A 42-year-old woman with a family history of Lynch syndrome presented with menorrhea. She was diagnosed with stage I endometrial adenocarcinoma based on clinical and radiological evaluation which included a positron emission tomography-computed tomography (PET-CT) examination. A hysterectomy was performed which contained a FIGO grade 3 endometrioid adenocarcinoma featuring extensive lymphovascular invasion, with depth of invasion 1.1 cm of 2.5 cm myometrium. The accompanying lymph nodes (12 right pelvic, one right para-aortic, eight left pelvic and 10 left para-aortic) were negative for tumor.
Immunohistochemical staining for DNA mismatch repair proteins of the hysterectomy specimen revealed retained expression of MLH1 and PMS2 accompanied by aberrant cytoplasmic expression and loss of nuclear expression of MSH2 and MSH6 in the tumor cells. Postoperatively, the patient underwent a genetic evaluation which revealed heterozygous MSH2 mutation c1906G>C (p.Ala636pro).
Three months postoperatively, a follow-up PET-CT examination revealed a new 4.4-cm hypermetabolic lesion in the gastric wall with mucosal and mural involvement. No other lesions were detected. An endoscopic biopsy of the gastric lesion was performed and diagnosed as “undifferentiated malignant neoplasm most consistent with gastric carcinoma with lymphoid stroma (lymphoepithelial-like carcinoma/medullary carcinoma)”. An endoscopic ultrasound examination was consistent with uT3N1Mx gastric carcinoma.
The patient was referred to our oncology service and her biopsy slides were reviewed in consultation. Based on the referral diagnosis of gastric carcinoma, the plan was to administer neoadjuvant chemotherapy followed by surgical resection of the gastric lesion.
As shown in , H&E-stained sections of the gastric lesion revealed a poorly differentiated carcinoma characterized by dyscohesive tumor cells with a solid growth pattern, prominent necrosis, high nuclear-to-cytoplasmic ratios, large, round to oval nuclei, prominent nucleoli, frequent mitoses and variable amounts of cytoplasm. No obvious gland formation was identified. Scattered intratumoral lymphocytes were noted and confirmed by immunohistochemical staining for leukocyte common antigen (LCA). Referred immunohistochemical stains of the tumor cells were focally positive for AE1/3, diffusely positive for CAM-2 () and negative for S100, LCA and CDX-2 (). Additional immunohistochemical stains performed in our laboratory were diffusely positive for PAX-8 () and focally positive for estrogen and progesterone receptor proteins. Because of doubts regarding the referral diagnosis, the biopsy slides were compared with slides from the hysterectomy specimen. This disclosed a moderately differentiated endometrioid adenocarcinoma accompanied by a portion of poorly differentiated carcinoma with tumor necrosis and extensive lymphovascular invasion (). Based on the morphological similarity of the latter component to the biopsy tissue and the immunohistochemical findings, the gastric neoplasm was diagnosed as metastatic endometrial carcinoma.
The patient underwent chemotherapy with 5-fluorourcil, leucovorin, oxaliplatin and docetaxel (FLOT) starting 1 month after the biopsy. A partial gastrectomy performed 2 months later showed no residual carcinoma.


A 64-year-old Caucasian lady with recently diagnosed Sjogren’s disease and no prior history of coronary artery disease presented to the hospital with worsening fatigue and progressive generalized weakness over past few weeks. Review of systems was positive for diffuse joint pains; she denied shortness of breath, chest pain, palpitations, orthopnea or paroxysmal nocturnal dyspnea. Hypertension was her only chronic medical problem. She had quit smoking 5 years ago. In the emergency department, she was found to be hypotensive with a blood pressure of 78/40 mm Hg; pulse rate was 100/min, regular. Laboratory tests revealed acute kidney injury (blood urea nitrogen (BUN): 40 mg/dL, creatinine: 3 mg/dL) and hyponatremia (sodium: 129 mEq/L); potassium was 4.9 mEq/L, chloride: 93 mEq/L and bicarbonate: 23 mEq/L. Complete blood count, TSH and liver function tests were normal. Electrocardiogram (ECG) showed sinus tachycardia with a rate of 106/min. On review of medications, it was discovered that she had recently been tapered off prednisone and had started feeling worse since then. The patient was treated empirically for adrenal crisis with “stress dose steroids” (100 mg hydrocortisone every 6 h). She was hydrated aggressively with normal saline; initially she felt better, but a few hours later developed worsening shortness of breath. She was found to be in congestive heart failure. Pro-BNP was elevated at 30,000 pg/mL. She denied any chest pain or palpitations. EKG showed sinus rhythm and T wave inversion in anterolateral leads (). Echocardiogram showed left ventricular ejection fraction (LVEF) of 20-25% with anteroseptal, inferoseptal, apical, and inferolateral akinesis (). Cardiac enzymes were mildly elevated with a peak troponin of 1.7 ng/mL, peak creatine kinase (CK) of 73 U/L and peak CK-MB of 10.74 ng/mL. The patient was diagnosed as having non-ST elevation myocardial infarction (NSTEMI), and transferred to our institute for cardiac catheterization.
Cardiac catheterization revealed non-obstructive coronary artery disease and severely reduced left ventricular systolic function with an estimated LVEF of 20%, along with wall motion abnormalities consistent with takotsubo cardiomyopathy on ventriculogram (). She was treated in the coronary care unit for heart failure with standard medical therapy and she improved gradually. She was transitioned from hydrocortisone to oral prednisone. She was subsequently discharged in a stable condition. She continues to follow up with a cardiologist and is doing well 6 months later with improved LVEF between 45-50%.


A 63 years old lady had a right total knee replacement (TKR) in 2013 using the Vanguard® knee system - Biomet implant. She was admitted into hospital in March 2018 - approximately five years following her initial TKR. She presented with an insidious and acute onset of worsening right knee pain and swelling, not associated with any trauma. The pain was affecting her mobility, limiting her ability to weight bear on that joint.
On clinical assessment, she had an erythematous and fluctuant right knee with a moderate joint effusion. Along with this, she had a tender joint line with a limited range of movement. There was no evidence of wound breakdown, equally in 2013 following her primary procedure, she had an uncomplicated recovery period. She had a core body temperature of 37.3 °C, with no accompanying fevers or rigors, and the rest of her physiological markers were unremarkable.
Her initial blood investigations revealed significantly raised inflammatory markers with a white cell count (WCC) of 20.27 × 109/L, neutrophils of 16.68 × 109/L and C - reactive protein (CRP) of 186 mg/L, suggesting an acute infection. Radiographs of the knee showed a relatively well positioned in-situ TKR, with no evidence of loosening, with the possibility of a joint effusion (Figure and B).
Given this patients history, examination and biochemical findings, a right knee septic arthritis could not be excluded, and as such she was taken to theatre for a knee arthrotomy with a view to debride the joint, and potentially replacement of the polyethylene liner.
After the initial arthrotomy was made, significant purulent, dark coloured fluid extruded from the joint. The knee joint was formally opened and at this point no pus was seen, however there was a significant amount of metallosis debris deeply embedded into the soft tissues surrounding the knee prostheses (Figure ). On further inspection, it was clear that the metal clip which is normally used to secure the polyethylene insert to the tibial base plate had broken and dislodged (Figures and C). Despite this broken metal clip, the polyethylene liner was still in its original position, and on further examination the femoral, tibial and patella implants were all well fixed with no evidence of loosening. There was also no evidence of significant macroscopic wear of the femoral and tibial components.
The broken metal clip was retrieved successfully and in whole (part being dislodged and part being well fixed in the polyethylene liner). The Vanguard® TKR system is no longer used in our trust, and consequently we were unable to replace the liner and metal clip. This lady therefore went on to have a thorough soft tissue debridement of her metallosis and lavage with copious normal saline solution. She later had a second staged procedure (after a total of 18 d) at which point we were able to obtain the correct implants, and thus provide her with a new polyethylene liner and metal clip to secure it in place. In the interim, between stages, she was prescribed a course of two grams of intravenous flucloxacillin antibiotics (to complete a six week course) and was restricted with her weight bearing, to prevent polyethylene liner displacement.
Superficial and deep tissue samples from the time of her 1st procedure did not grow any organisms. The histology report demonstrated areas of black necrosis with reactive fibrosis, a giant cell foreign body reaction triggered by black, irregular metallic particles, confirming the diagnosis of metallosis.


A 53-year-old man presented with left back pain for 1 month. Laboratory investigation revealed increased C-reactive protein (CRP) and elevated erythrocyte sedimentation rate. The results of serum tumor markers showed raised carcinoma antigen 125, squamous cell carcinoma antigen, cytokeratin 19 fragment antigen 21-1 (CYFRA21-1), and ferritin (Table ).
A contrast-enhanced computed tomography (CECT) scan showed a moderately enhancing mass with a necrotic area in the upper left lobe of the lung and a filling defect in the interventricular septum suggestive of tumor.
A staging 18F-FDG PET/CT scan (Discovery STE; General ElectricHealthcare Technologies, Waukesha, WI) was performed 1 hour after the injection of 286.38 MBq (7.74 mCi) of 18F-FDG with a blood glucose level of 5.9 mmol/L. The PET/CT images demonstrate tracer concentration at the mass in left lung, left pelvic lymph node, and multiple cardiac lesions (Fig. ). Axial fused PET/CT image showed intense 18F-FDG uptake (SUVmax: 13.41) in the cardiac region corresponding to the hypodense lesion on axial CECT image and elevated pathologic 18F-FDG uptake (SUVmax: 2.86) in the left ventricular corresponding to a small tumor with soft-tissue density which was slightly less enhanced by contrast medium than normal myocardium on CECT. No abnormal finding was showed in the right atrium on CECT. However, there was intense focal 18F-FDG uptake (SUVmax: 5.28) in the right atrium detected on axial PET/CT image.
Two-dimensional transthoracic echocardiography only identified a large well-delineated mass (2.9 × 2.8 cm) attaching to the endocardial surface of interventricular septum (Fig. ). And left ventricular function was preserved.
A CT-guided needle biopsy was performed on the mass in the upper left lobe of the lung. Based on histologic findings, a diagnosis squamous cell cancer of the left lung was made. Therefore, the patient was diagnosed as having nonsmall-cell lung cancer with multiple cardiac metastases.
The patient was treated with Gemcitabine chemotherapy. After 18 months, the follow-up CECT scan revealed the patient achieved stable disease status according to the Response Evaluation Criteria In Solid Tumors (RECIST) guidelines.
Informed consent was obtained from the patient for publication of this report and accompanying images.


A 52-year-old male with a history of end-stage renal disease and atrial fibrillation presented to the emergency department with acute hypotension. The patient had chest pain, presyncopal symptoms, and a blood pressure that was too low to be obtained by manual blood pressure cuff. He was initially in atrial fibrillation with rapid ventricular response, featuring intermittent 10–15 s runs of ventricular tachycardia. The remainder of the patient's medical history was unknown. A focused bedside echocardiography was immediately obtained to assess the patient's cardiac status. On ultrasound, the patient was noted to have “severe-to-critical aortic stenosis” and moderate mitral stenosis. The decision was made to immediately bolus the patient with fluid and to perform synchronized cardioversion at 200 joules. Subsequently, the patient returned to normal sinus rhythm with a blood pressure of 121/79. The reader is referred to Figures and for key details of the sonographic appearance of critical aortic stenosis in this particular case.
The patient described herein underwent a comprehensive transthoracic echocardiogram after admission which redemonstrated the findings made on ultrasound in the emergency department.
Causes of ventricular tachycardia include long QT syndromes, hyperkalemia, cardiac ischemia, heart failure, and aortic stenosis. In patients with unstable ventricular tachycardia, treatment involves synchronized cardioversion and an amiodarone infusion. In a patient on hemodialysis, other potential causes of arrhythmias such as hyperkalemia, fluid overload, or other metabolic disturbances can cloud the clinical picture when choosing emergent treatment in the setting of hemodynamic instability. As this case demonstrated, bedside ultrasound can help identify cardiac abnormalities which can focus a broad-based differential into a specific treatment plan.
Aortic stenosis should be suspected in patients presenting with syncope, angina, and heart failure. Atrial fibrillation and nonsustained ventricular tachycardia are common arrhythmias associated with aortic stenosis.[] Patients with aortic stenosis often have ventricular tachycardia during syncopal episodes.[] It is critical to remember that patients with aortic stenosis are preload dependent and require aggressive fluid support to maintain their cardiac output. Atrial fibrillation typically causes more severe symptoms in the setting of aortic stenosis due to the noncompliant left ventricle and the resulting greater need for atrial contraction.
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Nil.
There are no conflicts of interest.


A 69-year-old man with no significant history was admitted for ampullary adenocarcinoma. A PD was performed by laparotomy using the Whipple procedure, followed by a Child reconstruction. The patient was considered high-risk for PF, according to the Wirsung duct size of ≤ 3 mm and presence of soft pancreatic parenchyma; thus, a preventive treatment (octreotide) was given. The postoperative course was marked by PF development on the 3rd postoperative day, which was treated with somatostatin and conservation of the nonaspirating drain placed intraoperatively. A control CT scan was performed on the 7th postoperative day and showed absence of active bleeding or pseudoaneurysm, absence of hematoma, and good placement of the drain (with contact with the pancreaticojejunal anastomosis). On the 12th postoperative day, the patient presented hemorrhagic shock with hemodynamic instability. The CT scan revealed an active bleeding arising from the stump of the gastroduodenal artery, with formation of a noncompressive hematoma. The drain had migrated and was no longer in the area of the pancreatic anastomosis. The PF was scored as grade C, according to International Study Group of Pancreatic Fistula classification. Endovascular exclusion of the gastroduodenal artery was performed by interventional radiology, along with placement of a covered stent in the hepatic artery.
Severe acute liver failure and acute renal failure developed immediately. Blood test showed cytolysis above 10 N (aspartate aminotransferase at 2000 UI/L, alanine aminotransferase at 1738 UI/L), cholestasis (alkaline phosphatase at 336 UI/L, gamma-glutamyltransferase at 388 UI/L), total hyperbilirubinemia (at 43.8 μmol/L), decreased prothrombin rate (by 36%), decreased factor V (by 32%), and a creatinine rate of 152 μmol/L. On the repeat CT (abdominal injection of iodinated contrast), the liver presented a heterogeneous enhancement, with a defect of enhancement in the left liver on portal time. Concerning liver vascularization, the portal trunk, the hepatic veins and the hepatic artery were permeable, with absence of intrastent thrombosis and of active bleeding. However, the inferior vena cava was compressed in its retrohepatic and suprahepatic segments by a hematoma located in the lesser omental sac (Figures and ).


This study has been approved by our institutional review board, and the need for written informed consent was waived due to retrospective study of medical record.
A 79-year-old woman was admitted to hospital with gait disturbance and cognitive dysfunction. Previously, she had a 4.5 mm aneurysm on the right middle cerebral artery for 1-year, and radiological follow-up was performed without treatment. Her symptoms began to worsen 20 days before the admission. She had a confused mental state without specific motor weakness and was not ambulatory. Brain magnetic resonance imaging (MRI) revealed a multi-lobulated mass, 1.8 cm in size, on the posterior third ventricle, which exhibited low- to iso-signal intensity on T1-weighted images and high signal intensity on T2-weighted images (Fig. A and 1B). The mass was homogeneously and strongly enhanced after gadolinium administration (Fig. C). Obstructive hydrocephalus developed due to the presence of the mass on the posterior third ventricle (Fig. D). Regional cerebral blood volume was slightly increased on perfusion magnetic resonance images. The provisional diagnosis was meningioma or lymphoma. Neuronavigation-guided endoscopic third ventriculostomy (ETV) was performed on the tuber cinereum between the mammillary bodies. Ventriculostomy was done using a monopolar coagulator and a balloon catheter; the arteries were atherosclerotic (Fig. A). Endoscopic biopsy (Bx) of the lesion on the third ventricle was obtained. Intraoperatively, the mass was pinkish in color and friable, with mildly increased vascularity (Fig. B). After surgery, her gait disturbance was improved, and she ambulated using a walker. The resected specimen was a cellular tumor that was composed of densely packed, round monomorphic cells exhibiting a solid growth pattern (Fig. A). The nuclei were round to oval and exhibited fine granular chromatin (Fig. B). Acellular neuropil islands were also observed and were positive on glial fibrillary acidic protein (GFAP) immunohistochemistry (Fig. C). Tumor cells were strongly immunopositive for synaptophysin (Fig. D) and negative for CD3 and CD20, which are representative T cell and B cell markers. The tumor was diagnosed as central neurocytoma. One week following surgery, GKR was performed using a radiosurgery planning software (Leksell Gamma, Elekta Instruments AB, Stockholm, Sweden). The prescribed dose was 14 Gy with 50% isodose lines, and the target volume was 1.62 cc (Fig. A). Three months after GKR, brain MRI revealed a decrease in the size of the multi-lobulated strong enhancing mass in the posterior third ventricle from 1.8 cm to 1.4 cm (Fig. B), and her confusion was improved. She did not undergo additional treatment including radiotherapy or chemotherapy. The patient had been followed-up 8 months with no signs of neurological deterioration.


A 13-year-old girl sustained an open BBFF. The laceration was volar, the deformity was seen in apex anterior, and both bones had a short oblique fracture pattern. She underwent irrigation and débridement with intramedullary nail fixation. Her pain was well controlled, and her compartments were soft. She had transient decreased sensation of her index finger only. One week after the surgery, she was noted to have difficulty flexing her index finger and making a fist. Therapy was initiated at 4 weeks postoperatively as a result of incomplete extension of all her fingers. At 8 weeks, she could only extend her wrist 10° before finger flexion occurred; some puckering of the skin at the scar of the volar open wound was observed. Despite improvement with therapy, at 1 year, she was unable to fully extend the proximal interphalangeal (PIP) joint of each finger with the wrist fully extended (Figure , A and B). She was referred to us. The contracture with the wrist maximally extended included the index (PIP, 40°), long (PIP, 60°), and ring (PIP, 25°) fingers. She underwent myotenolysis of flexor digitorum superficialis of index, long, and ring fingers, which were adhered to the volar scar and each other (Figure , C). A culture was obtained because of her open fracture and remained negative. Full passive extension was obtained with 90° of wrist extension intraoperatively (Figure , D). At 1 week postoperatively, she had full extension and flexion of her fingers with 70° wrist extension. By 1 month, she had full finger flexion and extension at 90° of wrist extension (Figure , E). She later presented with newly occurring limited flexion of her thumb consistent with an extensor pollicis longus (EPL) contracture. She underwent implant removal and was found to have a partial EPL rupture adjacent to the prominent radial intramedullary implant. The implant was removed, and the EPL was débrided tenolysed. She achieved full mobility.


A 16-year-old female patient sustained BBFF and underwent open reduction and internal fixation at another institution. She presented to us after 6 months with a significant flexion contracture of the thumb interphalangeal joint, which worsened with wrist extension and resolved with wrist flexion (Figure , A and B). Her other fingers were also involved but less severely. She also had ulnar nerve dysfunction with 50% subjectively decreased sensation, interossei wasting, and clawing of the ring and small fingers. She had intact median motor function; however, she reported mildly subjectively decreased median nerve sensation. Her findings had not changed with therapy. She underwent plate removal, myotenolysis of the flexor pollicis longus (FPL), and flexor digitorum profundus to each finger. The video shows FPL adherent and limiting thumb extension (Video 1, ). Her muscles appeared pink and viable, without signs of previous ischemia. A neuroma in continuity of the ulnar nerve was identified, and we performed a neurolysis; it was not found to be entrapped in bone. Her median nerve was intact. Full passive motion of FPL with wrist extension was achieved intraoperatively as shown in the video (Video 2, ). Intraoperative findings in response to treatment confirmed clinical entity of psuedo-Volkmann contracture, independent of ulnar nerve lesion. Postoperatively, she had an unchanged neurovascular examination and full thumb extension (Figure , C and D). She did have a residual minor contracture of the small finger with wrist extension, but this not bothersome to the patient, and she was very happy with her result.


A 25-year-old man was admitted with trichoblastoma in the nuchal area with frequent recurrences since birth. The mass gradually increased to walnut-size, and the first excision surgery was performed in a local medical center (LMC) 3 years ago. The mass recurred at the same location and the patient underwent a second excision surgery at the LMC and was diagnosed with trichoblastoma after biopsy. After excision, the mass recurred with an increased size, and a third excision was performed in the LMC. However, when the mass recurred at the same site for the fourth time, the patient was transferred to our department (). The patient’s history, family history, and results of the laboratory study were unremarkable. A palpable lymph node was found in both, the internal jugular and popliteal cervical areas, and ultrasonography-guided aspiration was performed, but no metastasis was observed. The pathological diagnosis after the third excision surgery in the LMC was adnexal tumor with hair follicle differentiation with nonmalignant potential with involvement of the base. Immunohistochemistry results were positive for cytokeratin (+), p53 (−), and Ki-67 (1+). For accurate diagnosis, we requested for the specimen to be examined again in our pathology department. The specimen was identified as a skin adnexal carcinoma, of hair follicle origin and lowgrade malignancy (). The preoperative neck magnetic resonance image (MRI) revealed lobulated soft tissue lesions involving superficial fascia and infiltrating into both proximal trapezius muscles (). Positron emission tomography-computed tomography (PET-CT) revealed three hypermetabolic mass lesions about 4 cm in size on the subcutaneous layer of the posterior neck, and no distant metastases was observed. In the plastic surgery department, wide excision including a 1.5-cm safe margin and reconstruction with a free anterolateral thigh flap were performed. After extensive excision, histological examination revealed skin adnexal carcinoma, originating from the hair follicles, and low granular malignancy, consistent with trichoblastic carcinoma, with clear resection margin (). Even though partial flap necrosis had occurred, it was treated with debridement and split thickness skin graft. Neck MRI performed at 6 months postoperatively and PET-CT at 1 year postoperatively showed no remnant mass, recurrence, or distant metastasis. There was no palpable mass 5 years postoperatively, and there was no recurrence on follow-up of 5-year neck CT and PET-CT ().


A 34-year-old male came to the emergency room presenting with moderate to severe low back pain that limited ambulation and was partially controlled with the administration of non-steroidal anti-inflammatory drugs. He had a previous chemonucleolysis of L5–S1 due to a discopathy, and radicular compression of the nerve and left renal enlargement, all found on magnetic resonance imaging (MRI). Otherwise, his clinical history was unremarkable. Abdominal examination did not reveal any discomfort or palpable mass. Lumbar movements and palpation only reproduced the same discomfort, which was also evident upon asking the patient to perform Valsalva’s maneuvers. Both testicles were found normal upon inspection and palpation. The rest of the physical examination was unremarkable.
The lumbar spine MRI obtained previous to the chemonucleolysis reported a discopathy and lymph node enlargement in the retroperitoneal area. Although the discopathy was resolved, the persistence of lumbar pain called for a different approach. During the workup, an urotomography scan was performed, which confirmed multiple retroperitoneal masses in the left paraaortic region measuring 10 × 8 × 6 cm3. There were satellite lymph nodes around the retroperitoneal mass and the left psoas causing lateral displacement of the left kidney, compressing the pyelocaliceal system conditioning hydronephrosis (Fig. ). Next, a testicular sonogram showed the left testicular heterogeneous parenchyma, with high vascularity and irregular borders, with a size of 28 × 23 × 14 mm3 and a volume of 4.9 cm3. Evaluation of the right testicle was unremarkable. These findings were suggestive of a primary TGCT. Laboratory studies revealed a serum alpha fetoprotein of 15 115 ng/dL (normal value <20 ng/dL), β-human chorionic gonadotropin (β-HCG) of 11 IU/L (normal <0.5 IU/L) and lactate dehydrogenase of 394 U/L (normal value <250 U/L). As part of treatment, the patient underwent left radical orchiectomy without any complication and the specimen was sent for histological analysis. Pathology results showed subtotal atrophy of the testis with extensive fibrosis, multifocal calcifications, focal hemorrhage and Leydig’s cell hyperplasia. Extensive recent hemorrhage in the spermatic cord and epididymis was evident, without pathological alterations. There was no evidence of germ cell tumor, confirming spontaneous tumor regression (Fig. ). After reassessment, a cystourethroscopy with placement of a double J catheter was performed to resolve the secondary hydronephrosis due to obstructive uropathy. Subsequently, the patient began first-line chemotherapy with four cycles of bleomycin, etoposide and cisplatin (BEP) protocol. Hiccups, nausea, constipation and alopecia presented as adverse events that were managed with symptomatic medications. By the time of the submission of this case report, the patient had concluded his fourth BEP administration.


A 6-month-old girl was brought by an ambulance to our tertiary care hospital with difficulty in breathing and severe stridor. It was decided to perform airway assessment by ENT surgeon to determine the possible causes of stridor due to failure of improvement despite maximum medications given by pediatrician. Preoperative assessment showed an infant with mixed stridor requiring about 4 L of oxygen to maintain oxygen saturation above 90%. Suprasternal and intercostal recessions with conducted sounds could be heard on the chest. Chest X-ray was normal. No premedication was given and she was shifted to the operation theatre.
Supraglottic airway assessment was done awake with topical anesthesia using flexible fiberoptic endoscope which was normal. Subglottic endoscopic examination was decided under general anesthesia. She was induced with sevoflurane to maintain spontaneous ventilation for dynamic airway assessment. The spontaneous ventilation was assisted with great difficulty after loss of consciousness. The ENT surgeon used pediatric rigid endoscope. It revealed subglottic mass occluding 90% of the area, and it was not possible to bypass the mass with the smallest endoscope available (size 2.7 mm) []. The infant started to desaturate after endoscopic manipulations with difficulty to ventilate. Intubation failed with the smallest tube size 2. Ventilation was tried but was not effective. The saturation and heart rate started to drop with the scenario of cannot intubate and cannot ventilate. Atropine was given and external cardiac massage started as saturation dropped to less than 50% and heart rate fell to less than 60 beats per minute. Emergency tracheostomy was done successfully in 7 min and saturation improved to 99%. Infant regained consciousness and spontaneous breathing. Computed tomography was done which revealed a small hypodense area measuring 0.5 cm in diameter in the region of glottis. LASER marsupialization of the subglottic cyst was done successfully after 2 days from emergency tracheostomy.
Unfortunately, there is no definitive algorithm to follow for difficult airway in case of patients aged less than 1 year of age. Difficult airway society (DAS) published algorithm of cannot intubate and cannot ventilate in a paralyzed anesthetized child aged 1–8 years in 2015.[]
In the present case, we skipped insertion of supraglottic devices, percutaneous transtracheal jet ventilation (PTJV), rigid bronchoscopy ventilation, and percutaneous cannula cricothyroidotomy (PCC) for different reasons. Supraglottic devices cannot be used due to distal mechanical obstruction. PTJV is relatively contraindicated due to near total airway obstruction below vocal cord.[] In addition to risk of serious complications such as air embolism, extensive cervical emphysema, pneumothorax, and damage to the esophagus occur if jet ventilation is tried with misplaced cannula.[] Rigid bronchoscopy ventilation was impossible as the smallest endoscope of size 2.7 mm could not bypass the mass. PCC is not easy in infants. Moreover, it is challenging to obtain a proper angle to insert PCC without the risk of perforation of posterior tracheal wall.[] Emergent tracheostomy should be considered as the first step if an ENT surgeon is available.[]
The management of cannot intubate, cannot ventilate scenario needs vast experience in airway assessment, unshaken confidence, with extreme cooperation between anesthetists and ENT surgeons.
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Nil.
There are no conflicts of interest.


A 63-year-old female having diabetes and hypothyroidism, controlled on medications, presented in the pulmonary medicine outpatient department with complaints of dyspnea (NYHA grade 4) and B/L wheeze in chest. Her pulmonary function test showed severe restrictive abnormality (FEV1 = 55%, FVC = 60%, FEV1/FVC = 99%). She was diagnosed with asthma 5 years ago and her symptoms were poorly controlled on multiple medications. She was on tab. Wysolone (prednisolone) 50 mg OD, MDI Foracort (budesonide + formoterol), and MDI Tiova (tiotropium) puffs in the preprocedure period. Considering her long history with poorly controlled symptoms of asthma, she was planned to undergo BT.
After taking informed written consent, she was premedicated with 0.5 mg of alprazolam PO in the night before BT to allay her anxiety and advised to take her usual medications of asthma till the morning of the procedure. After taking the patient to the table, appropriate monitors were applied including three-lead electrocardiogram, continuous pulse oximetry (SpO2), and noninvasive blood pressure. Her baseline heart rate (HR) was 94 beats/min, SPO2 97%, and blood pressure 149/84 mmHg. A 20-G IV line was secured. Inj. glycopyrrolate was given in the doses of 0.2 mg intravenously and patient was nebulized with duolin (salbutamol and ipratropium) before starting the procedure.
She was preoxygented with 100% oxygen for 3 min. Induction was done with IV fentanyl 100 μg, propofol 120 mg, and atracurium 30 mg. Once the adequacy on ventilation was confirmed, supraglottic device (i-gel 3#) was inserted and ventilation was resumed. Balanced anesthesia was maintained with O2/air mixture with FiO2 0.3 and propofol infusion keeping BiSpectral Index values between 40 and 60 with intermittent boluses of inj. fentanyl (1 μg/kg) and inj. atracurium. A flexible bronchoscope was placed through the supraglottic device and a bronchial thermoplasty catheter was placed through the bronchoscope to perform thermoplasty of the right lower lobe []. The entire procedure was uneventful with FiO2 of 0.3, except for one episode of desaturation with SPO2 dropping down to 82% and tachycardia, and HR reaching up to 180/min. The episode of desaturation and tachycardia was observed during the first activation of thermoplasty catheter []. This was immediately informed to the pulmonologists and it settled down once the activation was stopped. The procedure lasted for about 45 min. After completion of the procedure, muscle relaxation was reversed with neostigmine and gylcopyrrolate. i-gel was removed after the patient was fully awake and following commands. She was shifted to the intensive care unit on supplemental oxygen via face mask and monitored for postprocedural complications. The patient was followed up to 1 week after procedure and she did not develop any respiratory complications.


A 40-year-old female patient presented with a nontender lump in the left breast measuring 8 cm × 6.5 cm × 6.0 cm, since the past few months. The swelling was large, nodular, with ill-defined borders, soft to firm in consistency. Skin overlying the swelling was fungating and ulcerated. The nipple was retracted and puckered. Ipsilateral lymph nodes were palpable. Mammography showed ill-defined hypodense area within the left breast with focal hyperechoic regions. Fine-needle aspiration cytology (FNAC) was done from the breast swelling as well as from the lymph nodes. Smears stained with Giemsa and papanicolaou stain were highly cellular and revealed ductal epithelial cells arranged in groups, tight clusters, and scattered singly. Cells were large, having pleomorphic round to oval nuclei with prominent nucleoli []. No myoepithelial cells were seen in the aspirate. Cellular dissociation was Grade II with good number of cells seen scattered singly. The background showed polymorphonuclear inflammatory infiltrate along with hemorrhage. Along with these tumor cells, sheathed microfilariae of W. bancrofti having multiple, coarse, discrete nuclei extending from the head to the tail, except in the small terminal portion of the caudal end were present []. Based on these features, a diagnosis of ductal carcinoma of the breast (Robinson's Grade II having a score of 12) with coexistent microfilarial infestation was given.
Based on radiological and cytological findings, total radical mastectomy was done through pectoralis muscle dissection. Two lymph nodes were identified and dissected out. Histopathology of the excised tissue showed, infiltrating duct carcinoma of the left breast (T4bN0M0 stage) [], with focal areas of giant cell reaction []. On serial sectioning sheaths of W. bancrofti were evident, along with eosinophilic infiltrate and granulomatous reaction, which proved the cytology findings [Figure and ]. Sections from lymph node tissues showed reactive hyperplasia only. The patient was referred for radiotherapy and chemotherapy but was lost to follow-up. Estrogen receptor (ER), progesterone receptor (PR), and Her2neu were applied on the sections, which showed ER positivity, PR positivity, and Her2neu negativity. The findings of cytology and histopathology were concomitant.


A 22-year-old male was intubated and admitted to the intensive care unit of Sultan Qaboos University Hospital, Oman, in March 2014 after being involved in a motor vehicle accident with multiple injuries, which included his lower limb, ribs, and maxillofacial fractures. Facial bone computed tomography (CT) showed lower anterior dentoalveolar fracture with lingual displacement, bilateral Le Fort I fractures of the maxillae, and medially displaced and fractured right condylar neck [].
As emergency management, the patient underwent closed reduction of the dentoalveolar fracture and open reduction and internal fixation (ORIF) of the bilateral maxillary fractures under general anesthesia along with orthopedic surgical repair. Three days later, the patient underwent ORIF of the right condylar fracture. Following the completion of the ORIF, severe intraoperative bleeding was encountered from the posterior medial aspect of the condyle. All local measures of packing failed to arrest the bleeding, and the patient underwent emergency angiography to identify and treat the possible source of bleeding, which was anticipated to be from the right internal maxillary artery. However, the angiogram did not show any major source of bleeding in relation to the internal maxillary artery, but identified a large DA of the extracranial part of the right ICA []. The vascular surgeon attempted surgical repair of the identified DA. However, due to the additional intracranial extension of the lesion this was difficult []. At this time, no active bleeding was found from the surgical site of the right mandibular condyle. Accordingly, a decision was taken to arrange for repair using an endovascular arterial stent, thus avoiding ligation of the ICA. The wound was thus closed in layers.
Six days later, through the femoral approach, the patient underwent endovascular insertion of a 50 × 6 mm self-expandable covered arterial stent with no distal carotid embolic protection, which resulted in complete resolution of the vascular lesion with no complications []. At nine months follow-up, the patient showed satisfactory dental occlusion and mandibular movements with no vascular or cranial abnormalities.


The patient is a 35-year-old male with bipolar I disorder who presented initially to his family physician with complaints of low mood and so was started on sertraline. When he presented to psychiatry 4 months later, his mood was significantly elevated and he reported symptoms of mania including gross overspending and sexual indiscretions and had committed several crimes and so was admitted to an inpatient forensics psychiatric facility. He was started on aripiprazole 10 mg PO daily and eventually given aripiprazole 400 mg IM and was discharged with follow-up with a mood disorders specialist.
Approximately 5 days after discharge from the forensics facility, the patient attempted suicide by means of overdose and lacerations to his wrists. He was admitted to the Intensive Care Unit (ICU) with a Glascow Coma Score of 3. Electroencephalography (EEG) showed an abnormality possibly associated with anoxic brain injury. Once discharged from the ICU, the patient was transferred to an acute care Psychiatry service. He was noted to be dystonic on transfer with several movement concerns. He described muscle contracture in his arms which kept them angled at 90° and a consistent need to walk around the unit due to restlessness. He displayed repetitive movements of the arms and hands and reported stiffness in his neck and back. At times, the movements of his hands would display a tremor. He was started on regular benztropine.
On the acute care Psychiatry unit, the patient was started on lithium up to 900 mg PO QHS for mood stabilization, which he initially tolerated well. Vortioxetine was added for antidepressant effects at a starting dose of 10 mg PO QHS. Due to continuous complaints of poor sleep, quetiapine, clonazepam, oxazepam, temazepam, nozinan, zopiclone, and lorazepam were all trialed with only lorazepam effective. He required as needed benztropine throughout his stay. Approximately 64 days after receiving IM aripiprazole and 41 days after starting lithium, the patient developed another acute dystonic reaction, and all medications were discontinued. Librium, clonazepam, and benztropine were trialed to treat the symptoms with only mild relief.
Neurology provided two consults with the impression that the patient was sensitive not only to antipsychotics but also to lithium after suffering an anoxic brain injury after his suicide attempt. A magnetic resonance imaging (MRI) head was completed at the time and was found to be unremarkable. The patient was then transferred to a Mood Disorders Inpatient specialty facility for further treatment.


A 13-year-old boy with a pertinent medical history of only allergic rhinitis was hospitalized for septic shock with fever of unknown origin. He had gone diving 10 days prior to admission (PTA). Six-day PTA, he had a fever (38°C) followed by headache, nausea, and vomiting but no diarrhea. Pertinent serologic examination at another hospital revealed white blood cells (WBCs) 10,170/μL, segments 92.6%, and C-reactive protein (CRP) 28.67 mg/dL. The chest radiograph and urinalysis showed no abnormalities. The family refused a lumbar puncture. Intravenous (IV) penicillin was given and the fever gradually subsided. Four-day PTA, right neck pain occurred without a history of trauma or any particular findings in the aforementioned area. One-day PTA, the fever rose to 39°C; right neck pain progressed and he became drowsy. Upon admission, his body temperature was 36.9°C, pulse rate 96/min, respiratory rate 18/min, and blood pressure 70/30 mmHg. Physical examination showed no abnormalities except tenderness on the right side of the neck level II of the submandibular angle without nuchal rigidity, cervical lymphadenopathy, wound, or skin discoloration. Dopamine was given for his shock status on admission. Laboratory data were WBC – 7510/μL, bands – 49%, segments – 32%; platelets – 13,000/μL; CRP – 31.21 mg/dL; slightly elevated fibrinogen/D-dimer; and a normal prothrombin time/activated partial thromboplastin time (PT/aPTT). Fiberscopic examination revealed no evidence of deep neck infection. Under suspicion of atypical infection, IV penicillin and levofloxacin were started and his clinical condition improved. Dopamine was discontinued on the 2nd hospital day (HD), and his fever subsided on the 5th HD. However, right neck pain persisted accompanied by right peripheral facial palsy and ptosis but no visual impairment. Tests for serum Lyme antibody IgG and IgM were normal. Brain magnetic resonance imaging (MRI) on the 6th HD showed a right sphenoid sinus mucocele with a right cavernous sinus and internal jugular vein thrombosis []. Endoscopic incision/drainage was performed. Pathology revealed chronic sphenoiditis. Blood cultures grew Peptostreptococcus; anaerobic pus cultures grew Prevotella loescheii, both sensitive to penicillin. Pus acid-fast stain and tuberculosis cultures were negative. After completing a 4-week course of penicillin and ceftriaxone (levofloxacin was shifted to ceftriaxone due to elevating liver enzymes), he was discharged with full recovery of cranial nerve palsy and no neck pain.


A 38-year-old Caucasian gentleman with no prior significant history presented with headache, vomiting, and frequent falls over the course of 2 months. Physical examination revealed normal vital signs. Neurological assessment showed left-sided ataxia, dysmetria, muscular hypotonia, and difficult in coordination movements. No evidence of peripheral lymphadenopathy or hepatosplenomegaly was noted on physical examination.
Routine laboratory analysis showed no abnormal findings. Magnetic resonance imaging (MRI) with intravenous contrast revealed an intra-axial lesion (13.7mm × 23.5mm × 21.1mm) compressing the fourth ventricular and leading to surrounding vasogenic edema and mass effect in the left cerebellar hemisphere. A homogenous hyperintensity was also seen postcontrast without central necrosis []. Differential diagnosis included a primary brain tumor, metastasis from other sites, and lymphoma. Computed tomography (CT) scan of the neck, chest, abdomen, and pelvis did not reveal any significant abnormalities.
In light of previous findings, the patient was deemed a candidate for surgical resection of tumor and underwent complete tumor resection.
Histopathological examination of the mass using hematoxylin and eosin-stained sections showed mixed cell background with multiple scattered RS cells. The RS cells were immunoreactive for CD30 marker and were negative for CD20 and ALK-1 markers. CD3 and CD5 markers highlight the small background lymphocytes []. The overall findings were most compatible with classical HL, mixed cellularity type.
Bone marrow biopsy was also obtained for staging and was found to be normal. Lumbar puncture revealed clear cerebrospinal fluid (CSF) with normal protein, glucose, and white blood cell count. No malignant cells were seen on microscopic examination of centrifuged CSF sample. HIV test was negative.
Postoperative course was uneventful. The patient received whole-brain radiation with a dose of 4000 centigray (cGy) followed by a boost of 1000 cGy, which was targeted toward the resection site. Chemotherapy containing two courses of adriamycin, bleomycin, vinblastine, and dacarbazine was given to prevent tumor recurrence and metastasis.
The patient was followed regularly with routine physical and neurological examination, laboratory tests (complete blood count, erythrocyte sedimentation rate, and lactate dehydrogenase), MRI of the brain, and low-dose CT scan of the neck, chest, abdomen, and pelvis at 3, 6, 12, 24, and 36 months postoperatively []. No evidence of recurrence was noted over the course of 7 years.


This is a 76-year-old female with a medical history of hypertension, hyperlipidemia, and cardiac arrhythmia who was found to have a large 20 mm × 24 mm × 22 mm (width × depth × height) left cavernous carotid wide-necked aneurysm during a workup for gait instability in 2016. The patient was taking rivaroxaban for her cardiac arrhythmia and smoked one packet of cigarettes per day. Given the morphology and location of an aneurysm, the treatment of an aneurysm using the PED was recommended. Seven days before the procedure, the patient was started on aspirin (325 mg daily), and immediately before the procedure, her aspirin assay was therapeutic (462 aspirin reaction unit [ARU]; <551 ARU was considered therapeutic). Her rivaroxaban was withheld 48 h before her procedure.
In March 2017, the patient underwent placement of two overlapping PED (4.5 mm × 20 mm and 5 mm × 20 mm) through the Marksman microcatheter (Medtronic Inc., Minneapolis, MN, USA) and Sofia intermediate catheter (MicroVention, Aliso Viejo, CA) for the treatment of her large left cavernous carotid aneurysm []. The first PED (4.5 mm × 20 mm) was deployed spanning from the supraclinoid ICA into the neck of the aneurysm. Then, the second PED (5 mm × 20 mm) spanning from the cavernous ICA, overlapping the distal PED, into the vertical segment of the petrous ICA was placed, covering the neck of an aneurysm. The entire flow-diverter stent construct spanned from the supraclinoid ICA to the vertical segment of the petrous ICA []. Final postprocedural control angiogram demonstrated significant contrast stasis within the aneurysm sac [] while fully heparinized. The patient was continued on her aspirin and restarted on her rivaroxaban following the procedure.
The patient returned for a follow-up angiogram at 4 months following treatment, which demonstrated remodeling of the ICA with only minimal filling of the aneurysm measuring 7 mm × 8 mm × 7 mm at the anterior genu of the cavernous segment of the ICA []. Despite counseling, the patient continued to smoke during the follow-up period. In a subsequent angiogram, at 10 months after treatment, the aneurysm had regrown with interval expansion now measuring 25 mm × 28 mm × 18 mm []. Computed tomography (CT) angiogram demonstrated complete PED coverage of the aneurysm neck []. This patient underwent placement of another PED (5 mm × 25 mm), and interval follow-up at 3 months demonstrated persistent filling of the aneurysm.


A 36 year-old woman with Her-2 negative metastatic gastric adenocarcinoma currently on capecitabine and oxaliplatin presented for oxaliplatin infusion. Laboratory testing one day prior showed a platelet count of 237 × 109 and ahemoglobin of 10.9 g/dL with an MCV of 81.9 attributed to iron deficiency anemia, She had previously received 5-fluorouracil/leucovorin/oxaliplatin for 14 months and then was switched to single agent capecitabine for 2 months in the setting of stable disease. At progression of disease, oxaliplatin was added to capecitabine, which the patient had been on for the past 9 months.
Thirty minutes after the oxaliplatin infusion was started, the patient developed significant bleeding from her gums, epistaxis, and had 150 to 200 mL of bloody oral secretions. Laboratory testing showed a platelet count of < 5 × 109, white blood cell count of 2.6 × 109, hemoglobin 6.2 g/dL, PT 16.4, INR 1.4, total bilirubin 0.5 mg/dL, LDH 211 U/L. Peripheral smear showed few platelets and no schistocytes. The patient was admitted and received intravenous immunoglobulin 1 g/kg, dexamethasone 40 mg IV for 4 days, and oral aminocaproic acid, with resolution of bleeding after one day. No platelet transfusions were given. She received 1 unit of packed red blood cells. The platelet count improved to 77 × 109 after 4 days and normalized to 341 × 109 one month later. Oxaliplatin was definitively discontinued.


A 61-year-old woman had suffered from worsening neurogenic claudication for 1 year and low back pain with radiation to the legs. L3–L4–L5 spondylolisthesis was diagnosed with magnetic resonance imaging, which revealed spinal stenosis between L4/5 making L5 bilateral nerve root compression, more severe on the left side (). Microscopic transforaminal lumbar interbody fusion (TLIF) with cages had been discussed and planned. During the operation, L3/4/5 TLIF was performed through the left side under microscopy after paraspinal muscle dissection. A Kerrison rongeurs was then applied for L3/4 and L4/5 left-side laminectomy. However, one 3-cm ureter segment was clipped out unexpectedly (). We confirmed urine extravasation with an intraoperative portal X-ray taken 5 min after contrast medium injection, which demonstrated that urine leaked from the right upper ureter ().
Transperitoneal laparoscopic ureter realignment was attempted. Prior to repair, we indwelled a retrograde ureter catheter with ureteroscopy to make the distal ureter stump easier to recognize. One 10-mm periumbilical trocar was set up for the camera, followed by two working ports (10 and 5 mm) created along the right-side mid-clavicular line. With pneumoperitoneum and dissection, the avulsed two ureter stumps were found successfully. To reduce the gap between the stumps, we performed extensive mobilization of the right kidney, in which dissection was carried out along the kidney low pole, lateral side, hepatic flexure, and subhepatic area, with preservation of perirenal fat tissue, and great care of hilar vessels. Both stumps were trimmed out of the devitalized ureter tissue and spatulated well. The end-to-end anastomosis was conducted with care to minimize handling of the ureter adventitia; interrupted sutures were performed meticulously with 3–0 Vicryl in four stitches (). After this procedure, one retrograde double-J stent was placed under ureteroscopy, and a Jackson–Pratt drain was also left next to the anastomosis site.
In spite of the patient’s uneventful postoperative course, she received 14 days of parenteral ciprofloxacin to prevent adjacent spine infection. The Foley catheter was removed on the seventh postoperative day; she was discharged on the 15th day. The Jackson–Pratt drain was removed at the outpatient clinic 3 weeks after ureter repair, and the double-J was also removed 2 months after the anastomosis. However, excruciating back pain and vomiting developed, and hydronephrosis and an elevated creatinine level (increased from 0.67 to 1.87 mg/dL) were noted. Ureteroscopy revealed a short segment (<1 cm) of ureter stricture at the suture site (); therefore, this patient received long-term double-J stenting for ureter stricture. The associated flank pain and vomiting subsided once she received restenting in the repaired ureter.


A 53-year-old female patient with dyslipidemia was admitted to the Emergency Department with abdominal pain on the right iliac fossa and vomiting for 24 h. On arrival she was afebrile and haemodynamically stable. Abdominal examination disclosed increased abdominal tenderness with rebound located on right iliac fossa.
Blood tests revealed leukocytosis (14.500 white blood cells/μL) with neutrophilia (79%) and no C-reactive protein elevation; kidney and liver functions both were within normal range. Abdominal ultrasound showed some free fluid in the pelvis and a computed tomography scan was then performed and revealed a linear hyperdense foreign body located in distal ileum with intraperitoneal free air (Fig. ). A presumed diagnosis of intestinal perforation was established, and patient was taken to the operating theatre for diagnostic laparoscopy.
Intraoperatively the diagnosis of a perforated Meckel’s diverticulum by a fish bone with localized peritonitis was made (Fig. ) and a laparoscopic stapled diverticulectomy was performed, with the stapler applied to the base of the diverticulum, transversely to the longitudinal axis of the bowel (Figs and ).
Postoperative course was uneventful, and patient was discharged 4 days after surgery.
Histologic examination of the surgical specimen was consistent with perforated Meckel´s diverticulum, with no evidence of ectopic mucosa.


Patient is a 45-year-old female patient, with past medical history of gastritis. Six months before she sought medical attention, she was complaining of mild upper abdominal pain, however, due to her previous condition she was medicated with proton pump inhibitors assuming that the pain was due to her gastritis. In the last 3 months, she noticed a mass in her upper abdomen and the pain became more severe and started to affect her daily activities, thus she presented to a routine physical exam. No weight loss or other constitutional symptoms were noticed. Also no history of malignancy in her family was mentioned. On clinical examination, a 12 × 15 cm2 mass was discovered on her upper abdomen, mild pain was found on palpation but no tenderness was present. An abdominal ultrasonography revealed a 15 × 15 cm2 septate thin-walled giant cystic mass, it was anechoic and had a volume of ~735 ml. The cyst occupied most of the hepatorenal space and it was in intimate contact with the liver, right kidney and pancreas (Fig. A). Due to the size of the mass, CT was requested, it revealed well-defined 19.7 × 15 × 10 cm3 giant cyst, the cyst was located within the small bowel mesentery and it was in intimate contact with the liver, gallbladder, pancreas and right kidney (Fig. A). Nevertheless, the tomography could not rule out that the mass had some sort of communication with the bile duct or the pancreas. This is why a magnetic resonance cholangiopancreatography found that the cyst was attached but had no communication with the bile duct or the pancreas (Fig. A). CBC and blood work was normal.
Due to the size of the cyst and clinical condition surgery was planned. At laparotomy, a 19 × 15 × 10 cm3 mesenteric cyst was discovered (Fig. B), the cyst was near the root of the small bowel mesentery but did not compromise its main vessels, it had a yellowish appearance (Fig. B), and clear fluid was found within the cyst. Multiple adhesion were identified between the cyst wall and the transverse colon, liver, third portion of the duodenum and gallbladder. With these findings surgery was straightforward, complete resection of the cystic mass was performed, however, the cyst wall was completely attached to the body of the gallbladder and could not be resected without compromising it (Fig. B), so a cholecystectomy was performed as well. After this, the remainder of the procedure continued without any complication.
Pathology reported a giant primary mesenteric cyst, it was lined with a single layer of cuboidal epithelial cells and partially covered by adipose tissue and prominent vasculature, it had a yellowish wall and its thickness varied between 0.1 and 0.3 cm (Fig. C). Its interior had a white trabecular internal surface with brown patches it did not have any communication with other organs, and no areas of malignancy were found (Fig. C).
In the early postoperative period, a tachycardic patient with severe abdominal pain and tenderness was encountered, she became hypotensive an oliguric, thus an emergency re-laparotomy was performed. The 1000 ml of hemoperitoneum was encountered and after extensive washing of the abdominal cavity, an arterial vessel from the resected gallbladder was discovered and successfully managed. After this surgery patient fully recovered. Sips of liquids were initiated on the third postoperative day, and full diet was initiated a day after. She was discharged without any complications and, on follow up controls patient is doing well.


A 6-year-old female with a history of left FH and limb-length discrepancy presented for orthopedic evaluation of knee instability. Anterior tibial instability appeared to be the most pressing clinical issue with frequent subluxation episodes. The patient’s medical history revealed a left Achilles tendon lengthening at 11 months of age. Bilateral imaging of the legs revealed an absent left fibula (). The patient’s left leg was 3.5 to 4 in. shorter than the right with the left foot also smaller in size than the unaffected right side. On the affected left side, she was also ACL and PCL deficient. Physical exam revealed a normal straight leg raise with full range of motion, a grossly positive Lachman at 30° of knee flexion and a positive tibial sag at 90° of knee flexion. Varus–valgus stress tests in full extension and in 30° of flexion were normal.
Previous consultations with a pediatric orthopedic surgeon addressed procedures to potentially equalize the length of the legs through limb lengthening. Specifically, a tibial osteotomy of the left leg with the application of ring external fixator was recommended. It was also recommended that prior to the lengthening surgery, the knee ligaments should be stabilized. The patient was primarily symptomatic with instability from the anterior; this was visibly evident with anterior tibial subluxation episodes during walking. She was thought to be a candidate for ACL reconstruction using the Micheli procedure, a physeal-sparing technique utilizing the patient’s iliotibial band (ITB) autograft. However, due to the degree of anterior laxity and the expected small width and thickness of the ITB, graft augmentation procedures were considered.
In the operating room, the exam under general anesthesia again revealed a grossly positive Lachman with an excess of 2 cm of anterior tibial translation and a positive pivot shift. Her medial collateral ligament and laterlal collateral ligament were intact and stable and the PCL absent. A photo of the legs demonstrates the marked difference in limb length ().
After incision and exposure of the lateral thigh, a portion of the ITB was harvested producing a graft, 120 mm in length and 10 mm wide (). As the graft was considerably small in cross-section, and the anterior tibial laxity was quite significant, the decision to use a semitendinosus allograft to augment the reconstruction was made (). The allograft was baseball stitched to the ITB under tension.
Arthroscopic examination of the knee was consistent with the clinical examination finding of complete absence of both the cruciate ligaments (). In addition, she had a relatively small notch. The geometry of the notch was not altered at the time of surgery because of the relatively horizontal position of the ACL graft, nor was the posterior cruciate ligament deficiency addressed. The femoral portion of the graft was sutured to the intermuscular septum, while the tibial side was sutured to the periosteum of the proximal anterior tibia at 0° of extension after being passed intra-articularly. This patient was very young and therefore had a small transverse meniscal ligament. After intra-articular routing of the graft, it was decided to not place the graft under the intermeniscal ligament as is normally done in the Micheli procedure as a precaution to avoid damage to intermeniscal ligament. After the graft was secured to the tibia with sutures in the periosteum (), the Lachman exam was repeated and the anterior laxity of the tibia on the femur had been minimized. Anterior tibial translation was reduced to an appropriate 3 mm at 30° of flexion. The patient tolerated the procedure well and left the operating with the leg in full extension in a posterior splint. The patient returned to the clinic 13 months postoperatively. She subjectively reported that she has been very active playing on the playground with friends and feels that the knee is quite stable and strong. Her physical exam revealed full range of motion from 0° to 140° with no terminal flexion pain, a stable Lachman’s exam, good quadriceps contraction from a straight leg raise, and no tenderness to palpation along the ITB. Radiographic imaging of the knee and tibia revealed no growth alterations or damage to the physes on the proximal tibia or distal femur.


A 21-year-old male presented asymptomatically without any clinical sign and a nonspecific medical history. X-ray chest posteroanterior view showed asymmetrical cardiomegaly []. Transthoracic echocardiographic examination revealed that an intramyocardial hydatid cyst involved the anterior, posterior, and free lateral walls of the LV []. The left ventricular end-systolic and end-diastolic diameters were reduced. The rest of the echocardiographic variables were unremarkable. A smooth-surfaced cystic mass of 90 mm × 60 mm at the left ventricular lateral wall was also seen on cardiac computed tomography (CT) angiography [Figures and ]. The mass was localized inside the myocardial fibers. shows proximity of cyst with the left anterior descending (LAD) artery. There was no contrast intake inside the mass; the left ventricular volume was decreased due to bulging of the mass. No other cyst was detected in the body of the patient. His preoperative hematology and biochemistry investigations were within normal range. The patient was scheduled for off-pump removal of cardiac hydatid cysts. Intraoperatively, electrocardiography, pulse oximetry, EtCO2, invasive blood pressure (IBP) monitoring, central venous pressure (CVP) monitoring, and urine output and temperature monitoring were done. After securing an intravenous (iv) access with 16 G cannula in the right limb, left radial artery cannulated for IBP monitoring and right internal jugular vein cannulated for CVP monitoring. The patient was induced with iv injection midazolam 1 mg, iv injection fentanyl 100 microgram, and iv injection etomidate 8 mg and intubated with iv injection rocuronium 50 mg. Anesthesia was maintained with iv injection propofol infusion and intermittent iv injection vecuronium boluses. Heart was approached with left anterolateral thoracotomy. Stand-by cardiopulmonary bypass was considered for any intraoperative hemodynamic deterioration. After pericardium reflection, the mass with its pale yellow daughter cysts was visible []. The affected area was encircled with polyvinylpyrrolidone-iodine-embedded gauzes. After checking with a diagnostic aspiration to identify if there is any communication between cyst cavities and cardiac chambers, polyvinylpyrrolidone-iodine solution was injected into cysts to inactivate the scolices. The fluid content of the cysts was then aspirated, and the cavity was carefully opened. Multiple daughter cysts were removed []. Daughter cysts were best mobilized with a tablespoon. The area was then irrigated. Epicardium covering the cyst cavity was excised and the cavity was left open. He was discharged successfully 7 days after the surgery. During follow-up visits, he had no fresh complaints and echocardiography parameters were in normal range.


A 73-year-old Japanese man was transferred to our hospital with dyspnoea. He had no medical or family history of note. Blood pressure was 140/75 mmHg, heart rate 137 beats/min, and respiratory rate 24/min with oxygen saturation of 92% on room air. Electrocardiogram showed atrial fibrillation, ST depression, and inverted T waves in leads V3–V6. QRS width was 112 ms. Echocardiography showed mild left ventricular (LV) concentric hypertrophy (interventricular septum/posterior wall thickness of 11/11 mm, LV end-diastolic/end-systolic dimension of 46/25 mm, and LV mass of 180.6 g), LV ejection fraction of 60%, dilated left atrium (LA) with LA diameter of 50 mm and LA volume of 77 mL/m2, diastolic function at the upper limit of normal range (E/e′ 14.6), and preserved right ventricular (RV) systolic function (tricuspid annular plane systolic excursion of 20 mm and RV fractional area change of 44%). On laboratory examination, troponin T was 0.025 ng/mL, and B-type natriuretic peptide was 252.4 pg/mL. Spirometry showed an obstructive pattern [vital capacity of 3.28 L (103.7%) and forced expiratory volume in 1 second of 1.88 L (59.7%)] with normal diffusing capacity of the lung for carbon monoxide of 13.24 mL/min/mmHg (88.3%). Coronary angiography showed no significant coronary artery stenosis.
Right ventricular endomyocardial biopsy revealed diffuse interstitial amyloid deposits in the myocardium, with positive immunohistochemical staining for TTR (Figure
A–C). Genetic analysis revealed Val30Met mutation (GTG → ATG), indicating a diagnosis of hereditary TTR amyloidosis. The patient showed vitreous opacities and chronic glaucoma, suggesting ocular amyloidosis, without peripheral/autonomic neuropathy or carpal tunnel syndrome. The patient was started on tafamidis 20 mg per day for prophylaxis against progression of neuropathy.
To evaluate the efficacy of tafamidis treatment on cardiac lesions, the patient underwent 3 tesla CMR evaluations before and after 12 months of tafamidis treatment. CMR imaging before tafamidis treatment showed diffuse LV hypertrophy (Figure
D–F) and diffuse myocardial late gadolinium enhancement (Figure
G–I), which showed no obvious progression at follow-up (LV mass by CMR: 115.0 g before and 111.3 g at 12 months). As shown in Figure
, prolonged native T1 time (1387 ms) and increased ECV (42.0%) were observed before tafamidis treatment, and no obvious worsening was found at 12 months follow-up (native T1 time of 1356 ms and ECV of 40.4%). Troponin T and B-type natriuretic peptide levels were unchanged at 0.016 ng/mL and 271.5 pg/mL, respectively, after 12 months of tafamidis. Echocardiography showed no significant progression in LV morphological features (interventricular septum/posterior wall thickness of 12/12 mm, LV end-diastolic/end-systolic dimension of 43/25 mm, and LV mass of 184.1 g), with LV ejection fraction of 60%, as well as no obvious changes in LA size, diastolic function, or RV systolic function (LA diameter of 47 mm, LA volume of 73 mL/m2, E/e′ of 14.4, tricuspid annular plane systolic excursion of 18 mm, and RV fractional area change of 46%). Spirometry after tafamidis also showed no obvious change [vital capacity of 3.20 L (102.2%), forced expiratory volume in 1 s of 1.84 L (59.6%), and diffusing capacity of the lung for carbon monoxide of 12.46 mL/min/mmHg (89.2%)]. Comparison of electrocardiograms before and after tafamidis is shown in Figure
, which also showed no obvious change in QRS width or inverted T waves.


A 51-year-old male flight attendant complained of chronic lateral ankle pain without prior trauma or twisting injury.
Three-month history of left lateral ankle pain. He sought treatment at other Orthopaedic centres but failed conservative management on two separate occasion. He subsequently presented to our care after he exacerbated his lateral ankle pain and heard a “click” whilst alighting from a bus. He denied any traumatic or inversion injury.
Known history of gout and previous left total hip replacement secondary to left hip avascular necrosis.
None.
On clinical examination, he presented with an antalgic gait, swelling and tenderness over the posterolateral hindfoot. He demonstrated weakness in eversion
Not performed.
Radiograph of the left foot showed a proximally displaced os peroneum compared to contralateral foot (Figures and ). Peroneal tendon pathology was suspected and magnetic resonance imaging (MRI) of the left foot revealed a full-thickness rupture of the PLT distal to the os peroneum with underlying tenosynovitis (Figure ).


A 66-year-old man was diagnosed in March 2016 with occluding colonic cancer, immediately proximal to and partially involving the splenic flexure. Due to the presence of liver metastasis and peritoneal carcinomatosis with ascites, a 22 mm/6 cm through-the-scope (TTS) SEMS (WallflexTM, Boston Scientific) was placed through the stenosis, and chemotherapy with fluorouracil/folinic acid/irinotecan was immediately started. Six months later, an occluding intra-stent tumor ingrowth (with responsive systemic disease) was treated by the placement of a colonic stent-in-stent (22 mm/9 cm TTS SEMS; WallflexTM, Boston Scientific), and chemotherapy resumed 2 d after.
After more than 1 year of substantial disease stability (although bevacizumab was added to the chemotherapy regimen 18 mo after diagnosis), the patient experienced symptoms of intestinal occlusion in January 2018 (+16 mo from the second stent). Physical examination revealed abdominal distension, hyper-tympanism on percussion, and tinkling bowel sounds. An abdominal X-ray showed ileocolic dilation proximal to the correctly located previous stents (Figure ), and colonoscopy showed new intrastent tumor ingrowths (Figure ).


A 59-year-old male with a history of concomitant laryngeal squamous cell carcinoma and lung adenocarcinoma referred to our laboratory for a whole-body bone scintigraphy for the evaluation of bone metastasis. During history taking and physical examination, we realized that shoulders were asymmetric in size, left side seemed to be smaller than opposite side. The left upper limb was weak and to some extent abnormally positioned. The patient stated that these skeletal abnormalities were congenital and did not use much his left upper limb. The patient has also been limping since his previous motor accident. A planar whole-body bone scintigraphy and spot view [Figures and ] were performed at 2 h after intravenous injection of 740 MBq of 99mTc-methylene diphosphonate. As shown in , significant asymmetric size of scapulae but the normal-appearing shape and slightly higher position of the left scapula are detected. Other findings were mild cervicothoracic scoliosis as well as slightly asymmetric upper limbs. Focal uptake at midshaft of the right tibia was compatible with a recent trauma.


A 46-year-old woman with a passive smoking history who presented with dyspnea and unintentional weight loss underwent chest computed tomography (CT) scanning that revealed a right middle lobe mass (51 x 61 mm) and multiple thorax and bone metastases. Her clinical stage was T4N2M1b (stage IV). Morphologically, immunohistochemistry showed a poorly differentiated adenocarcinoma that was diffusely positive for thyroid transcription factor 1 (TTF-1) and focally positive for Napsin A (Fig a–c). The tumor harbored a classic EGFR exon 19-deletion mutation, as shown by qualitative detection (amplification refractory mutation system PCR) (Fig a–d). The woman was subsequently treated with gefitinib and experienced significant regression of the mass.
Six months after her first exposure to gefitinib, the primary mass and metastatic nodules exhibited obvious enlargement, accompanied by gradually increasing bone pain. The patient subsequently underwent CT-guided percutaneous lung biopsy, which revealed SCLC transformation (Fig a). Given that sufficient biopsy tissue was not obtained for immunohistochemistry staining and next generation sequencing (NGS), a blood sample was collected for driver gene testing and revealed that she harbored a new EGFR-T790M mutation (Fig b). She was then administered osimertinib therapy and experienced excellent improvement.
However, approximately five months after initial exposure to osimertinib, CT and whole-body bone scanning revealed further deterioration. Another CT-guided percutaneous lung biopsy specimen presented SCLC morphology with neuroendocrine markers, including diffuse positivity for Syn and focal positivity for CgA and CD56 (Fig ). Additionally, peripheral blood was collected, and we defined circulating tumor cells (CK+/CD45-/4′,6-diamidino-2-phenylindole [DAPI]+) and white blood cells (CK-/CD45+/DAPI+) (Fig a). RB1 and TP53 inactivation mutations were definitively identified in this SCLC transformation (Fig b). Additionally, tissue NGS also revealed that the EGFR exon 19 deletion (81.18%) and EGFR T790M mutation (3.10%) were retained, and some new mutation positions were detected, including CTNNB1, FGFR2, HRAS, PIK3CA, and RET mutations. The patient was administered a standard chemotherapy strategy with an intermittent etoposide-cisplatin regimen (EP) and continued to take osimertinib after each cycle of chemotherapy. After six cycles of chemotherapy, chest CT revealed obvious clinical responses, including shrinkage of the primary lung mass and metastatic nodules. The patient continued to take osimertinib, and achieved progression-free survival (PFS) of four months. In March 2018, the tumor progressed with a chest mass and multiple brain metastases. After written informed consent was obtained, a fourth biopsy of the progressing mass was performed, revealing Syn-positive, CgA-positive, and CD56-positive SCLC with no evidence of adenocarcinoma histology (Fig a–d). Molecular analysis revealed that the T790M mutation was retained, and a new EGFR C797S mutation was identified (Fig e). Detailed driver gene information and biopsy, treatment, and image scanning history are presented in Figures and .


A 41-year-old woman was referred for the investigation of a progressively growing, large-sized lesion involving the gingiva and the palate, since the last 8 months. The patient gave a history of an oral surgery at the site of the current lesion, 8 years back; however, the patient was unaware of the histopathological diagnosis. Therefore, we could not assert if it was a recurrent or de novo lesion. There was no relevant medical history or any extraoral signs. The intraoral examination revealed a well-defined, lobulated nodule covered by normal mucosa, measuring 3.0 cm, extending from the palatal gingiva of the right first and second molars to the hard palate (). The lesion was firm on palpation, painless and presented slight mobility. Additionally, there was a sign of mild trauma in the premolar region, caused by a removable partial prosthesis (). The panoramic x-ray examination was normal.
An incisional biopsy was performed. The specimen collected was rubbery, soft to moderately firm, and white-gray colored. The histopathological examination showed a well-delimited but non-encapsulated lesion, characterized by a myxomatous connective tissue presenting spindle-shaped fibroblasts interspersed with short bundles of collagen (). An Alcian Blue staining (pH = 2.5) showed strong staining of the myxoid areas, suggestive of hyaluronic acid and was negative in the dense connective tissue areas (, and ). Immunohistochemical reaction for S100 protein was negative, ruling out neural tumors.
As per the clinical, histopathological, and immunohistochemical features, the case was diagnosed as OFM, following which, the lesion was excised (). The patient showed no signs of recurrence in the follow-up after 8 months ().


An 80-year-old Caucasian man presented to an outside hospital with one month of non-productive cough, fatigue, low-grade fever, 2.5 kg weight loss, and a syncopal episode. His past medical history was significant for hypertension, hyperlipidemia, nephrolithiasis, benign prostatic hyperplasia, and Lyme disease. He had a 22 pack-year smoking history, quitting 45 years before the admission. He was diagnosed with Lyme disease one year prior and was treated successfully. Of note, he had a tick bite three months before the current admission for which he was prescribed amoxicillin. His symptoms improved slightly but recurred, and he was started on doxycycline. The patient reportedly did not finish the course of antibiotics.
On admission, the patient had a low-grade fever of 38,2C and a platelet count of 66,000/mm3 (reference range [RR]; 141-320 × 103/mm3). His hospital course was complicated by progressive anemia and thrombocytopenia. Computed tomography (CT) scans of the head, chest, abdomen, and pelvis showed no evidence of central nervous system (CNS) lesions, lymphadenopathy, hepatosplenomegaly, or other altered finding. Small bilateral pleural effusions were noted. Bone marrow biopsy was unrevealing, and flow cytometry showed no immunophenotypic evidence of a clonal cell population.
The patient developed hypotension and tachycardia and was transferred to the medical intensive care unit at our institution after 16 days at the outside hospital. A panel of labs was performed on admission, revealing elevated glucose, lactic acid, D-dimer, BUN, AST, and unconjugated bilirubin; low sodium, CO2, ionized calcium, albumin, prealbumin, total protein, total T3, free T4, and amylase. He was mildly anemic with hemoglobin of 12.2g/dl (RR; 13.8 – 17.3g/dL). White blood cell count was 6,870/mm3 (RR; 4.0-10.4 × 103/mm3), with 76% neutrophils, 16% lymphocytes, 8% monocytes, and 1% nucleated red blood cells. Peripheral smear showed mild anisocytosis, ovalocytosis, and macrocytosis. Platelet count was 13,000/mm3. The physical exam revealed the patient had a blanching, tan-pink maculopapular rash on the right lower extremity.
He was transfused with two units of platelets, which temporarily elevated his count to 39,000/mm3; however, he required platelet transfusions throughout his stay. Multiple services were consulted for expertise in this difficult case. Lyme titers were negative, as were HAV, HBV, HIV, syphilis, and rheumatologic serologies. Cardiac function was normal for age. Central hypothyroidism was considered due to low TSH and free T4; however, imaging showed a normal pituitary and no evidence of hemorrhage.
With multiple specialties involved in the patient’s care, the differential diagnosis was still broad, and an infectious process such as ehrlichiosis was thought to be most likely. Serologies for ehrlichia were sent, as well as CSF studies for HSV, Cryptococcus, and Lyme titers. The patient was placed on a regimen of antibiotics (vancomycin, doxycycline, piperacillin-tazobactan) to cover ehrlichiosis or other tick-borne illness, pneumonia, and abdominal processes.
On hospital day 3, the patient required 14 liters of fluid over 18 hours due to worsening lactic acidosis and hypotension. CT scan of the abdomen revealed anasarca and possible peritonitis. Due to the patient's condition and poor prognosis, care was withdrawn, and the patient passed away on the morning of hospital day 4.


A 49-year-old African American male presents with a large mass on the left shoulder that has been rapidly enlarging for the past 2 months. The mass grew over a presumed keloid scar, which developed approximately 1 month following a motor vehicle accident 12 years prior. During the accident, he suffered a contusion to the left shoulder that first bruised and subsequently formed a golf ball-sized mass. There was no breakage of skin on the left shoulder. He sought medical attention for the skin lesion at that time and was diagnosed with keloid, which was readily accepted as he had past medical history and similar family history. No treatment for the lesion was performed at that time. Since then, the lesion had been stable without any change in shape, color, or size until 1.5 years prior to evaluation, when he suffered a minor trauma to the lesion during a work-related injury that did not break the skin barrier. Following this event, he noticed that the lesion slowly increased in size under the skin without apparent cutaneous changes in appearance. Two months before the clinical encounter, he noticed a new rapidly growing nodule on the surface of the initial mass. He noticed no changes in symptomatology other than left shoulder pain and limited range of motion of the neck that became more prominent as the mass increased in size.
On examination, there were three discrete protuberant tumor nodules, gray-white, involving the skin and subcutis. The largest nodule measured 16 × 15 × 7 cm and the smallest nodule measured 7 × 6 × 3 cm ().
The tumor was ulcerated and necrotic without apparent attachment to underlying structures. Anterior cervical, posterior cervical, supraclavicular, and axillary lymph nodes were not palpable bilaterally, and there were no other masses observed. CT of thorax suggested the masses were superficial with no attachment to underlying bone or great vessels, and there was no evidence of metastatic disease or adenopathy. A wide excisional biopsy of the lesion was performed. The histological examination revealed a fascicular architectural pattern composed of plump spindle cells with high nuclear grade atypia and numerous mitoses leading to the diagnosis of high-grade fibrosarcoma arising from DFSP (). The spindle cells diffusely express CD34 ().
There were areas showing a transition from scar to DFSP (), and focal areas were consistent with keloid.
There was also invasion of the lesion into the underlying skeletal muscle as well as focal areas at the deep surgical margin. The post-op course was uneventful. Due to the location and extent of the invasion, further excision was not feasible. A multidisciplinary approach including radiation oncology will be pursued for further treatment. The current plan involves the placement of a skin graft over the incision site followed by radiation treatment to target the remaining lesion. The patient will continue to be observed for recurrence of the tumor to allow for early resection.


The first patient is a 54-year-old Hispanic female with poorly controlled diabetes mellitus with a hemoglobin A1C of >10 since diagnosis in 2011. She was treated with oral agents and insulin shortly after diagnosis, given her poor glycemic control. She initially did not have overt DN, but gradually started developing albuminuria and renal function decline. Her serum creatinine first started rising to 123.79 μmol/L (1.4–1.6 mg/dL) over 2014–15 and her proteinuria rose from 1000 μg albumin/mg creatinine (1000 μg albumin/mg creatinine = 1 g albumin/g creatinine) to 2000–3000 μg albumin/mg creatinine. Her hyperglycemia remained persistent in spite of her medication regimen. She began to take nonsteroidal anti-inflammatory drugs (NSAIDs) a few times a month, but as her renal function declined, she was instructed to stop NSAID use in 2016–17. Urine protein:creatinine ratios were not obtained in the Kaiser Permanente (KP) system, so trends of albumin:creatinine ratio (ACR) were followed at the University of California Los Angeles Health System.
She was examined in KP’s ophthalmology clinic and was noted to have worsening glaucoma and proliferative DN. She started treatment with bevacizumab every 4 weeks as needed in January 2016. She required a monthly dose of 1.25 mg of bevacizumab over the next 13 months in either one or both eyes over a total of 10 separate visits, with the indication of proliferative diabetic retinopathy (DR). Thus the full dose administered was 12.5 mg of bevacizumab over 10 injections during this period. A notable increase in the slope of proteinuria was noted, with an increase in ACR to 4000 μg/mg and ultimately to 7000 μg/mg (see for trends of renal function decline and worsening proteinuria in this patient). The patient’s blood pressure did not rise beyond her usual range of 140–150 mmHg and, as such, it was not plotted.
It was noted that her renal function seemed to worsen more rapidly in the year after bevacizumab was started. A full serological workup was performed, but was unrevealing. Due to the more rapid than expected decline in renal function, a renal biopsy was performed. The biopsy showed nodular diabetic glomerulosclerosis and hypertensive nephrosclerosis without any histological features suggestive of other glomerular disease. The timing of proteinuria exacerbation corresponded with the first few months after starting intravitreal bevacizumab injections. The mechanism of renal function decline may be due to worsening proteinuria and acute tubular necrosis. Given the severity of the patient’s DR, a change to a less potent agent, like ranibizumab, was not immediately feasible. The patient was managed with renin–angiotensin–aldosterone system (RAAS) blockade with plans to add a non-dihydropyridine calcium channel blocker (i.e. verapamil or diltiazem) for proteinuria control, with continuing attempts to optimize hypertensive control.


The second patient is a 53-year-old Asian male with a history of type 2 diabetes mellitus that was diagnosed in 2010. His medical history also includes hyperlipidemia, severe uncontrolled hypertension and advanced renal disease with Stage 4 CKD just before the need for intravitreal anti-VEGF therapy was noted. He had poor compliance with his prescribed diabetic diet. His hemoglobin A1C ranged between 10% and 11% at the time of initial diagnosis and remained consistency high for years afterwards. He was on oral agents for his diabetes mellitus since he declined insulin therapy despite elevated blood sugar levels and had a history of NSAID use earlier in his history that likely contributed to his CKD progression. As his renal function declined, he reduced his NSAID usage significantly and would only use NSAIDs during infrequent gout flares. His metformin was stopped in March 2017 and changed to a sulfonylurea due to his declining renal function.
He had an estimated glomerular filtration rate (eGFR) of 17 mL/min at the initiation of bevacizumab injections on 1 July 2017. He had a nearly linear decline in eGFR (mL/min) as measured by the Cockroft–Gault equation. His proteinuria had been stable at 2800–3000 μg albuminuria/mg creatinine (= 2.8 g albumin/g creatinine), but after starting bevacizumab injections for proliferative DR his ACR increased to 4500 μg albumin/mg creatinine.
Within the first 2 months of initiating therapy he received four injections of 1.25 mg of bevacizumab at an interval of every 2 weeks alternating between each eye. His injections were planned so that he waited at least 1 month between injections in the same eye. The total dose delivered over these four injections was 5 mg, and within that short interval, his renal function deteriorated to the extent of needing renal replacement therapy (hemodialysis).
His renal function had already been declining prior to anti-VEGF therapy, but after starting therapy his creatinine rose from a baseline of 338 μmol/L (3.83 mg/dL) to 688.8 μmol/L (7.79 mg/dL). His blood pressure at baseline was 180–200 mmHg systolic (SBP) and 100–120 mmHg diastolic (DBP). There was no discernible change in the SBP or DBP, though his blood pressure was already severely elevated. The increase in urine protein from baseline to higher levels after the anti-VEGF injections and renal function trends are depicted in .


The third patient presented is a nondiabetic, 65-year-old female who was diagnosed with AMD. She had normal renal function at 56.59 μmol/L (0.64 mg/dL) with no measurable proteinuria. She started bevacizumab in January 2015 and continued receiving anti-VEGF injections every 4–6 weeks. After one dose of bevacizumab (1.25 mg) she was switched to aflibercept because of the need for a stronger antiproliferative agent. Initially the patient only met the criteria for prehypertension, with an SBP within the 130–140 mmHg range and normal DBP. However, we noticed her blood pressure began to rise from her recorded baseline after initiating injections. She was monitored until July 2016, when her SBP was routinely 170–200 mmHg and antihypertensive therapy was initiated. Thus she received 1.25 mg of bevacizumab and 16 injections of 2 mg aflibercept in the period between January 2015 and July 2016, for a total dose of 32 mg of aflibercept.
Despite multidrug regimens, her SBP rarely dropped below 150 mmHg. Her secondary hypertension workup for renal artery stenosis and hyperaldosteronism was negative. She had a borderline elevated urine cortisol test, but it was too low to be diagnostic of hypercortisolemia, and the lack of weight loss, potassium wasting or finding of an abdominal mass did not suggest another endocrine cause for the observed hypertension. (Refer to for blood pressure trends and antihypertensive regimens needed to control increasingly resistant hypertension in this patient.) A recommendation was made to change the patient to ranibizumab if possible. Some difficulties arose from the ophthalmology perspective, however, given the severity of her macular degeneration (MD) and the lower potency of ranibizumab. The plan of care was to work to optimize this patient’s blood pressure management with the goal of minimizing anti-VEGF intravitreal injections as able and to switch to a lower potency agent, like ranibizumab, when clinically feasible.


The present case was a 39-year-old woman, gravida 0. She had a past medical history of hypertension. She fainted following acute abdominal pain at home and awakened by herself but did not consult a doctor. Two days later, she visited a physician with the chief complaint of fainting episodes and epigastric pain and genital bleeding. Because anemia had progressed to 8.7 g/dl hemoglobin compared with 13.7 g/dl 5 months previously, she was recommended to visit a gynecologist. The next day, she presented to our department. She denied pregnancy, but her serum human chorionic gonadotropin level was 55713 mIU/ml. Transvaginal sonography showed no gestational sac in the uterus and low echoic legion in the Douglas pouch suspected of intraabdominal hemorrhage. An approximately 2-cm mass was found on the left side of the fundus of the uterus, and the tumor might have had subserosal fibroids, but there was no other site of ectopic pregnancy. Accordingly, we considered pregnancy in the left interstitial fallopian tube or isthmus of the left fallopian tube. Emergency laparoscopic surgery was performed with the diagnosis of rupture of ectopic pregnancy. The right tube, but not the left side, was remarkably swollen and raised toward the head, but this was not able to be identified by transvaginal sonography []. A large amount of hemorrhage was found in the peritoneal cavity, and adhesion suspected of being Fitz–Hugh–Curtis syndrome was observed on the liver surface. During the operation, grasping forceps penetrated the area of pregnancy, which resulted in intensive bleeding. Bleeding was uncontrolled. Therefore, the assistant gripped the suspensory ligament of the right ovary to reduce the amount of bleeding. We rapidly confirmed the right ovary while tracing the suspensory ligament and identified the mesosalpinx. Right salpingectomy was performed with bipolar forceps and an ultrasonic energy device, and the right tube was collected in a specimen pouch. The specimen was extracted from the abdominal cavity via a 12-mm port in the umbilicus. Contrary to expectations, we found placental tissue and a fetus measuring approximately 2.5 cm in biparietal diameter, and this was nearly equivalent to 13 weeks’ gestation [].


A 23-year-old female presented with several months of worsening right upper and lower quadrant abdominal pain with radiation to the right anterior thigh accompanied by paresthesia and numbness. She also reported right-sided neck pain with numbness radiating into the right arm involving the ring and middle finger. Four months before this visit, she was treated with a cholecystectomy to address her abdominal pain: the gallbladder proved to be normal. Next, a computed tomography (CT) of the abdomen and pelvis demonstrated multiple lesions within the psoas muscle and mesentery of the lower abdomen [Figures and ]. She was referred to the neurosurgery clinic and on examination demonstrated hyperpigmentation in the axilla with mild freckling. Additionally, she had diminished sensation in the right C8 distribution. She underwent neural axis magnetic resonance imaging (MRI) using the neurography protocol (MRN). It revealed multiple neurofibromas involving the right brachial and lumbar plexuses [Figures –]. Within the lumbar plexus, neurography demonstrated multiple neurofibromas involving the nerve roots throughout the plexus and involved both the femoral and sciatic nerves bilaterally. Given the extent of involvement, the patient was medically managed.


An 83-year-old lady with a past medical history of ischaemic heart disease, asthma, hypertension and ex-tobacco smoking, presented to emergency department with a sudden-onset severe epigastric pain. The pain was described by the patient as burning in nature and radiated through to the back, and was associated with nausea and vomiting. On examination, the patient’s vital signs were normal. There was severe epigastric tenderness on palpation, as well as moderate right upper quadrant tenderness.
Serological investigations showed elevated white blood cell count of 12.6 × 109/L and C-reactive protein of 170. Moreover, the serum lipase was 13 000, confirming the diagnosis of acute pancreatitis. Liver function tests were mildly deranged but with a normal bilirubin of 12 μmol/L, ALT of 92 U/L, AST of 146 U/L, ALP of 89 and GGT of 117 U/L.
An abdominal ultrasound (Fig. ) demonstrated a distended gallbladder with multiple subcentimeter gallstones. There was diffuse gallbladder wall thickening up to 7 mm and associated probe tenderness, consistent with cholecystitis. The common bile duct diameter measured up to 7.4 mm without any evidence of choledocholithiasis, thus did not require ERCP. However, the pancreas was not well visualized. A follow-up CT abdomen (Fig. ) was performed, which demonstrated evidence of pancreatitis with moderate peripancreatic fat stranding without any features of complications including necrosis, abscess or pseudocyst.
The diagnosis of concomitant acute cholecystitis and gallstone pancreatitis was made based on the radiological and biochemical findings.
The patient underwent an uncomplicated laparoscopic cholecystectomy following successful conservative management of both cholecystitis and pancreatitis. The histopathology confirmed cholelithiasis with acute on chronic cholecystitis.