A 58-year-old woman presented at age 42 with syncope and blood glucose measuring <30 mg/dL. A 72-hour fast demonstrated blood glucose of 46 mg/dL, insulin of 50 mIU/mL (2.6–24.6), and C-peptide of 7.0 ng/mL (1.1–4.4). Her symptoms were managed with frequent small meals. CT showed a 2.4-cm lesion in the pancreas tail. MRI showed two metastatic lesions in the right hepatic lobe. She underwent distal pancreatectomy, splenectomy, and hepatic wedge resection, with radiofrequency ablation of liver metastases. Follow-up CT showed two new lesions in the liver and she underwent chemoembolization with resolution of her symptoms. Symptoms returned by age 48, with MRI showing new lesions throughout the liver (Fig. ). She was started octreotide 20 mg IM monthly, and her symptoms resolved soon afterward. Since then, she has had stable annual imaging via MRI and well-controlled symptoms.


A 48-year-old woman presented at age 37 with episodes of mental fog and paresthesia when exercising or skipping meals. Her serum fasting glucose was 36 mg/dL. The 72-hour fast was stopped early when she developed neuroglycopenic symptoms. Blood glucose was 43–46 mg/dL, with insulin of 10.0 μIU/mL (2.6–24.6), proinsulin of 56.8 pmol/L (0–18.8), and C-peptide of 1.5 mg/mL (1.1–4.4). CT, MRI, and endoscopic ultrasound did not localize a mass. 18F-DOPA-PET showed increased uptake in the head of pancreas, concerning for insulinoma, and increased activity in the tail. Exploratory laparotomy with intraoperative ultrasound and palpation of the pancreas did not localize a mass. A second surgery, with 75% removal of the distal pancreas, including tail and body, did not resolve her symptoms. Calcium-stimulated arteriography demonstrated 10-fold increase in the pancreas head. She tried several different medication regimens (Table ). Verapamil 80 mg TID (monotherapy), combination of verapamil 80 mg TID with diazoxide 50 mg TID, and octreotide 50 μg BID subcutaneously did not control her symptoms. Diazoxide 150 mg BID caused fluid retention and tachycardia; therefore, the dose was decreased to 100 mg BID and hydrochlorothiazide (HCTZ) was started, but symptoms persisted. She started prednisone, initially at 5 mg in the morning and 2.5 mg in the afternoon, continuing diazoxide and HCTZ. Her symptoms resolved and blood glucose normalized. She could exercise without symptoms, and blood glucose ranged from 60 to 80 mg/dL. By age 42, she self-decreased her prednisone dose to 2.5 mg daily while continuing diazoxide and HCTZ. She stopped checking her blood glucose and endorsed symptoms with increased activity, but believed they were manageable taking glucose tabs as needed.
At age 44, an MRI and nuclear medicine study in a clinical trial showed findings consistent with a 9-mm insulinoma in the pancreas head; however, exploratory surgery did not find a mass. Presently, she remains on prednisone 2.5 mg daily, diazoxide, and HCTZ. She adheres to a strict vegan diet, with frequent meals, endorsing only rare hypoglycemic symptoms. Surveillance anatomic/functional imaging studies remain stable with no identified lesion (Fig. ).


A 64-year-old male patient with unremarkable previous history was hospitalized for the investigation of persistent low-grade fever and malaise during the past month. Systemic inflammatory markers were elevated, but repeated blood and urine cultures were negative. The patient received different combinations of broad-spectrum antibiotics (including an antistaphylococcal regimen), without signs of clinical or laboratory improvement. No abnormal findings were detected on transesophageal echocardiography or chest and abdomen computed tomography (CT) imaging, and HIV testing was negative.
The patient was an immigrant originated from a country with TB incidence 18/100 000 and had a family history of tuberculosis (TB). He had been assessed 2 years ago, due to close household contact with an active pulmonary TB case. At that time chest X-ray was normal, and tuberculin skin test (TST) was negative.
At admission, a new TST test and an interferon-γ assay (IGRA) were both positive. Sixty minutes after intravenous injection of 268 MBq (7.2 mCi) of 18F-flurodeoxyglucose (18F-FDG), a whole-body PET/CT scan (18F-FDG PET/CT) was performed as part of the investigation for FUO which revealed diffusely elevated metabolic activity (Standardized Uptake Value, SUVmax 7.0) in T11 vertebra (, arrows). Since no other hypermetabolic foci were detected on the whole-body imaging (), the test was considered compatible with isolated vertebral osteomyelitis (VO). Interestingly enough the patient had never reported focal myoskeletal pain in the affected area and neurologic examination was normal.
As the patient denied confirmatory diagnosis by means of vertebral biopsy, empirical first-line anti-TB treatment (isoniazid, rifampicin, ethambutol and pyrazinamide) was initiated soon after the PET/CT imaging, leading to rapid decline of the fever and improvement of inflammatory markers. A follow-up 18F-FDG PET/CT with 280 MBq (7.6 mCi) of 18F-FDG which was performed after 6 months of anti-TB treatment was normal (), thus indirectly confirming the diagnosis of TB osteomyelitis. The patient received a total of 9 months of anti-TB treatment.


This was a case of a 53-year-old male patient who presented with major complaints of severe abdominal pain and approximately 100 pounds unintended weight loss, over the course of 3 months. Additional history taking revealed the presence of intermittent dyspnea and a productive cough over the same period. He also complained of subjective fevers and night sweats, but was afebrile at presentation. He was a former smoker with 20 pack years smoking history and denied any sick contacts at presentation. He had no history of joint pains, connective tissue, respiratory, or granulomatous disease.
On examination, he was in moderate distress, and his abdomen was tender to light palpation with decreased bowel sounds but without rigidity, guarding, or rebound tenderness. Respiratory examination revealed decreased air entry with poor inspiratory effort, crackles in bilateral lung lower lobes, and decreased tactile vocal fremitus in bilateral lower lung fields. The examination of other systems was noncontributory.
Blood tests revealed an elevated lipase at 220 U/L and an elevated aspartate aminotransferase at 88 U/L. There was no leukocytosis. Blood cultures, respiratory cultures, urinalysis and culture, serum Aspergillus antigen, HIV antibody, tuberculosis, syphilis, C3, C4, erythrocyte sedimentation rate, urine legionella antigen test, cyclic citrullinated peptide, rheumatoid factor, hepatitis A, hepatitis B, and hepatitis C antibodies all returned negative. Autoantibodies, including Anti-ds DNA, ANCA, Anti-JO-1, anti-SM, anti-SSA, anti-SSB, anti-SCL70, myeloperoxidase, and serine protease 3, were also all negative. Bronchoalveolar lavage and fungal cultures were also negative. Computed tomography (CT) of the abdomen revealed no evidence of bowel obstruction. CT of the thorax was performed, and the radiologic impression was suspicious for multifocal pneumonia or aspiration pneumonitis. With the constellation of his symptoms, signs, and radiologic findings, he was diagnosed with pancreatitis and pneumonia and was placed on bowel rest and broad-spectrum antibiotics. In light of his significant weight loss, an additional whole-body CT scan was performed but revealed no covert malignancy.
However, his hospital course quickly deteriorated, and he developed severe respiratory compromise. He was given hyperbaric oxygen, developed acute respiratory distress syndrome and required intubation. Despite optimal ventilator settings and pronation, his condition worsened, and he died after 10 days on admission.
The significant findings at autopsy were bilateral enlarged lungs with bibasilar pulmonary consolidations. Histologically [], sections from both lungs showed extensive interstitial fibrosis, with the presence of fibroblastic foci present in multiple lung lobes. There were areas of focal hyaline membranes and dense interstitial inflammatory infiltrates consisting of lymphocytes, neutrophils, and plasma cells. Prominent intra-alveolar macrophages and type 2 pneumocyte hyperplasia were also seen. There were focal areas of interalveolar and interstitial edema, with prominent pulmonary congestion. In addition, focal areas of honeycomb lung were seen in the left lower lobe, right upper lobe, and right lower lobe. However, there was no subpleural honeycombing.
In summary, the patient's primary cause of death was determined to be severe respiratory failure secondary to a mixed IIP pattern of diffuse alveolar damage (DAD), superimposed on extensive interstitial fibrosis, with features of honeycombing, consistent with advanced interstitial/end-stage lung disease.


A 26-day-old girl presented to our department with persistent vomiting, which started initially as non-bilious and became bilious in the previous 2 days. She was delivered via caesarean section at 33 weeks of gestation to nonconsanguineous parents and her birth weight was 2.25 kg. Her parents reported that they sought medical advice 2 weeks previously because of the persistent non-bilious vomiting and received supportive treatment, but it was not successful. On examination, she showed signs of dehydration and failure to thrive, and weighed only 1.6 kg. The abdomen was distended and non-tender.
An upper gastrointestinal series showed a hugely dilated stomach with secondary reflux up to the level of the cervical oesophagus and malrotation, where the duodenojejunal flexure was positioned in the right midabdomen (). After resuscitation, the patient was prepared for surgery.
Exploration confirmed malrotation, and consequently, she underwent Ladd’s procedure. The small bowel length was 40 cm from the pylorus to the ileocecal junction (). The length of the small bowel was assessed from the pylorus because the duodenojejunal junction was not clearly identifiable after kocherisation of the duodenum. After 3 months of follow-up, the patient had a small increase in weight (approximately 120 g) and still suffers from infrequent attacks of non-bilious vomiting every several days. She is currently receiving enteral feeding via a gastric tube, which started at a low concentration and increased to 0.67 kcal/mL. However, the patient is still dependent on parenteral nutrition.


This study was approved by the Ethics Committee of The Second Xiangya Hospital of Central
South University, and the patient provided consent to publish this case report.
A 43-year-old woman with bilateral nanophthalmos was referred to our clinic because of
decreasing visual acuity (VA) and shadow in her right eye that had persisted for one month.
Family history revealed that, among their relatives, only the patient and her brother had
nanophthalmos.
Clinical examination of the patient showed that VA was limited to counting fingers (CF)/10
cm in the right eye. Both eyes were deeply set in the orbits, with narrow palpebral fissures
and corneal diameters of 11.2–11.4 mm. Examination with IOL Master 500 (Carl Zeiss Co.,
Ltd., Shanghai, China) revealed an axial length of 15.34 mm in the right eye and 15.15 mm in
the left eye. Fundus examination revealed the presence of smooth, bullous retinal
detachments (); tortuous
retinal vessels and fine macular folds were also observed. A diagnosis of nanophthalmos with
ERD was made, and the patient was treated with 80 mg prednisolone once-daily for 1 week;
however, the ERD persisted. Therefore, we performed one-half thickness sclerectomy with
central sclerostomy in each quadrant of the right eye (), as described in a prior report. At the 1.5-month follow-up, the retina was completely reattached (), and VA in the right eye had
improved to 1/50. The patient’s VA remained stable, and there was no evidence of UES during
a three-year follow-up period.
Subsequently, the patient experienced reduced VA for 10 days, and returned to our clinic
for treatment. ERD was observed, and VA in the right eye was again limited to CF (). Because of the risks of
surgery, the patient refused additional procedures; considering that steroid therapy was
ineffective, we selected minimal treatment of topical nonsteroidal anti-inflammatory drugs
(NSAIDs) and observation. Surprisingly, fundus photography examination showed that the
retina had partially reattached within 7 days. Thus, we chose to observe the patient’s
progress without additional treatment. At the 1-month follow-up, the retina had completely
reattached and VA had recovered to 1/30; notably, VA remained stable throughout a 3-month
follow-up period ().


A 76-year-old woman was undergoing a routine follow-up outpatient visit after surgery. She had no complaint and routine computed tomography (CT) revealed an abdominal mass.
Two years prior to the routine outpatient visit, the patient had been admitted to our hospital complaining of melena. Upper gastrointestinal endoscopy revealed a submucosal tumor (SMT) with ulceration located at the greater curvature of the gastric body. CT revealed inhomogeneous density and an extramural mass measuring 4.5 cm. She underwent laparoscopic local resection of the gastric SMT with a non-touch lesion-lifting method called CLEAN-NET. Immunohistochemical examination showed c-kit- and CD34-positive cells. The tumor was 4.5 cm × 4.0 cm in size, and the mitotic count was under 5 mitoses per 50 high-power fields (HPF). The patient was diagnosed with gastric GIST with intermediate recurrence risk. Therefore, adjuvant imatinib therapy was not administered. After surgery, she underwent regular outpatient visits and routine periodic examinations. Two years after the operation, periodic CT revealed an abdominal mass.
The patient’s medical history included hypertension for more than 5 years.
The patient had no subjective symptoms, such as abdominal pain or bloating. Physical examination revealed normal abdominal findings, and the intra-abdominal mass could not be palpated.
A laboratory examination showed a decreased level of hemoglobin (Hb = 11.5 g/dL). Blood tests for liver and kidney function and electrolyte levels showed results within the normal range.
CT revealed an abdominal mass between the dorsal side of the right hepatic lobe and the right kidney (Figure ). The tumor size was 12 mm with uniform enhancement. CT did not show any other intraperitoneal masses or ascites. Diffusion-weighted magnetic resonance imaging (MRI) showed a tumor with high signal intensity with uniform contrast (Figure ). Positron emission tomography/CT (PET/CT) showed the accumulation of fluorine-18 2-deoxy-2-fluoro-D-glucose (FDG) in the tumor, with a standardized uptake value of 5.5; no other definitive intra-abdominal lesions were noted (Figure ). Other imaging tests did not reveal any additional abnormalities.
Based on the clinical course, we suspected a solitary recurrence of gastric GIST but could not distinguish whether the source of the suspected metastases was from the liver or retroperitoneum.


A 22-year-old man was admitted to our emergency department following a road traffic accident and presented with a slight cough and a small amount of bloody sputum. Approximately 37 h after admission, he developed severe chest tightness, chest pain, dizziness and haemoptysis. His was 178 cm in height and 82 kg in weight.
The patient experienced multiple traumas when his motorcycle collided with a truck. On admission to our emergency department, he was conscious and had a slight cough and a small amount of bloody sputum. His blood pressure and breathing were stable, with an oxygen saturation (SpO2) of 95%-97% at 5 L/min of mask O2. Whole-body computed tomography (CT) showed a left fifth rib fracture and mild PC (Figure ) as well as fractures to the left clavicle and scapula, pubis, left femoral shaft and right ulna. After plaster fixation of his right upper arm, he was admitted 18 h after the onset of mild PC to the orthopaedic ward for further surgical treatment. There he received an analgesic, antibiotics and left tibial tuberosity traction treatment. However, he developed severe chest tightness, chest pain, dizziness and haemoptysis 19 h later. Clinical examination revealed severe hypoxia with an SpO2 of 68%, tachypnoea (respiratory rate: 36 breaths/min) and tachycardia (heart rate: 157 bpm). Endotracheal intubation was subsequently performed, and a large amount of bloody sputum was suctioned from the endotracheal tube. The patient was transferred to the intensive care unit (ICU) 15 min later.
The patient was free of relevant medical history.
When transferred to the ICU, the patient received volume-controlled ventilation and the following parameters were set: Fraction of inspired oxygen, 100%; positive end-expiratory pressure, 15 cm H2O; tidal volume, 420 mL (6 mL/kg); and respiratory rate, 20 breaths/min. The patient was maintained under deep sedation (Richmond Agitation-Sedation Scale: -3 to -4) to reduce respiratory distress, and a lung recruitment manoeuvre was performed to open his airways. Nevertheless, he developed refractory hypoxemia (SpO2: 78%) and hypotension (invasive blood pressure: 10.5/5.5 kPa). Physical examination revealed coarse, moist rales that pervaded the lung. No apparent abnormalities were found in the heart or abdomen. Both legs were deformed and swollen, and multiple skin abrasions were observed all over his body.
Arterial blood gas analysis revealed a pH of 7.44, partial pressure of CO2 of 5.2 kPa and partial pressure of O2 of 7.9 kPa. Routine blood examination indicated mild leucocytosis (15.3 × 109 cells/L) and a reduction in haemoglobin (from 12.3 g/dL at admission to 10.3 g/dL after transfer to the ICU). Coagulation function test results showed a normal prothrombin time, activated partial thromboplastin time and thrombin time; however, his fibrinogen level was low (1.4 g/L). Biochemical examination revealed a glutamate transaminase level of 74.2 U/L and glutamate transaminase level of 44.9 U/L, indicating slightly abnormal liver function.
Bedside chest X-ray showed diffuse infiltration on both sides (Figure ). After ECMO was established, chest CT and pulmonary artery imaging were performed, at which point there was no evidence of a pulmonary embolism, but substantial consolidation was noted in both lungs (Figure ). Fibreoptic bronchoscopy revealed diffuse and profuse blood in all bronchopulmonary segments and fresh bleeding was observed in the trachea and right bronchus.


A 41-year-old male came to the hospital for fatigue, satiety and abdominal distension in March 2018. Palpation revealed that the lower edge of his spleen reached the umbilicus level. His chest computed tomography (CT) scan showed no abnormality. Bone marrow biopsy showed remarkably increased age-adjusted cellularity with granulocyte proliferation, decreased erythropoiesis, a large number of megakaryocytes atypia, grade 0 fibrosis, and the JAK2V617F mutation. He was diagnosed with Pre-PMF. His Dynamic International Prognostic Scoring System (DIPSS) risk group was intermediate-1. He was started on rux (20 mg, twice daily).
Fever and productive cough started in early July and lasted approximately one week. He was hospitalized on 12th July for antibiotics. Laboratory tests showed white blood cells (WBC) 16.11×109/L, erythrocyte sedimentation rate (ESR) 40 mm/h, hypersensitive C-reactive protein 107.7 mg/L, and procalcitonin (PCT) 0.76 µg/L. Blood lymphocyte subsets showed an absolute total T cell count of 347/μL (normal range: 995–2860/μL) and CD4+ T cell count of 208/μL (normal range: 550–1440/μL). Sputum acid-fast bacilli (AFB) smears were negative, but interferon gamma release assay (IGRA, T-SPOT.TB) was positive. Transient syncope unexpectedly occurred the next morning. Multiple deep venous thrombosis was later confirmed by ultrasound in his left lower extremity. Enhanced CT showed pulmonary thromboembolism in his right upper and inferior pulmonary artery, bilateral pleural effusion, pulmonary infection, multiple enlarged mediastinal lymph nodes and soft tissue shadows that surrounded his left main bronchus ( and ). CT also revealed frontal lobe hemorrhage. He received low molecular weight heparin instantly, and rux was discontinued from then on. To prevent the occurrence of lethal complications, he was transferred to vascular surgery for inferior vena cava filter implantation. A bronchoesophageal fistula on his left main bronchus was later discovered by iodine contrast esophagogram in response to persistent dry cough, and then he received nasal jejunal nutrition ().
Hydroxyurea was introduced to control the WBC count in September. Given that infection work-up was negative, fiberoptic bronchoscopy was chosen to determine whether he was infected with TB. However, bronchoalveolar lavage fluid (BALF) specimens tested negative for culture, AFB and GeneXpert assay. A tracheobronchial lymph node biopsy finally confirmed Mycobacterium tuberculosis (MTB) by polymerase chain reaction. He was diagnosed with tracheobronchial tuberculosis (TBTB) and received a 12-month antituberculosis therapy (ATT) involving isoniazid, rifampicin, ethambutol and levofloxacin. Another two bronchoalveolar lavages were performed during ATT. BALF was negative for all relevant results, including mycobacterial ribonucleic acid (RNA) and deoxyribonucleic acid (DNA). The mediastinal lymph nodes’ size also decreased (). In July 2019, rux (10 mg, twice daily) was reintroduced due to splenomegaly and abdominal distension. His DIPSS was intermediate-1 at that time.


A 66-year-old male was diagnosed with PMF in December 2010 at a local hospital. Bone marrow biopsy showed megakaryocytic proliferation, grade 3 fibrosis and the JAK2V617F mutation. Because rux was not available in China at that time, he received regular interferon therapy for 7.5 years. To mitigate the progression of splenomegaly, rux (20 mg, twice daily) monotherapy started in late June 2018. The DIPSS risk group was intermediate-2. The single dose was adjusted to 25 mg in early August owing to an unsatisfactory reduction in spleen size.
Unexplained fever started on 20th August and lasted until September (Tmax 39.2°C). Laboratory tests showed WBC 14.14×109/L, hemoglobin 78 g/L, platelet 198×109/L, PCT 0.65 μg/L, and ESR 60 mm/h. Blood samples were positive for T-SPOT.TB and TB antibody. His purified protein derivative (PPD) test was strongly positive. Chest CT scan presented small diffuse nodules in the bilateral lungs, pleural effusion, adhesion, and enlarged lymph nodes in the retroperitoneum. He was diagnosed with disseminated TB (DTB).
His temperature gradually stabilized when 12 months of ATT (isoniazid, levofloxacin, rifapentine and amikacin) started in October 2018. Considering the potential progression of PMF, rux (20 mg, twice daily) was retained under close monitoring of liver function. Nevertheless, accompanied by the reappearance of fever, his left hip joint began to hurt, and a neck mass was found by palpation on the same side. Imageology examinations confirmed the existence of neck and bilateral psoas abscesses and Schmorl’s nodes at L4 and L5 (). During debridement, a 3×15.6×2.8 cm focus on the left, a 3×10×2 cm focus on the right, and a 4×3 cm focus of the neck were found. All three contained yellow pus and caseous necrosis, in which the DNA and RNA of MTB were detected as positive. Amikacin was replaced by ethambutol in November.


A 43-year-old male presented for more than 2 years of left-sided C8 root symptoms/ signs following an avulsion injury sustained due to a motor vehicle accident (MVA). He developed a CRPS type II lesion, treated with venlafaxine, lisdexamfetamine, quetiapine, cyclobenzaprine, and lidocaine patches, multiple cervical interlaminar epidural injections, and physical therapy; none of which resulted in significant improvement. On physical examination, he had left upper extremity 3/5–4/5 motor deficits in the C6–C8 distributions, intolerable C8 dysesthesias, and tactile allodynia. He also had a 2.3° reduced temperature regionally in the left arm compared to the right arm.
The MRI demonstrated abnormal signals ventral to the C8–T1 level consistent with an avulsed C8 nerve root. Electrodiagnostic tests including electromyography revealed sensory and motor conduction abnormalities for pre- and postganglionic involvement of the C8 distribution.
The patient met the Budapest Clinical Diagnostic Criteria for CRPS type II. The patient received an initial left-sided, ultrasound-guided stellate ganglion block 30 months after the avulsion injury; it resulted in 50% pain relief. He underwent a series of five additional SGBs performed 2–3 weeks apart, ultimately experiencing 75% improvement in pain and strength []. Six years later, the patient continues to have significant pain relief with SBGs performed 4 times/year.


A 39-year-old male from the state of Assam, India, presented with intermittent fever for 3 months associated with generalized weakness due to which he was bedbound for 2 months with a history of passing high colored urine. He was on regular medications for diabetes mellitus for 6 years. He was treated as a case of septic arthritis elsewhere.
On examination, he was febrile (body temperature = 102° F), icteric, dehydrated, hypotensive (blood pressure: 90/70 mmHg), tachypneic (respiratory rate: 50 cycles/min), and had tachycardia (heart rate: 128/min). On auscultation, crackles were heard on both sides. The spleen was mildly enlarged (4 cm below the costal margin) with no evidence of free fluid in the abdomen. No neurological abnormality was noted. On local examination, he had multiple skin lesions over the right forearm [] and a Grade 3 bedsore in the left gluteal region.
Blood investigations showed pancytopenia and elevated C-reactive protein levels. Diagnostic workup for vasculitis was negative. Ultrasound study of the abdomen showed mild ascites with bilateral pleural effusion and splenomegaly. Laboratory investigations are listed in . Chest X-ray [] showed multiple lobulated pleural-based opacities along the left lateral pleura projecting into lung parenchyma, i.e., into left hemithorax and a similar smaller lesion along the right lateral pleura.
Whole-body 18-fluorine-fluorodeoxyglucose positron emission tomography–computed tomography (18F-FDG PET-CT) scan was performed, which showed 18F-FDG-avid multiple destructive lytic lesions with soft-tissue component and necrosis involving the entire axial and appendicular skeleton, bilateral pulmonary nodules, and hepatosplenomegaly with no focal FDG uptake [Figures -].
Blood culture and sensitivity workup showed the growth of B. pseudomallei [].


A 46-year-old male from the Andaman and Nicobar Islands, India, presented with high-grade fever for 4 months associated with burning micturition and increased frequency of urination. The patient had a history of diabetes for 14 years.
On examination, he was febrile (body temperature: 104° F), normotensive, and had tachycardia (heart rate: 132/min). Normal vesicular breath sounds were heard. Per abdomen examination was normal. No cardiovascular or neurological abnormality was noted.
Fusion PET/CT imaging was performed, which showed bulky left kidney with ill-defined collections [] and para-aortic, interaortocaval, and retrocaval nodes.
Following the 18F-FDG PET-CT, ultrasound-guided renal abscess aspiration was performed that was sent for culture and sensitivity. VITEK 2 method revealed B. pseudomallei on culture.


A 28-year-old woman presented with secondary infertility despite regular sexual life after the previous CS done 6 years ago.
Her day 3 hormonal profile and her husband's semen analysis were completely normal, while the hysterosalpingography showed left tubal obstruction. The transvaginal ultrasound showed an irregular intrauterine lesion closed to the scar of the previous CS, most probably endometrial polyp or intrauterine foreign body (FB) because of its irregularity.
The preoperative investigation of the studied woman including blood picture, liver and renal function tests, and coagulation profile was normal. In addition, the markers of infection and the high vaginal swab for the common sexually transmitted diseases as gonorrhea and chlamydia were negative.
Departmental decision was taken to proceed for postmenstrual combined hysteroscopic and laparoscopic assessment after patient's counseling and written consent.
Combined hysteroscopy and laparoscopy showed intrauterine sutures attached to the scar of the previous CS [Figures and ] and omental adhesions attached to the anterior abdominal wall with obstructed Fallopian left tube (negative dye test).
The intrauterine sutures were incised and released from its attachment to the uterine wall using the hysteroscopic scissors under direct laparoscopic vision [], followed by laparoscopic adhesiolysis for the omental adhesions and left salpingostomy for the obstructed left Fallopian tube. The patient had a smooth uneventful postoperative period and was discharged from the hospital on the 4th postoperative day for follow-up in the infertility specialized outpatient's department.
The studied woman was enrolled in the ovulation induction (OI) protocol for 3 months, and she is currently on OI protocol and intrauterine insemination (IUI) for another 3 months. According to the departmental protocol, the studied woman was enrolled in vitro fertilization and embryo transfer program if the OI and IUI failed to achieve pregnancy at the end of the 6th month.
A departmental ethical committee approval (IRB No. OBGYN_REC_19.04.02) and written consent were obtained from the studied woman to use her data for scientific education and publication as a case report.


A 30-year-old P0 + L0 female presented with severe dysmenorrhea and pressure symptoms. She was a known case of multiple uterine myomas and endometriosis for which she had already tried medical management with no significant improvement in symptoms. She was also anxious for conception. She was also hypothyroid and morbidly obese (BMI 42 kg/M2, Class III Obesity). On clinical evaluation, her uterus was irregularly enlarged to 22 weeks gestation uterine size. The cervix was pulled up and could not be visualized. On preoperative magnetic resonance imaging (MRI), the myomas were noted to be on the anterior, fundal, posterior, and lateral uterine walls, measuring 12 cm (Type 4), 10 cm (Type 5), 6 cm (Type 6), and 5 cm (Type 7), respectively (as per the International Federation of Gynecology and Obstetrics classification system).[] The two largest ones were intramural and the small ones were subserous in location. The 12 cm myoma was multilobulated and had undergone degeneration and was extending from the uterine fundus to isthmus. The myomas were also causing mass effect on the endometrial cavity [-MRI images]. She also had a 5 cm endometriotic cyst in one ovary.
After preoperative workup, she was counseled and consented for robotic myomectomy. This was done using the DaVinci Xi surgical system (Intuitive Surgical, CA, USA). Four ports for each of the robotic arms plus an assistant 12 mm Excel port were used. Port placement was standard as for DaVinci Xi docking for pelvic surgery, keeping the camera port 4 cm above the umbilicus to gain maximum working distance and port R1, R2, and R3 in a horizontal line 9 cm apart []. Robotic instruments used were Monopolar Curved Scissors, Fenestrated Bipolar Grasper, Mega Needle Driver, and Robotic Tenaculum (Intuitive Surgical, Inc., Sunnyvale, CA). Assistant port was used for vasopressin injection, needle pass, suction, and morcellation. No other traditional laparoscopic instruments were utilized. Before docking, vaginoscopic hysteroscopy was done. The cavity was distorted due to the large bulk of fibroids, and vaginal manipulation was also not possible due to the same reason.
After docking, intrapelvic adhesions (omental adhesions on the surface of myomas) as seen in were lysed. Myomas were enucleated after injecting vasopressin 0.4 U/ml in the capsule of each intramural myoma (Type 4 and Type 5). The Type 5 fundal myoma was first enucleated using an elliptical incision which was given at its base. The same incision was extended horizontally to enucleate the type 4 anterior myoma which was extending up to the uterine isthmus and was multilobulated and degenerated. After defining the cleavage plane between the myoma and uterine wall, dissection was accomplished with sparing use of cautery (which was used mainly at the base of the myoma) and pushing the myoma bed down and away rather than excessive traction on the myoma. As vaginal manipulation was not feasible due to severe cavity distortion, the robotic tenaculum was preferred, which had the advantage of lifting the myoma from various angles due to 360° range of motion (ROM) and ability to be used through any of the robotic ports as required, which would have been difficult with the conventional laparoscopic tenaculum. Lack of haptic feedback in robotic surgery did not affect the enucleation of the myomas as visual clues during surgery, and good preoperative MRI helped to map the fibroids accurately. The Type 6 and Type 7 myomas were pedunculated and were cut at the base using a combination of bipolar and monopolar energy.
Myoma bed and uterine surface were approximated with V-loc Absorbable Wound Closure Device1-0 (Covidien, UK) in 2–3 layers depending on the depth of incision. Blood loss was minimal as evidenced by the drop in post-operative Hb of only 0.1 g/dL. Endometrial cavity integrity was not breached, and the uterus was reconstructed successfully []. This was covered by an adhesion prevention barrier. She also had Grade III endometriosis that was tackled in the same sitting. Bilateral ovaries were adherent to each other and posterior uterine wall. Endometriotic cyst in the left ovary (4 cm × 5 cm) was drained and its base fulgurated. Endometriotic spots on the surface of the right ovary were fulgurated. The pouch of Douglas was partially obliterated by adhesions, which was also lysed to give her as normal a pelvic anatomy as possible. The myomas were removed after morcellation (in-bag) and weighed total 745 g []. Console time was 160 min (including suture of myoma bed and uterine reconstruction which took 40 min). The total anesthetic time was 320 min (which included patient positioning, docking, and morcellation). Morcellating the large myomas took the most of the other 160 min (nearly 100 min), docking took 10 min, positioning around 20 min, and anesthesia around 30 min. The patient made an uneventful recovery in the postoperative period and resumed normal diet and activity the next day. The final histopathology showed leiomyomata with varying degrees of degeneration. In the postoperative period, Gonadotrophin releasing hormone (GnRH) analog was given to suppress menses for one cycle, followed by ovulation induction. Both short-and longterm recovery were uneventful.


A 29-year-old female (gravida 2, para 0, abortion 2) had a history of polycystic ovary syndrome with irregular medication control presented to our outpatient department due to lower abdominal pain. No dizziness or sweating was noted. Per vaginal examination revealed a mass in the left adnexal area. Transvaginal ultrasound revealed a heterogeneous, septated mass over the left adnexa with approximate dimensions of 7.3 cm × 6.1 cm []. Laboratory data showed unremarkable results. The tumor marker CA19-9 was elevated (65.77 IU/mL); carcinoembryonic antigen and CA125 were not elevated (1.0 ng/mL and 9.1 IU/mL). An abdominal computed tomography (CT) scan showed a left pelvic mass with heterogeneous content []. Lymphadenopathy or splenomegaly was not noted. Ovarian germ cell tumor wasfirst suspected.
Due to the possibility of ovarian germ cell malignancy, laparoscopic surgery with left salpingo-oophorectomy (LSO) wasfirst planned and performed []. We made one single port (one 11 mm and one 5 mm trocars inserted into two fingers of the glove) and two accessory ports with a 5 mm trocar at the bilateral abdominal region. We did LSO by Ligasure electrocauterization. The left adnexa was then safely placed into the tissue bag. Then, we removed the tissue bag through a single port and did contained-morcellation in the bag.[] Frozen section of the tumor reported dysgerminoma. Then, we continued staging surgery through bilateral pelvic lymph node dissection, para-aortic lymph node dissection, omentectomy, right ovary biopsy, peritoneal random biopsy over bilateral gutters and pelvic cavity, and washing cytology.
A frozen section of the ovarian tumor wasfirst requested intraoperatively. A left ovarian tumor of approximately 8 cm in diameter with an irregular shape was noted. Grossly, the tissue was elastic and yellowish. Extensive necrosis and several viable hypercellular regions were noted. The surgeon thought the tumor may be a dysgerminoma. The pathologist confirmed the diagnosis of dysgerminoma according to the histology showed large open nuclei and fibroconnective tissue septa among the tissue.
At permanent sections, microscopically, the left ovary showed numerous malignant large lymphoid cells [], positive for CD20 (a B-cell marker) [] and a CD3 T-cell-rich background [], revealing a T-cell/histiocyte-rich large B-cell (THRLBCL) lymphoma with an activated B-cell subtype. The left fallopian tube, right ovary, left pelvic lymph nodes, and right pelvic lymph nodes were negative for malignancy. The para-aortic lymph nodes were also positive for lymphoma. The omentum showed one calcifying nodule. Other immunohistochemical staining showed that the tumor cells were positive staining for CD5, ki67 (>90%), BCL-6 (15%), and MUM-1 (50%) [] and negative for c-kit, CD10, cyclin D1, SOX-11, and CD30.
The patient was then indicated for oocyte preservation and referred to hematology for further chemotherapy.


A 15-year-old woman presented with head deformity 10 days after bilateral otoplasty under local anesthesia. She presented with a painful torticollis; the head was rotated to the right and tilted to the left side. Computed tomography (CT) showed NTARS [].
Reduction was achieved under anesthesia by transoral palpation of the dislocated C1 articular facet associated with manual head traction, followed by cervical halter traction. The anatomical relationship of C1–C2 was confirmed by CT [].
Two recurrence of the dislocation was observed after two attempts of closed reduction under anesthesia followed by cervical traction and hard collar immobilization. Open reduction and posterior atlantoaxial fixation with C1–C2 sublaminar wire and autologous iliac bone graft was performed, followed by hard cervical collar immobilization for 3 months [].
There was neither intraoperative nor postoperative complication. The patient remained neurologically intact, radiographic evidence of bone fusion was observed after 1 year follow-up, and the patient returned to normal activities [].


A 57-year-old right-handed female, with no significant past medical conditions presented with a 1-year history of progressively worsening weakness and reducing function of her left hand. This was associated with muscle wasting, which she noticed when she felt increasing difficulty to grip on objects resulting in frequent dropping of things from her hand. She eventually developed weakness to even lift up her fingers. She had denied any similar complaints in her other hand as well as bilateral lower limbs. She indicates that she has occasional neck pain since the last 1 year. However, she denied any history of cervical or head trauma, imbalance, falls, no right-sided or lower extremity symptoms, and bladder or bowel difficulties. She was referred to us for further evaluation as her treating physicians were concerned about amyotrophic lateral sclerosis (ALS).
On examination, left upper extremity strength was 5/5 except, hand grip was 2/5, finger adduction and abduction were 2/5 and dorsiflexion of the wrist and fingers were 2/5. Fasciculations, mild atrophy of the forearm and atrophy of the intrinsic hand muscles as well as both thenar and hypothenar muscles (with no evidence of split hand sign). Strength was 5/5 throughout the right upper and lower extremities, and the left lower extremities. Reflexes were 3+/4 in biceps, triceps, and brachioradialis bilaterally; and 3+/4 in bilateral knees and ankles. Hoffman and Babinski signs were present bilaterally. Sensory modalities such as pinprick, vibration and tactile sensation is equal and intact in both arms and legs.
Left upper extremity motor NCS (nerve conduction study) shows very mild prolonged distal motor latency (<120% upper limit of normal), significantly reduced median and radial nerve CMAP (compound muscle action potential) and borderline slow conduction velocity. Evoked response is absent in the left ulnar nerve. Motor nerve conduction studies of the right median, ulnar, fibular, and tibial nerves were found to have normal distal motor latency, evoked response amplitude and conduction velocity. Sensory evoked response is with normal limits in both arms but there was significant reduction of amplitude in medial and lateral antebrachial cutaneous nerve on the left hand. Electromyogram (EMG) was performed which revealed an active denervation in left first dorsal interosseous, abductor pollicis brevis, flexor digitorum profundus, and extensor indicis proprius. MUAP (motor unit potentials) could not be assessed due to lack of activation in these muscles. EMG of all other muscles tested in bilateral legs and right arm show no abnormal spontaneous activity, normal duration MUAPs and full or reduced recruitment on maximal or submaximal stimulus. Electrodiagnostic studies revealed medial and lower trunk left brachial plexopathy but did not show any evidence of motor neuron disease, generalized large fiber neuropathy. Magnetic resonance imaging (MRI) of the C-spine revealed severe kyphoscoliosis with spinal canal and neuroforaminal stenosis worse at C7-T1 levels, with a diffuse T2 hyperintensity extending from C5-T1 levels, and enhancement of the anterior nerve roots (Fig. ). MRI of the brachial plexus was found to be normal.
The patient underwent a combined anterior-posterior decompression, and instrumented fusion with cervical spine reconstruction was performed. Her post-operative recovery was uneventful. On 6-month follow-up, examination showed improvement in muscle bulk hand, muscle strength had improved to left wrist extension (4/5), hand grip (3/5), and finger abduction/abduction (3/5).


A 53-year-old gentleman presented with persistent headache in the past 2 years. He had previously hypertension history, was treated permantly by calcium blocker, without history of vision blur and seizure. He came to the Neurosurgery Department because of increasing headache and short-term seizure. Brain magnetic resonance imaging (MRI) showed a large AVM at right brain lobular, maximum diameter of the AVM nidus was 6.48 cm (Fig. ). In digital subtraction angiography (DSA), there were many large and high-flow supplying arteries (the largest was the right internal carotid artery) (Fig. ). The diagnosis was inoperative large AVM, Spetzler-Martin grade V, inappropriate for embolization. We decided to use VS-SRS with an interval time of 3–6 months. The AVM had been divided into two halves (anterior and posterior) based on the posterior edge of anterior clinoid as landmark. Dose to anterior half was 15 Gy and posterior half was 15 Gy after calculated doses for coverage and organs at risk. Planning target volumes were defined as GTV +2 mm (Fig. ). Simulation was performed by using specific radiosurgery thermomask. Computed tomography simulation and MRI were recorded by 1-mm slice thickness; plans were calculated by dosimetrists and software Monaco 5.1. MRIs and DSA were taken before treatment, between 2 stages, and 3, 6, 12, 18 months after the second stage. Follow-up time was 24 months at the time of report.
First fraction (first stage) was on September 28, 2017, with 15 Gy delivered to the anterior half of the whole AVM. Coverage was >95% prescriptive dose to 100% of volume, maximum dose was 1,847 cGy (<140% prescriptive dose) (Fig. ).
Forty-eight hours after the first fraction, he felt mild headache, without seizure or dizziness, and the symptom disappeared after 24 h treated by steroid (dexamethasone 8 mg b.i.d.).
After 4 months, he came for continous treatment. MRI before the second stage showed reduction of whole AVM toward treated half by 20% (Fig. ). We decided to make some modifications: alleated borderline between two halves anteriorly (toward treated half) by 2 mm, and decreased dose for second stage at posterior half to 13 Gy, to assure protection to organs at risk (chiasm, right optic nerve).
The second stage was performed on February 26, 2018 (5 months apart).


A 64-year-old, Asian male presented to the Department of Respiratory Medicine at our hospital (a tertiary care hospital) on May 16, 2020 for cough and sputum with dyspnea for six months. Before the patient’s visit, he had gradually aggravated dyspnea and presented chest tightness, chest pain, shortness of breath, edema of lower limbs and other symptoms, which had affected his daily life. However, he did not go to the local hospital for treatment. The patient reported a 5-year history of hypertension, up to 220/180mmHg, self-administered antihypertensive medication, and self-reported blood pressure control acceptable. He also had a 5-year history of previous cerebral infarction. No other history of disease has been reported. Physical examination showed a temperature of 36.4 C, apulse of 119 beats/min, a breath of 20 beats/min, and ablood pressure of 153/129mmHg. Sporadic wet rales can be heard in both lungs, no obvious abnormal heart sounds in the heart, and multiple enlarged lymph nodes can be touched in the neck, axilla and inguinal regions. The results of chest computed tomography (CT) (Day −2) with our hospital showed ( and ): right interlobar fissure, reticular nodular, diffuse thickening; right pleural effusion with partial package, scattered inflammation in the middle and lower lobes of the right lung with local external pressure atelectasis, scattered alveoli in both lungs; diffuse small nodular high density shadow in both lungs; plain strip shadow in the lower lingual segment of the upper lobe of the left lung. Laboratory examination results after admission: white blood cell 4.6 x 109/L, neutrophil% 88.0%, lymphocyte 0.19 x 109/L, eosinophils 0.00 x 109/L, procalcitonin 0.27ng/mL, N-terminal probrain natriuretic peptide (NT-proBNP) 295.00 pg/mL, D-dimer (D-D) 3.42 µg/mL, total protein (TP) 55.03 g/L, albumin (ALB) 27.81 g/L, no bacterial growth in blood culture (liquid culture), sputum culture (solid culture) for Streptococcus viridis (upper respiratory tract colonization bacteria). The detection of antibodies against Mycoplasma pneumoniae and Chlamydia pneumoniae showed that Chlamydia pneumoniae immunoglobulin G (IgG) 130.0 AU/mL, the rest of the antibodies were within the normal range, the respiratory pathogen spectrum antibody immunoglobulin M (IgM) test was negative, and the rest of the blood collection results were basically normal or abnormal results had no obvious clinical significance. Thoracic color Doppler ultrasound showed a 6.2cm dark fluid area in the right thoracic cavity, and cardiac ultrasound results showed aortic sclerosis, normal left ventricular systolic function measurements, and tachycardia. Based on the current findings, the patient was initially diagnosed with 1) right pneumonia, 2) right pleural effusion, 3) double pulmonary bullae, 4) hypertension. After initial diagnosis, the patient was given symptomatic and supportive treatment such as anti-infection, anti-inflammation, cough relief and phlegm elimination, blood pressure lowering and diuresis.
Refer to the diagnosis process of adult unilateral pleural effusion diagnosis guide, we consider further clarifying the etiology of pleural effusion in this patient, and performing puncture and drainage of right pleural effusion and submitting it for examination. The test results () classify the nature of pleural effusion according to Light criteria, and finally determine the exudative pleural effusion. Thereafter, relevant examinations were further improved to clarify the cause of exudative pleural effusion in this patient. Among them, immune-related tests: the results of anti-nuclear antibody series (17items) were negative, the results of anti-neutrophil cytoplasmic antibody (ANCA) series were negative, the results of anti-cyclic citrullinated peptide (CCP) antibody were 19.43 RU/mL, the results of immunoglobulin + complement + rheumatism suggested that complement C3 0.73 g/L, C-reactive protein 186.34 mg/L, all kinds of immune serological indicators were basically normal, only the slight decrease of complement C3, while the significant increase of C-reactive protein was considered to be associated with pulmonary inflammation, so it was not considered as immune-related pleural effusion. Fungi-related detection: serum galactomannan test (galactomannan) < 0.25, 1.3-beta-D glucan test 53.14 pg/mL (reference result: < 70 pg/mL indicates a lower risk of infection, 70–90 pg/mL is recommended for continuous monitoring, and > 95 pg/mL is highly suspicious of infection), and pleural effusion related to fungal infection was not considered according to the test results. Thyroid function test: among the five items of thyroid function, only triiodothyronine T3 was slightly reduced by 0.95 nmol/L, and the rest had no abnormalities, so pleural effusion caused by thyroid function changes was not considered. However, the interferon-γ release assay (T-SPOT) of tuberculosis infection was negative (-), and the multi-tumor markers were generally normal (among which the neuron-specific enolase was only slightly elevated, without reference significance). The two most common causes of pleural effusion are tuberculosis and tumors. Although current tests for tuberculosis and tumors were negative, the possibility of tumors or tuberculosis could not be ruled out. Therefore, further detection methods were needed to clarify the etiology of pleural effusion.
Unfortunately, on the 8th day of admission, the patient’s sudden dyspnea worsened, and NT-proBNP 2990 pg/mL and D-D 3.42 µg/mL were reexamined. The patient was transferred to intensify care unit (ICU) for treatment. After that, no venous thrombosis was found by venous ultrasound of lower limbs, no pulmonary embolism was found by computed tomography angiography (CTA) of the chest. Chest CT (Day 10) showed ( and ): decreased right pleural effusion, increased left pleural effusion, increased diffuse patchy and grid lesions of both lungs (considering the possibility of pulmonary edema combined with inflammation). Based on the above findings, we excluded the aggravation of acute dyspnea caused by pulmonary embolism. Considering that this aggravation may be due to acute heart failure and pulmonary edema induced by pulmonary infection, the symptomatic symptoms of dyspnea gradually improved after full anti-infection, recombinant human brain natriuretic peptide anti-heart failure, diuresis and other supportive treatment. However, the cause of the pleural effusion was still not clear at this time, and thus the additional left pleural effusion was sent for puncture and drainage (), and then the left and right pleural effusions were sent to NGS for testing respectively at this time.
A total of 39,575,303 reads were obtained from right pleural fluid samples, and 68 Mycobacterium tuberculosis complexes were detected ( and ). A total of 38,603,770 reads were generated from left pleural fluid samples, and 1 read of Mycobacterium tuberculosis complex were detected ( and ), covering 0.0010% (43/4,370,115) of the references genome. In order to validate the results of NGS detection, the detected specimens were also tested by real-time quantitative polymerase chain reaction (qPCR). The results of qPCR showed that Mycobacterium tuberculosis complex was positive in the right pleural fluid specimen, while no MTB was detected in the left pleural fluid specimen.
MTB was detected in both NGS specimens, and MTB infection was confirmed in qPCR of right pleural effusion specimen, so the patient was diagnosed as tuberculous pleurisy. At this time, after full anti-infection, anti-inflammation, cough relief, phlegm resolving, symptomatic support treatment, the patient’s symptoms of cough, expectoration, dyspnea and other symptoms have been better than those at admission, and the condition was relatively stable. Chest CT (Day 15) reexamination showed ( and ): absorption of left pleural effusion, reduction of right pleural effusion, improvement of bilateral pulmonary inflammation. According to the relevant national laws and regulations, tuberculosis is an infectious disease, and patients should receive designated treatment in infectious disease hospitals. In order to standardize anti-tuberculosis treatment and to prevent recurrence of the disease, the patient was discharged from the hospital and transferred to the tuberculosis infectious disease hospital for systematic treatment.
The patient’s condition improved after standard anti-tuberculosis treatment in Tuberculosis Infectious Disease Hospital, and the anti-tuberculosis treatment was effective, which confirmed the diagnosis of tuberculous pleurisy again. At this time, the patient was generally in good condition, and we contacted the patient to ask him to return for CT scan efficacy evaluation, but he just rejected the request and has not returned so far.


A 65-year-old Caucasian female with severe ascending aortic dilation and aortic regurgitation was scheduled for an urgent Bentall procedure. Her past medical history was remarkable for a recent laparoscopic cholecystectomy after which she developed MH in the immediate postoperative period. This required use of dantrolene and a prolonged ICU and hospital stay. Interestingly, her three prior general anesthetics for herniorraphy, hysterectomy, and orthopedic spine surgery had been uneventful. Family history revealed an aunt with a similar MH episode in the past. Because of the strong family history, immediate members of her family were advised to undergo the caffeine halothane contracture test. All tested positive.
Transesophageal echocardiography (TEE) was performed on the patient preoperatively. This was notable for a dilated ascending aorta measuring 61 mm at the level of the pulmonary artery, absence of aortic dissection and severe aortic regurgitation with a vena contracta of 7 mm and pressure half-time (PHT) of 165. During the TEE, the patient developed acute respiratory failure requiring emergent intubation facilitated by IV etomidate without use of muscle relaxant. There were no signs of MH following intubation. An urgent cardiac catheterization showed non-obstructive coronary artery disease (CAD) with a left ventricular end-diastolic pressure (LVEDP) of 22 mmHg.
The patient was urgently scheduled to undergo surgery. Since we do not have a dedicated anesthesia machine for MH- susceptible patients, we prepared our Drager Fabius anesthesia machine (Drager Medical, Telford, PA, USA) by removing all vaporizers, replacing CO2 absorbent, attaching a fresh anesthesia circuit, and running 10 l fresh gas flow with tidal volume 1 l for 2 hours. We also removed succinylcholine from the drug tray, and kept dantrolene available in the room. The vaporizer from the CPB machine (Terumo System One®, Terumo CVS Corporation, Ann Arbor, MI, USA) was also removed.
A combination of propofol and sufentanil infusions was chosen for maintenance of anesthesia. Rocuronium was selected for skeletal muscle relaxation. Invasive blood pressure monitoring, central venous and pulmonary arterial pressure monitoring, and continuous cardiac output with mixed venous oxygen measurements supplemented the standard ASA monitors through the case. Intraoperatively, temperature was monitored using both nasopharyngeal probe and indwelling Foley catheter. Median sternotomy was followed by ascending aortic cannulation beyond the dilatation and a three-stage venous cannulation of the inferior vena cava through the right atrial appendage in preparation for the CPB. During CPB, ABGs were drawn every 20 min with special attention to PaCO2 and base deficit. Heparin 300 Units/kg was administered and CPB was instituted after confirmation of activated clotting times of greater than 400 seconds. The patient was cooled to 33.1°C by the perfusionist to comply with surgeon's preference. Rewarming was uneventful, with strict maintenance of less than 1°C difference between nasopharyngeal and bladder temperatures. Following an uneventful CPB course, the patient was successfully weaned from CPB with infusions of epinephrine and vasopressin.
On postoperative day (POD) #3, she was successfully extubated. On POD #16, she was discharged from the hospital.


A 73-year-old male with past medical history of hypertension, diagnosed with COVID-19 infection 3 days prior to admission, presented to the emergency room with progressive worsening of shortness of breath. He endorsed 4 days of subjective fevers, chills, productive cough, generalized weakness, and decreased oral intake. On presentation to the emergency room, he was tachypneic to 35 breaths per minute with oxygen saturation of 85% on room air. He was immediately placed on a non-rebreather with improvement in oxygenation. Blood work showed elevated inflammatory markers with C-reactive protein of 25.85 mg/dL, ferritin 1847 ng/mL, and lactate dehydrogenase of 475 IU/L. Chest radiograph on day of admission showed bilateral peripheral infiltrates suggestive of COVID-19 without any signs of cavitary lesions (). Nasopharyngeal swab polymerase chain reaction for SARS-CoV-2 tested positive. Blood and respiratory cultures were drawn.
Due to progressive respiratory distress, the patient was initially placed on high-flow nasal cannula. Subsequently, he required intubation and was transferred to the medical intensive care unit. He started on remdesivir, dexamethasone, and received convalescent plasma based on current COVID-19 recommendations. With persistent fever spikes to 102 °F, he was initiated on broad-spectrum antibiotics. Respiratory cultures obtained at time of intubation grew methicillin-resistant Staphylococcus aureus, and antibiotics were narrowed. With worsening P/F ratios, the patient was proned for a total of 48 hours, per hospital acute respiratory distress syndrome protocol, with significant improvement in the gas exchange.
Despite appropriate antibiotics, the patient continued to have persistently high-grade fevers and progressively higher oxygen requirements. Computed tomography scan of the chest was performed 3 weeks after admission demonstrating extensive airspace disease with bilateral peripheral ground glass pattern, along with newly formed thin-walled cavitary lesions in the right middle lobe and left upper lobe ( and ). These cavities were occupied by fungal ball-like lesions, and subsequent respiratory cultures grew Aspergillus flavus, without any fungal growth in blood cultures, and aspergillus/galactomannan serum assay showed no results. The patient was then started on intravenous voriconazole for subacute invasive pulmonary aspergillosis. Due to persistence of the SARS-CoV-2 and severe acute respiratory distress syndrome complicated by pulmonary aspergillosis, the patient further underwent tracheostomy and was discharged to a subacute rehabilitation facility.


A 40-year old Caucasian female of French Canadian ethnicity presented with moderate pruritus on the thorax and oropharyngeal swelling shortly following ingestion of roughly 250 mg of mahaleb seed kernels. The symptoms resolved following self-treatment with diphenhydramine.
The kernels were not ground and not mixed with other ingredients, though it remains unknown whether it was raw or lightly roasted. The subject had not knowingly consumed mahaleb predating the reaction. The subject’s clinical history included 20+ years of pollinosis to birch and late onset food allergy to several types of nuts starting at age 19 which were later clinically confirmed by skin prick testing at age 24 and again at age 29. In particular, the subject had previously experienced anaphylaxis to walnut, pistachio, pecan, hazelnut, cashew, and Brazil nut marked by systemic hives, oropharyngeal swelling, facial swelling, and hypotension, and necessitating intervention with combined epinephrine and diphenhydramine, and in some instances, oral prednisone. The subject had additionally manifested food-dependent exercise induced-anaphylaxis following consumption of peanut and almond marked by oropharyngeal swelling, facial swelling and hives on the arms and chest that resolved with administration of diphenhydramine. There was no history of food allergies among immediate family members, though one immediate family member had a positive history for seasonal pollinosis.
At the time of presentation, the subject had been observing a strictly nut-free diet for many years, including elimination of all tree nuts and peanuts. The most recent prior episode of anaphylaxis (food-dependent, exercise-induced) had occurred roughly six and a half years earlier at age 34 following accidental ingestion of almond in a prepared food necessitating intervention with epinephrine and diphenhydramine. On account of the history of almond allergy and exposure to mahaleb, the subject was assessed for responsiveness to mahaleb proteins four days following the mahaleb exposure.


This 30 year old lady underwent IVF due to primary infertility of unknown aetiology. Hysterosalpingogram had showed patent tubes with ovulation confirmed by a normal day 21 progesterone level. Semen analysis of her partner was normal. Ultrasound pelvis showed a fundal fibroid with no other abnormalities. Following referral to a regional fertility centre she underwent IVF and day 5 single embryo transfer. She presented to our unit 26 days following this with light vaginal staining, diarrhoea and mild crampy abdominal pain. On examination her abdomen was soft and not tender on palpation. Serum BHCG levels at this stage were 8273. Transvaginal ultrasound showed an empty uterus with an extra uterine gestational sac. Within the sac was a yolk sac and a fetal pole measuring 5 weeks gestation with cardiac activity present (see )
Due to the presence of an extrauterine pregnancy with fetal cardiac activity a laparoscopy was performed. At laparoscopy the known fundal fibroid was noted and the ovaries and tubes were normal (). There was no evidence of uterine perforation. On evaluation of the pouch of Douglas an ectopic pregnancy was noted on the rectum (.) This was in keeping with the previous ultrasound findings. The ectopic tissue was adherent to the rectum and therefore a laparoscopic suction device was used to open the mass bluntly and remove the gestational sac. It was felt that removal of all ectopic tissue would come at a high risk of a rectal injury so this was not attempted.
As some tissue was left in the abdomen she was treated with intramuscular methotrexate the day following laparoscopy. Her BHCG levels fell from 8273 to 271 one week following methotrexate. Within two weeks they had fallen further to 40 and she was discharged.


A six-year-old boy initially presented to the ophthalmologist with a squint in the left eye, which was associated with facial asymmetry. The patient had the squint since the age of two. A computed tomography (CT) scan of the patient’s brain and orbit revealed non-enhancing soft-tissue density arising from the left posterior ethmoid sinus that breached the lamina papyracea () and extended into the maxillary infundibulum (). The left fovea ethmoidalis was also eroded. The left orbital rim was slightly smaller when compared with the right one. There were no neck swelling, nasal symptoms, eye symptoms, constitutional symptoms or fever. Further, the patient had not experienced any preceding trauma or previously undergone an operation. Upon examination, the ranges of movement of the left eye toward the upper outer gaze were found to be reduced. No neck node was detected.
The patient was subsequently referred for a nasoendoscopy, during which a bulging over the lateral wall of the left middle meatus, posterior to the uncinate process with a non-pulsatile prominent vessel was noted. Both fossae of Rosenmüller were normal.
The patient underwent an endoscopic biopsy. A whitish, friable, and non-vascularised mass was found to be bulging from the posterior ethmoid air cells. The parts of the mass attached to the lamina papyracea and the skull base were left undisturbed.
A microscopic examination of the specimen identified tumour tissue composed of spindle cells with variable cellularity that was embedded within a fibromyxoid stroma. The cells were arranged in storiform, C- and S-shaped patterns (). They had plump stellate (ovoid) vesicular nuclei with visible nucleoli. Mitotic figures were only rarely seen (). Blood vessels in different sizes characterised by perivascular hyalinization with scattered lymphocytes, eosinophils, and multinucleated giant cells were also identified (). The immunohistochemical staining with vimentin and smooth muscle actin (SMA) revealed positive results, while the staining with S100, desmin, h-caldesmon, CD34, and CK revealed negative results. The Ki-67 proliferative index was absent (0-1%). A pathological diagnosis of NF was made. The patient was placed on regular follow-up for almost one year, no evidence of recurrence was seen clinically during this time. We planned to repeat CT scan of the paranasal sinus at postoperatively first year.


A 21-year-old Caucasian woman was admitted to the neurosurgery department with severe visual impairment and proptosis in the right eye. About 9 months earlier, she was suffering from a headache on the right side of the head, which caused sleeping difficulty. Four months later, the patient noticed right-sided proptosis, but she did not ask for medical consultation for fear that the surgical intervention might affect her pregnancy at that time. The patient lives in a rural area in contact with dogs and sheep. Her past medical history was unremarkable.
On physical examination, the patient was conscious, responsive and oriented. Visual acuity was only a perception of light in the right eye, and there was a complete restriction in this eye movement with severe chemosis (). The exophthalmia was non-axial, painless, non-tender, irreducible and non-pulsative. Magnetic resonance imaging (MRI) revealed a well-defined cystic lesion that measures ∼42 × 36 × 32 mm, located in the right orbital cavity displacing the optic nerve laterally. The lesion showed low signal intensity on T1-weighted images () and high signal intensity on T2-weighted images ().
The diagnosis was an intraconal orbital hydatid cyst. Chest X-ray and abdominal ultrasonography revealed no abnormal findings, and there were no other abnormalities in the general examination. In addition, the left eye and laboratory tests were normal.
Ophthalmic consultation recommended eradication via a neurosurgical approach due to the risk of rupture because of the large size. The patient underwent surgery using fronto-orbitozygomatic approach in which we made an incision in the right frontal skin and removed the right orbitozygomatic bony flap. Then, we opened the roof of the orbit and removed the hydatid cyst successfully without rupture ().
During the surgery, the eye returned to the orbital cavity spontaneously, and the proptosis disappeared in the immediate postoperative period. On the first day after surgery, the patient was conscious with severe eyelid edema treated with dexamethasone. On the third day, the edema was subsided, and there was a noticeable improvement in the visual ability from a perception of light to the ability to count fingers at a distance of 1 m. The patient was discharged after 72 hours of the surgical procedure with a prescription of antibiotic, analgesic, antiedemic and albendazole (10 mg\kg once daily for 2 months). There was no clinical recurrence of proptosis after the 3 months of follow-up (), and her eye motility and vision returned to normal.


On the initial admission, the 64-year-old man had a 1-year history of chronic intermittent abdominal pain and episodes of subacute bowel obstruction. The patient had no history of chronic medication usage.
Initial investigations included magnetic resonance enterography that was normal and a capsule endoscopy that showed rare erosions, aphthoid ulcers and two ulcerated stenosis ().
One month later, he developed an acute small bowel obstruction, and a laparotomy was therefore undertaken.
The laparotomy revealed the presence of two transition zones between dilated and non-dilated small bowel. These zones were located within 40 cm proximal to the ileocecal valve, and they corresponded to a few millimeters thin lesions, with no evidence of a thickening in the bowel or mesenteric abnormalities (classic stigmata of stenotic Crohn disease). An enterotomy for one of the two lesions was undertaken, which showed no macroscopic abnormality, and then a stricturoplasty was made.
A diagnosis of ileal Crohn disease was suspected leading to the initiation of a treatment with biotherapy (adalimumab).
A second capsule endoscopy showed the same lesions.
One year later, he was readmitted with small bowel obstruction investigated with an abdominal computed tomography (CT) scan that showed no radiological finding of stenotic Crohn disease or other obstructive etiology ( and ).
The small bowel occlusion was resolved with non-operative management.
After a multidisciplinary team discussion, an exploratory laparoscopy was decided in order to explore the extraluminal aspects at the obstruction area and execute an enteroscopy in order to ensure the existence of intraluminal unique or multiple lesions.
At laparoscopy, the patient was found to have stigmata from the previous operation without any other extraluminal anomalies on the small bowel or the mesenteric fat. A conversion to a mini-laparotomy was undertaken, and using manual palpation, 2 mm thin strictures were suspected to be the possible zones of the small bowel obstacle.
No other particular anomalies were perceived and a small enterotomy was performed 35 cm above the Bauhin valve near the previous stricturoplasty. The peroperative enteroscopy reached proximally the duodeno-jejunal angle and distally the ileocaecal valve and the caecum allowing the exploration of the entire small bowel (). It showed multiple ileal diaphragm including three diaphragms with small ulcers (video). A 60 cm segmental resection was performed removing all the six lesions and the histological features found in the lesion were consistent with the diaphragm disease.


A healthy 50-year-old man experienced black widow spider (BWS) envenomation. After the bite, he manifested sweating, wrist paraesthesia, and pain at the initial bite site with inoculum spreading to the upper arms. Laboratory tests revealed leukocytosis and increased plasma levels of C-reactive protein, cardiac troponin-I, and brain natriuretic peptide (Table ). Arterial blood gas analysis, chest X-rays, and echocardiographic examinations were normal at admission; electrocardiogram (ECG) showed diphasic T waves in lateral leads (Fig. a) which were not present in previous outpatient ECGs.
Due to the lack of available antidotes, the patient was empirically treated with intravenous fluids for hydration, analgesics for the relief of pain, benzodiazepines for agitation, antibiotics to prevent infection, steroids, and anti-histamines for periorbital edema. On day 1 of hospitalization, the ECG showed negative T waves in lateral and inferior leads (Fig. b), abnormalities in the wall motion of the left ventricle (LV) in association with moderate systolic dysfunction (hypokinesia of the LV middle/basal segments of the inferior, lateral and inferior-lateral walls); and LV ejection fraction (LVEF) of 48%. The decrease in LVEF was confirmed by speckle tracking analysis: global longitudinal strain (GLS) showed a reduced LV contractile performance (− 14%). Angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics were administered. Cardiac magnetic resonance (CMR) was carried out on day 6 to confirm the diagnosis of myocarditis, with the results showing an LVEF of 51% and no signs of myocardial edema/diffuse fibrosis. A minimal area of focal fibrosis was detected at the junction between the left atrium and ventricle, although this finding was not specific (Fig. ). Coronary angiography excluded coronary stenosis (Fig. ).
On day 11, the echocardiographic findings (LVEF 55%, GLS − 19%) and cardiac enzymes were normal and the patient was discharged with medical therapy for heart failure.


A 17-year-old healthy male was referred from a local eye clinic due to painless visual obscuration in the right eye for 2 weeks; white dot syndrome was suspected. His best-corrected visual acuity was 20/20 in both eyes with a refractive error of − 1.5 D in the right eye only. He denied preceding viral prodrome and any systemic disease. No concurrent neurological symptoms were noticed. No pupillary or color defects were observed. Slit-lamp examination indicated no inflammation in the aqueous or vitreous humor. Funduscopic examination showed mild hyperpigmentation around the optic disc and a mild hyperemic optic disc with indistinct margin in the right eye. Static perimetry examination revealed an enlarged blind spot in the affected eye []. Fundus autofluorescence (FAF) imaging revealed zonal hyperautofluorescence around the optic disc. Optic disc staining and a window defect in the retinal pigment epithelium (RPE) were found on fluorescein angiography. Optical coherence tomography (OCT) demonstrated loss of the ellipsoid line at the corresponding hyperautofluorescent region []. A pattern visual-evoked potential (VEP) test recorded a delayed response of P100 in the right eye (normal P100 latency in our laboratory is approximately 110 ms; []. Despite the detection of T2-hyperintense signals at the retrobulbar optic nerve through magnetic resonance imaging, no contrast enhancement was found []. He showed a mildly decreased Arden ratio in the right eye (1.84) compared with that in the left eye (1.97), but both values remained within the normal limit. Electroretinogram (ERG) results showed that the amplitude of the photopic and scotopic a-wave was slightly reduced in the right eye compared with that in the left eye [].
His chest radiograph, routine blood cell counts, erythrocyte sediment rate, C-reactive protein, immunological profile (including antinuclear antibody, anti-double stranded DNA, antineutrophil cytoplasmic antibodies, rheumatoid factor, C3, and C4), serological test for Syphilis rapid plasma, Treponema pallidum particle agglutination assay, human immunodeficiency virus screening, and screening of antibodies related to viral infection (including herpes simplex virus, cytomegalovirus, toxoplasma, rubella virus, and Epstein–Barr virus) were all normal.
AZOOR was diagnosed in this patient, and he was started on 30 mg oral prednisolone daily (body weight: 70 kg; 7 weeks after symptom onset). Subsequently, his symptoms subjectively improved. However, 2 weeks after treatment, he developed skin folliculitis on both his arms. Because his parents were concerned about this and other side effects of steroid use, prednisolone was discontinued immediately. Apart from steroids, no other medication was administered. A visual field (VF) test, OCT, and autofluorescence imaging performed 6 months later, revealed no disease progression.


A 56-year-old woman (height 161 cm, weight 74 kg, body mass index 28) was scheduled to undergo neurolysis performed by a hand surgeon to treat median nerve palsy. She had suffered from numbness in her right thumb with increasing severity for six months. Her medical history included depression and osteoarthritis of the left knee and right hip. She had no abnormalities in the routine preoperative examinations that included blood tests, electrocardiography, and respiratory function tests. No apparent anatomical anomalies were declared. However, electrophysiological examination, which is conducted preoperatively in all hand surgery patients, revealed slow nerve conduction.
Total intravenous anesthesia was administered as a single bolus of 5 mg midazolam and 20 mg ketamine, followed by 2 mg/kg/hour propofol. Subsequently, the brachial plexus was scanned by an ultrasonographic scanner with a 15–6 MHz linear array transducer to assist in performing a nerve block for intraoperative and postoperative analgesia. Unexpectedly, ultrasonographic images revealed enlarged brachial plexus nerves (). Three nerve trunks were evident in the supraclavicular region, with cross sectional dimensions of approximately 6.3 x 4.4 mm (upper trunk), 6.3 x 5.3 mm (middle trunk), and 7.8 x 6.3 mm (lower trunk), with their respective cross-sectional areas (CSAs) being 21.8 mm2, 26.2 mm2, and 38.6 mm2.
Following consultation with the surgeon, it was decided to operate as scheduled. A PNB at the supraclavicular level was performed, and local anesthetics were injected as initially planned. After 10 mL 0.75% ropivacaine and 10 mL 1% lidocaine were injected around the nerves under ultrasonographic guidance, a good sensory and motor block ensued. Spontaneous respiration was maintained with a face mask (5 L/min oxygen). During the operation, anesthetic maintenance was straightforward, and the surgery proceeded uneventfully. The total surgery time was 57 minutes, and the total anesthesia time was 78 minutes. The postoperative course was uneventful, and the analgesic effects remained for 10 hours. The patient was discharged the following day.
Postoperatively, we consulted a neurologist, who further investigated the potential presence of an underlying neurological disorder. The neurologist suspected CMTD based on the characteristic nerve enlargement and foot deformity, which is pathognomonic of CMTD (). The patient’s foot exhibited high arches and claw toes, but were unnoticed by the patient.
Cervical magnetic resonance imaging (MRI) was performed without contrast medium (1.5 T, repetition time 3500 ms, echo time 127 ms). Gigantic bilateral brachial nerves were observed on a coronal T2-weighted image (). Genetic testing was performed, identifying duplication of the peripheral myelin protein 22 (PMP22) gene. This mutation is consistent with CMTD type 1A.


The patient was a 16-year-old male with a past medical history significant for severe factor VII deficiency who presented with a several months' history of iron deficiency anemia requiring multiple blood transfusions and positive Hemoccult stool tests. His history extends back to when he was around 10 years of age and was found to have severe iron deficiency anemia also with Hemoccult-positive stool, so that he was referred to pediatric gastroenterology for evaluation. An extensive workup was done at the time that included upper endoscopy, colonoscopy, Meckel's scintigraphy, a nuclear medicine bleeding scan, and capsule endoscopy. The nuclear medicine bleeding scan showed some increased uptake in the second portion of the duodenum, but his upper endoscopy was visually normal and the remainder of his workup all came back within normal limits. Throughout this time, he was treated with multiple, repeat blood transfusions and was managed by pediatric hematology.
At the time of presentation, he was receiving approximately 2–3 blood transfusions per week as well as iron transfusions, but his blood work continued to worsen. His hemoglobin level had dropped to 8.6 g/dL with a hematocrit level of 27.7%. His ferritin level had also reached a low of 12.7 ng/mL with a reticulocyte count elevated at 4.5%. His Hemoccult stool tests continued to remain positive. He underwent an upper gastrointestinal barium contrast study with small bowel follow-through in anticipation of a repeat capsule endoscopy for further evaluation that was ultimately read as normal. During capsule endoscopy evaluation, it was discovered that he had a large polypoid growth in approximately the third portion of the duodenum, just proximal to the ligament of Treitz, that was actively bleeding (Fig. ). At that point, it was decided that a repeat upper endoscopy would be performed with possible enteroscopy and polypectomy. The patient was admitted to the hospital the day prior to the procedure with pediatric hematology consulted for administration of NovoSeven RT to help with bleeding control due to his factor VII deficiency. During the upper endoscopy, a large polypoid lesion was noted near the ligament of Treitz that had a notable clot from a prior bleed but no other abnormal surrounding mucosa (Fig. ). The tissue was extremely friable, and based on the size of the lesion as well as its position in the duodenum, combined with the patient's bleeding disorder, it was felt that it would be safer to remove the polyp via surgery with partial bowel resection rather than endoscopic polypectomy. The lesion was biopsied once with cold forceps and was then tattooed and the patient was given several doses of factor VII for hemostasis. The next day, surgery was consulted, and the child was taken back to the operating room for robotic resection. A small 2- to 3-cm section of jejunum near the ligament of Treitz was ultimately resected and a primary end-to-end anastomosis was created with no significant bleeding or any other complications. The bowel section was sent to pathology and the patient recovered without concerns. He was started on high-dose proton pump inhibitor therapy and discharged home on postoperative day 4. The patient had a pediatric gastroenterology follow-up appointment approximately 2 months after surgery where he was found to be asymptomatic and was eventually weaned off his proton pump inhibitor with no further follow-up recommended. His intestinal pathology came back showing duodenal mucosa with gastric heterotopia that was negative for dysplasia or carcinoma. He continues to be followed by pediatric hematology but is no longer receiving frequent blood transfusions and no longer having any significant gastrointestinal symptoms.


A 59-year-old man was referred to the ophthalmology department due to a 3-day history of painless visual loss in his right eye. He also reported asthenia and occasional vomiting over the previous 3 months. He had no relevant medical history apart from a pack-a-day smoking habit for the past 45 years. His best corrected visual acuity was 20/63 and 20/20 (Snellen chart) and a subtle right relative afferent pupillary defect was noted. Visual field assessment revealed a severe diffuse defect in the right eye, while the left visual field was normal. The only pathological finding of the slit lamp examination was an oedematous right optic nerve disc. Neurological examination showed diminished reflexes and mild gait instability, so the patient was admitted to hospital for a complete work-up. Inflammatory markers (C-reactive protein, erythrocyte sedimentation rate) were performed and were normal. An infectious aetiology was excluded by negative serological results for Treponema pallidum, human immunodeficiency virus, hepatitis B virus, hepatitis C virus, Borrelia burgdorferi, Bartonella henselae, Coxiella burnetti, and Toxoplasma gondii. Further, samples were IgG positive but IgM negative for cytomegalovirus, Epstein-Barr virus, and varicella zoster virus. The QuantiFERON-TB Gold test and blood cultures were also negative. Visual evoked potential test showed increased latency in the right eye and magnetic resonance imaging of both the brain and orbits was anodyne. The patient was discharged without a definitive aetiologic diagnosis. During follow-up, visual acuity dropped to hand movement in his right eye and 20/25 in his left eye. A right relative afferent pupillary defect was noted, as well as bilateral optic disc oedema in the fundus examination, with unremarkable macular appearance. Neurologically, the patient had worsening instability and dysmetria of all four limbs, as confirmed by sensory evoked potentials testing and electromyography, hence the patient was admitted again to hospital. The neurological findings, combined with the bilateral optic disc oedema, prompted a lumbar puncture and cerebrospinal fluid (CSF) analysis, this finding an opening pressure of 170 mm of water, elevated protein content (137.5 mg/dL) and lymphocyte count (94%) but negative cytology and cultures. Additionally, an abnormal chest radiography led to a thoracic CT scan which showed mixed emphysema as well as a right hilar adenopathy with malignant radiological features for which an extended study was advised.
While waiting for the positron emission tomography-computed tomography to be performed, visual acuity worsened to 20/40 in his left eye. Slit lamp exams did not show any presence of anterior chamber cells nor flare. Fundoscopic examinations revealed vitreous haze (RE [+3] > LE [+2]) as per the Standardization of Uveitis Nomenclature classification [] and creamy-yellow deep retinal lesions showing bilateral macular involvement, distributed in a perifoveal circular pattern in the right eye and a placoid parafoveal lesion in the left eye. Fluorescein angiography (FA) showed papillitis and peripapillary phlebitis (Fig. ). SD-OCT of the right eye showed a severe disorganization of the outer retinal layers: Henle's fibre layer (HFL) and outer nuclear layer (ONL) revealed focal granular hyperreflectivity with perifoveal coalescence of larger round hyperreflective lesions that transformed into hyperreflective wedge-shaped and then band-like lesions at the fovea. Both the retinal pigment epithelium (RPE) and the ellipsoid segment (ES) layers showed a granular pattern. A greater disorganization of these layers was noted under the hyperreflective lesions in the HFL and ONL. In the fovea, atrophy of the outer retinal layers was noted, with deepening of the foveal depression and, below this, a hyperreflective deposit. Hyperreflective dots in the vitreous cavity corresponding to the vitreous cells were also noted. SD-OCT of the left eye showed vitreous dotted hyperreflectivity and a single hyperreflective tangential band at the fovea, with granular disorganization of outer retinal layers (Fig. ).
Based on the negative systemic work-up for an infectious aetiology, the anodyne cerebral and orbital MRI and the suspicious right hilar adenopathy, the differential diagnosis included a paraneoplastic syndrome, and hence, serological and CSF onco-neuronal antibodies were tested. Indirect immunofluorescence detected IgG for CRMP5, Hu and amphiphysin, which were confirmed by recombinant western blot analysis both in serum and CSF, this leading to the diagnosis of paraneoplastic syndrome. The patient received intravenous methylprednisolone 1 g/day for 4 days followed by oral prednisone 30 mg with tapering doses and visual acuity improved to 20/125 and 20/32 in the RE and LE at day 5 of follow-up. Multimodal imaging showed improvement in vitreous haze and shrinkage of the macular lesions. Positron emission tomography-computed tomography showed a hypermetabolic region in the hilum of the right lung. A bronchoscopy endoscopy with ultrasound was performed, and the histopathological analysis of the sample revealed the presence of atypical epithelial cell groups which were positive for CD-56, TTF-1 and synaptophysin, compatible with the diagnosis of a SCLC. According to the American Joint Committee on Cancer TNM staging system, the disease was classified as T3 N2 M0 (Stage IIIA) by our cancer committee. Given the localized malignancy and the patient's good performance status, the patient started a treatment consisting of concomitant chemotherapy (cisplatin and etoposide) and radiotherapy with a curative intent. The patient tolerated the treatment well and the hilar mass decreased from 20 to 13 mm in diameter, representing a partial response. Prophylactic cranial irradiation was also conducted. Ophthalmologically, a subtenon injection of triamcinolone was given in both eyes while maintaining oral prednisone 10 mg/day. Fundoscopy revealed bilateral persistent vitreous haze (+1 and +0.5, respectively), normalized optic nerves and a progressive fading of the yellowish macular lesions leading to atrophic changes. Right SD-OCT showed a subfoveal collapse of the ONL and ES layers, with granular appearance of the RPE. Interestingly, regression of the left macular hyperreflective band was noted, with suboptimal restoration of the outer retinal layers (Fig. ). In line with this, at 3 months of follow-up, visual acuity in the right eye decreased to 20/200, whereas in the left eye it improved to 20/25.


A 43-year-old male patient diagnosed with non-seminomatous mixed germ cell tumor (yolk sac 80%, teratoma 8%, and embryonal 2%) categorized as good risk with pulmonary metastasis underwent orchidectomy and 4 cycles of adjuvant bleomycin + etoposide + cisplatin (BEP) regimen. The patient received a cumulative dose of 270 IU of bleomycin, 400 mg/m2of cisplatin, and 2 g/m2of etoposide after 4 cycles of BEP regimen. The patient developed bleomycin-induced grade 2 pulmonary toxicity after 270 IU; hence, bleomycin was omitted from the fourth cycle of chemotherapy. After 4 cycles of BEP regimen, CT scan showed residual disease in the lung. As the patient was not willing to undergo surgery, he was planned and received a second-line VeIP regimen (vinblastine 9 mg + cisplatin 100 mg/m2+ ifosfamide 6 g/m2). The patient did not have any clinical signs or symptoms of peripheral neuropathy, and audiometry was normal before initiation of VeIP. Three days after completion of first cycle of VeIP regimen, the patient presented with complaints of severe abdomen pain and constipation. X-ray erect abdomen showed grossly distended large bowel loops with fecal matter and normal bowel gas pattern (shown in Fig. ). Blood investigations showed normal serum electrolytes and renal and hepatic function. Serum amylase and lipase levels were also within normal limits. There were no signs of active infection like fever or diarrhea, and blood counts were within normal limits. The patient was not on any medication known to cause paralytic ileus like anti-cholinergics, opioids or any anti-motility drugs. On physical examination, the patient had diffuse tenders distension of the abdomen with decreased bowel sounds. There was no evidence of free fluid on percussion. The patient was afebrile with a slightly elevated blood pressure of 154/90 mm Hg and had tachycardia with a heart rate of 122/min. All other vital signs were within normal limits. As the patient's abdominal pain was very severe (visual analogue scale 9/10) and did not respond to analgesics, a CT scan abdomen was done which showed extensive fecal loading in the caecum and ascending and transverse colon without any evidence of obstruction (Fig. ). Per rectal examination was done which showed an empty rectum. The patient was treated with laxatives, enema and fentanyl infusion for severe pain. With the above supportive measures, the patient gradually recovered and was relieved of his constipation and pain 1 week after the first cycle of VeIP regimen.
Chemotherapy with VeIP was discontinued, the and patient is planned for radiotherapy to residual lung lesions.


A 70-year-old man with a 6-month history of genital skin lesion presented with confusion. The patient's abnormal behavior of frequent call and polyuria developed 3 weeks ago. Eight days ago, he was admitted to a nearby hospital because of lumbago and difficulty in walking. The patient was referred to our dermatology unit for evaluation of the genital skin lesion. On inquiry, the patient was slowly replying and was disoriented. Physical examination revealed an eroded, erythematous plaque with a white-coated tumor on the scrotum and perineum (Fig. ).
Several enlarged inguinal nodes were readily palpable. The laboratory data on his first visit showed marked hypercalcemia: serum calcium 14.5 mg/dL, corrected Ca 15.3 mg/dL (normal range, 8.8–10.1 mg/dL), with PTHrP-intact 66.1 pmol/L (normal, <1.1 pmol/L), PTH-whole 5.9 pg/mL (normal range, 8.3–38.7 pg/mL), 1,25(OH)2vitamin D355.4 pg/mL (normal range, 20.0–60.0 pg/mL), 25-OH vitamin D314.3 ng/mL (normal range, 9.0–33.9 ng/mL), carcinoembryonic antigen 330 ng/dL (normal range, 0–5.0 ng/dL), and creatinine 1.63 mg/dL. A computerized brain scan revealed no occupying lesion suggestive of tumor or stroke. A computed tomography (CT) and magnetic resonance imaging (MRI) scan of the spine revealed a compression fracture of the 3rd lumbar vertebra, but not a pathological fracture indicative of metastasis. 99mTc-HMDP (hydroxymethylene diphosphonate) imaging and CT revealed no evidence of bone metastasis. Abdominal CT and echography revealed multiple metastases in the liver, and para-aortic, pelvic, and inguinal lymph nodes. Histopathology of a specimen taken from erythematous plaque showed a thickened epidermis occupied by neoplastic cells with large nuclei in the entire epidermis. Skin biopsy from the tumor showed infiltration of small, atypical cells arranged in nests and strands in the dermis (Fig. ). Atypical tumor cells had a high N/C ratio and occur singly or in clusters, some of which comprised cells with foamy cytoplasm. Immunohistochemically, tumor cells were positive for CK7 (Fig. ) and carcinoembryonic antigen, establishing the diagnosis of EMPD with invasive adenocarcinoma. Tumor cells were positive for PTHrP (Fig. ). In contrast, specimens taken from patients with EMPD without hypercalcemia were negative for PTHrP in the tumor cells (data not shown).
Initial treatment for hypercalcemia with saline, 20 mg/day of furosemide, and 3 mg/day of zoledronic acid hydrate reduced the level of serum calcium within the reference value. As a result, the level of consciousness was also slightly improved. Chemotherapy could not be performed due to a poor performance status (PS4). Radiation therapy with 30 Gy/10 Fr electron beam was effective to reduce the exudate and tumor size (Fig. ). However, hypercalcemia developed again on day 18 and the level of serum-corrected calcium elevated up to 18.2 mg/dL, in spite of all the treatment with 40 units of elcatonin, 40 mg of furosemide, and zoledronic acid. Concurrently, the liver metastasis was rapidly enlarged (Fig. ), and his general condition gradually deteriorated. The patient died on day 55. Figure summarizes the clinical course.


A 19-year-old female patient visited the outpatient wing of the department of periodontics with a complaint of spacing in the upper front tooth region associated with loosening of teeth for 3 months. She was otherwise healthy and had no significant medical issues. The patient provided a dental history of spacing between the left lateral incisor and the canine from childhood. She narrated that the lateral incisor and canine had become mobile because of the increased spacing with a preoperative probing depth of 9 mm around the involved teeth. To manage the condition, orthodontic treatment was initiated and suitable periodontal treatment was also planned.
The patient was prepared for surgery with the infiltration of local anesthesia on the labial and palatal aspects of the anterior maxilla. Full-thickness mucoperiosteal advancement flaps along the gingival sulcus on the labial side extending into the cleft were elevated [] as the incision would go all the way into the cleft. A similar process was done for the palatal aspect too. Careful elevation was performed by placing sharp periosteal elevators along the labial and palatal surfaces of the alveolus into the cleft, and two separate labial and palatal flaps were hence obtained. The epithelial attachment present inside the cleft was removed by debridement, and the cleft alveolus was exposed []. With the use of round and tapered fissure burs, holes of 0.5–1.0 mm diameter were driven adjacent to the cleft, both labially and palatally, from the coronal to the apical parts to ensure regional accelerated phenomenon.[] Ten milliliters of fresh autologous blood was obtained from the patient, and the PRF membrane was prepared according to the conventional Choukroun protocol[] []. To avoid a second site for the procurement of autologous bone graft, a demineralized freeze-dried bone allograft (DFDBA) was placed in the cleft area. The PRF membrane was mixed with the graft and the amnion membrane was placed over it and stabilized with sling sutures [Figures and ]. The two separate edges of the full-thickness flap were closed with interrupted sutures in the labial and palatal areas []. Subsequently, a pack was placed, proper postoperative instructions were given, and medications such as antibiotic amoxicillin 500 mg for 6 days and analgesics such as Imol and acecloren-p possessing both anti-inflammatory and painkiller properties along with chlorhexidine mouthwash for 15 days were prescribed. The case was followed up for a period of 2 weeks, 3 months, and 6 months [Figures -].


An 18-year-old female patient reported to Department of Oral and Maxillofacial Surgery, Sree Anjaneya Institute of Dental Sciences with the chief complaint of pain and paraesthesia on the left side of the jaw, which was noticed since 1 month. It was initially mild in intensity, which gradually increased to the present state and radiating along the distribution of inferior alveolar nerve. There was no relevant medical history and the patient was moderately built, well nourished, and no signs of pallor, icterus, cyanosis, and clubbing. On clinical examination, there was missing 37 and partly erupted 38. A panoramic radiograph was taken, which shows impacted 37 and 38 []. Both 37 and 38 were surgically removed and iliac crest grafting was performed from anterior iliac crest on left side; grafting was done using both cortical bone and the cancellous bone from the marrow, following which surgical closure was performed using Vicryl 3-0 sutures. Satisfactory healing of extracted socket was noticed after 1 week. A panoramic radiograph was taken after 2 months and satisfactory bone formation was noticed [].