Ms. N is a 23-year-old nulliparous woman with morbid obesity (body mass index (BMI) 40.3 kg/m2) who presented to the emergency room at our local community hospital. Her concerns were progressive exertional shortness of breath for two weeks and tachycardia for three days. She had access to a home pulse oximeter and had noted heart rates in the 120s with normal oxygen levels. Ms. N did admit to some mild shortness of breath at baseline but stated that the recent progression was much worse. The patient noted recent past medical history significant for COVID-19 infection that occurred six weeks prior to presentation, diagnosed by nasal swab. Of note, she was an employee at a local nursing home and believes she contracted the virus at the facility. Ms. N stated that the acute illness was treated at home with symptomatic treatment and that her COVID-19 symptoms of cough and fever had completely resolved following the acute illness. Her past medical history was otherwise significant for asthma, depression, and migraines. Her only regular medication was an oral contraceptive. She did relate a family history of heart disease but was not able to specify further.
At the time of the emergency room presentation, Ms. N was noted to have sinus tachycardia and tachypnea. Her brain natriuretic peptide (BNP) was elevated at 1082 pg/mL while serum myoglobin and troponin-I were normal. The patient’s COVID-19 immunoglobulin G (IgG) was positive. Pertinent presenting labs are presented in Table . Computed tomography (CT) of her chest revealed the absence of pulmonary embolism but the presence of multifocal lymphadenopathy throughout the chest. A representative image is shown in Figure .
EKGs revealed a normal sinus rhythm and were unchanged during her hospital stay. She was admitted to the hospital with a provisional diagnosis of acute decompensated systolic congestive heart failure, and the cardiology service was consulted. Presumptive heart failure treatment was initiated with valsartan, metoprolol succinate, and furosemide. Echocardiography revealed severely decreased systolic function with an ejection fraction of 10%-15%, grade I diastolic dysfunction, and severe global hypokinesis. Cardiac catheterization demonstrated normal coronary arteries and elevated left ventricular end-diastolic pressure of 38 mmHg. The consultant cardiologist believed Ms. N’s cardiomyopathy to have been due to her recent COVID-19 diagnosis.
Ms. N was managed as an inpatient with diuresis with an improvement in her presenting symptoms. She was discharged to home with prescriptions for furosemide, metoprolol succinate, and valsartan. The interval echocardiogram at one month redemonstrated an ejection fraction of 10-15%, and the patient was referred to cardiopulmonary rehab. Ms. N was also referred to a specialized heart failure clinic in our healthcare system; the cardiologist there believed that she had a pre-existent cardiac remodeling process that was made worse by her COVID-19 infection. The heart failure clinic ordered a repeat CT of the patient’s chest, which redemonstrated the bilateral hilar and mediastinal lymphadenopathy. Cardiac MRI performed two months after hospital discharge demonstrated a dilated left ventricle without ventricular wall hypertrophy; this was interpreted by the consultant radiologist and cardiologist as consistent with nonischemic cardiomyopathy.


A 35-year-old lady presented to the surgical outpatient department with complaints of a vague lump in the right breast for the past three months. The swelling was associated with an occasional pricking type of pain, which was non-radiating. The swelling was insidious in onset and slow-growing. She had no history of fever, trauma or nipple discharge. On examination, a vague 3x2 cm lump was palpable in the right breast upper inner quadrant with no associated erythema, tenderness or local rise in temperature. Ultrasonography of the breast was performed, which showed a hypoechoic cystic lesion of 3.4 x 2.1cm size with few focal areas of heterogenic solid parenchyma (BIRADS 4a). A core-needle biopsy of the lesion was performed under local anaesthesia to establish the diagnosis. No pre-biopsy antibiotic prophylaxis was given to the patient as per the institutional protocol. Four days later, the lady presented to the emergency with an increase in the size of the swelling at and surrounding the site of the procedure. She complained of severe pain and pus discharge from the location of the core-needle biopsy. She also had an intermittent high-grade fever for the past two days. She is a known diabetic with uncontrolled sugar levels at presentation. She had no other comorbidities. At presentation, her vitals were stable, and examination revealed a 10x6 cm swelling in the right breast upper inner quadrant with a necrotic patch over it and surrounding erythema (Figure ).
There was a presence of foul-smelling discharge from the swelling. She also had mild right axillary lymphadenopathy. The opposite breast was normal. Her initial blood investigations revealed elevated total leukocyte counts (TLC - 19,000/mm3) and an elevated C-reactive protein (CRP - 55 mg/dL). Renal and liver function tests were within normal limits. Histopathological examination of the initial core-needle biopsy was suggestive of benign fibrocystic disease of the breast.
The patient was immediately taken for debridement under general anaesthesia in the emergency after obtaining informed consent. Intraoperatively, a 10x7 cm necrotic skin with an underlying 100 mL pus was mixed with necrotic material, which was debrided from swelling sparing nipple-areola complex. The debridement was extended until fresh bleed was found on the skin edges until we reached healthy breast tissue in the deeper layers. No definite mass/lump was palpable during the debridement at the area of the biopsy. She was transferred to an intensive care unit and immediately started on intravenous piperacillin-tazobactam 4.5 g every eight hours and clindamycin 600 mg every 12 hours. Her fever subsided on the following day, and her intraoperative cultures showed the growth of group-A β-haemolytic streptococci. Her blood glucose levels were controlled with insulin infusion. Following the antibiotic course, her TLC and CRP levels normalized. The wound was managed with serial dressings. After seven days of the antibiotic course, she was discharged in a stable condition with oral trimethoprim-sulfamethoxazole 400 mg twice daily for seven days. Her wound healed completely by secondary intention and was asymptomatic even at six months follow-up.


A 74-year-old female underwent right-eye pterygium surgery approximately 13 years ago. She presented to our ophthalmology department with a six-month history of right ocular pain (Table ). Her right-eye best corrected visual acuity (BCVA) was 20/20. Marked scleral thinning with a 4.5 × 4.5 cm calcium plaque was observed medially on slit-lamp examination (Fig. A). No organism was isolated on microbial staining and culture. The patient was diagnosed with noninfectious scleritis following pterygium removal surgery. A preserved corneal lamellar patch (Halo; Eversight Inc., Palo Alto, CA) was grafted after calcium plaque excision. At 1 week postoperatively, ocular surface epithelialization was complete and inflammation was diminished. At 1 month postoperatively, vascularization had partially progressed with regression of inflammation (Fig. B). One year postoperatively, the graft had been vascularized and a stable surface had been maintained (Fig. C). Her BCVA remained at 20/20.


A 66-year-old female with ocular pain was referred to our department (Table ). Her right-eye BCVA was 20/20. On slit-lamp examination, scleral thinning with infection and a 5 mm × 3.2 mm exposed calcium plaque was observed on the nasal aspect of the right eye (Fig. D). Although the patient received anti-inflammatory medication before referral, scleral thinning had progressed. Bacillus species was isolated on microbial staining and culture. The patient was diagnosed with infectious scleritis with exposed calcium plaque. The calcium plaque was excised, and a preserved corneal lamellar graft (Halo; Eversight Inc., Palo Alto, CA) was transplanted. One week postoperatively, with topical application of 0.5% moxifloxacin (Vigamox, Alcon, TX), the graft surface was fully epithelized and her BCVA was 20/20 (Fig. E). One month postoperatively, the graft surface was stable and there was no infection or inflammation (Fig. F). Subconjunctival haemorrhages were noted after suture removal (Fig. F).


An 82-year-old male visited our hospital with a three-month history of severe pain and decreased visual acuity in the left eye (Table ). At the initial visit, his BCVA was 4/20. Slit-lamp examination revealed diffuse scleral infection, nasal scleromalacia with a large calcified plaque, an inferotemporal scleral nodule, and nasal corneal stromal oedema with endothelial infiltration. Severe anterior chamber inflammation was also observed. The nodule was filled with pus originating from the nasal side. Culture revealed Paecilomyces and Bacillus species. The patient was diagnosed with fungal scleritis with bacterial infection. Hourly topical administration of 0.5% moxifloxacin (Vigamox, Alcon Laboratories, Inc., Fort Worth, TX), 2.5% fortified vancomycin, 5% ceftazidime, and 1% voriconazole, as well as oral administration of 200 mg voriconazole twice daily and 400 mg moxifloxacin once daily was performed.
Five weeks later, although the infection was partially controlled, scleral necrosis had worsened compared to the initial visit. The defect size was 5 × 8 mm with iris prolapse at the inferonasal limbus that extended to the scleral defect (Fig. G). After calcium plaque (4 × 9 mm) excision, the patient underwent tectonic keratoplasty using a full thickness corneoscleral graft and patch grafting using preserved corneal tissue (Halo; Eversight Inc., Palo Alto, CA). Twenty five days postoperatively, inflammation was reduced and complete graft epithelialization was observed (Fig. H). Six months postoperatively, the graft was vascularized and stable (Fig. I). Although his BCVA was only light perception, infection had subsided and the eyeball was saved.


A 53-year-old man (height, 180 cm; weight, 76.6 kg), a heavy alcoholic, was admitted to a local medical center under the diagnosis of right acetabular and iliac wing fracture after falling from a tree. The patient was bedridden under conservative treatment. Three days later, he presented with abdominal pain and tenderness and was then transferred to our hospital for further evaluation and management. The systolic/diastolic blood pressure, heart rate on electrocardiogram, and body temperature were 160/94 mm Hg, 120 beats/min, and 37.5°C, respectively. Under the suspicion of dehydration and fracture-induced pain, fluid resuscitation was initiated with Hartmann solution and analgesics were administered. Nonetheless, the heart rate did not decrease. Hence, bisoprolol (5 mg per os) was administered once daily. Thiamine, haloperidol, and quetiapine were administered to treat alcohol withdrawal delirium. Every time the patient became responsive to verbal stimuli, he kept reporting abdominal pain. However, no pulmonary symptoms were present. Anteroposterior chest radiograph and transthoracic echocardiography (TTE) were normal. Abdominal CT revealed retroperitoneal and right iliacus hematoma. However, no injury was found in major vessels or organs. The laboratory findings showed increased levels of D-dimer (26.64 μg/mL), the normal range of which was < 0.1 μg/mL. Because he was immobilized after the injury with elevated levels of D-dimer, combined CT venography and CTPA was performed 7 days after the injury to rule out DVT and PTE; however, the results were negative.
Three days later (10 days after the injury), he presented to the operating room for open reduction and internal fixation of the pelvic bone fracture. Before anesthesia induction, the systolic/diastolic blood pressure, heart rate, and peripheral oxygen saturation (SpO2) were 142/92 mm Hg, 100 beats/min, and 100%, respectively. Anesthesia was induced with bolus administration of 130 mg propofol and continuous infusion of remifentanil at 0.1 μg/kg/min. Endotracheal intubation was facilitated with 50 mg rocuronium. The ventilator was set in the volume-controlled mode to deliver a tidal volume of 6 to 8 mL/kg at a respiratory rate of 10 to 12 breaths/min. The tidal volume and respiratory rate were adjusted to maintain end-tidal carbon dioxide concentration (EtCO2) between 33 and 35 mm Hg. Anesthesia was maintained with sevoflurane (1.5–2.0 vol%) in oxygen/air mixture (inspired oxygen saturation of 50%) to ensure bispectral index values between 40 and 60. The infusion rate of remifentanil (0.1–0.2 μg/kg/min) was adjusted to maintain blood pressure and heart rate within 20% of the baseline values. The right radial artery was catheterized for real-time monitoring of arterial blood pressure and arterial blood sampling. The right internal jugular vein was catheterized for real-time monitoring of central venous pressure, bolus administration of drugs, and continuous infusion of drugs. The results of arterial blood gas analysis after anesthesia induction were as follows: pH, 7.468; partial pressure of arterial carbon dioxide (PaCO2), 37.2 mm Hg; partial pressure of arterial oxygen (PaO2), 193.5 mm Hg; bicarbonate (HCO3−), 26.3 mmol/L; base excess, 2.6 mmol/L; hemoglobin, 8.2 g/dL.
At 10 minutes before the surgery, 100 μg phenylephrine was bolus administered twice at a 5-minute interval to ensure a systolic blood pressure of > 100 mm Hg. At the beginning of the surgery, phenylephrine was continuously infused at a rate of 0.2 μg/kg/min owing to the transient effects of its bolus administration. To compensate for intraoperative blood loss and preoperative dehydration, 6% hydroxyethyl starch, packed red blood cells, and fresh frozen plasma were administered at a rate of 8 to 10 mL/kg/min, and systolic blood pressure and heart rate were maintained between 90 and 100 mm Hg and between 100 and 110 beats/min, respectively. Ninety minutes after the surgery, systolic/diastolic arterial blood pressure and EtCO2 abruptly decreased from 100/60 to 30/15 mm Hg and from 29 to 13 mm Hg, respectively. The central venous pressure elevated from 10 to 29 mm Hg. The heart rate slightly increased from 105 to 115 beats/min. The normal sinus rhythm on the electrocardiogram turned into atrial fibrillation, after which bradycardia (49 beats/min) ensued. Under the impression of PTE, 3 cycles of cardiopulmonary resuscitation (CPR) were intermittently performed for 25 minutes until spontaneous circulation [systolic/diastolic blood pressure of 80–90/50 mm Hg and sinus tachycardia (115 beats/min)] was achieved (Fig. ). At the beginning of CPR, epinephrine and norepinephrine were infused at a rate of 0.1 μg/kg/min, and 3 mg epinephrine was bolus administered during CPR. Arterial blood gas analysis performed between the first 2 CPR cycles revealed hypercapnia (pH, 7.287; PaCO2, 55.8 mm Hg; PaO2, 98.7 mm Hg; HCO3−, 26.0 mmol/L; base excess, −0.6 mmol/L; hemoglobin, 8.8 g/dL). At the end of the last CPR cycle, the infusion rate of the fluid was reduced to 3 to 5 mL/kg/min, and a probe for transesophageal echocardiography (TEE) was inserted into the esophagus. TEE showed right ventricular dysfunction with paradoxical septal motion. However, no embolus was found in the main, right, and left pulmonary arteries. Intraoperatively, 500 mL of 6% hydroxyethyl starch, 1250 mL of packed red blood cells, and 450 mL of fresh frozen plasma were administered in total. The amount of blood loss and urine output was 700 and 100 mL, respectively.
Chest CT performed immediately after the surgery showed emboli in both the pulmonary arteries (Fig. ). The patient was taken back to the operating room and underwent surgical embolectomy under cardiopulmonary bypass with aortic cross-clamping and cardioplegic arrest. The incision was made in both the main pulmonary arteries, and emboli were removed (Fig. ). EtCO2 and central venous pressure were elevated from 20 to 31 mm Hg and reduced from 30 to 4 mm Hg, respectively, after weaning from cardiopulmonary bypass. Intraoperative TEE and postoperative TTE showed normalized right ventricular function and septal motion. Anticoagulation therapy with warfarin was commenced from the third postoperative day. The inferior vena cava filter was also placed. One month after the surgery, CTPA and CT venography revealed no DVT and PTE. The patient was then discharged from the hospital without any complications. The patient provided informed consent for the publication of this case.


A 30-year old male presented to the emergency department complained of hemoptysis as a first manifestation a year ago without obvious predisposing cause. The hemoptysis was manifested as bloody sputum, with a total volume of 50–100 ml. The accompanying symptoms included paroxysmal chest distress, shortness of breath, and palpitation. During his stay in the emergency department, the physical examination was unremarkable. The pulmonary CT (taken in another hospital) showed mild infection. The abdominal ultrasound and echocardiography were both normal. The reexamination of pulmonary CT showed normal. The diagnosis of pneumonia was suspected then. His symptoms were relieved quickly after hemostatic therapy and antibiotic treatment. The patient was discharged without further evaluation. After a year’s duration, those paroxysmal symptoms sometimes start with nausea and emesis. This time, he visited the emergency department complaining of a recent attack. He was well before, without a history of medication. Physical examination was unremarkable. He was conscious, afebrile, and oriented, with a blood pressure of 107/85 mmHg, a heart rate of 79/min, and a respiratory rate of 18 breaths/min.
A complete blood count revealed the following: white blood cell 23,720/mm, hemoglobin 18.1 g/dl, hematocrit 52%, and platelets 275,000/mm. Liver function test results were ALT 62 IU/L, AST 58 IU/L, and LDH 326 IU/L. His blood glucose was 297 mg/dl, and serum creatinine was 114 ummol/L. Prothrombin time and activated partial thromboplastin time were 10.7 and 29.2 s, respectively. The examination of the urine showed proteinuria and glucosuria.
At admission, the pulmonary CT scan showed patchy high-density shadow and ground-glass opacity, compatible with diffuse alveolar hemorrhage (DAH) (see ). The bronchoscopy confirmed the diagnosis. The bronchoalveolar lavage reported macrophage (86%), lymphocyte (1.5%), neutrophil (12.5%). Autoimmune diseases were suspected at first. Further laboratory tests showed anti-DNA (anti-double stranded DNA), c-ANCA (c-anti-neutrophil cytoplasmic antibodies), anti-MPO (anti-myeloperoxidase antibody), ANA (anti-nuclear antibody), and anti-GBM (anti-glomerular basement membrane) antibodies were negative. Blood and sputum cultures were negative as well. The cortisol levels were 2.5 µg/dl (0 AM), 12.3 µg/dl (8 AM, reference value 5–25 µg/dl), 11.6 µg/dl (4 PM, reference value 2.5–12.5 µg/dl). Moreover, CT reexamination showed the diffuse alveolar hemorrhage resolved completely 5 days after the initial CT without any targeted treatment.
Acute coronary syndrome and stress-induced cardiomyopathy were both suspected. However, the patient did not show any signs of pulmonary edema. Biomarkers of myocardial injury were normal at admission. The echocardiography was normal with favorable systolic and diastolic functions. The electrocardiogram revealed normal sinus rhythm. The blood pressure remained normal under close monitoring.
The paroxysmal symptoms indicated high levels of catecholamine. The abdominal CT scan discovered left adrenal mass with intravenous contrast (69 * 61 * 62 mm) (see ). The diagnosis of pheochromocytoma was confirmed biochemically by the elevated catecholamine and metanephrine levels in the blood [metanephrine 2,506.2 pmol/L (<605.9 pmol/L), normetanephrine 16,279.2 pmol/L (413.9–4434.2 pmol/L)], and urine (VMA 40.3 µg/24 h, reference value 1.9–13.6 µg/24 h).
The diagnosis was considered as “pheochromocytoma, diffuse alveolar hemorrhage”. The patient received treatment of phenoxybenzamine, doxazosin mesylate, and moxifloxacin. During the hospital stay, the patient’s condition was getting better without any symptoms. Two months after discharge from the respiratory intensive care unit, the patient revisited the urology surgery department. The left adrenalectomy was performed by laparoscopy. Pathology examination revealed pheochromocytoma with moderate atypia histological features, immunohistochemical staining [Syn (+), SDHB (+), CD56(+), Ki-67(−)] (see ).
We followed the patient for 6 months. His symptoms gradually improved, and he was discharged.


A 52-year-old Hispanic male with newly diagnosed diabetes mellitus, hypertension, and ischemic cardiomyopathy presented with a one-month history of nonradiating right thigh erythema, pain, and swelling. He worked as a warehouse clerk; however, due to the severe, debilitating pain to his right thigh, the patient was on disability. He required maximal assistance in ambulation and, at times, even a wheelchair. He denied a history of fever, physical trauma, or intravenous drug use. The patient reported several emergency department and urgent care visits prior to our evaluation with no significant improvement on oral antibiotics for presumed cellulitis. Vital signs on presentation included blood pressure 108/69 mm Hg, heart rate 77 beats per minute, temperature 37.5°C, respiratory rate 18, and 96% on room air. On physical examination, a hard, tender, erythematous 7 × 4 inch right anterior thigh mass with accompanying right upper thigh edema was noted (as shown in ). Distal pulses were 2+ on palpation. Right lower extremity had 3+ pitting edema, while the left lower extremity had 2+ pitting edema. Severe tenderness was also noted in the right groin region with associated painful groin lymphadenopathy.
White blood cell count was 10.7 × 10^3 cells/mcl; other laboratory tests did show signs of systemic inflammation including elevated erythrocyte sedimentation rate 49 mm and elevated C-reactive protein 7.98 mg/dL. Aldose value was 3.8 units/L. The patient had an elevated creatinine 1.31 mg/dL, blood urea nitrogen 25 mg/dL, urine albumin/creatinine ratio 1,342.8 mcg/mg Cr, and creatinine kinase 844 unit/L, hemoglobin A1c (HbA1c) was 10.3%, and blood cultures were negative. Laboratory values to diagnose polymyositis and dermatomyositis were negative. A venous Doppler ultrasound of the right leg was negative for deep vein thrombosis. Magnetic resonance imaging (MRI) without contrast of the femur demonstrated bilateral inflammatory changes with disproportionate enlargement and diffuse heterogeneity of the right vastus medialis muscle with patchy areas of intramuscular hemorrhage, extensive subcutaneous edema, interfascial free fluid, and severe myositis (as shown in ).
Due to lack of improvement of symptoms on antibiotics and poorly controlled diabetes, the diagnosis of diabetic muscle infarction was considered. The treatment consisted of analgesia, low-dose aspirin, bed rest, and close outpatient follow-up. Upon discharge from the hospital, the patient was referred to a tertiary center for muscle biopsy; however, this was delayed due to the coronavirus disease 2019 (COVID-19) pandemic. Three months after being discharged from the hospital, the patient endorsed a significant size reduction of right thigh mass, complete resolution of pain, and endorsed being able to ambulate without assistance. With time, rest, and excellent adherence to low-dose aspirin, he no longer required a biopsy due to complete resolution of symptoms.


This 25-year-old man (early follow-up published elsewhere) [] suffered from generalized acquired dystonia with choreoathetotic movements due to perinatal asphyxia. Upon clinical examination, he also had an action-induced tremor with myoclonic jerks, mild spastic tetraparesis and ataxic gait. He was wheelchair-bound for longer distances and was not able to drink or eat by himself independently. Furthermore, he had severe dysarthria. The Burke-Fahn-Marsden (BFM) motor score was 80.5 (assessing axial and more peripheral dystonic symptoms), disability score 19 (describing dystonia-related problems in daily life). The patient was under no specific medication.
He underwent implantation of quadripolar DBS electrodes (Model 3387; Medtronic Inc., Minneapolis) bilaterally in the ventral intermediate nucleus (Vim) of the thalamus and bilaterally in the posteroventral lateral globus pallidus internus (GPi) guided by CT-stereotactic surgery and microelectrode recording. Postoperative stereotactic CT demonstrated appropriate placement of all four electrodes. After test stimulation an implantable pulse generator (IPG) (Kinetra; Medtronic Inc., Minneapolis) was implanted and connected to the thalamic DBS electrodes. Postoperatively, he had improvement of tremor and dystonia, he was able to grip objects and was more independent (BFM motor score 67.5; disability score 15 at 17 months postoperatively). Stimulation settings and the further course are shown in .
After 38 months of Vim stimulation the IPG was replaced upon battery depletion, and the previously and simultaneously implanted pallidal electrodes were then connected to possibly obtain further benefit. The rationale were the phasic and dystonic symptoms of the extremities, especially with severe difficulties to put the feet with the sole on the ground, and cervical dystonia further affecting the ability to eat. While there was subjective improvement in fine motor skills (e.g. handling of his smartphone became somewhat easier), the BFM motor and disability scores remained unchanged (BFM motor score 67, disability score 15) compared to bilateral Vim stimulation (electrodes were disconnected but not removed).
When he was seen for a routine follow-up 76 months after implantation, there was stable improvement of dystonia. However, IPG check revealed battery depletion since 5 weeks ago. Since clinical symptoms were stable with still an improvement of about 15% in the BFM motor score compared to the preoperative situation, IPG replacement was postponed and he continued to do well. Two and a half years after battery depletion, both the BFM motor score (58,5) and the disability score (13) were even further improved. No confounding factors such as medication, life circumstances or additional treatments had been modified. In the further course, however, one and a half year later, he noted a mild deterioration of dystonia and the IPG was replaced, leading to a rapid improvement to the former level, which is now stable for more than a year.


The patient is a 69-year-old Caucasian female who reported asymmetry of her abdomen in early 2011. An abdominal mass was visualized with magnetic resonance imaging (MRI) (Fig. ). CT-guided biopsy was undertaken, and pathology was consistent with a T2b grade 3 (stage IIB) high-grade soft-tissue sarcoma arising from the lower rectus abdominis muscle. In March 2011, following surgical resection with concurrent interstitial high-dose-rate brachytherapy, she had external beam radiation therapy (XBRT). The patient was observed, and 2 years later a solitary metastatic lesion to the anterior lingula of the left lung was noted on follow-up CT scan. This mass was resected in May 2013. Follow up PET/CT in August and November 2013 revealed no further evidence of disease other than a pulmonary nodule in the apical left upper lobe that was not fluorodeoxyglucose (FDG) avid. After an observational period of nearly 2 years, follow-up CT scan of the chest, abdomen, and pelvis confirmed stability of the apical left upper lobe pulmonary nodule. However, there was development of a pulmonary nodule more caudally in the anterior segment of the left upper lobe concerning for a possible solitary lung metastasis. The anterior segment left upper lobe pulmonary nodule had enlarged on the subsequent, March 2015 PET/CT scan, measuring 1.8 × 1.1 cm and was metabolically active, having a standardized uptake value (SUV) of 5.9, which was consistent with solitary pulmonary metastasis (Fig. ). The patient received a left upper lobectomy in late March 2015. The specimen pathology was found to be metastatic PEComa and was sent for additional genetic testing.
In September 2015, CT revealed progression of disease with development of a subaortic lymph node metastasis, in the anterior mediastinum (Fig. ). In this case, surgical resection was deemed to not be a viable option. Therefore, systemic therapeutic strategies were instead considered. mTOR inhibitors were a potential choice of therapy, based on studies indicating some efficacy in this setting, but no clinical trials utilizing these agents were available [, , , , ]. Secondary to elevated expression of PD-L1 on IHC of the tumor, treatment with the PD-1 inhibitor pembrolizumab 2 mg/kg intravenously every 3 weeks was begun in October 2015.
After cycle 21, a little more than 1 year after commencing pembrolizumab therapy, the patient had a PET/CT scan with no metabolically active disease (Fig. ). At this time, the patient’s only complaint was shortness of breath on exercise, which was attributed to the prior lung resection. She continued on pembrolizumab treatment with no evidence of disease until April 2018 for a total of 40 consecutive cycles at which time she was placed under surveillance. She has been disease free off therapy for 19 months.


A 34-year-old Haitian man with no past medical history presented with initial complaints of ataxia. He reported an unprotected sexual encounter 4 years ago with a suspected HIV-positive partner and was subsequently newly diagnosed with acquired immune deficiency syndrome (AIDS). CD4 cell count was 37.56 cells/mm3 [6.83%], CD8 357.82 cells/mm3, CD4/CD8 ratio 0.1 and plasma HIV viral load 459,020 copies/mL.
Brain magnetic resonance imaging (MRI) on admission showed increased T2 FLAIR in the brainstem and cerebellum, as well as bilateral, but asymmetrical involvement of the cerebellar peduncles, not consistent with intracranial mass or acute stroke (). Lumbar puncture (LP) showed: white blood cells 2/μL, red blood cells 140/μL, glucose 51 mg/dL, total protein 48 mg/dL, lymphocytes 94/μL, monocytes 6/μL. The cerebrospinal fluid (CSF) polymerase chain reaction (PCR) for JC virus returned as 6400 copies/mL, suggestive of PML. Other CSF studies were unremarkable, including: Cryptococcus neoformans antigen, venereal disease research laboratory test (VDRL), Toxoplasma gondii PCR, meningoencephalitis panel, Mycobacterium tuberculosis PCR, Epstein Barr virus (EBV) PCR, cytomegalovirus (CMV) PCR, herpes simplex virus (HSV)-1 and -2 (PCR), varicella zoster virus (VZV) PCR, adenosine deaminase (ADA), angiotensin converting enzyme (ACE) and acid-fast bacilli culture and smear. Serum serological testing was positive for Toxoplasma gondii, but otherwise negative. Other negative blood tests include EBV PCR, CMV PCR, hepatitis panel, and interferon gamma release assay. CSF cytology and flow cytometry were negative for malignancy including B- or T-cell lymphoma.
High concern for PML was raised; less likely toxoplasmosis or IRIS, as the patient was not on ART at the time. Differential considerations for his imaging appearance included CNS lymphoma, neurosarcoidosis, and cerebritis-meningitis among others. The patient was initiated on bictegravir 50 mg/emtricitabine 200 mg/tenofovir alafenamide 25 mg and prophylaxis against opportunistic infections notably Pneumocystis carinii pneumonia. After 2 weeks of ART, the viral load decreased significantly to 1400 copies/mL.
Two months after the initial presentation and despite compliance to ART, the patient was re-admitted for progressive neurological complaints, including worsening ataxia, now unable to stand or walk without assistance. The physical exam was notable for right facial droop, decreased sensation over the right face, marked dysmetria with finger-to-nose testing, and dysdiadochokinesia. He had significant ataxic gait but full muscle strength and negative pronator drift or nuchal rigidity. Repeat CSF studies were unrevealing. Brain MRI was concerning for worsening of previous PML lesions with multifocal brainstem and cerebellar T2/FLAIR hyperintense lesions, new extensive leptomeningeal and perivascular enhancement, and mass effect (). Repeat T- lymphocyte subsets/HIV studies at this time showed: CD4 cell count 252 cells/mm3 [7.94%], CD8 2430.4 cells/mm3, CD4/CD8 ratio 0.1 and plasma HIV viral load decreased to 106 copies/mL. In the setting of radiologic and clinical progression of disease with recently diagnosed AIDS and ART initiation 1 month prior, paradoxical cerebellar PML-IRIS was diagnosed. While ART was continued, he was also started on an adjunctive intravenous methylprednisolone course 1 g daily for 5 days, followed by an oral prednisone taper 60 mg per day, with taper over 6 weeks and close outpatient follow up. The patient was discharged after 5 days of hospital stay.
Patient did not return to receive care at our institution, but had 2 readmissions at an outside hospital within 20 miles to our hospital facility. The first readmission after discharge from our institution occurred within one week with symptoms of nausea, vomiting and gait dysfunction. Brain MRI again showed right cerebellar vasogenic edema with enhancing lesions in the left cerebral peduncle and extension to the pons, left cerebellar peduncle and right medullary edema. Repeat LP studies at this time was positive for JC virus PCR. He was treated again with a course of intravenous corticosteroids. Follow up CD4 count was 101 cells/mm3 and sulfamethoxazole/trimethoprim was continued for opportunistic infection prophylaxis. The patient was subsequently discharged to a rehabilitation treatment center after 4 weeks hospital stay.
One month after leaving the rehabilitation program, the patient was readmitted again with symptoms of nausea, vomiting and blurry vision. Repeat brain MRI showed a new 6 mm enhancing focus in the medulla in addition to imaging findings very similar to his last hospital stay. Work up for lymphoma and other malignancy was negative even though CSF studies were positive for EBV PCR in addition to JC virus. Patient again got a course of intravenous steroids. A repeat MRI performed after completion of intravenous steroids showed significant improvement of lesions. He was discharged home with outpatient physical therapy and his functional status continues to improve as of the time of this report.


A 45-year-old South Asian woman presented with a progressively worsening of proximal muscle weakness. Initially there was a mild pain in her thighs and arms which was followed by a difficulty getting up from the seated position and inability of raising her arms. There was no dysphagia, regurgitation or difficulty in breathing. During this particular presentation there was no dermatological manifestations suggestive of dermatomyositis or mechanic’s hands. There was no history suggestive of Raynaud’s phenomenon or any joint pains. There was a mild nonproductive cough which developed a few weeks after the onset of the muscle symptoms without any notable shortness of breath of exertion or wheezing. There was no other evidence of any connective tissue diseases.
There was no ptosis, double vision or fatiguability to suggestive myasthenia. Patient appeared to be clinically euthyroid without any overt features of hypothyroidism. There was no history of statin use at the time of the presentation or prior to that. Patient denied any similar history previously nor was there a history of a similar disease among her family members.
Examination revealed bilateral symmetrical proximal muscle weakness with a muscle power of 4/5 in all four limbs. Reflexes were intact without any muscle wasting. There were no overt features of dermatomyositis. Auscultation of the lungs revealed a few bilateral basal fine end inspiratory crepitations suggestive an interstitial lung disease. Second heart sound was of normal intensity. A diagnosis of inflammatory myositis was considered with a concurrent interstitial lung disease. With this clinical text she was thoroughly investigated.
Creatinine phosphokinase levels were elevated with a value of 1435 u/l. Inflammatory markers were elevated with a ESR of 54 though the CRP was only slightly elevated. ANA was negative. Findings on electromyography was consistent with an inflammatory myositis. Muscle biopsy which was carried out revealed inflammatory cells in between the muscle fibers causing complete necrosis of some of the muscle fibers. Anti Jo-1 antibody was positive. HRCT revealed bilateral homogenous sub pleural basal ground glass opacification suggestive of non-specific interstitial pneumonitis (Fig. ). She was started on oral prednisolone 1 mg/kg/day with azathioprine 50 mg per day which was later increased to 100 mg per day. Subsequently her muscle power improved, CPK levels normalized and the cough which was present improved.
She attended her follow up clinic visits and was compliant with her medication. She was in remission for 2 years with low dose prednisolone and azathioprine. She was asymptomatic with no muscle pains, proximal muscle weakness and CPK levels were within normal range. She continued to be free from any cough or shortness of breath. ESR was persistently normal with values in the mid 20’s.
Following a period of unsatisfactory compliance of 4 weeks, she presented with fissuring and cracking of the fingers suggestive of mechanic’s hands (Fig. ) without any muscle pain or weakness. She denied any recurrence of the cough which she had during the initial disease presentation and did not have any shortness of breath. Her CPK was within normal limits at that time. Though there was no evidence of a systemic relapse, the steroid dose was up titrated while continuing azathioprine. However, the mechanic’s hands did not improve and subsequently in the following month she started to complain of a pain in her thighs and arms with a subtle weakness. Her CPK had risen to 1427 u/L and ESR risen to 47. Given the overall clinical picture it was decided that she required escalation of her immunosuppressive therapy. She was started on IV cyclophosphamide 500 mg every 2 weekly and after 3 doses the skin manifestations started to resolve and CPK had normalized (Fig. ). Hydroxychloroquine 200 mg daily was added as patient had prominent dermatological manifestations with photosensitivity (Table ).
Repeat HRCT revealed stable nonspecific interstitial pneumoniae without any radiological progression. Lung function tests revealed a restrictive lung disease with a FVC of 78% of predicted, FEV1 of 94% of predicted with FEV1/FVC of 124%. DLCO was 49%.


A 17-year-old male was injured in a fall while riding a motorcycle. He presented left knee pain, swelling and partial active mobilities. The extensor mechanism was intact, and he had no neurovascular deficits. At clinical examination, he presented a positive posterior drawer test and positive varus stress test with a soft endpoint. The radiograph (X-ray) and computed tomography scan (CT scan) showed a displaced avulsion fracture of the PCL tibial attachment, a displaced avulsion fracture of the LCL femoral attachment and a comminuted fracture of the inferior pole of the patella (Figures and ). The PCL tibial avulsion fracture was better characterized by magnetic resonance imaging (MRI) (). The limb was immobilized with a cast and the patient was proposed for surgical intervention.


A 25-year-old G3P0202 presented at 22w3d gestation for evaluation of a newly discovered retroperitoneal mass found during workup for abdominal pain. The patient had experienced one year of ongoing, worsening abdominal pain. She had a history of two prior preterm deliveries at 36 weeks gestation but otherwise was healthy with no chronic medical conditions.
Magnetic resonance imaging (MRI) evaluation revealed a 13 cm transverse by 8 cm anterior-posterior by 9 cm craniocaudal smoothly marginated mass inferior to the pancreas which encased the left renal vessels, displaced the inferior vena cava (IVC) anteriorly, and partially encased the abdominal aorta (). A computerized tomography (CT) guided biopsy was unable to be performed due to the surrounding anatomy and gravid uterus; therefore, a laparoscopic biopsy was planned. CT of the chest was performed showing no evidence of metastatic disease. The patient was readmitted for planned laparoscopic biopsy at 27w2d gestation. She was given corticosteroids for fetal lung maturity prior to the procedure due to the increased risk of preterm birth. Continuous fetal monitoring was performed throughout the surgery and was noted to be reassuring for the gestational age.
Histopathology from the retroperitoneal biopsy demonstrated high-grade spindle cells with areas of herringbone pattern and small round blue cells (). Frequent mitoses were noted (8/HPF). Immunohistochemistry (IHC) revealed tumor cells to be CD56+, bcl-2+, weakly TLE1+, partially CD34+, and focally S100+. Cells were negative for pankeratin, CAM 5.2, EMA, CD99, SOX10, SMA, desmin, synaptophysin, SALL4, CD10, CD31, CD117, WT1, and estrogen receptor. Fluorescence in situ hybridization (FISH) was positive for SYT (SS18) gene rearrangement. While the IHC profile was not specific, the morphologic features and positive SYT rearrangement result were consistent with a diagnosis of poorly differentiated synovial sarcoma, clinically staged IIIB (T3N0M0).
The case was discussed at a multidisciplinary sarcoma tumor board in consultation with Surgical Oncology, Medical Oncology, Radiology, Pathology, Teratology, and Maternal-Fetal Medicine with decision for neoadjuvant chemotherapy with doxorubicin and ifosfamide with modified dosing during the prepartum period as described in Mir et al []. The patient was admitted at 29w6d for cycle 1 of chemotherapy and at that time had a repeat baseline MRI which redemonstrated the now 15.5 × 10.2 × 10.6 cm mass encasing right renal pelvis and aorta, displacing left renal vessels posteriorly and IVC anterolateral (). She received doxorubicin (50 mg/m2 day 1) and ifosfamide (2.5 g/m2/day, days 1-2) with standard mesna rescue without notable maternal side effects or fetal complications. She continued to follow closely for prenatal care and serial fetal growth ultrasounds. The timing for delivery was determined through multidisciplinary discussion with neonatology, maternal-fetal medicine, and oncology. Fetal antenatal testing was overall reassuring with normal fetal growth; however, the amniotic fluid index (AFI) was found to be borderline low (5.9 cm, with maximum vertical pocket (MVP) of 2.3 cm) and decreased from an AFI of 15.3 cm with an MVP of 5.7 cm prior to cycle 1 of neoadjuvant chemotherapy. Further, the patient had a prior history of two spontaneous preterm deliveries at approximately 36 wks. There was therefore a concern that delaying delivery for a second cycle of chemotherapy could result in a spontaneous delivery close to the administration of the chemotherapeutic agents which theoretically would increase the risk of neonatal adverse effects. Given the above considerations, the decision was made to proceed with a scheduled induction of labor (IOL) 3 wks after cycle 1 of neoadjuvant chemotherapy and to proceed with the remaining cycles postpartum. She was given a second course of corticosteroids for fetal lung maturity prior to her IOL, and she then underwent an uncomplicated IOL resulting in a vaginal delivery of a 1870 g (32nd percentile) male neonate with APGAR scores of 8 and 9 at 1 and 5 minutes, respectively. The patient had an uncomplicated postpartum course and was discharged home. The neonate's NICU course was complicated by mild respiratory distress syndrome requiring continuous positive airway pressure (CPAP) on admission which was weaned to room air by day of life (DOL) 7 as well as hyperbilirubinemia requiring 2 days of phototherapy. Otherwise, he had an uncomplicated NICU stay, was advanced to full PO feeds, monitored for temperature stability and adequate weight growth, and was discharged home on DOL 20 (corrected gestational age 36w0d).
The patient continued with neoadjuvant chemotherapy with cycle 2 beginning 1 week postpartum. She received doxorubicin (25 mg/m2/day, day 1-3) and ifosfamide (2.5 g/m2/day, day 1-4) with standard mesna rescue for the postpartum cycles. Restaging CT was performed following cycle 3 demonstrating marked decrease in the size of the retroperitoneal mass (). She went on to complete three additional neoadjuvant chemotherapy cycles (6 total) without significant complication with restaging imaging again demonstrating substantial reduction in tumor size, then measuring 3.7 cm × 6.3 cm in greatest dimension ().
Following completion of neoadjuvant chemotherapy, she received neoadjuvant external beam radiation therapy consisting of 5750 cGy in 25 fractions, which was completed without significant complication. She then went on to undergo radical resection of the retroperitoneal tumor including en bloc resection of infrarenal IVC and aorta and portion of omentum with 10 cm × 14 mm aortic reconstruction with tube graft and omental flap coverage of aortic prosthetic reconstruction. Her surgical recovery was unremarkable except for requirement of packed red blood cell transfusion twice for asymptomatic anemia with hemoglobin < 7 gm/dL on postoperative day numbers 3 and 7 with adequate response. She was discharged on postoperative day number 7 in good condition.
Pathology from the resection specimen demonstrated a 6 cm mass that on histologic evaluation exhibited marked treatment effect with only microscopic foci of residual synovial sarcoma in a background of necrosis, pigment deposition, histiocytic infiltrate, and inflammatory cells (). The tumor focally invaded the soft tissue surrounding the proximal aortic resection margin with all other margins uninvolved by tumor.
Following resection of her sarcoma, the patient was followed with routine surveillance CT imaging including the chest, abdomen, and pelvis at 3-month intervals. Unfortunately, she developed an isolated pelvic recurrence 13-month postresection. As of this writing, she is undergoing salvage chemotherapy with neoadjuvant intent. Her 23-month-old son is healthy and has achieved appropriate developmental milestones.


A 29-year-old Caucasian male sought medical attention due to face swelling and foamy urine for the past 3 months. He denied a family history of kidney disease, consanguinity, or Asian ancestry, and reported hypothyroidism with continuous use of levothyroxine 150 μg qd. His physical examination revealed blood pressure within the normal range and 2+/4+ lower-limb edema.
Urinalysis showed proteinuria (4+/4+), dysmorphic hematuria (54/high power field) and 24-h proteinuria of 12.5 g. Serum laboratorial tests included creatinine 0.94 mg/dL, eGFR 109 mL/min/1.73m2 (CKD-EPI), total protein 3.6 g/dL, albumin 2.3 g/dL, cholesterol 284 mg/dL, LDL 200 mg/dL, HDL 49 mg/dL, and triglycerides 175 mg/dL. Blood cell counts, serum complement and hydroelectrolytic parameters were within the normal ranges. Hepatitis B and C and HIV serologies were negative as well as the screening for diabetes and auto-immune diseases. Serum and urine protein electrophoresis did not detect anomalous proteins and echography revealed kidneys with normal size and features.
The patient underwent a kidney biopsy (Fig. ) with light microscopy evincing 12 glomeruli, two of them globally sclerosed. All glomeruli with open capillary loops showed increased volume and mild expansion of mesangial matrix, with slight hypercellularity. Intraluminal deposits of hyaline material were observed in glomerular capillaries with a compact appearance, pale and laminated, leading to loop distension consistent with lipoprotein thrombi. Basement membrane thickening was detected in some capillaries, while tubular atrophy and interstitial fibrosis were present in approximately 30% of the cortical area and a mild lymphocytic infiltrate was seen in fibrotic areas. Immunofluorescence was negative for immunoglobulins and complement fractions. Electron microscopy revealed dilated glomerular capillary loops with luminal obstruction by thrombi formed by acellular and transparent material associated with vesicle formation, a pattern consistent with lipoprotein thrombi. The diagnosis of LPG was therefore established.
Serum apolipoprotein E was 7.2 mg/dL (normal range: 2.3–6.2 mg/dL). An investigation with next-generation sequencing applied to a gene panel directed to familial hypercholesterolemia identified the pathogenic variant c.527G > C, p.Arg176Pro in APOE, called Osaka/Kurashiki [–], in heterozygosity (Fig. ). This variant is not described in the gnomAD, 1000 genomes or ABRAOM databases, and the corresponding amino acid (aa) position is conserved in mammals. This variant is classified as likely pathogenic according to the American College of Medical Genetics and Genomics criteria [], reaching high pathogenicity scores on SIFT (0.01) and DANN (0.996), and a moderate score on Polyphen2 (0.89). The patient remains on simvastatin 20 mg qd and ezetimib 10 mg qd after 3 years, with serum creatinine of 2.37 mg/dL and 24-h proteinuria of 3.7 g.


A 34-year-old Caucasian man came to a nephrology service for renal dysfunction and systemic hypertension. The patient reported intermittent episodes of lower-limb edema for the last 3 years. He denied Asian ancestry, but referred a family history of renal disease, affecting his sister, aunt and cousin. His physical examination revealed hypertension, but an absence of lower-limb edema.
Laboratorial tests showed BUN 99 mg/dL, serum creatinine 10.7 mg/dL (CKD-EPI 5.6 mL/min/1.73m2), absence of electrolytic imbalances, metabolic acidosis (venous gasometry with pH 7.25 and bicarbonate 12 mEq/L), hemoglobin 6.2 g/dL, cholesterol 155 mg/dL, HDL 22 mg/dL, LDL 79 mg/dL, triglycerides 277 mg/dL, serum albumin 3.1 g/dL, and 24-h proteinuria 2.7 g. Serologies for hepatitis B and C and HIV and screening for auto-immune disorders and diabetes were negative. Serum and urine electrophoresis did not show abnormal protein peaks. Echographic analysis revealed a mild reduction in renal size and increased echogenicity.
A kidney biopsy showed 16 glomeruli, 14 of them globally sclerosed (Fig. ). The two non-sclerosed glomeruli displayed endothelial cells with expanded volume obstructing the capillary lumen, cells with foamy cytoplasm, and segmental mesangial expansions. Interstitial fibrosis and tubular atrophy were diffuse and associated with hyaline arteriosclerosis. Sudan staining in a frozen specimen was positive in endothelial cells. Immunofluorescence showed C3 (+ 3/+ 3) and IgM (+ 2/+ 3) with segmental and global distribution following an entrapping pattern. Electron microscopy revealed dilated glomerular capillary loops with lipid droplets of variable sizes in the capillary lumen, a finding consistent with lipoprotein thrombi. These findings were consistent with advanced chronic nephropathy secondary to LPG. The patient progressed to renal replacement therapy after 2 months of conservative management. Whole exome sequencing also revealed the APOE c.527G > C, p.Arg176Pro variant in heterozygosity (Fig. ). The patient was transplanted a year ago after 4 years on RRT.


A 40-year-old male with no past medical history was found unconscious by bystanders after he had been out for a recreational jog. Upon the arrival of medical services, the patient was found to be in VF cardiac arrest and required two shocks before the return of spontaneous circulation. The downtime was reported to be about 15 minutes. Per history obtained from family members, the patient had never experienced any cardiac symptoms such as palpitations or chest pain and had no COVID-19 symptoms.
The patient had no significant personal medical history, took no medications, and exercised regularly with no difficulties. Family history was notable for coronary artery disease (CAD) in his brother, which had been diagnosed at age 50, and myocardial infarction (MI) in his father at age 72. There was no family history of sudden cardiac death.
Given the patient’s young age and absence of underlying cardiac issues, the differentials for his VF arrest were broad. Etiologies considered included ischemic heart disease, structural heart diseases such as hypertrophic cardiomyopathy, anomalous origin of coronary arteries, myocarditis, arrhythmogenic right ventricular cardiomyopathy, primary electrical abnormalities such as long QT syndrome, and Brugada syndrome, and non-cardiac etiologies such as a massive pulmonary embolism (PE).
A basic metabolic panel showed no significant electrolyte abnormalities. The initial troponin-T level was within normal limits. Electrocardiogram (ECG) on admission showed normal sinus rhythm, non-specific T-wave changes in anteroseptal leads, and a QTc of 445 ms (Figure ). A transthoracic echocardiogram (TTE) showed normal LV systolic and diastolic functions with no valvular pathology or regional wall motion abnormalities. A chest CT with PE protocol showed no significant pulmonary emboli. Per institutional policy, the patient was tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via nasopharyngeal swab polymerase chain reaction (PCR) test, which returned positive. A subsequent SARS-CoV-2 antibody test was also positive.
The patient was emergently intubated for airway protection and taken to the catheterization lab where coronary angiography showed non-obstructive proximal left anterior descending (LAD) artery disease with 55-60% stenosis and flow distal to the lesion with Thrombolysis in Myocardial Infarction (TIMI) score of 3. Left circumflex and right coronary arteries were disease-free (Figures , ). The left ventriculogram showed normal systolic function with no wall motion abnormalities. The patient was then admitted to the ICU for therapeutic hypothermia. He received convalescent plasma, remdesivir, and dexamethasone for his COVID-19 infection. During his ICU stay, he had one episode of monomorphic ventricular tachycardia (VT) in the setting of agitation and hypoxia that terminated spontaneously in less than three seconds. He continued to improve and was eventually extubated and discharged home.
Later on, an outpatient single-photon emission CT (SPECT) pharmacological myocardial perfusion scan showed no anterior ischemia or scar (Figure ). A subsequent cardiovascular magnetic resonance (CMR) imaging showed normal LV and RV sizes and functions with no late gadolinium enhancement. The patient eventually received a single-chamber VVI implantable cardiac defibrillator (ICD) for secondary prevention of VF. Subsequent outpatient genetic testing with INVITAE® Arrhythmia and Cardiomyopathy Comprehensive Panel (Invitae, San Francisco, CA) revealed no genetic variants known to cause arrhythmia. At the one- and four-month follow-ups, the patient remained asymptomatic and ICD interrogation revealed normal sinus rhythm with no episodes of arrhythmia.


A 5-year-old Caucasian female presented to our hospital with an intense dry cough and dysphagia for 2 weeks before the visit with no other symptoms. Her personal history was free of diseases. She was born second of her siblings by third-degree relative parents. Clinical examination revealed small enlarged lymph nodes at the level of the neck and immobile mass at the level of her right axilla with light edema. There were diffused café au lait spots all over her body. Auscultation revealed pulmonary wheeze sounds with a midsystolic murmur 2/6. The rest of the examination was within normal limits. Her weight (W) was 20 kg and her height (H) 110 cm. Complete cellular blood count (CBC) was completely normal. Because chest X-ray (CXR) showed a mass in the mediastinum, chest computed tomography (CT) was performed. Chest CT revealed a big mass along the mediastinum (Fig. ). She underwent a surgical biopsy. The histological results (Fig. ) revealed T-cell lymphoblastic lymphoma, and the malignant lymphocytes showed positivity for CD3 and terminal deoxynucleotidyl transferase (TdT), whereas CD20, myogenin, cytokeratins (CK), epithelial membrane antigen (EMA), desmin, and WT1 were negative. Ki67 was 50%. The girl went into a coma during the resection surgery and stayed in the intensive care unit (ICU) for 10 days, then died from cardiac arrest. We suggest that the fatality was due to compression on the air track by the mass after the anesthesia.


An 18-month-old Caucasian female was admitted to a private clinic with a productive cough that was diagnosed mistakenly as bronchitis. Based on that diagnosis, she took many medications (antibiotics and pain relievers) and showed partial improvement. She came to our hospital because of the increasing dyspnea. Her personal history was free of diseases. She was born third of her siblings by third-degree relative parents. Clinical examination revealed the following: diffused café au lait spots all over her body and congenital Mongolian spots with enlarged submaxillary lymph nodes without any palpable visceral enlargement. Chest auscultation revealed diffuse pulmonary crackles. The rest of the examination, laboratory tests, brain CT, and bone marrow biopsy were all within normal limits. Her weight (W) was 10 kg and her height (H) 78 cm with head circumference 48 cm. Complete cellular blood count (CBC) was completely normal. Computed tomography (CT) revealed an enlarged palatine tonsil and enlarging in the mastoid lymph nodes and submaxillary lymph nodes. The nodes measured no more 11 mm. CT also showed a mass in the mediastinum (Fig. ). In addition, there was a hyperplasia in the thymic area extending to the front of the heart. Mild hepatomegaly and enlarged paraaortic lymph nodes were also found. The histological results (Fig. ) revealed T-cell lymphoblastic lymphoma with positivity for CD3 and TDT, whereas CD20, myogenin, CK, EMA, Desmin, and WT1 were negative. Ki67 was 50%. The girl has been undergoing chemotherapy (cytarabine, vincristine, ifosfamide) till now, and she is getting well, with no respiratory symptoms.


A 71-year-old female presented to our hospital with gradually worsening balance, ataxia, and dizziness for one year. Six months later she started having a new-onset headache which was progressively getting worse, was not relieved with over-the-counter medications. Headache was associated with loss of peripheral vision without any focal weakness, dysphagia, bladder or bowel incontinence, irritability, and apathy. She came to the emergency department for evaluation. Vital signs including body temperature, blood pressure, and heart rate were within normal limits. On neurological examination muscle strength was 4 out of 5 in all four extremities, gait was impaired, and rest examination was normal. Computed tomography (CT) scan of the brain demonstrated a hyperdense focus within the right posterior parietal lobe (Figure and Figure ).
This was followed up with a magnetic resonance imaging (MRI) of the brain that demonstrated a new homogeneously enhancing lesion abutting the grey-white matter of the right parietal lobe concerning brain metastases versus primary brain neoplasm. Therefore, extensive imaging was carried out to look for extracranial disease and distant metastases. A CT scan of the chest, abdomen, and pelvis was normal. On evaluation by the neurosurgery team, the patient was advised to undergo a brain mass biopsy to confirm the diagnosis. She refused the biopsy; hence she was presumed to have a benign tumor and was followed up with a repeat MRI in one month. A repeat MRI two months later showed significant interval enlargement of the lesion with significant edema surrounding the lesion along with interval development of hemorrhage (Figure ).
As there was significant enlargement of the tumor over the course of two months, and she had a left hemianopsia with deficit to the right visual field. Hence patient was admitted and underwent right craniotomy with resection of the tumor. She had no immediate post-operative complications. Histopathology was confirmatory for diffuse large B-cell lymphoma, non-germinal center B-cell type (Figure ). Fluorescence in situ hybridization (FISH)/cytogenetics was negative for CD10, MYC, and IGH-BCL2 fusion but positive for rearrangement of BCL2.
A postoperative CT head was negative for any mass, mass effect, midline shift, hemorrhage, or large vascular territorial acute infarct (Figure ).
She was doing well post surgery, her physical exam was at baseline. Three days after the surgery she was discharged to a rehabilitation facility with a recommendation to continue dexamethasone 4 mg every 6 hours. Three weeks after surgery, she was seen by medical and radiation oncology team for discussion regarding the initiation of systemic therapy. On oncology evaluation she complained of persistent left-sided visual field deficits, however no further episodes of persistent headaches since her surgery. She continued to have quite a significant gait ataxia and was ambulating using a walker at home, and a wheelchair while going out of the home. On examination, she was ill-appearing, lethargic, minimally verbal, and wheelchair-bound.
As primary CNS lymphoma is an extremely rare tumor with generally aggressive biology compared to nodal lymphomas there was discussion regarding all the treatment options including combination chemotherapy. Generally, the mainstay of treatment is induction therapy with intensive combination chemotherapy using high-dose methotrexate, typically in combination with anti-CD20 agent rituximab or other chemotherapy agents, followed by consolidation with either whole brain radiation or autologous stem cell transplant in select individuals. These types of treatments are typically administered in the inpatient and require quite a frequent lab monitoring of drug levels. As these treatments were not available at our institution patient was referred to the larger tertiary care center.
Other alternatives for induction, especially in elderly patients with poor performance status, include either rituximab + temozolomide or whole brain radiation therapy (WBRT) as monotherapy. We discussed that the data for rituximab + temozolomide is mostly retrospective and studied in patients with progressive, refractory disease, and there is little or no data to the upfront setting, however, it is a reasonable option to consider in patients who were otherwise ineligible for more intensive approach. Alternatively, local therapy with WBRT can be utilized, although it is associated with long-term neurotoxicity, and may be reserved for the second-line setting. After extensive discussion with the patient and family about all the treatment options, the patient declined the second opinion and agreed with starting treatment with temozolomide and rituximab, using a similar dosing schedule as was used in the relapsed/refractory setting (Temozolomide 150 mg/m2 once daily for five days every 28 days, initially in combination with rituximab (for four cycles), followed by temozolomide monotherapy: 150 mg/m2 once daily for five days every 28 days for eight cycles).
The patient was still deciding on treatment options and came for follow-up with oncology in one month. Since her last visit, she had a progressive functional decline, had three hospital admissions with failure to thrive, weakness. She was requiring significant assistance with any degree of activity. She was wheelchair bound, had been experiencing significant difficulty performing any tasks, including standing up from her wheelchair. Given the patient's relative frailty and inability to travel to a facility where she will be treated with high-dose methotrexate, a plan was made to continue with a less aggressive alternative like rituximab, temozolomide, and lenalidomide. The patient's functional status continued to decline, and any treatment moving forward was unlikely to provide any clinically meaningful benefit; hence the goal of care was discussed, focusing on prognosis, aggressive treatment vs. pursuing hospice care. After informed discussion, the family and the patient decided to continue with hospice.


A 38-year-old woman from Southeast Asia, recently known to have been diagnosed with TB and SLE, who started on treatment, was brought to our hospital via Emergency Medical Services (EMS) due to fever, recurring seizures, and decreased level of consciousness.
She had arrived from her home country four months prior and was shortly later admitted to the hospital for an incidental diagnosis of active TB discovered due to chest X-ray findings on pre-employment screening. Her hospital admission, however, was significant for an observation of a baseline mild neutropenia and lymphopenia and upon initiation of first-line anti-TB medications, she had severe worsening of neutropenia and development of neutropenic sepsis attributed to rifampicin. During this admission, she was noticed to have a malar rash and subsequent testing revealed a positive antinuclear antibody (ANA) of 1:1280, positive anti-double stranded DNA (anti-dsDNA) antibody, positive anti-smith antibody (anti-Sm), positive anti-Ro antibody, positive antinuclear ribonucleoprotein (anti-RNP) antibody, and low complement levels. Subsequently, she was diagnosed with SLE and started on hydroxychloroquine. She was discharged on second-line anti-TB medications to avoid isoniazid for its association with drug-induced lupus and rifampicin due to its association with neutropenia which she had previously developed.
However, the patient was found to have stopped her anti-TB regimen and her hydroxychloroquine by herself after discharge which was subsequently resumed a month, later on, follow up. Her subsequent course before the current presentation was also eventful for hospital admission due to severe Clostridium difficile sepsis requiring ICU admission. However, the patient was discharged in a healthy condition with no residual neurological deficits.
A month later, the patient was discovered at home to be unresponsive after an episode of vomitus followed by a tonic seizure aborted with medication. She was also found to have a fever of 39.8 degrees Celsius. She had another focal seizure before arrival to hospital and upon arrival, was observed to have repeated convulsions varying from generalized tonic-clonic seizures to focal seizures lasting minutes aborted with IV lorazepam. No collateral history regarding events before this could be taken. She was neither known to have had any seizures in the past nor was there any history of alcohol or drug abuse.
Upon initial assessment, she had a Glasgow Coma Scale (GCS) of 8/15 (E2 V2 M4) with hemodynamic stability. She was noted to have bilaterally equal and reactive pupils, three millimeters in size. She had obvious neck stiffness present. The remainder of the exam was unremarkable. Blood investigations showed a mildly elevated neutrophil predominant leukocytosis, with normocytic normochromic anemia. Aside from hypokalemia on initial presentation, all electrolytes were within normal limits. Initial imaging included a CT scan of the brain (Figure ) which revealed bilateral subcortical and deep white matter hypodensities along with bilateral temporal lobe hypodensities suspicious of viral encephalitis.
She subsequently underwent a lumbar puncture (LP) which revealed a clear and colorless cerebrospinal fluid (CSF). The analysis of CSF is as follows: leukocytes cell count was 27/μL with 60% neutrophils and 1013/μL red blood cells (RBC). Glucose was decreased at 2.06 mmol/L (serum glucose 5.6 mmol/L) with an elevated CSF protein (1.89 g/L normal range 0.15-0.45 g/L). Polymerase chain reaction (PCR) testing for common viruses including HSV-1/HSV-2 were all found to be negative, along with a negative screen for TB PCR and acid-fast bacilli (AFB) smear from CSF. Considering a provisional diagnosis of acute meningoencephalitis of possible viral, bacterial or tuberculous origin, she was started empirically on ceftriaxone, ampicillin, vancomycin, acyclovir, and dexamethasone all intravenously and her home TB medications were resumed. She was initiated on IV levetiracetam for seizures. Following negative Gram stain results, vancomycin was stopped and remaining medications were continued.
MRI of the brain (Figure ) was done and it showed diffuse areas of diffusion restrictions with no definitive intracranial vascular occlusion.
These findings along with the history of SLE, the low complement levels, and the positive Anti-dsDNA (235 IU/mL reference range for positive test > 15 IU/mL) and anti-SmD (23 U/mL, reference range for positive test > 10 IU/mL) raised the possibility of SLE meningoencephalitis, however, due to the lack of a definitive diagnostic test and the fear of TB dissemination with high doses of immunosuppressant medications; no treatment for SLE other than the hydroxychloroquine was initiated at that time.
Despite the treatment directed toward TB and bacterial meningitis, the patient’s condition continued to worsen and her agitation and confusion were difficult to control despite using high doses of antipsychotics and benzodiazepines.
Due to the lack of improvement, it was decided to redirect the treatment towards SLE as a cause of the patient’s neuropsychiatric manifestations and methylprednisolone 500 mg intravenously was given once daily for three days along with the other ongoing treatment over the next few days, while no significant improvement in the clinical state of the patient was noted. Repeat MRI of the brain (Figure ) showed mild regression of the previously seen diffusion restricted areas and based on these findings it was decided to continue the treatment for SLE with IV cyclophosphamide 500 mg.
Over the two weeks after the first dose of cyclophosphamide the patient remained in a state of confusion, however, she became less agitated, and smaller doses of antipsychotics and benzodiazepines were needed to control her agitation. Hence, the treatment with cyclophosphamide was continued and the patient received four more doses with an interval of two weeks between every other dose along with the prednisolone and the TB treatment. The patient subsequently showed remarkable improvement as she became less confused, started to be able to take care of her basic needs, recognize her name, and follow simple commands.
Fortunately, the patient did not develop any signs or symptoms to suggest dissemination or worsening of her previous TB infection.


A 36-year-old female patient initially presented with recurrent attacks of upper abdominal pain, having been diagnosed with alcohol-related chronic pancreatitis. She had a past medical history of depression, pulmonary embolism, portal vein thrombosis, sickle cell trait, and pituitary microprolactinoma. Her medications included furosemide, pregabalin, methadone, omeprazole, pancreatin, thiamine, and vitamin B. She had 15 pack-years of smoking history and consumed about 42 units of alcohol per week. She was also an intravenous (IV) drug abuser. On examination, she had epigastric tenderness with marked ascites. There were no signs of jaundice or stigmata of chronic liver disease.
Liver function tests were remarkable for raised alkaline phosphatase (ALP) of 337 U/L (normal range: 30-130) and mildly raised alanine aminotransferase (ALT) of 96 U/L (normal range: 0-50). Notably, total bilirubin, albumin, amylase, C-reactive protein (CRP), renal function test, and full blood count were normal. Tumor markers including carcinoembryonic antigen (CEA) and cancer antigen 19-9 (CA 19-9) were within normal limits. Fecal elastase level was 23 ug/g (normal range: >200), suggestive of severe pancreatic insufficiency. HbA1C was 111 mmol/mol (normal range: <42), suggesting type 3C diabetes mellitus.
CT scan of the abdomen and pelvis with contrast revealed features of chronic pancreatitis along with a 7 x 4.5-cm fluid collection inferior to the uncinate process of the pancreas with intra and extrahepatic biliary dilatation. MRI of the pancreas and abdomen confirmed findings of 8 x 6 x 6-cm pseudocyst in the pancreatic head causing mass effect (Figure ), leading to marked dilatation of the pancreatic duct (PD) at about 6 mm, prominent common bile duct (CBD) of about 11 mm with dilatation of the intrahepatic biliary tree. Moderate ascites was also seen.
100 ml of blood-stained, straw-colored ascitic fluid was obtained under ultrasound guidance. Fluid was sent for cytology and microbiology. Microscopy showed leucocytes of 472/mm3, lymphocytes of 5%, and neutrophils of 95%. There was no bacterial growth on culture. serum-ascites albumin gradient (SAAG) was 5 and ascitic fluid amylase was 24 U/L, suggesting reactionary ascites that was infected. Cytology of the fluid revealed fluid predominated by neutrophilic polymorphs and reactive lymphoid elements. The patient was treated conservatively with intravenous antibiotics for infected ascitic fluid and was also started on subcutaneous insulin and oral metformin for glucose control. Her symptoms improved on conservative management, and hence she was discharged with outpatient follow-up.
She re-presented after a couple of months with obstructive jaundice (markedly raised bilirubin and ALP). On this occasion, magnetic resonance cholangiopancreatography (MRCP) revealed dilatation of the intrahepatic biliary tree, dilatation of the CBD to 13 mm, and dilated PD up to 7 mm secondary to extrinsic obstruction at the level of the pseudocyst in the head of the pancreas (Figure ).
Endoscopic ultrasound (EUS) was performed and showed a 2.6-cm thick-walled cyst in the head of the pancreas with a 1.5-cm soft tissue nodule in the cyst wall. There was freely floating organized material within the cyst. No locoregional lymph nodes were seen. The coeliac axis and portal confluence were normal. The CBD and main PD were dilated by the cyst. There were no major EUS signs of chronic pancreatitis based on Rosemont criteria. The cyst was aspirated to dryness by EUS guidance with a 20-gauge EchoTip ProCore® needle (Cook Medical, Bloomington, IN). Hemorrhagic, non-mucinous fluid was obtained for chemistry and cytology. The soft tissue nodule was sampled with a 22 GF AcquireTM fine-needle biopsy device (Boston Scientific, Marlborough, MA). The findings from EUS, fluid biochemistry, and the biopsy of cyst nodules were consistent with a pseudocyst. There was no evidence of malignancy or infection. After EUS-guided aspiration of the cyst, her jaundice improved with a significant fall in bilirubin and ALP levels.
After six months, the patient presented with pruritus, worsening abdominal pain, abdominal distension, jaundice, pale stools, and dark urine. She had still been drinking about 30 units of alcohol per week. Examination revealed icterus and uniformly distended abdomen with epigastric tenderness, no guarding or rigidity, and normal bowel sounds.
Her full blood count, renal function, and electrolytes were within normal limits. CRP was mildly elevated at 34 mg/L (0-10). Liver function profile showed albumin of 32 g/L (35-50), protein of 72 g/L (60-80), total bilirubin of 128 µmol/L (0-22), ALP of 844 U/L (30-130), ALT of 53 U/L (0-50) with normal prothrombin time (PT) and activated partial thromboplastin time (aPTT). Renal function and electrolytes were within normal limits.
CT abdomen suggested recurrence of the pseudocyst in the pancreatic head, causing compression of the CBD and PD leading to dilatation of upstream PD, CBD, and intrahepatic biliary ducts. There was a further large cyst measuring 6.6 x 3.7 cm posterosuperior to the pancreas along with a larger right renal cyst. MRI confirmed evidence of chronic pancreatitis and two pancreatic pseudocysts. One of the cysts in the head of the pancreas measuring 4.8 x 4.6 cm was causing local pressure effect on the CBD, and there was intra and extrahepatic biliary dilatation with the CBD measuring up to 15 mm (previously 13 mm) (Figure ). The cyst was also causing compression of the pancreatic duct, which was dilated to approximately 7 mm. The other large peripancreatic cyst measuring about 7 x 4 cm located posterosuperior to the body of pancreas had ruptured causing collection sized 12.9 x 11.2 x 13.0 cm, compressing on the right renal capsule (Figure ).
Ultrasonography-guided percutaneous drainage of the cyst was performed. The fluid obtained from the drainage was turbid and bloody with no growth of microorganisms on culture and negative for malignant cells on cytology. Following the drainage, an endoscopic retrograde cholangiopancreatography (ERCP) was performed that showed a distal CBD stricture, which was stented using a fully covered self-expandable metal stent. Brushings retrieved during ERCP did not show any evidence of malignancy.
Outcome and follow-up
Following the CBD stent insertion and the percutaneous drainage of the ruptured pseudocyst, her symptoms markedly improved. ALP and total bilirubin levels returned to normal and she was discharged with follow-up in gastroenterology outpatient clinic. She remained well for a while before she re-presented in a couple of months with severe right loin pain and nausea. On this admission, she was febrile with a CRP of 291 mg/L (1-10) and a white blood cell count of 16.9 x 109/l (4-11). CT abdomen was suggestive of infected residual collection at the site of the previous drainage with a significant reduction in the size of the pseudocysts and preserved patency of the metallic biliary stent (Figure ). She responded well to IV co-amoxiclav and was discharged from the hospital. The patient remained well thereafter, with no further recurrences of obstructive jaundice during the one-year follow-up. Stent removal was planned in a few months but was delayed due to the current coronavirus disease 2019 (COVID-19) pandemic.


This report is based on the informed consent of the patient and the approval of the appropriate ethics committee.
We report a case of a 56-year-old man with an olfactory neuroblastoma. The patient's chief complaint was nasal obstruction and left epistaxis. Magnetic resonance imaging showed that the tumour occupied mainly the left olfactory cleft and was isointense on T1 and high intense on T2 and showed no thickening of the left dura mater or invasion of the middle cranial fossa (shown in Figures and ). The left frontal sinus was filled with secondary mucus, and no tumour component was observed. However, both sides of the frontal sinuses were hypoplastic, with thickening of the septum of the frontal sinus and a difference in the anteroposterior (AP) diameter of the frontal sinus between the right and left sides (shown in ). The AP diameter was 9.6 mm on the right and 5.9 mm on the left, and the skull base-frontal sinus angle (SBA) was 126° on the right and 107° on the left (shown in Figures and ).
The patient underwent endoscopic anterior cranial resection for treatment. To determine the anterior tumour resection line, the outside-in EMLP was selected. First, the first olfactory fibre was identified on the right side (non-tumour side) (shown in ), and the depths of the right frontal sinus and the right anterior skull base were confirmed by Draf 2B (). Subsequently, Draf 2D [] was used to approach the left frontal sinus from the right frontal sinus via the septum of the frontal sinus (shown in ). At this time, the first olfactory fibre was identified on the left side (tumour side), and a space was observed on the left side at the same depth as the right frontal sinus, and the space was opened as if it was the frontal sinus. After opening the space by 4 mm, CSF leakage was observed, and the skull base was judged to be damaged (shown in ). When the position of the frontal sinuses was reoriented and the bilateral frontal sinuses were converted to a single sinus, the left anterior skull base protruded more than the right anterior skull base, and it was confirmed that the protruded region was damaged (shown in ). Fortunately, the injured area of the skull base overlapped with the resected area of the tumour (shown in ), and the skull base was reconstructed to be water-tight by suturing the dura mater to the fascia with 11 stitches of 6-0 proline (shown in ). Additionally, the fascia and nasal septal cartilage were in-layed between the dura mater and the skull base (shown in ). Finally, the nasoseptal flap was over-layed to complete the operation (shown in ). The postoperative course was good without CSF leakage or intracranial haemorrhage, and the patient was discharged one week later. There was no recurrence or higher-order functional disability observed 1 year after surgery.


The patient was an 82-year-old woman (146 cm, 44 kg) diagnosed with hypertensive heart disease with no known history of allergy. Upon being diagnosed with empyema, she was scheduled for video-assisted thoracic surgery decortication and wedge resection of the lung. Pre-procedural electrocardiography revealed a normal sinus rhythm. Cardiac echocardiography showed a left ventricular ejection fraction of 71% and impaired left ventricular relaxation. Abnormal laboratory data demonstrated a white blood cell count of 15500/uL and C-reactive protein level of 220.7 mg/L. Vital signs were unremarkable except for oxygen saturation being around 90% to 95% on room air.
Routine monitoring included electrocardiography (lead II), noninvasive blood pressure, pulse oximetry, end-tidal carbon dioxide measurement, entropy, and the use of neuromuscular transmission monitors (NMTM). General anesthesia was induced with thiamylal (225 mg), rocuronium (50 mg), lidocaine (40 mg), fentanyl (75 mg), and glycopyrrolate (0.1 mg). The patient was intubated with a 32 Fr left double-lumen tube, and inspected using a fiberoptic bronchoscope. Following tracheal intubation, a right radial arterial line and central venous catheter were inserted. Anesthesia was maintained with sevoflurane (0.5–0.9), minimum alveolar concentration and propofol (20 mL/h) ti4trated to effect under entropy. In addition, the patient received a continuous dose of rocuronium (15–10 mg/h) under NMTM. Ventilation was adjusted to maintain an end-tidal carbon dioxide of 35 to 45 mmHg. The surgery was completed uneventfully in 2 hours and 40 minutes. At the completion of the procedure, arterial blood pressure of the patient was estimated to be 124/85 mmHg; heart rate, 65 beats per minute (bpm); SpO2, 99%; NMTM count, 4; and train-of-four (TOF) ratio, 64. The patient regained consciousness and spontaneous breathing. A dose of 200 mg sugammadex was next administered. One minute following sugammadex administration, the patient developed sinus bradycardia with 34 bpm without diffuse ST depression, hypotension (67/34 mmHg), hypoxia (SpO2: 65%), with an NMTM count of 0, and TOF ratio of 0. The patient was immediately administered atropine (0.5 mg) intravenously, following which her hemodynamics improved, with a corresponding heart rate of 65 bpm, SBP of 89/50 mmHg, and SpO2 of 93%. Subsequent administration of glycopyrrolate (0.1 mg) and neostigmine (1 mg) improved the TOF ratio to 69. Arterial blood gas values were as follows: pH, 7.291; PaO2, 75 mmHg; PaCO2, 51.4 mmHg; HCO3−, 22.8 mmol/L; lactate, 1.1 mmol/L; hemoglobin, 12.6 g/dL; and hematocrit, 36.7%. The anesthesiologist replaced the double-lumen tube with a single-lumen 4endotracheal tube, following which the patient was transferred to the intensive care unit for further care. The patient was extubated and discharged 4 and 10 days post-surgery, respectively, without any sequelae.


A 33-year-old married male, from urban Manipur, of middle socioeconomic status, diploma holder in pharmacology and unemployed (previously working as a pharmacist), was admitted in our tertiary psychiatric facility. He presented with insidious onset and continuous progressive illness of 8-year duration, characterized by heroin use in a dependence pattern, associated with harmful use of tobacco (cigarette smoking). The first exposure to heroin was 8 years back as an experiment with friends. After a month of daily use of injectable heroin, the patient started buying heroin for himself spending up to Rs 500 per day (which was 90% of his average daily income). He started using heroin alone, up to 0.5 gram per day, which was more than twice the amount of initial use, to get the desired effects of relaxation and euphoria. Over the next 2 years, he started to develop withdrawal symptoms after 6-9 hours if he did not take heroin. These symptoms included body ache, back pain, runny nose, stomach cramps, feeling restless, with lack of appetite and sleep, and constipation. The patient had been married during this time but was unable to abstain from heroin consumption despite his spouse's multiple pleas. He was therefore admitted to a deaddiction facility where he stayed for 1.5 months. However, he relapsed within a week postdischarge due to craving. In the last 8 years, there were four episodes of overdose requiring hospitalization, and several of his friends expired due to heroin overdose during this time. However, he was unable to refrain from the same, with a maximum period of abstinence being 1.5 months and three previous relapses. Thus, the patient was admitted at our center and started on opioid substitution therapy after obtaining informed consent. At the time of admission, multiple injection marks with thrombosed veins were noted on his upper limbs, and he was in a preparation stage of motivation.
The patient was started on 2 mg BPN built over 1 week to 18 mg along with nicotine patch 21 mg daily. From the third day of his admission, the patient was referred to the yoga facility in the institute. A 60-minute validated yoga program for ODS was included as an adjunct in his routine []. The program included practices of physical postures, sun salutations, relaxation techniques, regulated fast and slow yogic breathing practices, mantra chants, and yoga-based lifestyle counselling. One to one supervised yoga was taught for 5 days per week for the first 2 weeks, followed by tele-yoga practice of the same module (3 times per week) plus home practice postdischarge (with recorded videos) up to the 3rd month. After that, he continued practicing yoga on his own. An online booster session was offered to the patient every month after the 3rd month. The patient was followed up on a monthly basis over phone and was motivated to continue practicing yoga.
To evaluate how well the patient learnt yoga, the yoga performance assessment scale (YPA) [] was applied by the yoga therapist on each follow-up assessment. Plasma beta-endorphin levels were also assessed at baseline, after 2 weeks, and at the end of 9 months. The patient was followed up for the next 9 months with assessments of several clinical parameters including Buprenorphine dosage. Plasma beta-endorphin levels were also assessed at the baseline and after 2 weeks of supervised practice. Clinical assessments were performed by a psychiatrist. Standard procedures were followed for assessing endorphin levels []. Written informed consent was obtained from the patient.


A 29-year-old female with a past medical history of SLE was brought to the emergency department with fluctuated mentation, fatigue, anorexia, and psychomotor retardation for the last week. She also complained of incoherent speech and intermittent choreiform movement in the upper part of the body. She was diagnosed with SLE four years back, having urticaria and erythematosus rash with itching, scaling of the palm of hands, and hyperkeratosis of the sole, for which she was taking hydroxychloroquine and prednisone. She was admitted to the hospital three weeks back due to worsening dyspnea, fever, and cough. She had tachypnea, wheezing, and a chest X-ray revealed diffuse infiltrates in both lungs. Her COVID-19 polymerase chain reaction (PCR) test was positive, and she was commenced on azithromycin and 6mg dexamethasone for five days. Her condition improved gradually, and she was discharged six days later.
On clinical examination, she looked anxious with poor speech. She had a temperature of 99oF, respiratory rate of 23/minute, heart rate of 87/minute, blood pressure of 110/70 mmHg, and oxygen saturation of 96%. Her cardiovascular and respiratory examination was unremarkable, with normal vesicular breathing and heart sounds. Neurological examination revealed psychomotor agitation, intermittent choreiform movements of upper limbs, and poor speech. She had no signs of meningeal irritation, muscle strength loss, seizure episodes, and any history of trauma and illicit drug use. Her repeat COVID-19 PCR test was negative; however, serum immunoglobulin G (IgG) antibodies were positive against COVID-19.
Her initial blood investigations revealed thrombocytopenia and mild elevation of creatinine (Table ). Infectious workup was negative for any organism. The urine screen was negative for any illicit drug use, and the result of her repeat autoimmune screening is shown in Table . Her brain magnetic resonance imaging (MRI) revealed hyperintense signals in the bilateral parietal and temporal lobes, suggestive of lupus cerebritis (Figure ). She was diagnosed with lupus cerebritis, an exacerbation of SLE due to COVID-19 infection. CSF analysis was not performed because she refused lumbar puncture.
Her initial management included 1g methylprednisolone for three consecutive days, 30mg of prednisone daily, and 5mg of olanzapine daily for two weeks. The patient was also placed on monthly 1g intravenous cyclophosphamide. Her condition started improving gradually, and she was stable on day six of hospitalization. She was discharged on maintenance oral steroid therapy with follow-up.


A 58-year-old female with a remote history of coronary artery disease (CAD) with PCI to ostial RCA with bare-metal stent 19 years ago presented with chest pressure radiating into her shoulders concerning for unstable angina. EKG showed ST-segment depressions in the anterolateral leads. Nuclear medicine pharmacological stress test that was performed few days prior showed diffuse ST-segment depression but no myocardial perfusion defects. She was transferred to our tertiary care center for cardiac catheterization. Left heart catheterization (LHC) showed 90% stenosis of the previously stented ostial RCA. The LHC also demonstrated that the previously placed ostial RCA stent was dislodged with only 3-4 mm within RCA and the remainder 10-12 mm in the ascending aorta (Figure ).
In addition, transthoracic echo (TTE) during this admission showed moderate to severe mitral regurgitation (MR), presumably due to RCA lesion. Thus, PCI was deferred at that time, in case the patient needed mitral valve replacement or repair plus single-vessel coronary artery bypass graft surgery (CABG). For workup, a transesophageal echocardiogram (TEE) was performed and showed only moderate MR. However, an echodense structure was noted in the right coronary cusp (RCC) of the aortic valve that was fairly immobile. Upon further investigation, this material was thought to be the dislodged RCA stent (Figure ).
Finally, given that her MR intensity was only moderate, complex PCI of ostial RCA was performed. Extra effort was made to flare the old ostial stent to try to oppose the old stent as much as possible to the aortic cusp before reintervention to the ostial RCA with a new stent. The 90% stenosed ostial RCA was ballooned and stented with 3 x 12 mm XIENCE™ (Abbott, Chicago, USA) drug-eluting stent (DES) reducing 90% stenosis to 0% residual. The mid LAD had 70% eccentric calcific disease that was proven to be hemodynamically significant with an instantaneous wave-free ratio (IFR) of 0.62, which was reduced to 0% with 3 x 12 mm Xience DES.


A 54-year-old woman was admitted to our hospital for the management of a growing, 50-mm, painless, elastic, left cervical mass. The patient had a medical history of panic disorder, with no history of alcohol abuse, smoking, or drug allergies. Blood laboratory examinations demonstrated normal thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxine (fT4) levels, elevated thyroglobulin level of 684 ng/mL (normal, ≤33.7 ng/mL), elevated anti-thyroid microsomal antibody level of 334 IU/mL (normal, <16 IU/mL), and elevated anti-thyroglobulin antibody level of 175 IU/mL (normal, <28 IU/mL). The patient was diagnosed with chronic thyroiditis. Chest radiography ruled out tumor growth in either lung.
On US, a heterogeneous mass showing a well-defined border, measuring 41 × 45 × 24 mm (width × length × depth), with a cystic internal lesion was identified in the left lobe of the thyroid gland. On CT (), the mass showed a low density with enhancement similar to that of the thyroid parenchyma, except in the cystic portion. In addition, the trachea was displaced to the right by the tumor. FNA revealed chronic thyroiditis on two occasions, and the possibility of malignancy could not be ruled out. Accordingly, left thyroid lobectomy was performed.
The resected specimen showed an encapsulated tumor measuring 25 × 21 × 35 mm (width × length × depth), with evidence of cystic degeneration. The tumor cells possessed abundant eosinophilic cytoplasm, oval to polymorphic nuclei and many intranuclear inclusion bodies (). PAS-positive puncta with immunohistochemical positivity for collagen type IV were found between the trabecular structures. No yellow bodies were observed. Ki-67 was positive for cytoplasm and negative for the cell membrane, and the nucleus was nearly negative. The histopathological examination revealed an HTA.
Two weeks following the surgery, the thyroglobulin level showed negative conversion and was detected as 14.2 ng/ml on the first postoperative exam. Eighteen months later, at the time of writing this report, there was no evidence of recurrence or metastasis with negative thyroglobulin level.
Informed consent for publication of this report was obtained from the patient.


A 57-years-old female was admitted to the emergency department due to a motor vehicle accident. The patient suffered from multiple severe injuries. After clinical and radiological evaluation, a moderate cerebral contusion (GCS 11), multiple rib fractures with pneumothorax, right supracondylar femoral fracture (AO classification type C3), left ankle fracture (AO classification type C) and a segmental left humerus fracture were diagnosed. Humeral injury included a sub-capital fracture (type 11B1), a shaft fracture (type 12A2b) and a supracondylar fracture (type 13A3.3) (Figure ). A distal undisplayed clavicle fracture (type 151A) and a fracture of the body of scapula were treated conservatively.
Neurovascular status of the injured limbs was normal []. After the initial evaluation, and expertise trauma unit coped with the pneumothorax using Büllau thoracic pipe and immobilized fractured limbs with splints according to the advanced trauma life support (ATLS) protocol. The patient was hospitalized in the ICU and six days later, definite surgical treatment of fractures was performed. Intramedullary nailing of the femur and open reduction with internal fixation of the ankle fracture took place initially. In order to avoid the risks of a long-lasting operation, EIN was selected for the humeral shaft and supracondylar fractures fixation, together with two Kirschner wires (K-wire) 2.0 for the sub-capital fracture which was induced percutaneously after closed reduction (abduction and internal rotation) (Figure ). Image intensifier and radiolucent table were used for this procedure.
Two 2-cm long skin incisions and a hole with a 2.5 mm drill on bone cortex were made over medial and lateral humeral epicondyle and a nail was introduced from each insertion point into the medullary canal. The two elastic nails were then, advanced by rotational movements, taking care to pass the fracture site by keeping the fracture reduced and the bone aligned under fluoroscopy. The tip of each nail was anchored to the cancellous bone of proximal humeral metaphysis. A long arm splint was applied for four weeks. The patient was discharged from the ICU after 20 days and afterwards, treatment was continued at a rehabilitation centre for two months. During the postoperative follow-up period, regular radiological evaluation took place (Figures -).
There was no neurovascular deficiency. Elastic nails were removed from the humerus four months postoperatively after clinical and radiological evidence of the fractures’ consolidation, and a month later, the patient was able to have almost a full range of motion of her shoulder and elbow (Figures -). Pendulum exercises of the shoulder had begun after the removal of the K-wires. Simultaneously, the elbow’s passive flexion and extension up to the pain limit was encouraged. Active exercises and muscle strengthening were commenced after the third post-operative month.
The patient has a full range of movement in her left upper limb joints and is absolutely pain-free 55 months after the accident (Figure ). She copes with daily-living activities except for over-head lifting of heavy objects (above 10 kg), and pushing a heavy object (more than 40 kg) with one hand. The patient's disabilities of the arm, shoulder, and hand (DASH) score was 2.5/100 and the American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form (ASES) score was 97/100 [-].