14.2 × 103/μL (normal value 4.0–10.0 × 103/μl), and glycaemia was 14.81 mmol/l (normal value 4.40–6 mmol/l), while other biochemical parameters were normal. The CECT of the abdomen revealed splenomegaly and splenic abscess in the upper pole of the spleen (Fig. ). No abscesses elsewhere in the body were detected. Systemic hematologic disorders are excluded. Initially, the patient was treated by imipenem- cilastatine. After the admission, on the fourth day, patient underwent open splenectomy. Enterococcus faecalis has been isolated from splenic abscess. On the seventh postoperative day the patient was discharged. The patient was in very good condition a month later after splenectomy. For the lesions on lower legs, based on clinical examination, necrobiosis lipoidica as a diagnosis was confirmed. The disease was in later stage and histopathologic examination was not necessary. This patient was treated by topical administration of steroid cream (Exevate cream 0.05%). After a 2 months follow-up, this treatment was not effective, but continuous to be under surveillance of dermatologists.


The patient is a 55-year-old female who presented to the emergency department with stabbing lower abdominal pain. Her examination revealed focal peritonitis in the left lower abdomen. Patient’s laboratory testing was remarkable for a leukocytosis. Computed tomography demonstrated left-sided uncomplicated acute diverticulitis. The patient was admitted for medical management with intravenous antibiotics and bowel rest. On hospital Day 3, she continued to complain of severe pain and was subsequently offered surgical intervention. She underwent a sigmoid resection with end colostomy, and after an uneventful postoperative course she was discharged home.
Three months after her initial surgery, the patient presented to the office requesting a colostomy reversal. An outpatient colonoscopy showed mild diverticulosis but was otherwise unremarkable. She underwent a laparoscopic colostomy reversal using a 28-mm end-to-end anastomosis (EEA) stapler. Again, her postoperative course was unremarkable, and at the time of discharge she was tolerating a regular diet and had appropriate bowel function.
The patient presented to her gastroenterologist 1 year after her colostomy reversal with constipation associated with diffuse abdominal pain and bloating. There was no report of weight loss or hematochezia. A colonoscopy was performed that revealed a near-complete stenosis of the rectal anastomosis. The patient was referred back to our clinic to discuss surgical options. Due to her favorable anatomy and the benign nature of her pathology, she was offered an open or laparoscopic stricturoplasty, endoscopic balloon dilation, or endoscopic transanal stricturoplasty. She elected to proceed with the latter after the risks and benefits of the procedure were explained.
After informed consent was obtained, the patient was brought to the operating room and positioned in the lithotomy position. A urinary catheter was inserted, and preoperative IV antibiotics were administered. A single-site transanal gelport (GelPOINT® Path Transanal Access Platform by Applied Medical) was positioned transanally. Low pressure pneumorectum was achieved and 0° bariatric scope was introduced through the anus into the rectum. The previous anastomosis was noted to be 15 cm from the anal verge and was clearly stenotic (Fig. ). Following gentle spreading of the stricture, a 60-mm purple load Endo GIA stapler was advanced under direct visualization across the anastomosis where one blade was position across the afferent limb and the other blade was positioned in the blind pouch (Fig. ). Firing the stapler led to the creation of a widely patent anastomosis (Fig. ). The patient was admitted to the general ward for observation. She was discharged the next day after tolerating a regular diet. Four weeks postoperatively, she reported completed resolution of her symptoms. She underwent a surveillance colonoscopy 6 months after the stricturoplasty, and a widely patient anastomosis was still observed (Fig. ).