A 44-year-old male patient reported to the clinic with the chief complaint of nasal obstruction in the left nostril and feeling of hard mass inside the nasal cavity for 3 years. The patient's medical history was unremarkable, and there was no previous history of maxillofacial trauma or surgery. Anterior rhinoscopy revealed a white mass in the left nasal cavity. On probing, it was hard in consistency and was found to be firmly attached to the floor of the nasal cavity. On intra-oral examination, his dentition was found to be normal. Panoramic radiograph revealed a well-defined radio-opaque elongated structure in the floor of the left nostril. Radiograph of the paranasal sinuses showed a radio-opaque shadow in the left nasal cavity. Computed tomography (CT) scan revealed a smooth mass located on the floor of the left nasal cavity between the inferior turbinate and the nasal septum [Figure and ]. Nasal endoscopy showed a grayish white mass between the inferior turbinate and the septum surrounded by granulation tissue and necrotic debris in the left nasal cavity []. A provisional diagnosis of the ectopic tooth was made, and the extraction of the tooth was planned. The patient underwent trans-nasal endoscopy of the left nostril under local anaesthesia for the removal of the nasal mass [Figure and ]. The gross specimen resembled a conical-shaped tooth []. Histopathological examination revealed well-organized enamel and dentin with pulp cavity in the centre. At 6 weeks of follow-up, the patient was asymptomatic and no mucosal abnormalities were observed.


A 48-year-old African American female with a past medical history of hypertrophic obstructive cardiomyopathy (HOCM), obesity, hypertension, hyperlipidaemia, and diabetes mellitus. She underwent uncomplicated thoracotomy with septal myectomy 2 years prior to this presentation, in which 11.0 g of excised myocardium was removed leading to a significant improvement in her LVOT obstruction with no residual valvular dysfunction. The postoperative course was uneventful. She presented with acute stroke and her symptoms included slurred speech, right facial droop sparing the forehead, and right-sided hemiparesis/hemianaesthesia. Previously, the patient had stable follow-up with postoperative echocardiograms showing a normal left ventricular ejection fraction of 70%, with a regional wall motion abnormality characterized by akinesia of the basal anteroseptal, mid anteroseptal, basal and mid inferior wall, and basal and mid inferior septum. The last echocardiogram was performed 3 months prior to this presentation.
The patient had stable vital signs. National Institutes of Health Stroke Scale (NIHSS) was 8, and her exam revealed expressive aphasia with flaccid right upper and lower extremities. Lab work were within normal limits. The rest of her physical exam was unremarkable. Electrocardiogram did not show any acute ischaemic changes, bundle branch blocks, or dysrhythmias. Computed tomography (CT) and CT angiography of the head and neck revealed an acute occlusion of the left sylvian branch of the middle cerebral artery, with an acute infarction of the left insula and the left frontal corona radiata.
She was not a candidate for thrombolytic therapy and was subsequently started on dual-antiplatelet therapy with aspirin 81 mg daily and clopidogrel 75 mg daily. She was admitted to the neurological intensive care unit for further workup. Echocardiogram demonstrated an ejection fraction of 55% with a focally abnormal left ventricular function and akinesis of the basal, mid anterior, and inferior septum consistent with her prior echocardiograms. However, there was a protruding density not previously reported in the basal-mid interventricular septum, measuring 2.2 × 1.4 cm (). It had multiple associated sessile, mobile projections with poor perfusion pattern on definity contrast enhanced imaging, visualized at the site of the remote myomectomy (). Cardiac magnetic resonance imaging was attempted to further characterize the lesion; however, it was unsuccessful due to the patient body habitus. Electrocardiogram-gated contrast cardiac CT was then performed and revealed an ovoid hypodensity arising from the septal wall of the left ventricle, with no contrast enhancement and low Hounsfield units (). Given the septal akinesis, coronary angiography was performed to rule out ischaemia and showed normal coronary arteries with no evidence of obstruction.
Based on the lesion’s atypical location in the LVOT, its origin at the former myectomy site, and poor perfusion on definity contrast study, the final diagnosis was acute cardioembolic stroke secondary to a left ventricular thrombus. Notably, the patient had no previous history of thromboembolic events and work-up for a possible underlying hypercoagulopathy state was negative. It was therefore deemed appropriate to commence anticoagulation with heparin and there was subsequently no evidence of bleeding. She was successfully transitioned to oral dabigatran 150 mg twice a day and discharged in a stable condition. Her neurologic deficits improved and echocardiography 3 weeks later demonstrated resolution of the thrombus ().


A 38-year-old woman was diagnosed with ductal carcinoma in situ (T2N1M0) in her left breast based on a pathogenic variant in BRCA2 (c.1813dupA, p.(Ile605Asnfs*11) in exon 10; NM_000059.3). The treatment consisted of a radical mastectomy followed by adjuvant treatment with four cycles of doxorubicin (cumulative dose 222 mg/m2) and cyclophosphamide, 12 times weekly paclitaxel followed by tamoxifen. After treatment was finished, the patient presented with palpitations and dizziness. She had no medical history and her only cardiovascular risk factor was smoking. Her blood pressure was normal (110/70 mmHg), and the electrocardiogram (ECG) showed no abnormalities but the echocardiography displayed a dilated left ventricle (LV) with a reduced left ventricular ejection fraction (LVEF) of 40%. She was treated with heart failure medication including enalapril (5 mg once a day) and carvedilol (3.125 mg twice a day) titrated up to the maximum tolerated dosage until complaints of orthostatic hypotension occurred. Her LVEF recovered to 50%, where after she was discharged from further follow-up. Three years later, the patient presented with reduced exercise capacity and was referred to our cardiogenetic department. During this presentation, she showed no signs of fluid overload at the physical examination. Her N-terminal pro-b-type natriuretic peptide (NT-proBNP) was increased (2584 ng/L), and Troponin T (TropT) was normal (4 ng/L). Cardiological evaluation showed non-specific repolarization disorders on the ECG and the echocardiography showed a dilated LV with a reduced systolic function (LVEF 28%). Cardiac magnetic resonance imaging (MRI) showed a dilated LV with EF of 26%. Delayed enhancement was only seen at the RV–LV insertion. Heart failure medication was optimized during bi-weekly controls by adding eplerenone (25 mg 3 days per week) in addition to enalapril (10 mg two times a day) and carvedilol (12.5 mg two times a day). Thereafter, echocardiogram showed partial recovery of the LV function to a LVEF of 35% at 1-year follow-up. Family history revealed that her father died suddenly at the age of 56 years while being screened for heart transplant, possibly of a ventricular arrhythmia in the context of a dilated cardiomyopathy (DCM). DNA analysis of 61 genes associated with cardiomyopathy identified a paternally inherited likely pathogenic variant in the TTN gene (NM_133378.4(TTN):c.63850dup p.(Ser21284Phefs*2)).


A 57-year-old male was diagnosed with a diffuse large B-cell non-Hodgkin’s lymphoma stage 3 for which he was treated with chemotherapy consisting of six cycles of R-CHOP [rituximab, cyclophosphamide, doxorubicin (cumulative dose 300 mg/m2), vincristine, and prednisolone]. Complete remission was attained 6 months later. A year thereafter, the patient presented with near syncope. He showed no signs of fluid overload at the physical examination. His NT-proBNP was significantly increased (8439 ng/L) and his Trop T was slightly increased as well (26 ng/L). Dilated cardiomyopathy was diagnosed with an LVEF of 20% and non-sustained ventricular tachycardias were recorded on Holter monitoring. Furosemide was started and heart failure medication was initiated including ramipril (2.5 mg two times a day) and bisoprolol (5 mg once a day) with bi-weekly follow-up visits for up-titration to the maximum tolerated dosage and an ICD was implanted.
His brother was diagnosed with non-Hodgkin lymphoma at the age of 23 years and was treated with chemotherapy. Three years later, recurrence of the lymphoma occurred and cytostatic treatment was again initiated leading to remission (cumulative dose anthracycline 630 mg/m2). Six years thereafter, he developed symptoms of dyspnoea and was diagnosed with DCM most likely cardiotoxic due to a high dose of doxorubicin. He died at the age of 32 years of an acute pulmonary embolism while awaiting a heart transplant. Family history also showed a paternal grandmother who died suddenly at the age of 36 years during delivery.
Genetic testing of a cardiomyopathy panel containing 62 genes in our patient revealed a pathogenic variant in the MYH7 gene (c.5754C>G, p.(Asn1918Lys); NM_000257.2, and a likely pathogenic variant in the TTN gene (c.45823_45848del, p.(Ala15275serfs*4); NM_001267550.1). A genealogical study showed that his paternal grandmother (as well as his father who died at the age of 66 years following lung cancer) was an obligate carrier of the MYH7 pathogenic variant. The DNA test on the paraffin material of his father and brother was inconclusive due to the low quality of the isolated DNA.


A 60-year-old male patient reported to the outpatient department of the authors' institution with the complaint of pain and swelling in the lower front tooth region for 15 days. The patient gave a history of extraction 1 month back due to loosened teeth following which he noticed a soft-tissue overgrowth in his mandibular anterior tooth region. The patient had the habit of bidi smoking for 30 years. Extraoral examination did not reveal any significant findings. He also experienced dull pain associated with this overgrowth. The submandibular and submental lymph nodes on the ipsilateral side were palpable.
On inspection, a soft nodular growth measuring about approximately 5 cm × 3 cm × 2 cm was seen on the mandibular anterior region. The lesion was pinkish white in color and ulceroproliferative in nature. The lesion was extending labiolingually from labial attached gingiva to lingual attached gingiva and mesiodistally from mandibular left canine to mandibular right first premolar region []. The growth was tender and firm in consistency. Based on clinical findings, a provisional diagnosis of aggressive inflammatory lesion with a differential diagnosis of granulomatous lesion and carcinoma of gingiva was made. No significant findings were noticed in an orthopantomogram. After routine hematological investigations, an incisional biopsy was performed. The tissue specimen was routinely fixed and processed. The H- and E-stained sections showed dysplastic epithelium invading into the connective tissue stroma. Invaded epithelial cells were in the form of nests, islands, and sheets composed of basaloid cells showing hyperchromatic large nuclei and indistinct cytoplasm [Figures and ]. Areas of comedonecrosis were seen in between the sheets of cells []. Frequent mitotic figures were also evident. The stroma also showed numerous blood vessels with areas of hemorrhage. Based on the histopathological findings, a diagnosis of BSCC with differential diagnosis of adenoid cystic carcinoma (ACC) (solid variant) was made. To differentiate between the two tumors, periodic acid–Schiff (PAS) stain and immunohistochemical staining for pan-cytokeratin were done. The negative results of PAS and positive for pan-cytokeratin [] lead to the final diagnosis of BSCC. The patient did not comply with any further treatment and succumbed to the disease within 1 month.


A 65-year-old female obstetric nurse was first referred to our gastroenterology center for further management of obstructive transaminitis. The patient has a medical history of a 2.0 cm left breast estrogen receptor (ER)-positive, progesterone receptor-positive, and human epidermal growth factor 2-negative ILC diagnosed 4 years prior, with 7 out of 9 ipsilateral lymph nodes involved with cancer. She was treated with lumpectomy, chemotherapy using dose-dense doxorubicin and cyclophosphamide (AC) followed by paclitaxel (T), whole-breast radiotherapy, and was placed on hormonal therapy with anastrozole. Three years after her initial breast cancer diagnosis, she had an onset of abdominal bloating, fatigue, and early satiety that progressed, leading her to see her primary care physician (PCP). At this time, diagnostic work up including computerized tomography (CT) of the abdomen and pelvis using intravenous contrast was unremarkable. Symptoms resolved but later recurred with associated significant fatigue, nausea, occasional vomiting and decreased PO tolerance, leading her to return to her PCP 6 months after the initial onset of symptoms. Blood test results were unremarkable (Table ). Her PCP referred her for esophagogastroduodenoscopy (EGD) and colonoscopy which she completed 2 months later, and these studies were also unremarkable. She was subsequently treated for lactose intolerance with minimal improvement. She presented again 13 months after initial symptoms with similar complaints, and blood tests obtained were remarkable for elevated liver function tests compared to 6 months prior (Table ), and cancer antigen 19–9 at 39 (nl <34 U/mL). CT scan of the abdomen showed severe intra- and extrahepatic biliary ductal dilatation with the “double-duct” sign (common bile duct was 19 mm and main pancreatic duct was 4 mm) without an identifiable cause (Fig. ). Additionally, there was pericholecystic fluid without other gallbladder abnormalities and, colonic thickening at the hepatic flexure, with otherwise normal bowel caliber; the retroperitoneum, abdominal wall, and lymph nodes were normal. The patient was then referred to our gastroenterology center for management of obstructive transaminitis.
EGD with endoscopic ultrasound (EUS) and colonoscopy was performed. EGD showed a stricture in the second portion of the duodenum (D2) that appeared to be extrinsic. On EUS, the mucosal layer of D2 appeared thickened and a fine-need aspiration (FNA) specimen of this segment was obtained. Cytopathologic examination of the FNA specimen showed clusters of atypical cells in the background of duodenal epithelial cells and inflammation. Additionally, on EUS, dilation of the common bile duct and main pancreatic duct without evidence of an obstructing lesion was reaffirmed, and the ampulla and pancreas appeared normal. The colonoscopy results were unremarkable. A follow-up magnetic resonance imaging (MRI) of the abdomen with intravenous contrast was performed, and it also reaffirmed the previous CT and endoscopic findings but additionally showed gallbladder dilation with no evidence of cholelithiasis or choledocholithiasis. The differential diagnosis given by the radiologist reading the MRI included a distal ductal/ampullary stricture, a neoplasm including ampullary carcinoma and cholangiocarcinoma, or an occult pancreatic mass. The patient was then referred to pancreatic surgery.
Given her elevated cancer antigen 19–9 and the cellular atypia observed in the endoscopic FNA specimen from the duodenum, the patient was presumed to have a local periampullary cancer. She was then recommended a pancreaticoduodenectomy (Whipple procedure). At laparotomy, there were several unexpected abnormalities noted upon abdominal entry. The stomach and gallbladder were distended. The small bowel mesentery in its entirety was indurated, foreshortened, and had numerous nodules. One of the nodules was biopsied and returned a benign lymph node. The duodenum was adherent to the retroperitoneum, and the transverse colon was adherent to the head of the pancreas. The right colon was adherent to the abdominal wall and also indurated. Based on the extent of the abdominal findings, the surgeons concluded that disseminated malignancy was present and the Whipple procedure was aborted. No bypasses were performed to the patient's bile duct or the stomach because the small bowel mesentery was so foreshortened that it would not allow reach into the upper abdomen above the colon. Her gallbladder was then resected, and a partial omentectomy was also performed to provide additional tissue for pathologic examination. Histopathological examination results of specimens obtained from the surgery revealed findings consistent with metastatic lobular breast carcinoma (Fig. ). These results were confirmed by immunohistochemical staining (Fig. ) which additionally, demonstrated that the cancer cells were ER+, progesterone receptor−, and human epidermal growth factor 2+. Postoperatively, a percutaneous transhepatic biliary drain was placed by interventional radiology which relieved her biliary obstruction after failure of biliary stenting with endoscopic retrograde cholangiopancreatography; the duodenoscope could not traverse the stricture in D2 despite sequential dilation with a wire-guided dilation balloon.
After discharge from the hospital, the patient followed up with medical oncology. Anastrozole was discontinued and she received 2 months of weekly Taxol without significant response. Intercurrent with this, she was discovered to have a large intra-abdominal abscess near her percutaneous transhepatic biliary drain. The abscess was drained by interventional radiology. She was subsequently started on Fulvestrant and Palbociclib 2- and 4- months after her surgery, respectively. Significant disease regression occurred, all drains were removed, and she enjoyed an active lifestyle with full functional status. After 3 and half years of Fulvestrant and Palbociclib, she presented with left eye irritation. This progressed to diplopia with abnormal extraocular movements on exam 59 months after the initial onset of symptoms. MRI showed a large left retro-orbital mass, and a biopsy was consistent with her lobular breast cancer. Palbociclib and Fulvestrant were discontinued. She was radiated with external beam radiation therapy to the left eye. An analysis of ctDNA showed autonomously signaling ESR1 mutations. She is now enrolled in a trial that involves a new highly active SERD with Abemaciclib and remains well.


A 47-year-old female was referred to the hospital due to gradual abdominal enlargement accompanied by leg swelling lasting for 2 weeks. There was also a decrease in body weight about 10 kg in the last 8 months. The starting weight of the patient was 67 kg and reduced to 57 kg in the past 8 months. General weakness, pruritus, and decreased pubic and axillary hair were also noticeable. Eight months earlier, she had profound jaundice without abdominal pain. At that time, she got ursodeoxycholic acid and got better. After 2 months of treatment, the patient was lost to follow-up and never visited again to the hospital. She had no noteworthy medical or family history, including gastrointestinal bleeding or liver disease. On physical examination, the patient was alert, fully oriented, and the vital sign was stable. There were pale conjunctiva and icteric of the sclera. Her abdomen was round and soft with severe ascites. There was no abdominal tenderness. Mass or organomegaly was difficult to assess due to massive ascites. Bilateral pitting edema was present on both ankles.
Initial laboratory data are shown in Table ; it revealed that she had macrocytic anemia, thrombocytopenia, and leukocytosis. The liver function test showed an increase in bilirubin level with mainly direct hyperbilirubinemia with an increase in AST and ALT with AST/ALT ratio >1. ALP and γ-GT levels were normal. Hemostatic functions showed an increase in both INR and APTT. Albumin levels were decreased with an increase in globulin levels. Renal function tests were still normal, and the results of hepatitis B and C were negative. Compared to the laboratory results from 8 months ago, the AST and ALT levels were higher and also the levels of bilirubin more severe compared to the present admission. However, there was no anemia nor thrombocytopenia documented 8 months ago. Ascites fluid analysis showed that the fluid was clear and yellow colored with low levels of protein, LDH, leukocyte, and erythrocyte. SAAG was <1.1 mg/dL. Cytology of ascetic fluid analysis found some polymorphonuclear and mononuclear cells without malignant cells. The results of ascites fluid analysis are also shown in Table .
The urinalysis result showed that there was moderate bilirubinuria, but no proteinuria was found. We also found mild urobilinogen in the urine. We already excluded the cause of hypoalbuminemia was due to nephrotic syndrome because no nephrotic-range proteinuria was found based on the examination of protein-creatinine ratio or albumin-creatinine ratio. Compared to the results from 8 months ago, the bilirubin and urobilinogen in the urine were milder in this admission with the other results similar. The urinalysis results are shown in Table .
Abdominal ultrasound examination (shown in Fig. ) showed ascites fluid in perivesical, perihepatic, perisplenic, hepatorenal fossa, and peri-intestine regions. No mass or organomegaly was found. Previous abdominal ultrasound from 8 months ago showed no ascites, but there was a thickening of the wall of the gall bladder without a sign of biliary obstruction. Because of the high level of globulin in this patient, we performed plasma protein electrophoresis in this patient. It showed a monoclonal gammopathy with an M spike in the gamma region with an increased level of γ-globulin. The result of plasma protein electrophoresis examination is shown in Figure .
While it is unfortunate that there was a lack of data regarding the bone marrow analysis in this patient, we found no sign of organ damage related to suspicion of multiple myeloma regarding the hypergammaglobulinemia in this patient. There were no lytic lesion from bone survey, hypercalcemia, or renal dysfunction from this patient. Because we suspected the possibility of autoimmunity in this patient, we found that there was an increased level of serum anti-nuclear antibody (ANA) by ELISA.
Based on the current data, the ascites was thought due to portal hypertension that might be caused by AIH. The patient was restricted for sodium intake and was given spironolactone 100 mg QD, furosemide 40 mg QD, ursodeoxycholic acid 250 mg b.i.d., and prednisone 60 mg/day. She also underwent large-volume paracentesis for the ascites followed by albumin transfusion. We also administered vitamin K injection and transfusion of fresh frozen plasma to correct the hemostasis function; however, there was no improvement regarding prolongation of INR and APTT.
Clinical improvements were found for the ascites and the laboratory results after 1-week treatment. She visited the Gastroenterohepatology outpatient clinic 1 week later, and there was a clinical improvement for the ascites showed by the decrease in abdominal circumference with a decrease in body weight of 2 kg in 1 week. The monitoring of laboratory results is shown in Figure .
The patient was planned to do magnetic resonance cholangiopancreatography and liver biopsy afterward. However, 1 week later, she visited the outpatient Gastroenterohepatology clinic. She had a sudden decrease of consciousness in the morning with the suspicion of stroke with intracranial hemorrhage. She died because of brain herniation due to the intracranial hemorrhage.


A 50-year-old male patient was admitted to our institute for perianal swelling and discomfort.
The patient had become aware of anal pain and discomfort with no obvious cause 6 d prior to admission. He did not report abdominal pain, and there was no bleeding during defecation. He had visited the local hospital 2 d earlier for pain, at which time the doctor diagnosed a perianal abscess and performed an incision and drainage. One day later, the perianal swelling had not subsided and had spread to the base of the scrotum; a local incision showed yellowish gray necrotic tissue with a fishy odor. At the same time, the patient developed a high fever. He was admitted to our hospital with a body temperature of 38.2 °C, respiratory rate of 21 breaths/min, heart rate of 81 beats/min, blood pressure of 105/69 mmHg, and dysuresia.
On admission, the case was considered perianal necrotizing fasciitis extending to the perineal region. In contrast to conventional cases of necrotizing fasciitis, the patient denied any underlying diseases. In addition, his physical and laboratory examination confirmed no signs of type 2 diabetes, malignancy, or any of the other common diseases associated with necrotizing fasciitis.
The patient stated that he has no relevant family history.
Physical examination showed that the entire anal margin was swollen and the skin was in red and black. It was also found after palpation that the previous incision on the posterior of the anal margin had yellow-white frothy secretions overflowed. The patient complained of severe pain. The skin on both sides and the base of the scrotum felt tender and warm to the touch, and there was crepitus when palpating the level of the left pubic symphysis (Figure ).
Laboratory and imaging examinations were promptly performed upon admission. Laboratory examination results during the patient’s hospital stay are shown in Table .
A lower abdominal and pelvic computed tomography (CT) scan suggested necrotizing fasciitis based on the demonstration of gas in the tissue on both sides of the buttocks, left perineal area, the subcutaneous soft tissues of the groin and the root of the thigh. The scan also showed urine retention and multiple lymph nodes in the inguinal area (Figure ).


A 61-year-old female presented to the emergency room with intermittent chest pain and shortness of breath for the past one week. She described moderate-intensity, non-radiating chest pressure, that was associated with fatigue. Paramedics gave her aspirin 324 mg en-route to the emergency room, resulting in transient symptom relief. She did not relate any exacerbating factors. On arrival, her blood pressure was 107/57 mm Hg, pulse was 68 beats/minute. Cardiovascular exam revealed a regular rate and rhythm with no audible cardiac murmur. There was no jugular venous distention. Chest pain was not reproducible on palpation. No lower extremity edema present.
The patient had a history of polycythemia vera (JAK2-positive) treated with phlebotomy, hypertension and chronic kidney disease stage 3. She had a similar episode of chest pain eight months ago, diagnosed as myocarditis, wherein she was discharged on colchicine 0.6 mg daily. Since then, she presented to the emergency room twice for recurring intermittent chest pain episodes, diagnosed as recurrent myocarditis. She was a former smoker with 16 pack-years and had quit >10 years ago.
Complete blood count showed hemoglobin (Hb) of 13.5 gm/dl, hematocrit (Hct) 45.1% and platelet count of 397 000/mcL. Blood urea nitrogen (BUN) was 40 mg/dl (range: 9.8–20.1 mg/dl) and creatinine 1.7 mg/dl (range: 0.30–1.50 mg/dl). Troponin significantly elevated at 11.06 ng/ml (range: 0.00–0.02 ng/ml) and B-type natriuretic peptide concentration (BNP) 2232 pg/ml (range: 0.00–100 pg/ml). Her c-reactive protein (CRP) was 2.17 mg/dl (range: 0.00–0.50 mg/dl). Electrocardiogram () showed sinus rhythm with no acute ST-T wave elevation or depression. Chest x-ray findings were consistent with cardiomegaly with no hilar lymphadenopathy. Ejection fraction on transthoracic echocardiogram was 35% with apical-lateral hypokinesis and increased left ventricular cavity size. Her ejection fraction eight months ago was 55%.
Patient was started on low-weight molecular heparin. She underwent coronary angiography, which did not show any significant coronary artery disease or spontaneous coronary artery dissection. As she was previously presumed to have myocarditis, her respiratory viral panel was checked for adenovirus, SARS-COV-2, coxsackieviruses, which were all negative. Additional investigation was performed to identify the etiology of her cardiomyopathy. Urine protein electrophoresis did not show a monoclonal or polyclonal pattern. Serum Iron and ferritin levels were normal. Autoimmune and inflammatory markers, antinuclear antibody, anti-neutrophil cytoplasmic autoantibody, complement level, erythrocyte sedimentation rate (ESR), and interleukin-6 (IL-6) level were all within normal range (). Her BUN was 40 mg/dl, not elevated enough to suggest uremic myopericarditis. The patient denied alcohol or illicit drug use, with no exposure to chemotherapy to indicate toxic cardiomyopathy.
Given her history of polycythemia vera with persistently elevated troponin level, and chest pain relieved with aspirin, there was suspicion for microvascular ischemia. Due to chronic kidney disease, she had cardiac magnetic resonance (CMR) imaging without contrast during the prior admission, which was inconclusive. The patient was hesitant to undergo invasive endomyocardial biopsy. Therefore, CMR with contrast was ordered after an informed decision was made with the patient and her nephrologist. Patient underwent CMR with contrast, which confirmed microvascular ischemia with areas of first-pass subendocardial perfusion defects and additional areas of <50% subendocardial late-gadolinium enhancement extending from the left ventricular base to apex ().
In addition to carvedilol, aspirin 81 mg daily and clopidogrel 75 mg were initiated on Day 3 for treatment of microvascular ischemia. Her chest pain had completely resolved. Troponin level and BNP rapidly decreased to 1.97 ng/ml and 309 pg/ml on discharge, respectively (). At 1-week follow-up, the patient reported no new episodes of chest pain. Troponin level was 0.07 ng/ml and CRP level was 0.31 mg/dl.


A 24-year-old woman was admitted to our department with pain in the right buttock and lower back. Incisional biopsy was performed at another hospital and a microscopic pathological report indicated intramuscular schwannoma. A non-tender palpable lump was identified at the left L5-S3 level. Neurologic sensory deficit or motor deficit was not detected. The laboratory data were within the normal limits. A 3.7×2.7×7.0 cm oval-shaped mass was identified on MRI at the left multifidus muscle. It had a well-defined margin with low signal intensity on a T1 weighted image, intermediate signal intensity on a T2 weighted image, and a strong enhanced mass lesion was identified ().
Under general anesthesia, we performed total mass excision and a biopsy was taken for pathologic confirmation. An 8.6 cm, well-encapsulated, soft mass was excised from the multifidus muscle (). Histopathologic diagnosis identified the mass as desmoid fibromatosis (). The patient was discharged without any neurologic defects after surgery.


A 55-year-old man with a weight of 76 kg and height of 178 cm, suddenly experienced a nontraumatic loss of consciousness after a cough attack at an upright position as reported by a witness. Two months prior, he was diagnosed with pulmonary tuberculosis and had been receiving antituberculosis treatment. On arrival, the patient was unconscious with a Glasgow coma scale score of 6, blood pressure of 169/89 mm Hg, regular heart rate of 85 beats/minute, respiratory rate of 18/minute, body temperature of 36.5°C, SaO2 of 82% at room air, and capillary blood sugar of 110 mg/dL. Auscultation of the lungs revealed an inspiratory crackle at the left lung field. After rapid intravenous access and oxygenation, the patient was sedated, the trachea was intubated, mechanical ventilation was initiated, and conservative treatment was maintained in the intensive care unit. Urgent computed tomography (CT) of the brain was performed and showed multiple air shadows in both hemispheres and the right cerebral vessels (). These lesions suggest air embolism. Twelve hours later, a magnetic resonance imaging (MRI) of the head was performed and showed a diffuse ischemic stroke in the right and left frontoparietal cortical areas and multiple hypointense signals, which were consistent with cerebral air embolism ().
The brain perfusion images were normal. The chest CT performed at the emergency department showed pulmonary tuberculosis cavity associated with the destruction of parenchyma in the left upper lobe (). There was no evidence of cerebral hemorrhage. The diagnosis of cerebral gas embolism after sudden cough was retained, and immediate treatment was started including 100% oxygen and cardiovascular support while the patient was placed in a supine position. The transthoracic echocardiography was performed, and no patent foramen ovale was found. A lumbar puncture was performed to seek for tuberculous meningoencephalitis. The cerebrospinal fluid analysis was normal. Hyperbaric oxygen therapy was considered, but the patient’s condition was too unstable to support transfer to the hyperbaric oxygen center. One day later, his neurological status deteriorated. The patient died on the fourth day with multiple organ failure. No autopsy was performed based on his family’s wishes.


Our patient is a 24 year old male who was involved in a motor vehicle accident. He was an unrestrained occupant in the front seat of a truck when he sustained the injury. Upon arrival to our hospital, he was tachycardic and tachypneic and was managed accordingly with ATLS protocol.
He had severe pain over the pelvis and gross deformity over the the right leg with distal neurovascular structures intact on examination. He had degloving soft tissue injury over the right heel for which debridement was done at the hospital where he was referred from.
Pelvis x-ray and CT scan was taken and showed right side overlapping symphysis pubis associated with ipsilateral transverse acetabular fracture type (). The x-ray of the right leg showed a closed tibial shaft fracture.
The patient was unable to maintain his O2 saturation with atmospheric breathing at the emergency room. He was put on intranasal O2 support for a lung contusion injury he had. He had no urinary complaint or blood at the urethral meatus, therefore a Foley catheter was inserted with no need for cystourethrography. He was taken to the operating theater 10 days after the injury. Closed reduction of the locked symphysis was not attempted inorder to avoid further displacment of the ipsilateral acetabular fracture. The patient was positioned supine on the operating table and his pelvis and both legs were prepped and draped free. The symphysis pubis was approached through a Pfannenstiel incision 2 cm above the pubic tubercle with about a 10 cm incision width. The rectus abdominis was found to be partially contused and was further surgically splitted at the midline vertically to retract it laterally. The retropubic space was accessed with blunt dissection to expose the overlapped pubis symphysis and the rami ().
Then 3.5 cortical screws were applied on the opposing pubic bone bodies with an anterior to posterior direction, approximately 2 cm lateral from the center using them as a joystick to apply a reduction clamp. Using the Jung Bluth clamp on the inserted screws, rotational and disimpacting force was applied and reduction of the symphysis pubis was achieved. After achieving reduction, 3.5 mm size and 6-hole precontoured reconstruction plate was applied on the superior aspect of the symphysis. The plate was secured with three cortical screws on each side.
For the percutaneous fixation of the acetabulum, an entry point was identified laterally on the supra-acetabular area with the help of a fluoroscopy image aiming to the symphysis and a stab incision was made for a guide wire insertion. The guide wire was directed from the entry point towards the symphysis using the pelvic inlet and obturator oblique outlet views under fluoroscopy. A 4.5 cannulated drill bit was used to create a path for the screw. Then the transverse column acetabular fracture was fixed percutaneously, using a 6.5 mm size and 100 mm length partially threaded cannulated screw. A post-operative x-ray image was taken the day after surgery ().
Post-operatively, the patient was stable and followed in the ward with 72 hours of post-operative broad spectrum intravenous antibiotics and adequate analgesics. Prophylactic unfractionated heparin 7,500 IU subcutaneous twice a day was continued according to the hospital’s protocol.
The patient was discharged after 5 days of hospital stay, shifting the UFH to oral rivaroxaban 10 mg per day for 1 month and additional adequate analgesics. He had no access for center-based physiotherapy, hence was advised on home physiotherapy with hip and knee passive range of motion and non-weight bearing status of 6 weeks period due to the associated tibial fracture he had. On the 2nd week of his visit to the OPD, the surgical wound was in good condition and the stitches were removed. He was on bilateral axillary crutch support for bed to chair and home mobilization during the first 6 weeks of his post-operation period. At his 2-month follow-up, the patient had no pelvic pain and was able to partially weight bear with the help of a crutch. He had no urinary symptoms or suprapubic pain. At 6-months follow-up he was back to his normal pre-injury activity. Pelvic radiograph showed the hardware in a good position with fracture and dislocations staying reduced ().


A previously healthy 21-year-old man presented to our emergency department with an acute onset of bilateral throbbing headache, left ear pain, and tinnitus for 4 days, followed by fever and fatigue. There was no nuchal rigidity, jolt accentuation, allodynia, or neuralgia. On admission, otoscopy revealed hyperemia and exudate over the left tympanic membrane with mild bulging, suggesting acute otitis media. His white blood cell count was 6.3 × 103 cells/mm3, and C-reactive protein was <0.04 mg/dL. He was initially treated with intravenous ampicillin/sulbactam 3 g six-hourly. On day 3, the swab culture of the exudate grew methicillin-sensitive Staphylococcus aureus, and we switched his treatment to oral cefaclor 500 mg thrice daily. Although his fever subsided and headache improved gradually, otalgia, tinnitus, and dizziness persisted. On day 4, he developed dysgeusia and hearing loss, followed by ipsilateral facial paralysis on day 7 (Figure ). A head computed tomography scan did not show any bone involvement in the auditory ossicles or mastoiditis. There were no vesicles on the left pinna or external auditory canal. Since the otomicroscopic examination revealed no evidence of otitis media exacerbation, we suspected Ramsay Hunt syndrome (RHS) with grade Ⅴ/severe palsy (House-Brackmann scale) and started him on oral valacyclovir 1000 mg thrice daily and oral prednisone 60 mg daily. Valacyclovir and tapered prednisone were continued for 1 week, and his ear pain, tinnitus, and dizziness subsided. Serology testing for VZV revealed an immunoglobulin M (IgM) of 1.12 and IgG > 120 (normal values: IgM < 0.8 and IgG < 2.0), and the polymerase chain reaction (PCR) of the otic exudate for VZV was positive. An antigen/antibody test for human immunodeficiency virus was negative. During the treatment, no vesicle was observed in the auditory canal or on the auricle. These findings were consistent with the diagnosis of ZSH. Despite prompt treatment, grade Ⅲ (moderate) facial palsy persisted, four weeks following discharge.


A 57-year-old female presented to the orthopedic clinic with chronic, bilateral hand pain secondary to Dupuytren’s myofascial contractures. She had onset of pain at the triangular area of her left palm three years prior, with similar symptoms presenting in her right palm two years later. At the time of evaluation, she reported that her pain was constant, dull and worse on the left than the right. It was rated 4/10 on average and 9/10 at its worst using a numerical rating scale. The symptoms were exacerbated by pinching or grasping objects in her hands and relieved with rest and pain medication. She reported associated weakness and functional limitations in gripping and fine motor dexterity of her hands but denied numbness, tingling, triggering or pain in her neck, shoulders, elbows or wrists. She had a history of bilateral hand tendonitis and was currently unable to work as a dentist due to her symptoms.
Previous evaluations included that with a rheumatologist, who ruled out rheumatoid arthritis, and a hand surgeon, who administered cortisone injections with minimal, temporary relief. Other treatments she had tried included anti-inflammatory medications (ibuprofen and meloxicam), oral steroids, opiates (tramadol and hydrocodone-acetaminophen), physical therapy and acupuncture. She had not tried splinting, bracing or neuropathic medications such as gabapentin.
Pertinent physical exam findings included: palpable palmar nodules and cords without evidence of contracture (Tubiana Stage N) [], tenderness over the palm with deep compression bilaterally and limited active range of motion of her intrinsic hand muscles due to pain. Upper extremity strength and sensory examination was otherwise normal. Relevant imaging studies included bilateral hand and wrist MRIs which showed interosseous ganglion cysts bilaterally.
The patient returned to the clinic for injections of 50 units botulinum toxin A (incobotulinumtoxin A, diluted in 4mL of normal saline to 1.25 units per mL) into the palmar fascia of her left hand, followed by a 25 unit (0.625 units per mL) injection into her right hand one month later. Injections were placed just above the flexor digitorum tendons at 20 points along the palm (five points per digit, excluding the thumb) ().
These provided temporary, mild relief. Four months later she returned for 50 unit injections into her bilateral hands using the same technique, providing two to three months of relief. Four months later, she was injected with 100 units (2.5 units per mL) into each hand, resulting in three to fourth months of marked improvement in pain (1/10 on average, up to 2/10 at its worst), range of motion and function of her hands. Her only remaining limitation was in fine motor dexterity, but she was successfully able to return to work.


A 64-year-old female with osteoporosis, presented with a non-penetrating T11 traumatic spinal injury as a result of falling backwards downstairs. The computed tomography (CT) scan showed a T11, AO spine C classification, without a neurological deficit, ASIA – E [].
Three days later, she underwent a T11 hemilaminectomy to remove an epidural hematoma with T9 - T10 (5.5 mm × 40 mm screws) to T12 - L1 (6.5 mm × 45 mm screws) transpedicular instrumented fusion. Vertebral body augmentation with 1.5 mL of PMMA bone cement per transpedicular screw (distally fenestrated) was performed due to her underlying osteoporosis. When the fourth screw was placed, fluoroscopy showed leakage of PMMA cement into the paravertebral system []. We briefly stopped applying bone cement, but then resumed its application when we observed no intraoperative cardiorespiratory compromise. Fracture reduction was then performed with bilateral 5.5 mm × 36 cm rod placement. The intraoperative arterial blood gas showed respiratory acidosis with a moderate “oxygenation disorder” (pH, 7.31; pO2, 100 mmHg; pCO2, 48 mmHg; HCO3, 24 mEq/L; O2 saturation, 96%; PaO2/FiO2, 178 mmHg; lactate, 1 mmol/L, hemoglobin 11.5 g/dL). Thirty minutes after transfer to the recovery room, however, she suddenly developed hypoxemia with oxygen saturation of 45%, requiring ventilatory support.
The CT angiogram of the chest documented a cement pulmonary embolism []. She remained intubated for the next 2 days and was started on low molecular weight heparin 4 days postoperatively. Nine days later, she had a postoperative Chest X-ray that showed a radiopaque image in the right lung associated with cement emboli []. She was then discharged without supplemental oxygen or on anticoagulation.


An 18-year-old female was born with congenital pseudoarthrosis (CPT) of the right tibia with neurofibromatosis. She underwent three unsuccessful surgeries before presenting to us as Type 1 infected non-union [] of tibia with shortening at the age of 18 years. She had neurofibromatic nodules all over the body including the face (). The leg had multiple active draining sinuses, with evidence of healed sinuses and operating scars, adherent to the underlying bone () []. There was minimally painful abnormal mobility at the fracture site. The X-ray showed multiple diaphyseal sequestra with cavities, apparent fusion of the ankle joint and atrophic non-union at the distal third of tibia and fibula () [].
Prolonged morbidity made her socially isolated. She belonged to a poor family. Meeting her medical expenses became a great burden to the family. The guardians were true to their thinking that no modern science could salvage her limb. They started believing that amputation would be a viable option and with that feeling in mind, they approached us. The clinical setting was also conducive, in general for such an action. We knew that still a modern orthopedic technology called Ilizarov could settle down the morbidities in her favor. However, it was difficult to make them believe that a miracle might still be happening. After few sittings of counseling, they somehow agreed to give it a try.
After improving the general condition of the patient, extensive debridement was done. All dead tissues including bone, soft tissues, and sinuses were excised (). An all-wire Ilizarov frame was mounted with two rings on the proximal fragment and one ring in the small distal fragment. Bone was so osteoporotic that wires could be put by pushing with hand only. The fibula was left untouched. The wound was kept open under massive dressing to heal by secondary intention. The immediate post-operative period was uneventful. A corticotomy was done in the proximal metaphyseal area when the wound appeared healthy after about 2 weeks. Distraction was started after a latency of 7 days and an X-ray on the 10th day of corticotomy showed normal distraction () []. Subsequent X-rays at 1 month interval showed hyporegenerate (). Since the bone was grossly osteoporotic, instability was thought to be the cause of hyporegenerate. One more wire was added in each fragment and the apparatus was further reinforced with two long extension plates. Weight-bearing was encouraged with shoe raise. Two cycles of Accordion maneuver (AM) as per Baruah and Patowary protocol [] were done at the hyporegenerate site. The wires were tightened in each follow-up. The distraction rate was slowed down to half a millimeter a day in the initial period when bone failed to appear in the beginning.
Once the docking site was reached further distraction was continued to get few millimeters of invagination into distal fragment to improve stability at the docking site. Slowly the bone started showing in the regenerate in follow-up X-rays. After docking was achieved, further distraction was continued to gain the length of the limb by external bone transport. Apparatus was kept twice the period of distraction to consolidate the regenerate. It was removed when clinically there was no pain, abnormal mobility, and tenderness, and the X-ray showed three cortices () []. A walking patella tendon bearing cast was applied for 6 weeks to further consolidate the regenerate. She was allowed unaided full weight-bearing afterward ().


The patient is a 40-year-old male in whom DCM was diagnosed upon clinical, echocardiographic, and angiographic investigations, carried out in the Department of Cardiology, Rabta University Hospital, Tunis, Tunisia. Transthoracic echocardiography revealed a left ventricular end-diastolic diameter (LVEDD) of 65 mm; a fractional shortening (FS) of 23%; and an ejection fraction (EF) of 48%. Coronary angiography was normal. The control group comprised 100 healthy adult subjects. The study was approved by the Ethical Committee of the University of Tunis (SN745556).
Muscle specimens were obtained by open biopsy, frozen, and stored in liquid nitrogen. Biochemical measurement of the ubiquinone oxidoreductase (NADH) dehydrogenase (complex-I), succinate-cytochrome-c-reductase (complex-II and complex-III), cytochrome-c-oxidase (complex-IV) and citrate synthase activities were done as described previously [].
Total DNA was extracted from lymphocytes or from muscle tissue according to established methods. The fragment that overlapped the entire sequence of MT-CYB (14747-15887) was attained by using a polymerase chain reaction (PCR) assay with cytb-1F as the first forward primer (nucleotides 14667-14687), cytbTB-1R as the first reverse primer (nucleotides 15289-15269), cytb-2F as the second forward primer (nucleotides 15189-15209) and cytb-2R as the second reverse primer (nucleotides 15941-15921). PCR amplification was performed in a 50 volume containing 100 ng DNA, 10 pmol of each primer, 4 µL MgCl2, 5 µL dNTP, and 0.2 µL Taq polymerase. Conditions for DNA fragment amplification included 3 min at 94 °C, 30 cycles of 30 s at 94 °C, 60 s at 52 °C, 1 min 30 s at 72 °C, and 10 min at 72 °C.
Direct sequencing of PCR fragments was conducted using an ABI 3730 automated DNA sequencer (Applied Biosystems) by using a Big Dye Terminator V.3.1 cycle sequencing kit (Applied 4337455 (100 reactions)) according to the manufacturer’s recommendations. All sequences were numbered according to the L-strand (the coding strand) of the Cambridge reference sequence [].
Mutated protein structures change due to biochemical differences of the AA variants (acidic, basic, hydrophobic) or due to the variant changing the protein sequence and affecting the tertiary or quaternary structure or the active site. To distinguish deleterious from functionally neutral mutations we used the PolyPhen algorithm, which predicts the pathogenicity of a specific variant by using a set of empirical rules, based on sequence, phylogenetic and structural information characterizing the variant. In addition to sequence alignments, PolyPhen utilises protein structure databases, such as the Protein Data Bank (PDB), Protein Quarternary Structure (PQS), Dictionary of Secondary Structure in Proteins (DSSP), or three-dimensional structure databases to assess if a variant affects the protein’s secondary structure, the interchain contacts, functional sites, or the binding sites.
Biochemical studies of the muscle homogenate revealed low activities of complex-II and -III but virtually normal complex-I and complex-IV activities () indicating a complex-III defect. Molecular analyses of muscle and lymphocyte mtDNA revealed the transition thymine for cytosine at np14757 (), changing medium size and hydrophobic methionine (M) to medium size and polar (hydrophilic) threonine (T) (M4T). This mutation was not found in lymphocyte mtDNA of 100 healthy subjects without comorbidities or known genetic defect. A substitution of adenine for guanine at np15326, changing medium size and hydrophilic threonine (T) to small size and hydrophobic alanine (A) (T194A), was considered a neutral polymorphism based on previous reports [].
The patient benefited significantly from conventional treatment recommended for heart failure.
Short-term follow-up after 8 weeks showed complete recovery of heart failure.


A 48-year-old white male presented to the clozapine clinic for routine follow-up and monitoring. The past medical history was significant for schizoaffective disorder; tobacco use disorder; constipation; vitamin D deficiency; and metabolic syndrome characterized by obesity, dyslipidemia, and prediabetes. Current medications included clozapine 150 mg by mouth at bedtime, aspirin 81 mg by mouth daily, docusate 100 mg by mouth twice daily, and cholecalciferol 2000 units by mouth daily. He tried and failed multiple antipsychotics prior to initiation of clozapine 4 years ago. His mental health had been stable since initiating clozapine, and he resides in a group home. He gained 9.5 kg the year after clozapine was initiated, and then weight stabilized. He had difficulty controlling his diet at the group home and ate what was prepared for him. Despite lifestyle education, he continued to visit the vending machine frequently for soda (2 cans per day), candy bars (1 per day), and chips (1 bag per day). He was referred to a dietitian but was unable to successfully implement dietary changes. He did not have access to exercise equipment at his group home and did not walk outside due to inclement weather. He was referred to an exercise program located in the same facility as the clozapine clinic but did not attend the appointments. Metformin initiation for weight management and prediabetes was recommended at several appointments, but he declined because he preferred not to take more medications. He smoked half a pack of cigarettes per day and was not interested in smoking cessation services.
His resting BP was elevated at his past 2 appointments (136/84 and 136/86 mm Hg), so the nurse at his group home had been recording daily BP readings in a log. His BP log revealed an average BP of 138/86 mm Hg. Pertinent vital signs and fasting laboratory results from the appointment were as follows: height: 5 feet, 10 inches; weight: 104.5 kg; BMI: 33 kg/m2; BP: 138/88 mm Hg; pulse: 79 bpm; hemoglobin A1c = 6%; TC = 225 mg/dL; LDL = 136 mg/dL; triglycerides = 395 mg/dL; HDL = 27 mg/dL; clozapine level = 132 mcg/L; norclozapine level = 135 mcg/L; white blood cell count = 8.4 thousand cells/mcl; and absolute neutrophil count = 5.1 thousand cells/mcl.
Clozapine is considered high risk for causing increases in weight, lipids, BG, and BP. This patient had already tried and failed multiple antipsychotics, and his mental health had been stable for 4 years on clozapine. Switching to an antipsychotic with lower liability for metabolic AEs is likely not a feasible option for this patient. Lifestyle interventions are a first-line treatment approach, but the patient had been unsuccessful with altering his diet, exercising, or attempting smoking cessation. Therefore, medically treating the metabolic AEs was necessary.
Hydroxymethylglutaryl-CoA reductase inhibitors (statins) are considered the cornerstone of treatment for lipid lowering due to evidence demonstrating they can prevent ASCVD. There are 4 categories of patients that may benefit from statin therapy, including those with clinical ASCVD, LDL ≥190 mg/dL, diabetes aged 40 to 75 years, and estimated 10-year ASCVD risk score ≥7.5%. An online ASCVD risk estimator can be located at . Individuals with an ASCVD risk score of 7.5% to <20% are considered intermediate risk for a cardiovascular event, and a moderate-intensity statin can be initiated if risk enhancers favor it. Examples of risk-enhancing factors include but are not limited to metabolic syndrome, chronic kidney disease, inflammatory disease (rheumatoid arthritis, psoriasis, HIV), ethnicity (eg, South Asian ancestry), and persistently elevated triglycerides (≥175 mg/dL). Individuals with an ASCVD risk score ≥20% are considered high risk, and statin initiation should be considered with a goal to reduce LDL by at least 50%. Moderate-intensity statins are expected to lower the LDL by 30% to 49% and high-intensity statins by ≥50% ().
Statins are most effective for lowering LDL, but they can also lower triglycerides (22% to 45%) and increase HDL (5% to 10%). Fibrates and niacin are effective for reducing triglycerides but have a mild LDL-lowering effect, and there is not enough evidence to routinely support their use as add-on medications to a statin. Adding a fibrate or omega-3 fatty acids to a statin is recommended for patients with persistently elevated severe hypertriglyceridemia (≥500 mg/dL) to prevent pancreatitis. Fenofibrate is preferred over gemfibrozil in patients being treated with a statin due to lower risk of myopathy. The dose of the statin is another important consideration. The largest percentage of LDL lowering is achieved with the initial dose., Each doubling of the statin dose should then lead to an additional 4% to 7% reduction in LDL., Clinical experience indicates that starting statins at a low dose and titrating up does not lead to the same level of LDL lowering as starting at a moderate- to high-intensity dose. Initiation of a lower intensity statin may be considered if there is a history of statin intolerance.
Stage 1 hypertension is defined as systolic BP 130 to 139 or diastolic BP 80 to 89 mm Hg. Stage 2 hypertension is defined as BP ≥140/90 mm Hg. At least 2 resting BP readings obtained on 2 separate occasions should be used to estimate the BP. A log of home BP readings can provide a more accurate estimation of BP if proper techniques are used. For primary prevention of cardiovascular disease in adults, nonpharmacologic therapy and treatment with an antihypertensive is recommended for individuals with stage 2 hypertension or stage 1 hypertension and a 10-year ASCVD risk of 10% or higher. Initiation of 2 antihypertensive agents from different classes is recommended for individuals with stage 2 hypertension. A BP target of <130/80 mm Hg is recommended. Thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and calcium channel blockers (CCBs) are first-line treatments for hypertension due to evidence demonstrating that they reduce clinical events. There is inadequate evidence to support beta blockers as a first-line treatment for hypertension in the absence of certain cardiovascular comorbidities, such as heart failure or ischemic heart disease. Patient-specific factors, such as comorbidities, concurrent medications, age, race, and medication adherence, should be taken into consideration when selecting an initial antihypertensive.
The optimal treatment for hypertension in individuals with metabolic syndrome has not been clearly defined. Thiazide diuretics can increase insulin resistance and accelerate conversion to diabetes mellitus.,, They can also worsen dyslipidemia., The European Society of Cardiology and the European Society of Hypertension guidelines list metabolic syndrome as a possible contraindication for use of thiazide diuretics. The ACC/AHA guidelines note that small increases in BG levels are possible but also state there are no data available demonstrating deterioration in cardiovascular outcomes in patients with metabolic syndrome who are treated with thiazide diuretics. When no compelling indications or contraindications are present to help guide treatment selection, preference may be given to an ACE inhibitor, ARB, or CCB in patients with metabolic syndrome to help avoid increases in BG. Age and race can also help with treatment selection. Thiazide diuretics and CCBs are preferred in Black adults without heart failure or chronic kidney disease because they are more effective than ACE inhibitors or ARBs. Older adults may also respond better to thiazide diuretics and CCBs due to a declining number of nephrons and lower plasma renin levels.
Using an average BP of 138/86 mm Hg, the patient in this case had a 10-year ASCVD risk score of approximately 17.5%, placing him into a statin benefit group. His known risk-enhancing factors included metabolic syndrome, characterized by persistently elevated triglycerides, obesity, and elevated BP. He also smoked cigarettes. Lifestyle modifications continued to be encouraged, and a risk-benefit discussion about statin therapy was conducted. He was willing to initiate a statin and was started on atorvastatin 20 mg by mouth daily. A moderate-intensity statin was appropriate based on his 10-year ASCVD risk score. His triglycerides were elevated but not enough to warrant addition of a nonstatin therapy. His BP readings in the clinic and at home indicated he had stage 1 hypertension, and his 10-year ASCVD risk score was greater than 10%. The patient did not have any compelling indications or contraindications to help guide selection of an antihypertensive. Given his age, race, and history of metabolic syndrome, initiation of an ACE inhibitor, ARB, or CCB may be most appropriate. After review of the potential AEs associated with each medication class, the patient elected to start amlodipine 5 mg by mouth daily.


A 12-year-old female patient came to the department with a blackish discoloration in the right upper front tooth region for 1 month (). Her previous dental history showed that she had undergone trauma when she was 8 years old. She suffered tooth avulsion wrt to right and left upper central incisors. Her previous records depict she was treated with rigid arch fixation and was following up for apexification procedure. However, currently patient started noticing reddish turned black discoloration in the right front tooth for the past 1 month. There was no history of pain or tenderness. On clinical examination, there was grade II mobility with discoloration at the cervical margin of 11. However, 21, appeared to be clinically stable and lacking any signs of inflammation. On radiographic examination, there appeared to be marked oval-shaped radiolucency involving radicular pulp space and coronal third as well (). Following which a diagnosis of inflammatory perforating internal resorption wrt 11 and replacement resorption wrt 21 was made. Consecutively, a treatment plan for surgical intervention wrt 11 was made.
The treatment objective was:
To halt the process of root resorption wrt 11.
To provide stability for 11 and preserve alveolar bone wrt 11 to later receive implant prosthesis.
The procedure was started by administering an infraorbital and nasopalatine nerve block along with local infiltration to provide for profound anesthesia. Now using a 15 no. BP Blade vertical incision was given on the labial aspect of the 11 and 12 region and an envelope flap was raised. The site was thoroughly irrigated with normal saline. Upon inspection, the labial cortex of the maxilla and the labial root surface of the right maxillary central incisor had undergone serve root resorption (). A 90% aqueous solution of trichloroacetic acid was applied over the resorptive lesion for 1 to 2 minutes using a cotton pellet. Following this, curettage of the resorbed cavity was done to remove any devitalized tissue. An 80-no. gutta-percha cone was placed within the canal over which freshly mixed white MTA Angelus (Dental Avenue India Pvt Ltd., Mumbai, India) was placed to provide for the root form (). However, the cervical region of the crown defect was recontoured with resin-modified glass ionomer cement (GC Gold Label Inc. Corporation, Tokyo, Japan). The patient was prescribed analgesics along with antibiotic coverage and was recalled for suture removal after 1 week. Since the tooth manifested mobility, independent ligature wire splints were bonded to the tooth with their adjacent teeth. The glass ionomer cement placed at the cervical margin was later faced with filled composite resin (). As for the status of 21, radiographically, it appeared that there was ingrowth of bone with the pulpal space and replacement resorption was ensuing (). The patient reported for follow-up after 1 year ().


A 7-year-old female patient admitted to the pediatric intensive care unit (ICU) with a known medical history of GT was referred to a pediatric dentist for opinion and management for bleeding gums. The patient presented with a chief complaint of severe bleeding from the upper left back tooth region since the previous night. History of presenting illness revealed that the patient was apparently normal the previous day morning, after which spontaneous bleeding started by afternoon leading to severe blood loss and hypovolemic shock for which she was admitted to the ICU. Bleeding was continuous; there were no aggravating or relieving factors. Previous hospitalization history revealed she was admitted twice earlier within a period of 30 days, with a similar complaint of bleeding from the oral cavity leading to a significant decrease in the hemoglobin (Hb) levels. No dental treatment was performed in the earlier visits, as it was advised by the pediatrician to wait for a month for the complete recovery of the patient. The parent also gave a history of a similar episode of bleeding from gums, vomiting containing clots of blood 1 year back with decreased Hb level at the time of hospitalization. The patient was discharged without being referred to the dentist one year back. A family history of consanguineous marriage was present. On extraoral examination, purpuric spots were seen in the left leg along with crusting and bleeding from the lips. Intraoral examination revealed root stump in relation to 54, 65, dental caries in relation to 53, 74, 36, and mobile crown structure in relation to 75, 55. Spontaneous bleeding was evident from 54, 55, 21, 11, 12, 22, and 46 and the patient also had anterior tooth crossbite in relation to 11, 21 (). The provisional diagnosis was given as gingivitis and chronic irreversible pulpitis in relation to 55, 54, 65, 75.
Laboratory investigation revealed a hemoglobin level of 1.3 g/dL on the night of admission. The next day the prothrombin time was 18.2 seconds, partial thromboplastin time was 22.8 seconds, international normalized ratio (INR) was 1.70, and hemoglobin was 6 g/dL. On the day of performing the dental procedure (fourth day of admission) as mentioned below, the hemoglobin level was 11 mg/dL, platelet count was 141,000, and bleeding time was 16.5 seconds. Orthopantomogram (OPG) revealed root stump in relation to 54, 65, dental caries involving enamel, dentin, and approximating pulp in relation to 53, 74, and resorbed roots in relation to 75, 55 ().
Consent was taken from the pediatrician and hematologist. Treatment planned was oral prophylaxis followed by extraction of 55, 54, 65, and 75. Placement of soft splint with absorbable gelatin sponge (Ab gel, Sri Gopal Krishna Lab Private Limited, India) after extraction. Restorative treatment included deep caries management in relation to 53 and 74, followed by stainless steel crown in 74, glass ionomer restoration in 36, pit and fissure sealants in 16, 46, 26.
After being admitted to the ICU, two units of random donor platelet and two units of packed cell volume transfusions were performed and the patient was shifted to the ward after an increase in the Hb levels. Two units of random donor platelets transfusion were performed on the next day. The patient was advised to use tranexamic acid mouth wash (500 mg tablet mixed with 10 mL of water—5%) 6 times a day for 2 days before the procedure. Instructions regarding maintenance of good oral hygiene and use of a soft-bristled toothbrush with fluoridated toothpaste and brushing using the Fones technique were emphasized. The dental procedure was planned for the fourth day. Half a unit of single donor platelets was infused pre- and postoperatively. Impression was made using putty and a soft splint (1.5 mm thick) was prepared. Following buccal infiltration, extraction of 55, 54, 65, and 75 was done. Tranexamic acid (500 mg tablet) was then powdered using mortar and pestle, mixed with saline, and packed into the socket. A paste of tranexamic acid was made, placed on gauze, and held with pressure for ten minutes on the socket after which the gauze was removed. The patient was advised to swallow the remaining tranexamic acid paste. An absorbable gelatin sponge (Ab gel, Sri Gopal Krishna Lab Private Limited, India) was then packed into the socket () followed by splint placement. Post extraction instructions were given and the patient was advised to keep the splint in place. The patient has advised a liquid diet until the next day and intravenous (IV) paracetamol and tranexamic acid (200 mg) 6 hours once were prescribed to the patient. After 2 hours, the patient did not show any signs of active bleeding. The splint was removed, the next day. No active bleeding was evident from the extraction socket. The patient was advised to wear a soft splint for two more days except during meals.
The patient was instructed to stop using the splint from the seventh day of admission (3 days after the dental procedure) and no active bleeding was evident from the extraction sockets. Few hours after removal of the splint, there was spontaneous bleeding from 12, 11, 21, 22, 46 and an extraction socket of 55. One unit of random donor platelets was infused on that day followed by infusion of half unit of single donor platelets the next day. Intermittent spontaneous bleeding was evident from the 11, 12, 21, 22, and 46 region. On the tenth day (sixth day of dental procedure), the remaining dental procedures were performed after infusion of one unit of random donor platelets pre- and postoperatively. Oral prophylaxis followed by deep caries management in 53, 74 with stainless steel crown in 74, glass ionomer restoration in 36, and type VII glass ionomer sealant in 16, 26, 46. Postoperatively, oral hygiene instructions were reinforced and IV tranexamic acid 200 mg once in 6 hours was prescribed. Spontaneous bleeding was still evident from 11, 12, 21, 22, and 46 the next day. The pediatrician advised stopping the oral bleeding to discharge the patient. Hence, on the eleventh day (the seventh day after the dental procedure), it was decided to use tranexamic acid paste (crush 500 mg of tranexamic acid and mix with saline) in the area of bleeding on the splint () and then place the splint intraorally. The patient was advised to keep the splint in place for 2 hours after which they were instructed to remove the splint and swallow the remaining tranexamic acid paste. The parent was advised to do the same whenever spontaneous bleeding occurred. The parent was also advised not to use more than two tablets of tranexamic acid (500 mg) each per day based on its maximum permissible dosage. Bleeding was completely reduced after 2 days of using this technique and the patient was discharged from the hospital.
Diet counseling was done. Stringent oral hygiene instructions were advocated by the patient. The patient was advised to use a soft-bristled toothbrush, fluoridated toothpaste, and gargle after every meal. Also, the parent was advised to use the soft splint with tranexamic acid paste whenever bleeding occurred.
Postoperatively, a 1-week follow-up revealed no active bleeding from gums. The patient has been reviewed every month for 4 months. The parent gave a history of using soft splint with tranexamic acid paste in the first 2 months during the eruption of the premolars with no history of hospitalization. Sealants were placed in relation to the premolars in the subsequent follow-up visits. At 7 months follow-up, there was no active bleeding and no history of hospitalization (). Loss of sealants was evident in relation to 16, 15, and 26 which was replaced.


A 25-year-old asymptomatic woman was sent to echo lab for routine echocardiography evaluation before discharge. She underwent surgical atrial septal defect (ASD) closure with median sternotomy approach 5 days ago. Her vital signs were stable, with unremarkable physical findings. An echocardiogram showed normal chambers and functions; an ASD patch was visualized with no residual ASD shunt. An echo-lucent mass (2.9 × 1.9 cm2), suggestive hematoma, was visualized at the pericardial space near the right atrium (RA) (). It was mildly compressing the RA, but no abnormalities on intracardiac hemodynamic were observed. The patient was sent for cardiac computed tomography (CT) scan to confirm the diagnosis; CT scan showed distinct hematoma without any sign of compression of cardiac structures (). Considering that the patient was asymptomatic and hemodynamically stable, she was discharged from the hospital and planned for monthly follow-up.
In the following few months, the patient came to the outpatient clinic monthly. She was asymptomatic and hemodynamically stable, with no remarkable physical findings. She was also sent to the echo lab for monthly evaluation. An echocardiogram revealed the hematoma was expanding and slightly compressing the RA ( and ()), with no intracardiac hemodynamic abnormalities. The patient was informed about her condition. Although stable, we suggested her to undergo hematoma evacuation due to fear that expanding hematoma will deteriorate her hemodynamic, but she refused and was discharged by her consent.
Three months later, the patient came to the outpatient clinic complaining of shortness of breath during daily activities, headaches, and coughs. On physical examination, the blood pressure was 110/70 mm Hg, heart rate 80×/min, respiratory rate 20×/min. Her physical examination showed increased jugular vein pressure with positive hepatojugular reflux. The cardiac examination showed cardiomegaly without muffled heart sound. The electrocardiography showed sinus rhythm, incomplete right bundle branch block, and the chest x-ray showed cardiomegaly without lung edema. The laboratory results were within normal limits. An echocardiogram revealed normal intracardiac hemodynamic without a sign of tamponade. Taking these findings into account, we suspected great vessel compression.
The patient was sent for a thorax CT scan, which revealed expanding hematoma compressed the SVC with dilation of the proximal vessel. Collateral vessels were also detected. The hematoma extended anterosuperiorly to the level of the aortic arch (). The patient was diagnosed with SVCS due to pericardial hematoma compression and sent for urgent surgery for evacuation. The patient then underwent a sternotomy, which found a large hematoma and hemostatic agents at the pericardium around the SVC, and the hematoma was successfully evacuated.


A 2-year-6-month-old male child, born to non-consanguineous parents, presented with persistent facial swelling, abdominal distention and reduced urine output for 6 weeks. He had recent onset breathing difficulty. He was a known case of NS being treated with prednisolone 2 mg/kg/day. His antenatal and postnatal history were uneventful. His nutrition and immunization status were appropriate for his age. He had nil significant family history.
On examination, the child was active and alert. Anthropometric examination recorded findings appropriate for his age. Examination of vitals revealed tachycardia (heart rate: 108/min), tachypnoea (respiratory rate: 27/min) and oxygen saturation of 93% in room air. He had elevated blood pressure of 130/90 mmHg (>95th percentile for his age and height) and pitting pedal edema.
Routine blood investigations, including renal and liver function tests were within normal limits. His baseline coagulation study and thyroid function test were normal. Urine analysis revealed nephrotic range proteinuria (4+ on dipstick and elevated protein creatinine ratio of 15.78) and microscopic hematuria. He also had hypoalbuminemia (1.4 g/dL) and hypercholesterolemia (1427 mg/dL). Ultrasound showed moderate pleural effusion, ascites and enlarged hyperechogenic kidneys. Suspecting SRNS, renal biopsy was performed, which revealed features of FSGS (). In view of severe anasarca and respiratory distress, he was initiated on albumin infusion with 20% albumin, 1 g/kg followed by diuretics, furosemide 1mg/kg/dose. After 2 sessions of combined albumin and diuretic therapy, edema settled and albumin level increased to 2 g/dL. Genetic study using targeted exome sequencing, revealed heterozygous missense mutation in exon 14 of ANLN gene that results in amino acid substitution of methionine for threonine at codon 821 (p.Thr 821Met;ENST00000265748.7). Currently, he is being treated with tacrolimus 0.1 mg/kg/day and enalapril 0.3 mg/kg/day, along with normal protein and no added salt diet. His parents have been counselled about the disease course, trial of immunosuppressive therapy and the need for renal transplantation in future.


A 7-year-old boy presented to the emergency services with purpuric rashes and bruises. Peripheral blood smear showed thrombocytopenia and neutropenia. No abnormal cells were seen. Bone marrow aspiration revealed markedly hypocellular bone marrow (5% cellularity) and no abnormal cells, leading to the diagnosis of aplastic anemia. He was referred to the pediatric ophthalmology service due to recent onset of headache, nausea, vomiting, and diplopia. Parents had noticed intermittent esodeviation. There was no history of transient visual obscurations or tinnitus.
Ophthalmic examination revealed visual acuity at 1.0 in both eyes (OU). Color vision (tested with Ishihara chart) was found to be normal OU. The pupils were normal in size and reaction to light. No relative afferent pupillary defect was noticed. Orthoptic evaluation showed an alternating intermittent esotropia of 18 prism diopters (PD) at near and 14 PD at distance. Extraocular muscle movements were normal. In particular, no abduction deficit was noted. Dilated fundus examination revealed bilateral disc swelling []. Cycloplegic refraction showed moderate hypermetropia of +6.0 D right eye (OD) and +5.75 D left eye (OS). Spectacle correction (full cycloplegic refraction) was advised. Humphrey visual showed enlarged blind spot OU []. Fundus fluorescein angiography was done and showed hyperfluorescence due to leakage, confirming the disc swelling to be due to papilledema []. Optical coherence tomography (OCT) showed increased average retinal nerve fiber layer (RNFL) thickness, normal macular contour, and macular ganglion cell layer (m-GCL) thickness [m-GCL; ].
Clinical examination by the pediatric neurologist was unremarkable. Magnetic resonance imaging (MRI) of the brain and orbits showed the absence of mass lesion and characteristic features of IH including prominent subarachnoid space around both optic nerves []. Magnetic resonance venogram (MRV) of the brain showed bilateral transverse sinus stenosis []. Lumbar puncture was performed and CSF opening pressure was found to be 50 cm H2O with normal CSF contents. The diagnosis of SIH was thus confirmed, and the child was started on oral acetazolamide (25 mg/kg/day – 250 mg, TID). Sodium bicarbonate 8.4% injection (35 ml) was added to combat metabolic acidosis. Intravenous dexamethasone (1 mg QID) and oral furosemide (7 mg TID) were added to aid resolution.
Follow-up after 5 weeks showed good response to the above treatment with resolution of headache, vomiting, and diplopia. Ophthalmic examination showed orthotropia with full stereopsis with glasses and flat optic discs []. OCT showed a marked reduction in the RNFL thickness and preserved m-GCL []. Bone marrow transplantation (BMT) was performed from a fully matched sibling. The post-BMT follow-up was uneventful for over 6 months.


A 62-year-old female presented to the emergency department at 13:30 with a 6 h history of oropharyngeal edema and dyspnea. She had a medical history of essential hypertension, chronic obstructive pulmonary disease, and gastroesophageal reflux disease. In 2019, she had undergone an invasive coronary angiogram performed for angina-type symptoms. This demonstrated no obstructive coronary atheroma [Videos and ]. Regular medications were esomeprazole 40 mg, perindopril/indapamide 5 mg/1.25 mg, and aclidinium bromide 322 mcg all once daily, and had not changed for 2 years. She was a retired teacher, an active smoker with a 40 pack-year history, and consumed 14 units of alcohol per week. She denied significant family history and was unaware of any known allergies.
Airway obstruction was observed secondary to oropharyngeal oedema. No skin changes were observed and she remained normotensive. Her bloodwork revealed a general blood count within the normal limits and a biochemical profile with no major abnormality. Eosinophils were normal at 0.29 × 109/L. Tryptase on the day of admission was 7.5ug/L (<13.5). The patient was administered intravenous hydrocortisone 200 mg, chlorphenamine 10 mg, and subcutaneous adrenaline (0.5 mg of 1:1000). Following interval resolution, several hours later oropharyngeal edema re-occurred necessitating subcutaneous adrenaline (0.5 mg 1:1000). Advanced airway was not deemed necessary, and the patient was monitored in the high dependency unit. The differential diagnosis considered at this stage was bradykinin-induced angioedema secondary to ACE-inhibitor, acute hereditary angioedema, idiopathic angioedema, or atypical allergic reaction secondary to mast cell activation. Given the subsequent good clinical response to glucocorticoids and epinephrine hereditary oedema was later felt to be less likely. Similarly, when it was known that the tryptase level was normal, atypical allergic reaction was no longer felt to be a strong differential diagnosis. After 48 h she was discharged from the hospital with a diagnosis of angioedema secondary to ACE inhibitor use. Perindopril/indapamide was replaced with the calcium channel blocker amlodipine 5 mg once daily.
Three days after discharge, she re-presented with nonpleuritic chest pain and intermittent dyspnea. 12-lead electrocardiogram showed t-wave inversion in leads I, II, aVl and V2-V6 []. Septal Q-waves were present, however, these were previously noted in 2016. Troponin level was 0.04ug/L (<0.01), and 0.04 after six hours. A chest X-ray showed bilateral pleural effusions. The d-dimer was elevated at 668 ng/ml FEU. Clinical concern at this point was a healthcare-acquired lower respiratory tract infection or pulmonary embolus. A computed tomography pulmonary angiogram did not demonstrate a pulmonary embolus, but again showed bilateral pleural effusions. To investigate her hypervolemia a transthoracic echocardiogram was filmed: it revealed a dilated, generally, hypokinetic left ventricle with the poor overall function was demonstrated []. Sigmoid septal hypertrophy was also noted, and ejection fraction was estimated to be at 15%–20% via the Simpsons method.
Due to the global nature of the myocardial dilation and nondynamic cardiac enzymes, the clinical suspicion of both a symptomatic dilated cardiomyopathy and stress-induced cardiomyopathy arose. A cardiac magnetic resonance imaging (MRI) without stress perfusion demonstrated a normal indexed left ventricular volume with moderately impaired ventricular function. There was moderate circumferential hypokinesis from mid-ventricle through to the apex, with appearances in keeping with a resolving takotsubo cardiomyopathy [Videos and ].
The patient was commenced on intravenous diuresis with the loop diuretic furosemide and once euvolemic, was discharged home. During her admission, the angiotensin-blocking receptor agent valsartan 80 mg, along with bisoprolol 2.5 mg were both introduced once daily and continued on discharge. A maintenance oral diuretic of frusemide 40 mg once daily also continued during recovery. Follow-up echocardiogram 1 month later revealed resolution of left ventricular systolic function to 50%–55%. Clinical follow up at 3 months postevent demonstrated euvolemia and symptomatic recovery. A full timeline of events is available [].


An 80-year-old male patient with a history of diabetes mellitus presented to the emergency department complaining of shortness of breath and cough. His vital signs on presentation were as follows: temperature, 37°C; heart rate, 112 beats/min; blood pressure, 120/75 mmHg; respiratory rate, 28 breaths/min; and oxygen saturation, 90% on supplemental oxygen. There were no significant points in the general examination. His bilateral lower extremities were normal, and his bilateral popliteal, posterior tibial, and dorsalis pedis arterial pulses were palpable. On laboratory testing, the following values were noted: white blood cells, 7×109/L (reference, 4.5×109-11.5×109); hemoglobin, 13.6 g/dL (12-16); hematocrit, 37.3% (35%-45%); platelets, 210×109/L (140×109-440×109); glucose, 378 mg/dL (70-105); creatinine, 1.4 mg/dL (0.6-1.40); blood urea nitrogen, 11.3 mg/dL (7-23); D-dimer, 248 ng/mL (<0.5); prothrombin time, 20 sec (12.2-14.9); international normalized ratio, 1.1 (<1); partial thromboplastin time, 40 sec (21.3-35.1); C-reactive protein, 151 mg/L (<10 mg/L); and erythrocyte sedimentation rate, 88 mm/h (0-32); lupus anticoagulant, negative; interleukine-6, 76 pg/mL (5-15). His nasopharyngeal swab was positive for the severe acute respiratory syndrome coronavirus-2, and high-resolution computed tomography showed bilateral extensive interstitial lung infiltrates. As such, the patient was admitted to the intensive care unit (ICU) and was treated with Ziferon (Interferon-1b, 250 mg/mL; Zist Daru Danesh, Tehran, Iran) every two days via subcutaneous administration, dexamethasone 8 mg/day via intravenous administration, Remdesivir (100 mg/20 mL; Actoverco, Tehran, Iran) 200 mg on the first day followed by 100 mg/day, and heparin 5,000 units subcutaneously every 6 hours. On the ninth day after admission, with the patient still complaining of shortness of breath (O2 saturation: 89%), he experienced sudden pain in the right lower extremity with coldness, ischemic discoloration, paralysis, and lack of femoral pulses of the limb (). Computed tomography angiography revealed the total occlusion of the right common iliac artery with no distal run-off (). Electrocardiography did not show any arrhythmia, and the platelet count was normal on the day of the event and after. The patient underwent an emergency thromboembolectomy with spinal anesthesia via a femoral incision. A long thrombus with a cohesive, tubular consistency emerged from the iliac, femoral, and tibial arteries (, Supplementary Video 1). After the successful thrombectomy, the ischemia resolved, and the patient was transferred to the ICU. In the ICU, the patient experienced respiratory acidosis (pH, 7.27; PCO2, 55; PO2, 90; HCO3, 14.4; base excess, –2.1) but had adequate urine flow. He also received intravenous heparin at a dose of 1,000 units per hour. The right lower extremity was warm, and the symptoms of ischemia resolved. In addition, necessary measures were taken to prevent reperfusion syndrome. Ten hours after the operation, the patient’s respiratory distress worsened despite receiving 100% oxygen. He eventually suffered from cardiopulmonary arrest and died.


A 49-year-old woman presented with increasing dyspnea on exertion for 3 wk, occasionally accompanied by chest pain and cough.
No special history of past illness.
Physical examination was notable for stridor at rest.
After she was admitted to the local hospital in March 2015, a chest computed tomography (CT) scan showed a soft tissue mass surrounding the inner surface of the upper trachea, leading to irregular lumen stenosis of the trachea (Figure and ). Thus, she was referred to our hospital, in order to initially undergo resection, which is considered the most effective treatment for tracheal tumor. The patient experienced stridor at rest. Bronchoscopy revealed that a large polypoid intra-luminal mass, with its surface presenting rich vascular networks and nodular protrusions, was present in the upper trachea extending caudally 2 cm to 7 cm of the glottis (Figure ).


Case 1: A 63-year-old woman was admitted with a perforating skin defect of the nasal dorsum.


Case 2: A 31-year-old man was visited our hospital with a perforating skin defect of the nasal tip.


A 25-year-old woman, homemaker, came to outpatient department (OPD) with complaints of eating mud for 2 years, increased for the past 1 month, decreased appetite for 6 months, and occasional apprehension. The patient was apparently asymptomatic around 2 years back when she started eating mud. At first, she had around 2–3 pinches. She continued to have pinches for around 1 year when she felt a need to increase the amount of mud she used to have daily. Thereafter, the amount of mud increased to 20–40 g/day. She preferred dry mud. She stated that the mud eating was preceded by an irresistible urge and simply that she enjoyed having mud. She did, however, note that once she began eating mud, she would have the need to eat more. Since the past month, the urge to have mud had increased to such an extent she started buying mud from the market to eat. She used to have around 100 g of mud daily. Whenever she tried to avoid eating mud, she would feel the need to eat something hard and could not control the urge to have mud and at times used to have apprehension. To control the apprehension, she used to eat mud. On enquiring, she said that she knows eating mud was not a right thing, but her urge was so strong that she was unable to stop herself from eating mud that made her distressed. She is also experiencing decreased appetite for the past 6 months. Earlier, she used to eat three meals in a day with a mid-day snacks. In each meal, she used to have two chapattis with a bowl of rice and a bowl of vegetable and pulses. For around 6 months, she has started missing her mid-day snacks and only eats one chapatti with a bowl of pulses. On asking by spouse and parents-in-law, she said that she does not feel like eating food. No significant past and family history was reported. She presented as a well-orientated, cleanly dressed lady with normal speech and appropriate replies. Her mood was generally warm and friendly. She had no abnormality of thoughts or perceptions and scored 30/30 on a Mini Mental State Examination. She was prescribed fluoxetine that was gradually increased to 40 mg along with multiple sessions of psychotherapy and showed a significant improvement in her condition.


A 30-year-old female, married for the last 11 years, educated up to 10th standard, came to the psychiatric OPD with complaints of eating nonnutritional substances for the last 10 years. The patient was apparently well 10 years ago when she was pregnant with her first child, and during third trimester, she started having craving for eating chalk pieces. One day, she went to a shop near her home and bought one box of chalk pieces. She ate the whole box in 1 day. It reduced her craving and she felt satisfied. After that, she started buying one box of chalk every day and eating it. With time, her craving and daily intake of chalk boxes increased, and within 5 years, she was eating 3 boxes per day. During her second pregnancy 5 years back, she as usual went to buy chalk box, but saw a box of “multani mitti” (MM), and decided to try it. She bought 250 mg of MM. She liked the taste of it. After that, she stopped eating chalk box and started eating MM only. Six months ago, the patient tried to stop eating MM. She experienced craving for it, and after 1 month of stopping, she gave in to the craving and started eating MM again. She was kempt, cooperative, in touch with reality. Talk was relevant and coherent. Mood was euthymic. No features of psychosis were noted. Memory, orientation, and insight were unimpaired. She was treated with sertraline 75 mg along with multiple sessions of psychotherapy and showed a significant improvement in her condition.


This is a single case report of a 3-year-old girl child with 20% total body surface area with scald burns over trunk and right thigh, managed at the tertiary burn care center of our institute. The depth of scald burn wound was mixed, having areas of second-degree superficial and second-degree deep burns. There were multiple blisters formed over second-degree superficial burn areas. Some of the second-degree superficial burn and all of the second-degree deep burn wounds were exposed and were not having intact skin or blisters over them. On arrival to the burn center, the child was managed according to the WHO (World Health Organization) burn management guidelines. After stabilization, she was shifted to burns procedure room for wound management. All the wounds were cleaned with warm saline carefully keeping the blisters intact. Intact burn blisters were aspirated in sterile way using 1-mL syringes, and the overlying skin was kept intact over the wound []. Quantity of burn blister fluid aspirated was 3 mL. The aspirated blister fluid was sprayed over the exposed parts of second-degree superficial burn areas immediately []. These areas were around 5% of the total body surface area. After that, all the wounds were covered with bovine collagen dry sheets, followed by a non-adherent layer, then a layer of absorbing dressing with connections for regulated oxygenation and negative pressure therapy, and a last layer of occlusive dressing. During postoperative period, fluid resuscitation and supportive treatment was provided to the child. After 5 days of burn injury, the child was taken to the operation theater, and her wounds were reassessed. Wounds were cleared of debris from dead skin and collagen sheets, using hydrojet debridement. It was found that the second-degree superficial wounds were healing well []. Only patchy areas were having deep burns, which were debrided, and pixel grafting was carried out to minimize donor-site problems. All wounds were provided adjuvant wound therapy using low-level laser, autologous platelet-rich plasma (APRP), and regulated oxygenation and negative pressure therapy. On 11th post-burn day, the wound was again opened, and it was found that all areas of second-degree superficial burns were completely epithelialized []. The pixel graft had started proliferating over the deep burn areas. On 18th post-burn day, complete wound was found to be healed []. Postoperative scar therapy was provided using silicone sheets and compression garments. The child was discharged with physiotherapy and nutrition counseling.


A 67-year-old woman presented with subacute epistaxis and diffuse bone pain. Her past medical history included poorly differentiated triple-negative infiltrating ductal carcinoma of the left breast and melanoma of the upper lip. Both malignancies were diagnosed and treated 20 years prior to her current presentation. For her breast cancer, she underwent left modified radical mastectomy followed by chemotherapy with doxorubicin and cyclophosphamide and then paclitaxel. Her breast cancer was successfully treated with no evidence of recurrent disease. For her melanoma, she underwent resection but no systemic therapy afterward. There were no other records regarding the details of her melanoma treatment, and no genetic workup appeared to be performed for inherited cancer predispositions.
The patient presented to her outpatient medical oncologist, who treated her for breast cancer, to further evaluate her symptoms. Her labs included a white blood cell count of 13.6 × 103/µL, hemoglobin 9.4 mg/dL, and platelet count 22,000/mm3. Her platelet count was normal approximately 5 months prior to presentation. Complete blood count differential showed absolute neutrophil count 2,900/µL, lymphocytes 3,800/µL, eosinophils 100/µL, and increased monocytes 2,200/µL. There were also increased metamyelocytes (1,000/µL), myelocytes (700/µL), and immature blasts (400/µL). Differential diagnosis for her anemia and thrombocytopenia included chemotherapy-related pancytopenia, hemolytic anemia, rheumatological disease, and vitamin deficiency. Serological workup for these differentials was unremarkable, so bone marrow biopsy was performed. Preliminary results of the bone marrow biopsy demonstrated small-round-blue-cell tumor (shown in Fig. , ).
She was subsequently admitted to the hospital due to concern for acute leukemia, especially given her prior chemotherapy. However, initial bone marrow biopsy results showed replacement of the bone marrow by metastatic tumor with expression of neuroendocrine markers (INSM1, CD56, synaptophysin, and chromogranin). Further evaluation of the bone marrow showed diffuse staining for muscle markers (myogenin and desmin), strongly favoring an alveolar rhabdomyosarcoma with some neuroendocrine differentiation. Noncontrast CT of the head demonstrated a large trans-spatial infiltrative mass in the left nasosinal cavity. Further advanced imaging, including MRI of the brain, noted that this mass extended into the skull base and cavity along with widespread lymphadenopathy. CT of the chest, abdomen, and pelvis demonstrated diffuse metastatic disease, including along the spine, thoracic rib cage, lungs, adrenal glands, and spleen. Nuclear bone scan demonstrated heterogeneous appearance of the marrow in the bilateral humeri and proximal femurs.
The biopsy from the left sinonasal mass revealed a malignant epithelioid neoplasm growing deep to the respiratory mucosa (shown in Fig. ). There were irregular, pleomorphic nuclei with nuclear hyperchromasia and a variable amount of cytoplasm (shown in Fig. ). A minor population of the cells had eccentrically located eosinophilic cytoplasm, imparting a rhabdoid appearance. The tumor cells had strong nuclear expression of myogenin (shown in Fig. ) and membrane expression of desmin (shown in Fig. ). FISH and molecular testing on the bone marrow, performed at an outside institution, demonstrated a FOXO1 gene rearrangement, consisting of a PAX3-FOXO1 fusion. Altogether, these findings confirmed the diagnosis of stage IV alveolar rhabdomyosarcoma.
Due to the widespread nature of her disease, she was started on chemotherapy with vincristine (1.5 mg/m2), actinomycin-D (0.045 mg/m2), and cyclophosphamide (1,200 mg/m2) (VAC) once the PAX3-FOXO1 fusion returned positive. It was approximately 2 weeks between initial bone marrow biopsy and positivity for the fusion study before treatment was initiated. She remained persistently thrombocytopenic, which was complicated by epistaxis and melena during her hospitalization and required multiple transfusions of platelets. The patient experienced acute hypoxic respiratory failure secondary to mucus plugging and aspiration requiring transfer to the intensive care unit. At that point, she declared that she wanted to stop all treatment and proceed with hospice care. Unfortunately, she died prior to discharge home.