A 45-year-old man presented to us with growth and foreign body sensation in his right eye. On examination, his best-corrected visual acuity was 20/20 in both eyes. Slit-lamp examination of the right eye showed nasal pterygium on the cornea approximately 3 mm from the limbus, with scarring at its margins. In both eyes, tear film height was adequate, and the ocular surface was moist. The rest of the examination was unremarkable. His ocular and medical history were unremarkable.
The patient underwent right eye pterygium excision with CLAG with fibrin glue (TISSEEL Lyo, Two-Component Fibrin Sealant Vapor heated, Baxter AG, Austria) under peribulbar anesthesia. Postoperatively, he was started on prednisolone acetate eye drops 1% four times daily, carboxymethyl cellulose 0.5% eye drops four times daily, and ciprofloxacin 0.3% eye drops four times daily, and was advised to apply a patch in between topical treatments. There were no concerns or complications noted for the first 15 postoperative days. On postoperative day 16, the patient presented with nasal corneal dellen (Figure ).
The steroid drops were stopped, lubricants were increased to an hourly rate, and he was advised to apply a patch in between topicals. Two days later, corneal thinning increased, and he underwent cyanoacrylate glue with bandage contact lens under topical anesthesia. Four weeks after the cyanoacrylate glue procedure, the glue and bandage contact lens were removed, and the dellen was found to have healed. Topical steroids were restarted four times a day, along with antibiotic eye drops four times a day, and lubricants two hourly. One week later, however, the dellen reappeared (Figure ).
Topical steroids were stopped; lubricants and antibiotics were continued. A systemic workup showed no underlying connective tissue disorder. Slit-lamp examination revealed poor tear flow to the area of dellen. This was attributed to mild graft edema nasally, which prevents tears from reaching the nasal cornea over the dellen. Option of temporary punctal plugs was discussed with the patient, but the patient refused the same for monetary reasons. Thermal punctal cautery was then applied under topical anesthesia to both the upper and lower puncta to achieve punctal occlusion. After five days, the dellen resolved with complete healing. Two years after the surgery, eye examination showed nasal corneal scarring with no recurrence without much epiphora (Figure ).


A 60-year-old Caucasian female with no significant medical history received 2 HA injections (a Restylane Silk injection and a Restylane Lyft injection, Galderma Laboratories, LP) in the horizontal nasal crease, maxilla, and nasolabial folds. She had received HA injections in the same facial areas without complication 9 months earlier. Two days after the injections, she was treated for ecchymosis with a 532 nm laser. The next day, she experienced pain in the left nasolabial fold and left eye and reported blurred vision in the left eye. She presented to the emergency department; an optometrist diagnosed her with keratitis and started her on erythromycin ointment twice daily in the affected eye.
The following day, the patient returned to the dermatologist's office and reported increasing pain in the left cheek and worsening redness, irritation, and continued vision loss in the left eye. She described severe pressure and pain on the left nasal crease extending up the left side of the nose and to the globe of the eye. She had a 1 cm reticulate patch and a firm nonvisible 3.5 × 1.5 cm area of swelling on palpation in the glabellar region (). She was treated with 450 units of hyaluronidase (Hylenex, Halozyme Therapeutics, Inc.) to the nasolabial fold, the left side of the nose, and the glabella. She was also given aspirin 81 mg and ibuprofen 800 mg. She reported an 80% improvement in the pressure and pain within 15 minutes after administration of the hyaluronidase. She was instructed to apply 2% nitroglycerine ointment to the affected areas and was referred to an ophthalmologist for the evaluation of her decline in vision.
The patient had an ocular history of dry eye, for which she had been using cyclosporine until the day of the injections. She had no history of contact lens use, herpetic eye disease, or recent rashes. Ocular medication was erythromycin ointment that she had started one day prior. Snellen visual acuity with correction was 20/25 in the right eye and 20/125 in the left eye and 20/40 with pinhole. Right eye examination and pressures were within normal limits. Examination of the left eye revealed no afferent pupillary defect, full extraocular movements and confrontational fields, 1+ left upper lid edema, 2+ conjunctival injection, intraocular pressure of 20 mmHg, and stromal opacity (keratitis) nasally with punctate fluorescein staining. The anterior chamber showed no cells and trace flare, but regularly shaped globules suspended in the aqueous were present. Retinal examination was within normal limits, and fluorescein angiography showed full vascular filling with a hazy view because of media opacity ( and ). The patient was advised to start ofloxacin antibiotic drops 4 times daily, continue erythromycin, and start cyclopentolate for discomfort.
Twelve hours later, the patient reported a dramatic decrease in her vision. Visual acuity with correction in the left eye was 20/200 with no improvement on pinhole testing. She had generalized 2+ corneal edema, sparing a small area of the temporal cornea. The anterior chamber clear globules were no longer visible, and the keratitis appeared unchanged with persistent punctate staining of the epithelium. The view of the fundus was hazier, but the retina and the retinal vasculature appeared normal, and intraocular pressure was in the normal range. The patient was treated with 75 units of hyaluronidase to the inferior periocular region and 75 units to the glabella and left nasal sidewall (150 units total). Because of her acute vision deterioration, she was referred for emergent HBOT for possible anterior segment ischemia and keratitis ().
The patient underwent nine 90-minute HBOTs and stated that her vision began to improve within 20 minutes of the first session. Her visual acuity measured by near card in the hyperbaric facility improved from 20/200 at the start of treatment to 20/60 at the 20th minute. On day 2 of her HBOT, the patient's visual acuity was 20/60, and intraocular pressure was 12 mmHg. Corneal edema and keratitis were significantly decreased; the area of stippled staining was smaller, approximately 2 × 1.5 mm; the anterior chamber was clear; and the fundoscopic examination was normal.
On day 3, the patient stated that her vision fluctuated but was gradually improving overall. She perceived that her vision improved during and immediately after each HBOT but that the effects of each treatment had decreased by the time she had the next session. Visual acuity was 20/200 in the left eye and 20/60 with pinhole. The keratitis was nearly resolved, but a corneal infiltrate measured 1.5 × 1.5 mm ( and ). The patient was started on fortified vancomycin 25 mg/mL and tobramycin 15 mg/mL drops 4 times daily, GenTeal ointment (Novartis Pharmaceuticals Corp.) every night, and valacyclovir (Valtrex) 500 mg 3 times daily to account for the possibility of an atypical herpetic component.
She continued to improve with each 90-minute HBOT. On day 10, her vision was 20/20, and the infiltrate had nearly resolved (). A small stromal scar, approximately 1 mm in diameter, corresponded to the site of the ulcer in the nasal cornea. One month later, the patient reported that her vision had returned to baseline. Her visual acuity with correction was 20/20. The cornea was clear, and her eye examination was normal ().


A 73-year-old woman (53 kg, 147 cm, and body mass index, 24) was presented to the operating suite for total thyroidectomy for bilateral papillary thyroid cancer. She was diagnosed with thyroid cancer on sonography during a routine medical checkup. A case of bilateral papillary carcinoma of thyroid was confirmed by computed tomography scan and fine-needle aspiration biopsy. Thereafter, she was transferred from the endocrinology department to the otorhinolaryngology department for operation. Examination by an otorhinolaryngologist was indicative of the presence of right vocal cord palsy and metastases. On enhanced thyroid scan, invasion of the right tracheoesophageal groove was observed. Her past medical history included diabetes and hypertension for more than 10 years, and she took an antihypertensive (losartan potassium, 50 mg), medications for diabetes (glimepiride, 2 mg; metformin, HCl 500 mg; alogliptin benzoate, 34 mg; thioctic acid, 600 mg), and cilostazol (200 mg). Her HbA1c value was 6.2% (reference range, 4.0%–6.0%), and her blood sugar levels ranged from 84 to 110 mg/dL preoperatively. She underwent an appendectomy 40 years ago without any anesthetic complications. Her preoperative electrocardiogram showed a first degree atrioventricular block, and echocardiography showed left ventricular hypertrophy and moderate diastolic dysfunction with normal ejection fraction (70%). Her airway was categorized as Mallampati Class 1. Endoscopic view of the larynx, as viewed by an otorhinolaryngologist, was normal.
After monitoring the electrocardiogram, blood pressure, pulse oximetry, and bispectral index (BIS), we preoxygenated the patient thoroughly. After administration of propofol (80 mg), rocuronium (50 mg), and confirmation of appropriate level of BIS for intubation, we tried to intubate the trachea with a 7.0-mm (internal diameter, 7 mm) neural integrity monitor standard reinforced EMG tube under videolaryngoscopic assistance. Because the tube was too thick for the patient's trachea, we successfully intubated her with an ID 6.0 mm EMG tube. Adequate depth of the tube was confirmed by videolaryngoscopy and auscultation. The cuff pressure of the tube was adjusted to 20 cmH2O using a manometer. We anesthetized the patient with total intravenous anesthesia using a target-controlled infusion pump (Orchestra with Base Primea, Fresenius Kabi, France) to infuse remifentanil and propofol with BIS and Train of four monitoring. After beginning the operation, we checked for spontaneous recovery from a neuromuscular blockade with a train of four watch, without disturbing the neuromonitoring. Total thyroidectomy, tracheal wedge resection, and end-to-end anastomosis were performed. Intraoperatively, the right-sided recurrent laryngeal nerve attached to the tumor was sacrificed. Furthermore, the right-sided tracheal wedge was resected and anastomosed because of the metastases into the trachea at the level of the 3rd to 5th tracheal rings. The mechanical ventilation was under control without any circuit leakage.
After completion of the surgery, anesthetic infusion was stopped and sugammadex (200 mg) was administered for reversal of the neuromuscular blockade. After confirmation of the patient's recovery, we tried to extubate her trachea after deflation of the tracheal cuff but felt strong resistance after withdrawal of the tube for 2 to 3 centimeters. Deflation was attempted again but the balloon did not shrink completely, and the resistance to extubation persisted. Therefore, a deeper anesthesia was induced with sevoflurane and the surgeon's opinion was sought for the possibility to anchor the tube by stitching it to the tracheal wall. The surgeon expressed the possibility of intraoperative damage to the cuff by sharp scissors during tracheal dissection; however, was strongly against the anchoring of the tube because the suture site was more proximally situated (closer to vocal cord) to the cuff of the tube. A consensus was achieved that the EMG tube was already withdrawn 2 to 3 cm, sufficient to pass through the sutured portion. Endoscopic examination through the tracheal tube or videolaryngoscopy revealed no abnormal findings. For the subsequent attempt at extubation, emergency surgical airway devices along with a videolaryngoscope and an ordinary ETT was kept ready. After the induction of a deeper anesthesia, we tried to extubate the EMG tube slowly under videolaryngoscopic view. With a moderate amount of force, the EMG tube was finally extubated, apparently in a fully inflated state. Thereafter, we intubated the trachea with an ID 6.0-mm ETT under videolaryngoscopic view; the laryngoscopic view was normal without the presence of any bleeding or laceration. Subsequent recovery and extubation were uncomplicated. The patient complained of slight soreness in the throat after recovery. She suffered from dyspnea for several days, caused by an arytenoid swelling seen on fiberoptic laryngoscopy, airway narrowing (1.4 × 0.7 cm), and mild dependent atelectasis in the bilateral lower lobes, which was documented on computed tomography. Finally, she was discharged on the 9th postoperative day after improvement of symptoms.
We examined the extubated EMG tube and found a tear in the cuff tear on its right shoulder, which corresponded with the surgical site (Fig. ). Deflation of the cuff caused it to shrink marginally; however, it expanded spontaneously to its original cylindrical shape. We concluded that the vocal cord obstructed the torn cuff during extubation, preventing the air inside the cuff from escaping (Fig. ).
This case report was approved by the Institutional Review Board of St. Mary's Hospital, The Catholic University of Korea (approval number SC19ZESE0080). The patient provided written informed consent for publication of this report.


The index case, a 44-year-old gentleman, who had been on a business trip to Italy for 12 days, returned to New Delhi on 25 February. He alighted a flight of more than a hundred passengers from various countries. At the international airport screening, he was found to be asymptomatic and was advised home quarantine. On 26 February, ignoring his quarantine instructions, the apparently fit man travelled by bus from Delhi to Agra, Uttar Pradesh – around 230 kms away. There were about 40 other passengers in the same bus. The index case reached his home and met his aged parents (73 and 64 years old), his wife (37 years) and son (16 years). The next day, he invited his close friend and his wife for dinner. During this whole time, he felt he was a healthy man.
On 1 March, he noticed a mild cough and fever. When a visit to the local practitioner did not relieve his symptoms, he approached a tertiary care centre a day later where he was rightfully suspected as a case of COVID-19 and referred to our hospital. The transportation back from Agra to New Delhi was in a dedicated ambulance after wearing full personal protective equipment (PPE). At our hospital, he was placed in an isolation room at the designated COVID-19 facility. His nasopharyngeal and oropharyngeal swabs were taken and sent for COVID-19 testing by polymerase chain reaction (PCR)-based test, the only approved test at the time. He was confirmed positive on 3 March.
The contact tracing was immediately initiated. Subsequently, his parents, wife and son also tested positive. Three days later, his close friend and his wife, with whom he had dined not a week back, both tested positive. All seven cases, three of them symptomatic, stayed in isolation ward of our hospital. The timeline is summarized in .
One hundred thirty-six contacts of this index case were traced and tested for COVID-19, all of them were negative, including the housemaid and her family, bus passengers, neighbours and the local doctor consulted and patients in the clinic at that time.
All seven patients admitted, two of them elderly, recovered completely. However, even on the 14th day since return, the index case continued to be PCR positive along with his son. They were kept admitted till two nasopharyngeal swabs were reported negative for COVID-19 as per national policy. The other family members had turned PCR negative and were discharged accordingly.


A 45-year-old Hispanic man presented to our institution with a progressively enlarging mandibular mass for two years. His medical history was significant for localized MGCT of the lower lip that was diagnosed five years ago in Mexico, for which he underwent surgical resection followed by radiation therapy (RT) and reconstructive surgery. He had a local recurrence one year after initial diagnosis but was lost to follow-up after an excisional biopsy. He presented for medical care two years later to discuss treatment options for the tumor, but it was deemed unresectable. He was treated with palliative chemotherapy (carboplatin, paclitaxel and cetuximab) for unknown number of cycles with no response and was advised hospice. Due to lack of further therapeutic options in Mexico, he presented to us to seek treatment for his advanced disease.
Physical examination revealed a large, tender exophytic fungating mass approximately 15 cm in size encompassing entire lower lip, extending inferiorly to the chin and inferior angle of mandible on right side and eroding deep into the floor of mouth (Figure ). Areas of erosions and ulcerations were scattered over the mass expressing serosanguinous discharge. It was associated with decreased tongue mobility, muffled voice and drooling of saliva. However, he was able to swallow soft food and pills. He was not in any respiratory distress. Laboratory workup was unremarkable except for hemoglobin of 10.6 gm/dL (normal 12.9-16.8 gm/dL).
Computed tomography (CT) scan (Figure ) and magnetic resonance imaging (MRI) of the neck and brain (Figure ) demonstrated a large infiltrative destructive soft tissue mass involving the right hemimandible, anterior part of left hemimandible, floor of mouth, right oral tongue, masticator space, right temporomandibular joint, skull base, foramen ovale, right Meckel’s cave and cisternal segment of the right trigeminal nerve abutting the pons and bilateral cervical adenopathy. No evidence of metastatic disease was seen on CT scan of chest, abdomen and pelvis. Biopsy of the tumor confirmed MGCT, and it was deemed unresectable. A gastric tube (G-tube) was placed for nutritional support.
The incurable nature of the disease was explained, and he was started on half the usual dose of pazopanib (400 mg) orally due to ongoing bleeding from the tumor, based on the limited available data. It was then increased to 75% of the dose (600 mg) after two weeks. There was a significant improvement in facial swelling, bleeding, discharge and size of the tumor within one month. However, the tumor started to slough off exposing midline part of lower jaw and the tongue resulting in increased pain and trouble swallowing pills (Figure ). His medications were switched to be taken by G-tube and based on pharmacokinetic data of pazopanib that showed an increase in area under curve by 46% of a crushed tablet, he was prescribed 400 mg (1/2 dose) crushed by G-tube daily.
A CT scan performed after six weeks of treatment initiation revealed a decrease in the size of primary lesion (from 135 x 104 x 127 mm to 105 x 58 x 104 mm) and cervical adenopathy along with improved intracranial extension (Figure ). Gradually, his tumor stopped sloughing and stabilized. Secretions and facial swelling continued to diminish and pain was well controlled with narcotics. Repeat CT scans done at three months after the initiation of pazopanib showed overall radiological improvement of local disease and a slight decrease in intracranial extension.
After four months of treatment, he developed diplopia and right lateral rectus palsy. MRI brain and neck revealed interval increase in intracranial disease, invasion of right cavernous sinus, pons and abducens nerve, while redemonstrating a decrease in extracranial tumor burden, especially in the infrazygomatic masticator space (Figure ). He was treated with dexamethasone, 9 Gy of RT and tarsorrhaphy. Pazopanib was increased to 600 mg daily. At nine months, his CT scan showed stable intracranial disease, while his extracranial disease became more necrotic. He did not report any adverse events from pazopanib. He passed away suddenly at home 10 months after the initiation of pazopanib. The family refused an autopsy.


A 31-year-old male with no past medical or family history of disease presented with intermittent abdominal pain lasting almost 2 months, and he was admitted to the local hospital on February 28, 2017. Positron emission tomography (PET) showed isolated high metabolic nodules during the pancreatic uncinate process that were likely to represent malignant disease (Fig.a, b).
The patient then underwent radical pancreaticoduodenectomy on March 9, 2017. Pathological examination after radical excision showed poorly differentiated ductal adenocarcinoma associated with UC-OGC at the head of the pancreas (Fig.a-d). Immunohistochemistry staining revealed that the cells were positive for CD68 and CK7, whereas the cells were negative for vimentin and S-100 (Fig. e, f). The tumor was measured to be 3 × 3 × 2 cm in size and exhibited invasion of the nerves, nearby pancreatic tissues, duodenum and the lower part of the common bile duct. The surgical margins were negative, and there was no discovery of lymph node metastasis. The surgical-pathological staging of the tumor was IIA (T3N0M0) according to the 7th edition of the American Joint Committee on Cancer (AJCC)/Union for International Cancer Control (UICC) TNM staging system.
Adjuvant chemotherapy with gemcitabine and albumin-bound paclitaxel was administered starting on April 10, 2017 for six cycles, and the toxicity was acceptable. However, the patient developed a backache 2 months after the termination of adjuvant chemotherapy. The contrasted computed tomography (CT) scan performed on November 27, 2017 showed multiple lymph node metastases in the mesenteric region (Fig. c) and peritoneum (Fig. d) with a serum CA199 level > 900 U/ml. Exploratory laparotomy was performed on November 29, 2017, and affirmed peritoneal metastasis was confirmed by peritoneal biopsy. The patient afterwards received systemic chemotherapy with the FOLFIRINOX regimen (combination of oxaliplatin, irinotecan, fluorouracil and leucovorin) for two cycles. Unfortunately, the serum tumor marker CA199 level was elevated to 1595 U/ml after two treatment cycles, and the patient’s condition deteriorated due to obvious myelosuppression and digestive tract toxicity caused by the chemotherapeutic drugs. Finally, he had to suspend chemotherapy and was admitted to our hospital on January 11, 2018.
WES analysis was performed, and the KRAS p. G12D (c. 35G > A) and somatic BRCA2 p. R2896C (c. 8686C > T) mutations were detected in both surgical formalin-fixed paraffin-embedded (FFPE) tumor tissues and plasma ctDNA samples. Additionally, WES indicated that the tumor did not show microsatellite instability (MSI) and did not present a high tumor mutational burden (TMB). Considering the poor condition of the patient and the fact that the polyadenosine diphosphate-ribose polymerase (PARP) inhibitor olaparib was not available, we administered apatinib combined with tegafur/gimeracil/oteracil potassium capsules (S-1) for his disease. However, the patient’s condition worsened rapidly with the occurrence of fever, jaundice and vomiting after 1 month of treatment with this regimen, and eventually he died on March 12, 2018. The disease-free survival (DFS), which was defined as the time from radical surgery to disease recurrence, was just 7.4 months. The overall survival (OS), which was defined as the time between the primary diagnosis of UC-OGC and death, was only 12.6 months.


A 67-year-old woman with remote history of endocarditis s/p tricuspid valve repair and mechanical aortic valve replacement was referred for second opinion and management of new severe symptomatic tricuspid valve stenosis resulting in progressive debilitating congestive heart failure (HF). The patient was approved by the heart team to undergo redo open heart for surgical repair of the tricuspid valve. Intraoperative technical challenges were met to repair the tricuspid valve. In turn, the native valve was resected and a 33 mm On-X mechanical valve prosthesis (On-X Life Technologies, Austin, TX, USA) was implanted.
The patient’s post-operative course was complicated by recurrent haemoptysis related to endotracheal tube trauma, prolonged mechanical respiratory support, acute kidney injury, and cardiogenic shock. While unable to anticoagulate, increasing requirements of inotropic and vasopressor support were noted. On the fifth post-operative day, 2D examination revealed single leaflet fixation of the tricuspid mechanical prosthesis resulting in severe stenosis, along with moderate size iatrogenic ventricular septal defect (VSD) not previously seen and later confirmed on transesophageal echocardiography (TEE) (Figure ). The mechanism for the leaflet dysfunction remained unclear. There appeared to be no evidence of leaflet thrombosis. The left ventricle and mechanical aortic valve function remained preserved. Using a heart team approach, it was felt that surgical re-exploration to address the dysfunctional mechanical tricuspid valve and VSD would be prohibitive. A transcatheter assessment with ad hoc intervention was considered. Upon obtaining consent from the patient’s next of kin, the patient was emergently taken to the cath lab for further evaluation and management.
The patient was transferred to the cardiac catheterization laboratory in severe haemodynamic collapse. Initial fluoroscopic examination of the heart confirmed the echocardiographic results of an immobile septal leaflet of the recently implanted mechanical tricuspid valve (Figure ). A 9 Fr St. Jude Viewmate intracardiac echo-catheter was used to further assess the TV function and assist with transseptal puncture. Transseptal access allowed for LV and RV intracardiac pressure assessment across the VSD. Similarly, simultaneous right atrium (RA) and RV pressure gradients obtained confirmed the presence of severe TS with a mean gradient of 11 mmHg (Figure ).
Initial attempts were made to force open the fixated tricuspid valve leaflet with a 6 Fr multiple purpose catheter from the right femoral vein (Figure ). Despite several attempts using different angles and techniques, it was unsuccessful. ‘Valvuloplasty’ was therefore pursued. A 0.035” Terumo angled-glidewire was carefully manoeuvered antegrade across a 6 Fr MPA catheter, between the aperture of two mechanical leaflets and into the pulmonary artery. The Multipurpose (MPA) catheter was then exchanged for an 8 × 40 mm Mustang OTW angioplasty balloon (Boston Scientific, Natick, MA, USA) was then advanced across the mechanical valve and inflated gradually at nominal pressure (8 ATM). A single inflation resulted in successful restoration of valve leaflet function (Figure ). Fluoroscopic examination with repeat haemodynamics confirmed successful procedural results with complete normalization in valve function and no residual stenosis (Figure ).
Percutaneous closure of the VSD was subsequently pursued following balloon valvuloplasty. Significant temporary improvement in haemodynamic function ensued over the following days. Unfortunately, despite all heroic measures undertaken, the patient succumbed to her illness after multisystem organ failure 5 days later.


A 20-year-old woman with no smoking history presented a round-shaped shadow in the right middle lung field on a chest X-ray during her medical checkup on employment (Fig. a), while her chest X-ray 2 years ago had no abnormalities. She exhibited no symptoms and had no comorbidities. Contrast-enhanced computed tomography (CT) of the chest showed a lobulated solid mass in the hilum of the right lung measuring 3.5 × 3.0 cm in diameter, which was homogenously enhanced in the early phase scan without any intratumoral fat or calcification identified (Fig. b). FDG-PET revealed a high accumulation of FDG in the mass wherein the maximum standard uptake values were 7.1 and 8.4 in the early and delayed phases, respectively (Fig. c). The levels of all serum tumor markers of lung cancer such as carcinoembryonic antigen, cytokeratin 19 fragment, and pro-gastrin-releasing peptide were within normal ranges. Based on the radiological findings, the mass was suspected to be either an invasive lung cancer, a lymphoma, Castleman’s disease, a solitary fibrous tumor, or an inflammatory pseudotumor. A transbronchial lung biopsy was performed, but the specimen was too small for histological diagnosis. It was decided that the most likely diagnosis of the mass was clinical T2aN0M0 stage 1B non-small cell lung cancer as per Union for International Cancer Control (UICC) 8th edition criteria. Accordingly, the patient underwent anterolateral thoracotomy through the fifth intercostal space. Intraprocedurally, it was detected that the mass arose from the S3 of the right upper lobe and that its surface facing the interlobular space was covered with visceral pleura. The mass had not invaded the middle lobe, but it was close to the hilar vessels. Thus, wedge resection with the mass was considered to be difficult, and right S3 segmentectomy was performed. Intraoperative frozen section analysis revealed that the tumor contained branched gland ducts along with columnar epithelial cells with poor nuclear dysplasia arranged in papillary growth patterns. Therefore, the tumor was diagnosed as a benign pulmonary lesion (e.g., papilloma or adenoma), and the operation was completed without deploying any additional procedures.
Macroscopically, the mass was a solitary, white-colored, well-defined, and solid component measuring 2.9 × 2.5 cm in diameter (Fig. d). These findings were seldom found in conjunction with necrotic or hematomatous lesions. Microscopically, it consisted of abundant glands with single or double layers of nonciliated cells and bronchial structures that resembled the tubular epithelium of a fetal lung. Rounded morules of polygonal cells with eosinophilic cytoplasm were frequently observed (Fig. a). Immunohistochemistry showed that nuclei and cytoplasm of the tumor cells were positive for β-catenin (Fig. b) and negative for p53, nuclei of the tumor cells were positive for thyroid transcription factor 1, and the cytoplasm was positive for synaptophysin. Based on the abovementioned morphological patterns and immunohistochemical profile, the tumor was finally diagnosed as a WDFA.
At 1 month after the initial operation, the patient underwent completion right upper lobectomy and systematic lymph node dissection. Anterolateral thoracotomy was performed via the fifth intercostal space, same with the incision in the initial operation; further, the lower lobe and chest wall surrounding the wound were widely attached, and both the major and minor fissures were firmly adhered. Although peeling off the adhesions was difficult, the remaining upper lobe was successfully removed without any complications such as vessel injury, lung damage, and massive bleeding. According to the pathological findings, no residual tumor or lymph node metastasis was present, and the final pathological stage was pT1cN0M0 stage 1A3 (UICC, 8th edition). The postoperative course was uneventful, and the patient was discharged on postoperative day 6. She did not wish to receive any adjuvant therapy. At 1-year after the second operation, the patient was well without any evidence of recurrence.


A 9-month-old female infant (11.7 kg) was admitted to our hospital for a previously undiagnosed growing pulsatile mass at the lower chest that was present since birth and, according to family, had been gradually growing (Video ). She was otherwise asymptomatic, with no history of embolic events, syncope, arrhythmia, or heart failure. Physical examination revealed aplasia of the xiphoid process and lower sternum (Video ). The preoperative electrocardiogram was normal. Transthoracic echocardiography showed dextrocardia with the apex pointing to the right side, and a large contractile pouch arising from the apex, contracting in synchrony with the left ventricle (Video ). No other heart defects were identified. Enhanced computed tomography (CT) confirmed a protrusion extending beyond the apex and showing a wide connection with the left ventricular cavity (Fig. ). The infant was diagnosed with LVD and treated immediately by surgery, without a period of prior observation or conservative management, because it was growing.
The patient underwent surgical resection using cardiopulmonary bypass. Under direct visualization, the ratio of the diameter of the diverticulum “neck” (4 cm) to the maximum diameter of the diverticulum body (3 cm) was 1.3 (Fig. a and b). In addition, the left anterior descending coronary artery (LAD) was close to the ventricular connection (Fig. a and b). Given the vicinity of the LAD to the LVD and the wide ventricular connection, partial resection was undertaken by excising the distal half of the diverticulum, and the remnant was oversewn using an interrupted pledgeted 5–0 polypropylene suture (Prolene, Ethicon, USA) (Fig. c). The right pericardium was resected carefully to avoid damaging the phrenic nerve, and the left ventricular apex was successfully repositioned to the right thoracic cavity.
The postoperative course was unremarkable. Histopathology of surgical specimens showed the presence of all three layers of the heart (endocardium, myocardium, and epicardium), and no fibrotic tissue was identified anywhere in the lesion (Fig. ). During 8-month follow-up, the infant remained asymptomatic with good heart function. The last follow-up echocardiography showed normal left ventricular geometry without obvious evidence of apical outpouching. No thrombosis was identified (Video 3).


We report the case of a 70-year-old man who was neither treated for tuberculosis nor has had any recent tuberculosis contagion, and with no notable pathological history or chronic smoking. The patient has reported a productive cough for 2 months, with mucous sputum associated with stage III of mMRC dyspnea, without hemoptysis or chest pain. Moreover, for 1 month he had liquid dysphagia associated with regurgitations, in the context of apyrexia and deterioration of the general state.
Clinical examination finds a conscious patient, eupneic at rest, saO2 = 92% at ambient air, with a pleuropulmonary examination without particularities.
The posteroanterior chest roentgenogram showed homogeneous right hilar opacity with peripheral nodular opacity with speculated contours (). The thoracic computed tomography (CT) showed a right hilar tumoral process, extended to the posterior segment of the right upper lobe with irregular and spiculated contours, measuring 42 × 32 × 25 mm without contact with the esophagus, associated with a spiculated nodule of the right upper lobe measuring 20 × 19 mm, without lymphadenopathy mediastinal ().
A bronchial fibroscopy was made objectifying a budding mucosa of the right upper lobar bronchus whose biopsy concluded from an epidermoid carcinoma.
As part of the exploration of dysphagia, an oesophagoscopy was normal and an achalasia was evoked and confirmed by esophageal manometry.
Due to the significant alteration of the patient, the patient died before the initiation of treatment.


The 72-year-old Chinese woman attended a major city general hospital because of recurrent peculiar behaviors during sleep for 3 years. At the illness onset, her daughter witnessed the patient shouting, punching, kicking or even walking around her bedroom during sleep about once or twice per month, but the patient had no recollection of her behavior. Her symptoms worsened over time and in the last 12 months, she developed nightmares, dream-enactment behaviors and vocalization during sleep occurring almost nightly. The vivid dreams included violent scenes, and once she dreamt about chasing someone but in fact she was pacing up and down her room. No physical harm towards herself or others was reported.
The laboratory examinations such as routine blood test, liver and kidney function, thyroid hormones, tumor biomarkers, infectious diseases including HIV, syphilis and hepatitis B and C, were all unremarkable. The cranial magnetic resonance imaging revealed scattered ischemic lacunar lesions in bilateral paraventricular and semioval regions. The results of the assessment scales are listed in Table . An overnight polysomnography (PSG) showed that the total sleep time: 392.5 minutes; time in bed: 498.0 minutes; sleep efficiency: 78.8%; REM sleep: 73.0 minutes; apnea-hypopnea index: 0. The electromyography monitoring revealed that she had intermittent dynamic chin electromyographic activity and her REM sleep without atonia condition was obvious. Besides, the video also showed that she had trivial limb movements and swing actions during sleep. The patient had no concurrent medicine or alcohol/substance use or any family history of psychiatric diseases or neurodegenerative diseases such as PD. The PSG findings and clinical manifestations met the diagnostic criteria of RBD according to the International Classification of Sleep Disorders (ICSD)-3.[ She was initially prescribed with paroxetine 20 mg per day and melatonin 3 mg per night. A year later, her daughter noticed that her symptoms had partially improved but she still had nightmares and dream-enactment behaviors such as shouting and crying in sleep for about once a week. As such, paroxetine was discontinued and vortioxetine was initiated in a daily dose of 10 mg.
In terms of the Clinical Global Impressions Severity scale (CGI-S), score ranges from 1 for “normal” to 7 for “among the most extremely ill” were as follows: at the initial presentation, the CGI-S score was 5; when treated with paroxetine and melatonin for a year, the CGI-S score was rated 4; when treated with vortioxetine for 2 months, the score dropped to 2, and after 3 months of vortioxetine therapy, her CGI-S score dropped to 1. After taking vortioxetine 10 mg per day for 15 months, the CGI-S score of the patient remained 1 point and no obvious side effects of the drug were observed.
This case study was approved by the Institute Ethical Committee of the First Affiliated Hospital, Zhejiang University School of Medicine, and written informed consent was obtained from the patient and her daughter.


A 75-year-old male with a past medical history of hypertension and diabetes presented to the hospital with worsening shortness of breath, dry cough, fatigue, and fever for three weeks. On presentation, the patient was awake, alert, in moderate respiratory distress, and had left-sided wheezes. He was afebrile with a respiratory rate of 30, oxygen saturation of 95% on nonrebreather mask, blood pressure of 156/81, and heart rate of 86. Chest X-ray (CXR) showed airspace disease involving the left lung (Figure ). Electrocardiogram showed sinus rhythm with premature atrial complexes. Influenza antigen was negative. Laboratory testing was unremarkable. COVID-19 test was sent and the patient was started on azithromycin and cefepime. The patient had worsening of symptoms and the next day laboratory testing revealed: elevated D-Dimer, ferritin, troponin, lactic acid dehydrogenase, C-reactive protein, white blood cells, and a positive COVID-19 test. The patient was started on HCQ but shortly thereafter, he developed multiple episodes of nonsustained ventricular tachycardia, and HCQ was stopped which led to the resolution of the aforementioned rhythm (Figure ).


A 56-year-old COVID-19 positive female was admitted to the hospital for further management of her fever, fatigue, and mild shortness of breath. She denied any gastrointestinal symptoms. On presentation, she was awake, alert with diminished lung sounds bilaterally. She was febrile with a temperature of 100.5°F, respiratory rate of 18 with oxygen saturation 96% on room air, blood pressure of 127/83, and heart rate of 81. CXR showed bilateral patchy areas of multifocal infiltrate (Figure ). Electrocardiogram showed normal sinus rhythm. Influenza antigen was negative. Laboratory testing including white blood cell count, ferritin, lactic acid dehydrogenase, coagulation profile, liver function tests were within normal range. She was started on HCQ, azithromycin, and cefepime. Soon after initiation of therapy, the patient began complaining of nausea, vomiting, severe abdominal cramps, and unbearable watery diarrhea. HCQ was stopped after two days as per patient’s request and her symptoms improved with supportive care. Ultimately, the patient was discharged home on azithromycin and cefdinir upon improvement and resolution of respiratory symptoms.


A 56-year-old Japanese man was admitted to our hospital because of high fever and consciousness disorder. He developed drowsiness and did not respond well to simple questions. He had been diagnosed with lung adenocarcinoma of the right lower lobe with upper right hilar lymph node metastasis (cT2N2M0). He was a taxi driver and had smoked until he was 55 years old (1 pack per day × 35 years). He had no other medical history or family history. He underwent right lobectomy 10 months prior to admission and had been treated with three courses of chemotherapy with a combination regimen of cisplatin plus vinorelbine, although positron emission tomography showed disease progression with multiple new metastatic lung lesions. Subsequently, he received three cycles of chemotherapy with a combination regimen of carboplatin plus nab-paclitaxel. He had received his first treatment with atezolizumab 17 days earlier for metastatic lung adenocarcinoma. His fever occurred about 1 week prior to admission. Neurological examination showed a consciousness disturbance (Glasgow Coma Scale E3V3M6) and motor aphasia. He did not show signs of pyramidal tract involvement, involuntary movement, ataxia, sensory disturbance, or autonomic disturbance. No other abnormal findings, including nuchal rigidity, were found.
Magnetic resonance imaging with gadolinium contrast of the brain on admission showed no abnormalities (Fig. ). A cerebrospinal fluid (CSF) study demonstrated a cell count of 20/μl, protein of 166 mg/dl, and glucose of 73 mg/dl. The level of interleukin 6 (IL-6) in CSF was increased to 82.9 pg/ml (normal level < 8.7 pg/ml []). The CSF was negative for bacterial cultures and polymerase chain reaction for herpes simplex viruses 1 and 2 and cytomegalovirus. Serum antibody tests for paraneoplastic neurological syndrome including anti-Hu were negative. Thus, metastatic brain tumor, bacterial meningitis, herpes simplex encephalitis, and paraneoplastic neurological syndrome were ruled out. Our patient was diagnosed with encephalitis induced by atezolizumab, and steroid pulse therapy with 1000 mg of methylprednisolone for 3 days was started on the second hospital day. His symptoms including high fever, consciousness disturbance, and motor aphasia improved immediately the next day. After the steroid pulse therapy, oral administration of prednisolone 30 mg (0.5 mg/kg) was started and tapered. The CSF findings, except for mild pleocytosis (12/μl), were normalized on day 8. The value of IL-6 was decreased to 2.3 pg/ml. Oral administration of prednisolone ended on day 13. A subsequent CSF study on day 14 showed an almost normalized cell count (7/μl) and a normalized value of IL-6 (3.9 pg/ml) (Fig. ). He was discharged on day 16 without neurological sequelae. After discharge, he was treated with combination chemotherapy with a regimen of docetaxel plus ramucirumab for lung adenocarcinoma without relapses of encephalitis.


A 30-year-old South Asian male with no known co-morbid, presented with the complaints of involuntary, abrupt, and purposeless movement of left upper and lower limbs along with difficulty walking for two weeks, but could ambulate without assistance. These movements suppressed partially by rest, and disappeared completely during sleep but aggravated on performing tasks. The patient did not have urinary or stool incontinence. History of undocumented, unintentional weight loss was present, noticed due to the loosening of clothes. On detailed questioning, he denied a history of head trauma, tongue bite, unconsciousness, memory impairment, neuropsychiatric symptoms, fever, sore throat, heat intolerance, joints pain, oral ulcers, photosensitivity, or jaundice. Past medical, surgical, or history of blood transfusion was not significant. He declined the use of illicit drugs or any antipsychotic medications. His father was diabetic and hypertensive. There was no history of similar illness in family members. His sleep, appetite, bowel habits were normal, but noticed an increase in the frequency of passing urine lately.
Higher mental functions were intact. Mini-mental state examination revealed intact cognitive function. Pupils were bilaterally equal and reactive to light and no Kayser-Fleischer ring appreciated on naked eye examination. Cranial nerves were intact, muscle mass was normal, power five/five in all limbs. Deep tendon reflexes and the sensory system were intact, while planters were bilaterally flexors. Cerebellar signs were negative, whereas gait was abnormal due to hyperkinetic dance-like movements. Milk Maid grip sign and pronator sign were positive on the left side. We could not assess Romberg’s sign. All other systemic examinations were within normal limits.
Random blood sugar was 453 mg/dL, while HbA1c 15.13% on patient presentation. We have presented blood/serum laboratory reports in Table . Arterial blood gas parameters were within normal limits on presentation. Urine analysis was insignificant with no ketones but positive glucosuria only. MRI brain with contrast showed right-sided basal ganglia hyperintense lesion in lentiform nucleus on T1 weighted images (Figure ), but no ischemia or hemorrhages suggested. Hence, we diagnosed the patient with hyperglycemic-hemichorea (chorea-hyperglycemia-basal ganglia syndrome). We started our patient on insulin therapy along with haloperidol. His symptoms progressively improved and he was much better after 12 days of starting therapy. He improved completely after 55 days. Blood glucose levels remained under control and repeat HbA1c after two months was 8.24%.


An 80-year-old lady with a past medical history of hypertension, chronic obstructive pulmonary disease, atrial fibrillation, heart failure, chronic kidney disease, fibromyalgia, cerebrovascular disease and a non-active pituitary mass presented to the hospital with nausea, vomiting, fatigue and poor oral intake. Further workup revealed that she had panhypopituitarism, which was being managed in the hospital. During her hospital stay, she became lethargic likely secondary to delirium with electrolyte abnormalities from her pituitary disorder and required bilevel positive airway pressure (BiPAP) support for respiration. Her respiratory status continued to deteriorate with acute respiratory failure, which prompted further workup with a CT scan of the thorax. CT thorax revealed a finding of edematous changes isolated within the right breast area with several gas foci just superficial and inferior to the right clavicle (Figure ).
The patient did not have any pain or discharge from the right breast. She did not have any fevers or chills during the hospital stay. Physical examination did not reveal warmth, erythema, induration or crepitus over the breast. Labs showed normal leukocyte counts during this course. The finding of air in the breast was therefore not attributed to infection. She was thoroughly evaluated for other possible causes of air in the breast based on prior case reports. She did not have any procedures over the right chest wall during the hospitalization. She did not have a central line placement, was not intubated but was placed on BiPAP for respiratory failure. She did not have a history of breast cancer and no recent mammogram, but reported that her mammograms from several years prior did not show any abnormal findings. After a thorough chart review, it was found that there was a peripheral intravenous line placement on the day prior to the CT thorax over the right upper extremity. It was attributed to being the most likely source of the edema and gas foci. The surgery team was consulted to ensure no surgical intervention was necessary. No surgical intervention was warranted given her lack of infectious symptoms and they recommended a follow-up if she noticed any changes to her breast. The patient has not had repeat imaging done since then and has not followed up for any complaints with regard to her breast.


In July 2017, a 46-year-old man of Han Chinese ethnicity was referred from a local community hospital with complaints of fever of 2 weeks’ duration, along with hematuria, proteinuria, and rapidly deteriorating renal function. He was being treated with intravenous antibiotics and expectant treatment for his kidneys without any improvement. The patient had a 5-year history of hypertension without treatment (peak blood pressure 145/110 mmHg). In February 2017, he was diagnosed with pancreatitis, and he recovered after treatment. He denied any history of diabetes, alcohol intake, intravenous drug abuse, and smoking. He had no history of familial disease and no known environmental exposure. He was a farmer, was married, and had a daughter. He had not undergone any examination for infectious diseases, including HBV, HCV, or HIV.
On admission to our hospital, his mental status was normal. His body temperature was 36.9 °C, pulse rate was 92 beats/min and regular, respiratory rate was 18 breaths/min, and blood pressure was 116/78 mmHg. His physical examination revealed a systolic murmur (Levine classification 3/6) in the apex area and a diastolic murmur (Levine classification 2/6) in the aortic area. The result of his neurological examination was normal. A series of laboratory tests was performed after admission.
On the day of admission, laboratory results indicated 1+ proteinuria (1.28 g/24 h), 3+ urine occult blood with 2959.9 red blood cells per high-power field, a white blood cell count of 6.22 × 109/L, hemoglobin of 81 g/L, albumin level of 32.3 g/L, globulin level of 48.7 g/L, serum creatinine level of 196 μmol/L, and blood urea nitrogen level of 7.7 mmol/L. His hepatitis B surface antigen, hepatitis B e-antigen (HBeAg), and hepatitis B core antibodies were positive. His DNA level of HBV was 1.38 × 104 IU/ml. The findings for rheumatoid factor, HCV antibody, and HIV were negative. The level of MPO-ANCA was normal, whereas that of PR3-ANCA was 170.4 relative units/ml (normal range, < 20). Blood cultures were obtained three times, and examination revealed the presence of Abiotrophia defectiva. Ultrasound cardiac examination revealed aortic and mitral valve vegetation (13 × 10 mm, 11 × 6 mm). Moderate regurgitation and turbulence could be seen in the diastole of the aortic valve orifice and the systole of the left atrial side of the mitral valve orifice (Fig. a–c). A chest computed tomographic scan showed no obvious pulmonary infection (Fig. ).
Given the clinical information provided, including the results of the blood culture and ultrasound cardiac examination, IE was identified. However, it was difficult to determinate whether HBV or more acute IE was the main cause of this patient’s ANCA positivity. Due to the patient’s rapidly deteriorating renal function, he was supposed to undergo kidney biopsy to clarify the type of glomerulonephritis (GN), but the results of echocardiography stopped us from performing a biopsy. The patient’s echocardiogram revealed mitral and aortic valve vegetation (11 × 6 mm, 13 × 10 mm) and regurgitation. Doctors in the cardiothoracic surgery department suggested valve replacement surgery be considered to avoid systemic bacterial emboli. Severe regurgitation and heart failure due to valvular destruction was another consideration. Because of these complex conditions, the patient’s diagnosis was a challenge.
When the patient was admitted to our hospital, he had a fever the first night. He was treated with antibiotics because blood culture results indicated A. defectiva infection. The patient’s temperature decreased gradually (Fig. ). Meanwhile, he was given other medications, including niferex (150 mg once daily by mouth), folic acid (5 mg three times daily by mouth), and medicinal charcoal tablets (1.2 g three times daily by mouth). On the 15th hospital day, the patient underwent mitral and aortic valve replacement and was then treated with warfarin (2.5 mg once daily by mouth) and antibiotics for more than 1 month (Fig. ). On the 57th hospital day, the patient was discharged. His urinary abnormalities and renal function were gradually recovering. Four months after being discharged, his PR3-ANCA levels had returned to the normal range. The patient’s whole clinical course can be seen in Fig. .


The patient is a 74-year-old female. She was diagnosed with diabetes mellitus. She presented an acute bullous skin eruption after some oral medication 30 years before, of which she had no records. She reported that the eye symptoms, including ocular pain and visual disturbances, began after that episode.
The patient has been in our care for 10 years. Her first visit diagnosis was symblepharon and dry eye syndrome in both eyes with corneal keratinization in the left eye. During the years, she had several acute episodes of corneal ulcer in the right eye (RE), which needed hospitalization, while the left eye (LE) was quiet. The LE had a visual acuity (VA) of light perception and presented an opaque cornea and ankyloblepharon, for which she was treated only with artificial tears.
The period of time between 2017 and 2018 presented a particular ocular evolution.
Thus, the RE presented several recurrent episodes of corneal erosions, severe corneal neovascularization and severe dry eye symptoms. The treatment consisted in 3 subconjunctival injections of Bevacizumab-Avastin 0,05 ml (1,25 mg), artificial tears and monthly soft contact lens. Meanwhile, she developed cataract in this eye and the visual acuity became “count fingers”. She was told that cataract surgery had poor prognosis. However, she still underwent cataract surgery with posterior chamber IOL implantation. The surgery took place in September 2018. On the other hand, the LE maintained the same biomicroscopic aspect, with no further symptoms or complications.
Nonetheless, in December 2018, 3 months after having the cataract surgery, the RE developed corneal ulcer with aggressive evolution to descemetocele. Local antibiotics, mydriatic and steroids were administrated. No perforation of the cornea happened, instead it healed with a central scar after three weeks.
In the next period, March-April 2019, the RE developed several inflammatory episodes with ocular pain, blurred vision and enlargement of the corneal neovessels. The therapeutic plan included 3 peribulbar injections of 4 mg dexamethasone, one per week. No relief of the pain was observed.
In May 2019, the patient complained of recurrent and short (30 minutes) episodes of acute loss of vision. She was hospitalized because the RE cornea had a new ulcer and was so hazy that the pupil and posterior pole could not be examined. Treatment consisted of antibiotics and dexamethasone in peribulbar injections every 2 days. After one week, some part of the retina could be examined and several retinal hemorrhages were observed. We concluded that it was a retinal venous branch occlusion, but we could not exclude diabetic retinopathy. Neurological and cardiological examinations along with cerebral MRI showed no signs of stroke or arrhythmias. The patient was discharged and the local treatment she continued at home consisted of artificial tears and soft contact lens in both eyes, while the general treatment included Aspenter. VA at that time was “counting fingers at 30 cm” in the RE and light perception in the LE.


The second patient is a 72-year-old female. She was diagnosed with arterial hypertension. Both eyes presented intense dry eye symptoms for the last two years with no relief from artificial tears.
The first visit in our clinic was in May 2018. VA in both eyes was 20/ 20 without correction. Both eyes presented inferior symblepharon, entropion with corneal erosions, and a severe dry eye syndrome. Schirmer 1 test was 0 mm/ 5 min and the tear break up time was 2 sec. No corneal vascularization was observed (-).
We started bilateral treatment with local antibiotics, lipid artificial tears during day time and gel during night time, associated with topical steroids for 2 weeks. Because symptoms persisted, she was prescribed topical 1 mg/ ml cyclosporine (Ikervis), 1 drop per day in both eyes. Soon after introducing Ikervis in the therapeutic plan, the patient reported symptoms of ocular pain, hyperemia and blurred vision. Thus, the cyclosporine was discontinued after 3 weeks because the patient did not tolerate it. She continued the local treatment with lipid artificial tears, and in May 2019 she underwent surgery for entropion in both inferior eyelids. A conjunctival biopsy was sampled and examined by direct immunofluorescence, which was positive for IgA, leading to the diagnosis of Ocular cicatricial pemphigoid. The collaboration with a dermatologist led to the patient being immediately treated with immunosuppressive therapy, respectively azathioprine. Systemic oral corticoid treatment was also administered. After 3 months, the patient developed elevated transaminases and the immunosuppressive therapy was interrupted. At present, her treatment consists of lipid artificial tears along with oral corticoid therapy.


The third patient is 74-year-old male suffering from arterial hypertension. For the last 10 years, both eyes presented dry eye syndrome, corneal neovascularization, symblepharon, misdirection of the cilia and multiple episodes of corneal ulcers, the ulcers being predominant in the right eye. It must be noted that the misdirection of the cilia was present only on the superior right eyelid and the cilia were very soft and did not hurt the corneal epithelium. VA of RE decreased over the years mainly because of the cataract evolution, while VA of LE maintained at “count fingers at 1 meter” due to corneal opacification and neovascularization.
Patient asked intensively for cataract surgery in the RE, despite being strongly recommended not to, considering his pemphigus disease. He had cataract surgery with posterior chamber IOL implantation in March 2016, when his VA was 0,3. After surgery, VA was 0,6 for six months and then began to decrease due to cystoid macular oedema. The patient had 6 intraocular injections with Avastin (1,25 mg), and 4 with Triamcinolone the next year, but VA decreased significantly to “count fingers at 3 meters”. At present, his treatment consists of lipid artificial tears.


A 59-year-old man consulted our service due to a bilateral and painless visual loss. He started presenting blurred vision on his left eye (LE) the prior week, which became bilateral in 48 hours. He was a smoker of 52 packets/ year and he also reported high blood pressure, which was controlled with torasemide 5mg/ day and amlodipine 10mg/ day. He denied any other relevant medical history past.
Ophthalmic examination revealed a reduced visual acuity (VA), 20/ 125 in his right eye (RE) and hand movement in his left eye (LE). The slit lamp examination revealed a non-swollen anterior pole, but in the fundus examination we found a moderate vitreous cellularity (1+) on his RE and a dense vitreous cellularity (2+) on his LE. Moreover, we found a bilateral swollen optic disc (), an arteriolar narrowing and vascular tortuosity without sheathing retinal veins. Fluorescein angiography examination revealed a hyper fluorescence and leakage in the optic nerve without any vasculitis signs (). A CT-scan was normal and the chest X-ray revealed enlargement of both hila. With a suspicion of posterior uveitis with bilateral papillitis we initiated 1-gram Methylprednisolone x 5 days.
A total-body CT-scan only revealed enlargement of para tracheal bilateral nodes, and the cerebral MRI was normal. The purified protein derivative (PPD) skin test, Interferon-γ release assay, HLAB27, HLA B51 and Angiotensin-converting enzyme (ACE) were negative, with the rest of the biochemistry being unremarkable. Two different biopsies made by echo-endoscopy revealed necrotic areas without granulomas or evidence of malignancy. A new ophthalmologic examination showed a total resolution of the vitritis, without evidence of retinitis or choroiditis, with diminution of the swollen optic disc () and a fast recovery of his VA becoming 20/ 20 in OU during the first weeks, although an enlargement of the blind spot, and some peripheral scotoma in his visual field persisted ().
A CT-scan was repeated and multiple node enlargements in mediastinum and bilateral hilum were still identifiable, so we decided to perform a mediastinoscopy, which revealed a SCLC. Serologic evaluation of paraneoplastic autoantibody profile was positive to CRMP-5-IgG positive.
The patient was referred to the oncology department with a diagnosis of SCLC with limited involvement of the thorax. Initially, a concomitant treatment with cisplatin and etoposide together with radiotherapy was considered. However, due to the fact that all the affected territories could not be included in a single radiation field, an induction chemotherapy was started. After three cycles of treatment, a partial response was achieved, hence concomitant radiotherapy was at that point feasible. After three cycles of chemo radiation, a complete response was achieved.


A 30-yr-old woman with oligomenorrhea, clinical hirsutism, and a history of primary infertility for six years was referred to our institute from another province for oocyte retrieval. Laparotomy was performed 10 years prior for an ovarian cyst. The results revealed GTB and granulomatous disease with caseous necrosis. She underwent anti-TB treatment for six months.
At the first admission in our institute, she had a negative tuberculin test (PPD) and a normal chest X-ray with no clinical evidence of TB. Hormonal evaluation on day 3 of the menstrual cycle showed a follicle-stimulating hormone (FSH) level of 6.02 mIU/ml and luteinizing hormone (LH) level of 7.2 mIU/ml. Vaginal ultrasound results revealed a 10-mm hypoechogenic structure in the right adnexa that agreed with a right hydrosalpinx (Figure 1A). Hysterosalpingography (HSG) results showed a bilateral hydrosalpinx (Figure 1B). Infertility workup for the husband indicated that he had a normal sperm analysis according to the World Health Organization criteria (5). The patient underwent ovarian stimulation according to the standard long protocol where she received 0.1 mg/day Decapeptyl (Ipsen Pharma Biotech, France) from day 20 of the pre-stimulation cycle until the day of the hCG injection. Once the down-regulation was confirmed, from day 3 of the new menstrual cycle, she received subcutaneous injections of 2 ampules/day of Gonal-F (Merck Serono, Darmstadt, Germany). Follicular growth was monitored by serial transvaginal ultrasound and repeated until the detection of at least three follicles 18 mm in diameter. At that time, the patient received an intramuscular injection of hCG (10000 IU). After 36 hours, 21 oocytes were retrieved. Of these, 15 oocytes were fertilized and cleaved. Because of the risk for ovarian hyperstimulation syndrome, all embryos were frozen on the third day. After three months, the patient elected to undergo a laparoscopy/hysteroscopy due to hydrosalpinx (es). Laparoscopic findings included dense adhesions of the pelvic organs and a frozen pelvis. The surgeon could not perform a salpingectomy or proximal tubal occlusion so both ostium of the uterine tube were cauterized by hysteroscopy according to a previously reported procedure (6). However, direct smear and bacterial culture of endometrial tissue and evaluation of tissue by polymerase chain reaction (PCR) were negative for Mycobacterium TB. After eight months, the patient underwent FET. After GnRh agonist down-regulation, she received estradiol valerate (Aburaihan Co., Iran) as hormone replacement therapy in the following doses: 4 mg/day for the first six days, followed by 6 mg/day for another six days, until endometrial thickness reached 9 mm. When the optimal endometrial thickness was obtained, intramuscular progesterone (100 mg; Aburaihan Co, Iran) was administered and three days later, two good-quality embryos were transferred. The luteal phase was supported with estradiol and progesterone. However, she did not achieve pregnancy. One year later the patient underwent a laparoscopy. A skillful laparoscopist carried out the operation. There was a severe dense pelvic adhesion and frozen pelvis (Figure 2A). After adhesiolysis, she had a bilateral hydrosalpinx and both tubes were removed. The next day, the patient was released without any problem. Surgical specimens were collected and stained with hematoxylin and eosin and evaluated with light microscopy. We observed cystically dilated glands surrounded by hypertrophic smooth muscle fibers, which demonstrated bilateral hydrosalpingitis isthmica nodosa (Figure 2B). After one year, she underwent a second artificial FET, which was similar to the previous transfer. When the endometrial thickness reached 9.5 mm, we transferred three high-quality embryos. The luteal phase was supported by 100 mg of daily progesterone injections (Aburaihan Co., Tehran, Iran). Biochemical pregnancy was detected by a β-hCG test 2 wk after the embryo transfer and clinical pregnancy was confirmed by the presence of a gestational sac with fetal echoes at 6 wk after embryo transfer. The patient was followed and had a cesarean delivery at 38 wk of gestation. Her child was a healthy girl who weighed 3,100 g.
The patient signed the written informed consent for reporting this case.


A 57-year-old male with a history of heroin abuse, chronic hepatitis C, and advanced diffuse large B-cell gastric lymphoma with a contained perforation on chemotherapy presented to the hospital with dizziness, hematemesis, and abdominal pain. On arrival, the patient was noted to be hypotensive with a blood pressure of 79/50 mmHg and tachycardic with a heart rate of 139 bpm. On physical exam, the patient had epigastric tenderness, dull bowel sounds, and splenomegaly. Labs revealed hemoglobin (Hgb) 8.2 g/dL, international normalized ratio (INR) 1.6, and lactic acid 3.2 mg/dL. CT of the abdomen revealed a gastric mass in the greater curvature of the stomach with a 3.1 cm perforation along with free fluid and air in the abdomen. The patient was admitted to the intensive care unit (ICU), and resuscitation was initiated with intravenous pantoprazole and red blood cell transfusion. Esophagogastroduodenoscopy (EGD) was performed revealing a large blood clot attached to a giant ulcer in the great curvature of the fundus (Figure ) without active bleeding. No endoscopic intervention was performed, and oral sucralfate was added to therapy. The patient’s Hgb stabilized after blood transfusions, and the patient was transferred to the floor.
Two days later, the patient experienced massive hematemesis, abdominal pain, and decreased mental status. Vitals revealed hemodynamic instability with a blood pressure of 65/50 mmHg and heart rate 140 bpm. Labs revealed Hgb of 6.5 g/dL. The patient was intubated for airway protection and emergent blood transfusion was initiated along with inotrope therapy for the treatment of hemorrhagic shock. Given active bleeding, a visceral arteriogram was performed, revealing active bleeding from the splenic artery which was treated with embolization and coiling. After the procedure, the patient’s Hgb was monitored in the ICU.
Over the next day, the patient’s Hgb continued to decrease, requiring more blood transfusions. A repeat EGD showed a large crater ulcer in the fundus/greater curvature of the gastric body and a large perforation with evidence of recent bleeding (Figure ).
Initial attempts to approximate the edges of perforation using a dual grasper were unsuccessful due to the gastric mucosa being friable. Therefore, the suction method was used to approximate the edges, and two OTSCs (Ovesco, Tübingen, Germany) were used to close the perforation (Figure ).
At this point, Hemospray was deployed achieving hemostasis of the entire ulcer (Figure ).
After the EGD, CT abdomen revealed a decreased amount of intraperitoneal free air without evidence of new perforation and no active bleeding. Over the next 24 hours, the patient’s Hgb stabilized, and no further blood products were transfused. Repeat EGD two days later showed persistent contained perforation without any active bleeding. The patient was discharged home and was cleared to resume chemotherapy. A follow-up EGD was performed after two months of chemotherapy, which revealed a marked decrease in the size of the ulcer and nearly resolved contained perforation [].


We report a case of a 49-year-old female of Asian descent who presented to the emergency department with burning with urination, frequency, and sensation of incomplete bladder emptying. The patient has a history of acute cholecystitis diagnosed a few months earlier. At that time, she underwent cholecystectomy and pathology showed eosinophilic cholecystitis. After this, she had persistent abdominal pain; she underwent esophagogastroduodenoscopy with esophageal, gastric and duodenal sampling showing mild chronic gastritis. The patient’s peripheral blood count at that time was showing persistent eosinophilia. The total white blood cell (WBC) count was 21,900/mm3, while the AEC was 15,600/mm3. Work up for parasitic infections was all negative.
This presentation, the patient has been experiencing the burning and frequency symptoms for three weeks. Her symptoms were associated with lower abdominal pain. She denied any fever, bloody urine, nausea, or vomiting. She was diagnosed with urinary tract infection (UTI) as an outpatient and had received seven days of an unknown antibiotic, then was started on ciprofloxacin, which she administered for four days. However, her symptoms did not improve. On admission, the patient was afebrile and vitally stable. Her physical examination was noted for suprapubic tenderness. Her lab work showed elevated WBC of 25,000/mm3 with AEC of 19,000/mm3, hemoglobin of 14.4 mg/dL, and platelets of 301,000 cells/mm3. Urinalysis was positive for nitrites, protein > 500 mg/dL and RBCs > 100/HPF. The patient was admitted for complicated cystitis with sepsis. Ultrasound of the pelvis showed a trace amount of free fluid in the pelvis with diffuse wall thickening of the bladder (Figure ).
CT scan of the pelvis with oral and IV contrast showed multiple urinary bladder masses, the largest of which measured 2.5 x 6.6 cm with an anterior wall mass 1.7 x 2.2 cm (Figure (a, b)).
The patient was started on ceftriaxone for complicated UTI. Cystoscopy showed a bladder mass, which was resected. Pathology showed benign polyploid urothelium with reactive changes and extensive eosinophilic infiltrate, numerous histiocytes with eosinophilic crystal-like structures; there was no evidence of malignancy. The patient was then treated with prednisone 20 mg, which she continued for two months. The patient’s peripheral blood count showed a response to prednisone with a WBC count of 6,000 cells/mm3 and AEC of 300 cells/mm3. However, she continued to have urinary symptoms; hence, she was started on mirabegron for overactive bladder.
The patient returned for right-sided abdominal pain with tenderness on palpation. Lab work showed a WBC count of 7,800 cells/mm3, AEC 1903 cells/mm3, lipase 282 U/L, and amylase 144 U/L. CT scan of the abdomen and pelvis showed ill-defined fat stranding of the peripancreatic fat with no pancreatic masses or peripancreatic fluid. Moderate right and mild left hydronephrosis were also noted. No hepatomegaly or splenomegaly was detected.
Given her eosinophilia, the patient underwent bone marrow biopsy, which showed normocellular marrow with active trilineage hematopoiesis, eosinophilia, mild megakaryocytic hyperplasia with a few atypical forms and mild T-cell lymphocytosis. Flow cytometry showed no evidence of acute leukemia, or T-cell or B-cell lymphoproliferative disorder. FISH myeloproliferative neoplasm testing was negative for PDGFRA, PDGFRB, and FGFR1 rearrangement. Polymerase chain reaction (PCR)-based advanced sequencing assay of her deoxyribonucleic acid (DNA) did not detect any of the following mutations: Janus kinase-2 (JAK2)-V617F, calreticulin (CALR) exon 9, JAK2 exon 12, myeloproliferative leukemia (MPL) exon 10, or the receptor for colony-stimulating factor 3 (CSF3R) 14/17.
Tryptase level was within normal limits. However, her B12 level was elevated at 1,453 ng/ml.
She was started on a second course of prednisone; however, a month later, she developed abdominal pain again, and her CT scan showed ileo-ileal intussusception within the right lower quadrant with no evidence of bowel obstruction. Repeat peripheral blood counts showed WBC 11,300 cells/mm3 and AEC 4,700 cells/mm3. A higher dose of prednisone resulted in the patient having significant gastrointestinal upset and anxiety.
Since she was not responding to prednisone, and given the significant toxicity of interferon, she was started on imatinib, a tyrosine kinase inhibitor, at 400 mg daily. She received the treatment for two weeks and then stopped it due to developing side effects, which included periorbital edema, joint pain, rash, and fluid retention. Despite not having the FIP1L1-PDGFRA gene fusion, our patient responded to the treatment with a decrease in her absolute eosinophils count from 4,700/mm3 to 700/mm3. On her six-month follow-up, the patient had no fever or other signs of inflammation.


A nine-year-old boy with developmental delay presented with a progressive functional decline of three months' duration culminating in emergency department presentation for gingival bleeding, lethargy, and immobility. He had significant weight loss with malnutrition. On exam, significant vitals included a blood pressure of 99/37 mmHg and a heart rate of 58 BPM. He was lethargic with altered mental status. He had a soft S2 with grade III/VI decrescendo diastolic murmur, water hammer pulses, and contractures of all major joints. Laboratory workup revealed hepatic and renal failure, coagulopathy, pancytopenia, hypernatremia, and uremia requiring emergent dialysis. CT of the brain, obtained for the evaluation of mental status decline, demonstrated generalized atrophy (Figure ).
A transthoracic echocardiogram confirmed severe aortic regurgitation (Figure ). Throughout hospitalization, his hepatic and renal failure, coagulopathy, pancytopenia, hypernatremia, and uremia improved, but he continued to require blood products. Hospital course was complicated by methicillin-sensitive Staphylococcus aureus bacteremia with leukocytosis and episodes of tachycardia, which were managed with antibiotics and beta-blockers, respectively. Chest and abdominal radiographs demonstrated broad posterior ribs and beaking of the vertebral bodies (Figures , ); based on the imaging findings, the radiologist was the first to raise the possibility of MPS early during hospitalization. Genetic testing ultimately confirmed MPS-III, or Sanfilippo syndrome, type A. The patient developed hyperkalemia during the second month of hospitalization, and renin, aldosterone, and cortisol testing led to a diagnosis of hyperreninemic hypoaldosteronism with normal cortisol. Daily Kayexalate® (sodium polystyrene) and furosemide were required to normalize potassium levels, which eventually stabilized with hydrochlorothiazide and by mixing Kayexalate with his Ensure (Abbott Laboratories, Abbott Park, IL), a nutritional supplement, and decanting the low potassium supernatant.


An 85-year-old man presented to our institution complaining of recurrent fever and a mitral regurgitation murmur. He has a past history significant for atrial fibrillation being treated with apixaban status post leadless pacemaker implantation and AV nodal ablation 15 days ago, hypertension, hyperlipidemia, obstructive sleep apnea on continuous positive airway pressure, diverticulosis and diverticulitis, dental caries, melanoma in situ, and persistent pulmonary coccidioidomycosis on fluconazole.
He underwent a transthoracic echocardiogram which showed normal left ventricular size and no wall motion abnormalities, LVEF of 56%, severe mitral regurgitation due to incomplete coaptation of the mitral valve leaflets (Figures and ), mild right ventricular enlargement, systolic dysfunction with visible apical right ventricular lead, mild tricuspid regurgitation, and no pericardial effusion. A transesophageal echocardiogram confirmed restricted mitral valve leaflets resulting in incomplete coaptation and severe mitral regurgitation (Figures and ). No vegetations were seen. Blood cultures ruled out endocarditis as the cause of fever, and he was later found to have non-Hodgkin's lymphoma.
His cardiac history is notable for atrial fibrillation diagnosed 10 years ago which was treated with atenolol and warfarin. Despite this treatment, he had recurrent episodes of paroxysmal symptomatic atrial fibrillation with a rapid rate requiring multiple emergency department visits and hospital admissions (). Given difficulty to control the rate, he underwent AV nodal ablation and leadless pacemaker insertion 15 days prior to current presentation with resultant LBBB on his electrocardiogram (ECG) post implantation (). His echocardiogram days before pacemaker insertion revealed only mild mitral regurgitation and normal coaptation of the mitral valve leaflets ().
Given the absence of degenerative mitral valve abnormality and no evidence of cardiomyopathy, his diagnosis of new-onset severe mitral regurgitation is the direct result of abnormal electrical conduction related to iatrogenic LBBB due to AV nodal ablation and single-chamber paced rhythm.


A 28-year-old Asian female presented to her primary care physician (PCP) for follow-up due to progressively worsening dyspnea on exertion. The patient reported that the dyspnea was increasingly impacting her ability to perform her day-to-day activities. Prior to the onset of this dyspnea, she was an active young adult who swam routinely, yet now found herself unable to ambulate one block or up on flight of stairs without severe dyspnea. Additionally, she endorsed occasional palpitations with the dyspneic episodes, though the palpitations never occurred independently of such episodes. She denied the presence of lightheadedness, syncope, chest pain, cough, sputum production, hemoptysis, paroxysmal nocturnal dyspnea, orthopnea, lower extremity edema, wheezing, fevers, chills, night sweats, or weight changes.
Notably, this 28-year-old female was a relatively new patient of her PCP. At the time of her initial PCP visit, she had endorsed mild dyspnea for which the differential included physical deconditioning secondary to a low back injury, anxiety, premature atrial contractions, asthma, and pulmonary embolism (PE). Her past medical history was remarkable only for a remote history of asthma when she was a child, and her use of oral contraceptives (OCPs). Her social history was remarkable for immigration to the United States from China 10 years ago. She was encouraged to keep a diary to track her symptoms and began physical therapy for a mechanical low back injury. Her physical examination at that time was unremarkable and she was able to tolerate all her physical therapy appointments, even hiking for five miles without difficulty five weeks prior to her admission. Of note, the patient did experience an episode of hemoptysis after a paroxysm of coughing while experiencing cold-like symptoms.
On physical examination at her follow-up visit, she was noted to have visibly labored breathing, which resolved with rest and a normal cardiac exam, while her symptom diary showed progression in the severity of her symptoms. The differential diagnosis was expanded to include anemia in addition to the original differential. A chest x-ray was ordered, along with a complete blood count (CBC), D-dimer, and pulmonary function tests. The chest x-ray revealed prominent pulmonary vasculature concerning for PH (Figure ). Subsequently, her PCP had the patient present immediately to the emergency department for further evaluation and intervention.
The patient was admitted after further diagnostic tests to evaluate the concerning chest x-ray showed an enlarged right ventricle and an ASD on bedside ultrasound, confirmed with a CT chest with contrast (Figure ). On examination, there was a 3/6 systolic murmur present at the lower left sternal border, with no appreciable S1 or S2 splitting. Inspiratory and expiratory effort was normal with clear lung sounds, no signs of digital clubbing, no cyanosis, with the remainder of the exam completely benign. Her vital signs at rest included a blood pressure of 107/72 mmHg, heart rate 76 beats per minute, respiratory rate 18 breaths per minute, and oxygen saturation 92% on room air. During the interview and examination, the patient’s oxygen saturation was noted to fall to 72% without signs of dyspnea during the conversation, and she remained hypoxic despite 5L of oxygen via nasal cannula. The CT chest showed an ASD, 4.4 cm dilatation of the main pulmonary artery with dilatations of bilateral pulmonary arteries, segmental branches, and coronary sinus (Figure ). Transthoracic echocardiogram revealed an ejection fraction of 50%, severe dilatation of the right atrium and ventricle, dilatation of the coronary sinus, a pulmonary artery pressure of 132 mmHg with right atrial pressure of 8 mmHg, moderate tricuspid regurgitation, and moderate pulmonic valve insufficiency. Her laboratory chemistries were unremarkable except for her iron studies showing a slight iron deficiency of 34 ug/dL (normal 42-135 ug/dL) and iron saturation of 8% (normal 15-50%) with her hemoglobin (12.6 g/dL) within normal limits. Her electrocardiogram showed normal sinus rhythm with right axis deviation, concern for septal infarction of undetermined age, and ST abnormalities suggesting inferior subendocardial injury (Figure ).
She was transferred to a cardiac transplant center for further evaluation and potential heart-lung transplantation. Currently, she is stable on a medication regimen including ambrisentan and tadalafil. Her OCPs were discontinued. Since the initiation of pulmonary vasodilatory medications, she endorses improvement in her symptoms and is able to walk up to 10 blocks before becoming dyspneic. She is currently categorized as New York Heart Association Heart Failure Class 1.


A 63 year old woman with no known comorbidities, was evaluated in September 2017 for complaints of an insidious onset, gradually progressive painless swelling in the posterior aspect of right thigh. Magnetic resonance imaging scan revealed a well-defined, lobulated soft tissue lesion in posterior subcutaneous compartment of the right knee joint. She underwent excision biopsy of the primary lesion at a local hospital and histopathology was suggestive of undifferentiated pleomorphic sarcoma, with 14–15 mitoses per high power field, no necrosis and FNCLCC grade II (Fig. ). Subsequently whole body 18-fluorodeoxyglucose positron emission tomography with computed tomography (FDG PET-CT) scan showed metabolically active soft tissue mass in musculofascial plane of right lower thigh with FDG-avid right inguinal and external iliac lymph nodes, and multiple small bilateral lung nodules suspicious for metastases. In view of residual disease, she underwent wide local excision of the primary tumor along with right ilio-inguinal lymph node dissection. The tumor measured 8 × 5 × 5 cm, with all peripheral margins being negative. 10 out of 19 inguinal lymph nodes and 11 out of 22 pelvic lymph nodes showed metastatic tumor with extracapsular extension. On immunohistochemistry (IHC), tumor cells had a Ki-67 of 40%, and were positive for desmin, while being negative for SMA, S-100, CD34, CD99, Bcl2, MDM2, Desmin, H-caldesmon, cytokeratin, epithelial membrane antigen, Alk-1, HMB45, Melan-A, CK18, CK19, P63, ER, CD10, CK5/6, CK-HMW. She presented to our center at this point for further management and in view of metastatic disease, was advised doxorubicin-based chemotherapy. After discussion of the encouraging results from the phase 2 trial conducted by Tap et al. with the patient, the platelet derived growth factor receptor alpha antibody olaratumab was also added []. However, response assessment done after 4 cycles of doxorubicin and olaratumab showed progressive disease and she was then switched to gemcitabine and docetaxel regimen. She received 8 cycles of gemcitabine/docetaxel and had reduction in number and size of lung nodules, suggestive of partial response (Fig. a, b). Chemotherapy was stopped in view of unacceptable toxicity and she was kept on follow-up. After 3 months of treatment-free interval, she developed progressively worsening cough. A CT scan of the chest was done, which revealed disease progression (Fig. c, d). Biopsy blocks were reviewed for expression of programmed death ligand-1 (PD-L1) by IHC using the Ventana PD-L1 assay (SP263), which was positive, with a tumor cell score of 25 percent (Fig. ). She was then started on pazopanib 800 mg daily along with anti-PD-1 antibody pembrolizumab pembrolizumab (200 mg every 3 weeks). She had grade 2 infusion reaction with second dose of pembrolizumab, grade 2 immune-related hypothyroidism and grade 2 hypertension. There was significant improvement in her cough within one month of therapy and response evaluation done after 3 months of therapy showed regression of lung metastases (Fig. e, f). Same combination was continued with no unmanageable adverse effects, and a repeat evaluation done after 9 months of treatment showed further disease regression (Fig. g, h). Thus far, she has completed ten months of this combination therapy and continues to be in good general condition.


A 63-year-old woman with a history of alcohol use disorder, end-stage liver disease, and mycobacterial tuberculosis presented with one-month history of progressive diffuse weakness and altered mental status. The patient’s condition had progressed to the point of being unable to care for herself or make decisions. She was accompanied by her sister, the patient’s designated medical power of attorney, who provided informed consent for all tests, interventions, and treatments. T1-weighted post-contrast MRI and a T2-weighted MRI were obtained, which demonstrated an enhancing mass within the right foramen of Monro and findings suggestive of choroid plexus inflammation manifesting with right-sided trapped temporal horn syndrome. No abnormal signal was observed within the brain parenchyma, and the basal cisterns were preserved in appearance. MRI findings are shown in Figure .
Blood cultures acquired at patient presentation demonstrated positivity for Cryptococcus neoformans. Subsequently, an acute decline in the patient’s mental status was observed and the patient was taken emergently to the operating room for endoscopic biopsy and septum pellucidotomy. Under image guidance, an endoscope was extended through a burr hole and dural incision at the right Kocher’s point to the right frontal horn. Both the foramen of Monro mass and what appeared to be inflamed choroid plexus were biopsied. Using image guidance and anatomic landmarks, a small hole was made through the septum pellucidum using endoscopic graspers. The endoscope was used to expand the opening and was then passed into the left frontal horn. Cerebrospinal fluid (CSF) encountered on this side of the opening was observed to be yellow-green in color. Following biopsy and septum pellucidotomy, an external ventricular drain (EVD) was placed in the right frontal horn. Pathologic evaluation of the biopsied tissue demonstrated an abundance of budding yeasts with mucicarmine-positive capsules, most suggestive of Cryptococcus species, but not excluding differentials of Candida or Histoplasma species. CSF drawn intraoperatively as well as from the EVD was culture positive for Cryptococcus neoformans. In addition, a latex agglutination test of the CSF was positive and a serum cryptococcal antigen titer of 1:128 was suggestive of cryptococcal choroid plexitis in this setting. Pathology findings are shown in Figures , .
The patient was started on induction therapy IV liposomal amphotericin 5 mg/kg daily and flucytosine 1,500 mg q6h once the diagnosis was made. The altered mental status improved over the next few days. Ten days after placement of the EVDs, the patient underwent a clamp trial. The CT scans demonstrated unchanged ventricle size, so both EVDs were removed. The patient had no complications with regards to the choroid plexitis and was discharged 18 days following admission with a peripherally inserted central catheter (PICC) line in place for continuance of the amphotericin. The patient completed four weeks of amphotericin and flucytosine. The patient was prescribed consolidation therapy with fluconazole 800 mg for four weeks followed by a maintenance dose of 200 mg to be continued lifelong. Lifetime maintenance antifungal therapy was deemed necessary due to the patient’s multiple medical comorbidities and her poor likelihood of surviving a repeat cryptococcal infection of the CNS.


An 82-year-old Caucasian woman with a known history of metabolic syndrome (hypertension, dyslipidemia, type II diabetes, and hyperuricemia) developed atrial fibrillation 15 days before admission to our hospital and received 20 mg of rivaroxaban once a day, in addition to the usual treatment that she had regularly been undergoing for a long time and that remained unchanged, namely, moxonidine 0.2 mg/day, metoprolol 200 mg/day, losartan 100 mg/day, spironolactone 50 mg/day, furosemide 20 mg/day, simvastatin 40 mg/day, ezetimibe 10 mg/day, allopurinol 100 mg/day, 500 mg of calcium, and 400 UI of cholecalciferol/day.
Three days before admission, she noticed petechial lesions in the legs and developed progressive bilateral pitting edema in the lower limbs, associated with a weight gain of 4–5 kg, which made her fall twice at home. At admission, the clinical examination was remarkable for a petechial rash of the legs and the massively swollen lower limbs with pitting edema. The patient had low-grade fever with a temperature of 38.0°C. The blood pressure was 132/70 mmHg, heart rate was regular at 92/min, and oxygen saturation was 94%. The remainder of the exam was unremarkable. Diuresis was conserved at a rate of 0.55–0.60 ml/kg/hour. summarizes the results of the laboratory analysis performed at admission. There was marked acute renal dysfunction (serum creatinine = 215 µmol/l) with a moderate inflammatory response (C-reactive protein = 129 mg/l), a mild hepatic dysfunction, and a marked lymphopenia at 0.11 G/l (normal >1.0 G/l) but no eosinophilia. The urine exam showed massive leucocyturia (without eosinophils), no hematuria, and a mild tubular proteinuria of 0.72 g/day (25% albumin). The renal ultrasound and the posteroanterior and the lateral chest X-ray were normal. The echocardiography showed a normal ejection fraction (60%) without signs of diastolic dysfunction. As the patient had fallen before admission, a native cerebral CT scan was also performed and showed two small asymptomatic subdural hematomas (4 mm left-parietal and 1 mm right-parietal). The autoimmune screening was negative for antinuclear antibodies, rheumatoid factor, antineutrophil cytoplasmic antibodies, antiglomerular basement membrane antibodies, and cryoglobulins. C3 and C4 were within the normal range. The serologies for human immunodeficiency virus, hepatitis B, and hepatitis C were negative. The urine and blood cultures were sterile.
At admission, rivaroxaban was immediately stopped. In the first 48 hours of the hospitalization, the diuretics were stopped, and the patient received cautious intravenous hydration with vitamin K supplementation. Over the following days, we observed a rapid clinical and biological improvement. The petechial lesions in the lower limbs improved, while the edema affecting the legs rapidly diminished under low-dose diuretics (5 mg/day of torasemide), with a weight loss of 4.3 kg in five days. At the same time, the blood analysis showed a rapid and spontaneous improvement in the renal and hepatic dysfunction, as well as in the inflammatory syndrome (see and ). As the renal function rapidly and spontaneously improved, neither a renal biopsy was performed nor were steroids prescribed.


An obese, African American, 44-year-old female with a past medical history of hypertension and hyperlipidemia presented to the emergency department (ED) with a chief complaint of sharp, central chest pain radiating to the left upper extremity that awoke her from sleep. The patient arrived at the hospital within 30 minutes of symptom onset, with initial vital signs of blood pressure 172/86 mm Hg, heart rate 91 beats per minute, respiratory rate of 16 breaths per minute, oxygen saturation of 99% on room air and pain level of 9/10. Electrocardiogram (ECG) performed in triage was normal sinus rhythm without evidence of ischemia (Figure ). Initial labs revealed troponin elevated at 0.11 ng/mL (normal range 0.0-0.03 ng/mL); other lab values including those reflected in the complete blood count, complete metabolic panel, coagulation panel and human chorionic gonadotropin were within normal limits. Chewable aspirin, 324 mg, was immediately administered; 975 mg of oral acetaminophen, and a total of 1.2 mg of sublingual nitroglycerin over three doses were administered for analgesia, which reduced the patient’s chest pain to 3/10.
Posterioranterior and lateral chest plain films were without radiographic evidence of acute process. Two additional ECGs, which were performed within the subsequent 1 hour and 40 minutes of the initial study, remained unchanged, and repeat troponin demonstrated escalation to 0.59 ng/mL. Anticoagulation therapy with enoxaparin was administered subcutaneously at 1 mg/kg, and a diagnosis of non-ST elevation myocardial infarction (NSTEMI) was established. After cardiology consultation, the patient was admitted to the cardiac care unit. The patient underwent subsequent left and right heart cardiac catheterizations that revealed findings consistent with coronary artery dissection of the obtuse marginal 3 (OM3) branch of the left circumflex artery (Figure ). No underlying atherosclerosis was identified during the study. The remainder of the inpatient course was uneventful, and the patient was placed on daily oral 81 mg aspirin and her antihypertensive regimen was also optimized. While dual antiplatelet therapy was the original therapeutic plan, the patient was unable to tolerate clopidogrel due to a multisystem drug reaction, and it was unknown whether alternatives such as ticagrelor or prasugrel were considered. Outpatient CT angiography studies and rheumatology referral were ordered as part of the investigation for extracoronary vessel pathology including vessel narrowing and aneurysms that are often found in comorbid connective tissue conditions including fibromuscular dysplasia (FMD). Cardiac rehabilitation and short-term cardiology appointments were also scheduled. The patient continued to do well with no return to the ED within the next 30 days. The patient was ultimately not diagnosed with other comorbid vascular lesions or connective tissue disease including FMD.


A 13-day-old male child born full-term, weight appropriate for gestational age via normal spontaneous vaginal delivery was brought by the mother to our outpatient clinic for a follow-up visit. The neonate was found to have a 20% weight loss from his birth weight, which was quite significant. The infant was born to a teenage mother who received routine prenatal care. The mother’s laboratory results were negative except for gonorrhea and chlamydia, which were treated prior to delivery. The infant was exclusively formula-fed every 5-6 hours with a concentrated formula (2 scoops of formula powder mixed with 3 oz of water). The mother also reported "spit-ups" following feeds. The child had one to two bowel movements every other day and five to six wet diapers daily. Physical examination was significant for a cachectic appearing neonate with no subcutaneous fat appreciated. The abdomen was soft, non-distended, without palpable masses and bowel sounds were appreciated on auscultation. The child was subsequently admitted to the pediatric floor for further investigation and management due to his inadequate weight gain with clinical signs of malnutrition.
On the pediatric floor, the neonate was clinically stable with normal vital signs. Upon further investigation, the mother reported that the child had been vomiting “yellow” tinged partially digested milk, about one to two episodes daily since he started feeding. On the night of admission, the patient initially had one episode of non-bilious, non-bloody vomitus with partially digested formula after feeding. Initial laboratory testing which included a basic metabolic panel was significant for hypochloremic metabolic alkalosis (Table ).
The patient was then given 0.9% normal saline (NS) bolus and maintained on intravenous fluids D5 ½ NS with 10 mEq/L of potassium chloride. The patient had two recurrent episodes of “yellow” vomitus and an episode of red-currant jelly vomit. Oral feeds were held and a nasogastric tube inserted. The patient's initial abdominal X-ray showed stool in the bowel without free air or any sign of obstruction. A second abdominal X-ray showed prominent loops of bowel in the right side of the abdomen (Figure ).
On hospital day two, an ultrasound of the abdomen and pylorus was performed to rule out pyloric stenosis but the findings were inconclusive due to persistent vomiting during the study (Figure ).
An upper gastrointestinal (GI) series was then performed which revealed a partial obstruction at the level of the duodenum (Figure ).
The patient underwent an exploratory laparotomy on hospital day five. Exploration revealed stenosis of the third part of duodenum with mild adhesions to pancreatic tissue. There was no evidence of pyloric stenosis. The adhesions were lysed and a duodeno-duodenostomy was performed, approximating the second and fourth portions of the duodenum. The patient received inpatient post-operative care and was subsequently discharged home to the mother following recovery.