An 86-year-old man was diagnosed with a squamous cell carcinoma of the lung after further examinations of hemosputum and was referred to our hospital for surgical treatment. A chest computed tomography (CT) scan showed a cavitary nodule without mediastinal nodal metastasis (Figure ). The patient had a past history of brain infarction and atrial fibrillation 5 years previously, which was treated with medical treatment with apixaban. We replaced the anticoagulant drugs to intravenous heparin 7 days before his operation followed by a thoracoscopic right upper lobectomy and mediastinal lymph node dissection. The operation took 385 min because of intrathoracic adhesions and infiltrating hilar lymph nodes. We can detach the adhesion between parietal and visceral pleura except the part of the dorsal adhesion, in which the extrapleural detachment was required. The blood loss was 50 g. The pathologic staging was pT2aN0M0 stage IB. He progressed well after surgery, and the chest tube was removed on postoperative day (POD) 5. Regarding the administration of anticoagulant, we restarted the administration of intravenous heparin on POD 1 and switched it to apixaban on POD 5 (after removal of the chest tube). The chest X-ray on POD 11 showed a small pleural space with effusion on the apex of the thoracic cavity. He suddenly developed a right chest pain and a hemoptysis after straining at defecation on POD 15. An emergent chest CT showed a huge extrapleural hematoma on the right anterior chest wall ranged to thoracic apex and widespread ground glass opacification in the right lower lobe (Figure ). His vital signs were as follows: heart rate = 140 bpm, blood pressure = 85/52 mm Hg, SpO2 = 92% (nasal O2 2L), and hemoglobin = 11.1 g/dl. The patient suddenly went into cardiac arrest probably because of a hemoptysis. We decided to perform an emergent operation for an evacuation of EP immediately after resuscitation. We evacuated the hematoma through 15-cm incisions on the 4th and 7th intercostal space. The extrapleural space was occupied with a large amount of hematoma that ranged from thoracic apex to lower lateral thoracic wall. The bleeding point was revealed on the extrapleural thoracic apex after the removal of the hematoma to succeed in hemostasis by a suture ( S1). The volume of bleeding was 840 g. No approach was made to the thoracic cavity because of the formation of postoperative adhesions in the thoracic cavity. Fortunately, the hemoptysis stopped under an overnight ventilator control, and we could remove the endobronchial tube on the next day. Extrapleural chest tubes were successfully removed 10 days after surgery. No evidence of EP was found for 6 months.


A 35-year-old female presented to the clinic with a complaint of dull aching pain in the left flank region with occasional sharp episodes and no radiation. She had no history of fever, burning micturition, hematuria, and increased urinary frequency and urgency. She complained of occasional fatigue but denied nausea, weight loss, blurred vision, headache, neck swelling, excessive thirst, constipation, muscle and joints pain, mood changes, amenorrhea, and galactorrhoea.
She had a similar history of nephrolithiasis episodes in the past and had undergone left and right percutaneous nephrolithotomy (PCNL) surgery 15 and 10 years back, respectively. In addition, she had no family history of similar illnesses in other family members. She denied tobacco consumption but consumed alcohol occasionally.
Due to similar previous episodes, further studies were done revealing elevated serum calcium and parathyroid hormone (PTH) with 11.5 mg/dl (normal range: 8.8-10.5mg/dl) and 152.6 (normal range: 7.5-53.5pg/ml), respectively. The level of vitamin D was 22.7 ng/ml and was slightly in the level of the lower range. In addition, she had normal 24 hours urinary calcium level, prolactin, serum albumin, magnesium, phosphorus, lactate dehydrogenase, thyroid function test (TFT), and urine examination.
As part of the protocol, an ultrasound of the neck was solicited but was unexceptional. Hence, a 4D CT scan of parathyroid was commenced, which showed soft tissue density lesion at the posterior aspect of the lower pole of the right lobe of thyroid with hyperenhancement in arterial phase and washout in venous phase compared to the thyroid, and an inferior thyroid artery as a polar vessel - features suggestive of parathyroid adenoma (Figures -).
Later, Sestamibi parathyroid scintigraphy confirmed the right parathyroid adenoma. The bone mass density (BMD) was also performed which revealed normal spine and femur density. Hence, she was diagnosed with recurrent nephrolithiasis secondary to hypercalcemia due to primary hyperparathyroidism. As a result, she underwent Right inferior focused parathyroidectomy (Figures -).
The level of PTH one hour before the surgery was 187.2 pg/ml, and the level of PTH 20 minutes after the surgery was 21.6 pg/ml, which decreased significantly. However, PTH and corrected calcium levels were normal (21.5 pg/ml and 10.6 mg/dl, respectively) on the subsequent second postoperative day. She had recovered well after the surgery, and currently, she is in good health with no complications. She is on regular follow-up.


A 43-year-old healthy Caucasian female presented to primary care with short (7–10 days), recurrent flares of lower extremity tenderness, swelling, and redness over several months. She also reported myalgias in the upper back and neck, and a one-year history of headache with transient, reoccurring curtain-like visual disturbances in her right eye that ophthalmology diagnosed as ocular migraines. A rheumatologic workup was initiated. Labs were positive for an elevated sedimentation rate (ESR) 31 mm/H (normal 0–20 mmH), positive antinuclear antibodies (ANA), and an elevated ribonucleoprotein antibodies (RNP) 2.4 AI (reference <1.0 AI). Double-stranded (DS) DNA 1 IU/mL (<4 = Neg), antichromatin (AC), anti-Smith (SM), SM/RNP, and lyme disease antibodies were negative. Based on these results, the patient received a presumptive diagnosis of undifferentiated connective tissue disease (UCTD), started 20 mg of oral prednisone as needed for flares, and referred to rheumatology.
Two months after her initial evaluation, the patient continued to experience episodes or erythema nodosum of the lower extremities. She also began to experience early signs of Raynaud's phenomenon, chest pain, and visual disturbances concerning for amaurosis fugax. A personal symptom journal kept by the patient indicated transient episodes of fatigue and painful hand/finger swelling with petechiae and purpura. Magnetic resonance imaging (MRI) of the brain was ordered, and repeat labs done by rheumatology showed an elevated ESR, 39 mm/H; RNP, 1.8 AI; CRP, 3.7 (normal <0.8 mg/dL); and a negative antineutrophil cytoplasmic antibody (ANCA), myeloperoxidase antibodies, proteinase-3 antibodies, and ANA. Complement C3, 118 mg/dL (normal 90–180 mg/dL), and C4, 29 mg/dL (normal 16–47 mg/dL), were within normal limits. The patient was referred for further evaluation at an academic medical center.
The MRI showed a 6 mm lacunar infarct within the left cerebellum and a 12 mm hemorrhage along a cortical sulcus of the right frontal lobe. The findings were noted to be “abnormal” for a woman in her early forties, and a further work was recommended for vasculitis and/or connective tissue disease via magnetic resonance angiography (MRA). The MRA and ophthalmological assessment were unremarkable, and cardiology found no evidence of vascular disease on carotid ultrasound and no evidence of exercise-induced myocardial ischemia on stress echocardiogram.
A second rheumatological consult was completed where concern for possible evolving MCTD was raised; however, the diagnosis of UCTD was retained due to the negative ANA. Seven months following her initial presentation, the patient saw neurology where she reported worsening lightheadedness and 6-7/10 bifrontal/apical headaches lasting hours to days over the previous month. Despite the history of arthralgias/myalgias, purpura, chest pain, evidence of cerebral hemorrhage, and initial labs showing nonspecific inflammation and markers of autoimmunity, vasculitis was considered low on the differential due to a lack of a clear prodromal history and changes in cognition. Similarly, neuro-ophthalmology found no definite retinal vasculitis and believed her homonymous right visual field defect to be associated with the brain lesion previously appreciated on MRI and not amaurosis fugax. A nonemergent repeat MRI with contrast and an MR venogram of the brain were ordered by neurology to rule out thrombosis and evaluate for new lesions.
Approximately two months after her neurology appointment, the patient presented to the emergency room with a severe, right-sided headache with a left-sided visual disturbance. Shortly after arrival, the patient became delirious and exhibited seizure-like activity. A computerized tomography scan (CT) of the brain was conducted that showed a right parietal lobe intraparenchymal hemorrhage approximately 5 × 3 × 5 cm in size with secondary mass effect including mid- and hind-brain herniation (see ). A CTA showed multifocal narrowing and an abnormal “beaded” contour of the entire cerebral arterial vasculature consistent for vasculitis. Neurosurgical assets were not available, and the patient was transferred to a sister center where craniectomy was performed to evacuate intracerebral hemorrhage and treat intracranial hypertension (see ). Postoperative prognosis was poor, and palliative measures were initiated. The patient passed away peacefully surrounded by family several days later.


A 57-year-old female presented to the dermatology clinic for evaluation of an erythematous rash on the left forehead and ear. The patient reported that the rash had developed two months prior. She stated that it had been asymptomatic and stable, and denied the use of any new cosmetics or cleansers. Her medical history was significant for allergic rhinitis, gastroesophageal reflux disease, and chronic ultraviolet exposure secondary to sun tanning. Incidentally, the patient had been self-treating the rash on her face with betamethasone which was originally prescribed for a distinct eczematous rash with no improvement. On physical examination, multiple discrete pink macules were noted over the left forehead with similar lesions over the left ear. Proposed differential diagnoses included cutaneous malignancy, tinea infection, and contact dermatitis. The helical lesion was cultured to rule out infection, and a shave biopsy was performed on the preauricular area to assess for cutaneous malignancy. Figure shows the macular lesion on the left forehead of the patient.
Histologic examination of the lesion on the left preauricular area showed perivascular and periadnexal dermatitis, highly suspicious for a connective tissue disorder. Hematological examination including complete blood count (CBC), antinuclear antibody, and rheumatoid factor (RF) was unremarkable, except for RF which was elevated. Hydrocortisone cream 2.5% was prescribed for application to the affected areas, and a one-month follow-up was scheduled with an allergist to rule out contact dermatitis.
On follow-up, the patient reported no improvement of the rash and denied any associated pruritus. At this appointment, a diagnosis of seborrheic dermatitis was favored and treatment was initiated with ketoconazole 2% cream. The patient returned to the allergist one month later with no improvement in the rash following the trial of ketoconazole. She was then instructed to discontinue the ketoconazole and begin the application of pimecrolimus 1% cream to the affected areas. After this visit, the patient underwent allergy testing, but no relevant findings were noted. Due to the persistence of the rash, the patient requested reevaluation by dermatology.
The patient consulted a dermatologist two weeks later. The rash did not show any improvement and was not associated with any new symptoms of burning or itching sensation. After a detailed examination of the forehead, it was decided that a 3 mm punch biopsy of the affected area was warranted. Figure shows the full 3 mm punch biopsy taken from the left forehead. Figure and Figure show high-powered views of the biopsy specimen, significant for periadnexal inflammatory infiltrate consisting of intraepidermal mononuclear cell aggregates with enlarged hyperchromatic nuclei and irregular nuclear borders. These histologic findings were consistent with the diagnosis of pagetoid reticulosis. Following the diagnosis, a CBC, comprehensive metabolic panel, and T cell count were ordered, and the patient was instructed to apply Clobetasol 0.05% cream twice daily and return in one month for follow-up. Because the rash did not improve, the patient was referred to the Mayo Clinic where a trial of topical nitrogen mustard therapy was initiated without improvement of the rash. Furthermore, the patient noted spread to other areas of her body including the extremities and trunk. The patient’s current treatment regimen is light therapy three times per week with chlormethine topically.


A 77-year-old female presented with slurred speech, facial weakness, and left limb numbness and was admitted into our hospital. The patient had a history of hypertension and coronary heart disease, without diabetes or smoking. The patient’s hepatic function, renal function, coagulable state, and other laboratory tests were normal. Brain MRI without contrast revealed a subacute cerebral infarction near the right side of the lateral ventricle. The patient was given supportive treatment and improved. Nonetheless, an intracranial aneurysm of the left ICA was incidentally found on cranial MR angiography (MRA). Afterward, this patient underwent a diagnostic cerebral angiography and an additional therapeutic cerebral angiography.
After the second therapeutic angiography, the patient presented with right hemiplegia and aphasia when she was resuscitated from anesthesia. Neurological examination revealed mixed aphasia, left eye gaze, reduced pupillary light reflex, loss of right muscle strength (level 0/5), a positive right Babinski sign, and lack of response to painful stimuli. At first, we suspected stroke due to the clinical findings which mimicked a left middle cerebral artery (MCA) occlusion. According to the TOAST criteria, the “stroke” symptom could be classified as large artery atherosclerosis []. However, the patient’s clinical findings did not match the imaging results which showed a patent left MCA. Therefore, CIE was suggested. The patient was given 200 mg methylprednisolone QD IV, 124 mL of 20% mannitol Q8H and rehydration fluids after emergent CTA and MRI examinations. 54 h later, the patient suddenly developed a generalized tonic-clonic seizure lasting about half a minute. She achieved remission after symptomatic treatment. 72 h later, the patient’s right hemiplegia and aphasia began to improve, as the muscle strength of the right lower limb increased to 3/5 and the right upper muscle strength remained at 0–1/5. Finally, after fluid restriction dehydration, short-term corticosteroid treatment, and rehydration resuscitation, all neurologic deficits achieved complete remission on a postoperative Day 6.
The first diagnostic cerebral DSA procedure was conducted to further confirm the existence of the left intracranial ICA saccular aneurysm with a size of 6.9 × 6.0 mm, with a total of 150 mL nonionic, iso-osmolar Iodixanol (Visipaque, 320 mg I/ml, Bayer Healthcare, USA) IV. It also showed extracranial moderate stenosis (approximately 50%) in the initial segment of the left ICA. The internal carotid artery and vertebral artery angiography showed the anterior, middle, and posterior cerebral arteries. One week later, the patient underwent a second angiographic treatment for aneurysm embolization under general anesthesia. On this second procedure, the 6F intracranial support catheter (Navien, RFX072–105-08MP, EV3, America) was guided over the stenotic left ICA to the extracranial distal segment of ICA (the level of first cervical vertebra) without local artery vasospasm, stenosis, or the stasis of the contrast agent. A total of 160 mL Iodixanol was injected during the second therapeutic DSA.
After the second interventional DSA procedure, an emergent head CT angiography (CTA) scan showed the left cerebral hemisphere swelling, shallowing of the sulci, and diffuse high-density in the subarachnoid space without any cerebral artery occlusion or stenosis (Fig. ). 4 h later, brain MRI showed diffuse swelling in the left cortex with a normal signal on T2-weighted imaging (T2WI), fluid-attenuated inversion recovery (FLAIR), and mild hyperintense on diffusion-weighted imaging (DWI) (Fig. ). 20 h later, repeat brain CT showed the resolution of left cerebral hemisphere swelling and diffuse high-density (Fig. ). However, 28 h later, repeat non-contrasted brain MRI showed mild gyral hyperintense in the left hemisphere on T2WI, FLAIR imaging, and DWI with a normal ADC mapping (Fig. ). There were no indications of acute cerebral infarction.


A 62-year-old man with a history of hypertension and chronic rhinosinusitis presented to our clinic with complaints of subacute onset right-sided nasal obstruction. He first noticed his symptoms six months ago; however, he noted a rapidly growing mass in his right nostril over the past two months which was causing his symptoms to become more bothersome. Apart from nasal obstruction, he noted recurrent right-sided epistaxis as well as a mass on the right side of his neck that had gotten progressively larger.
On exam, he had notable facial asymmetry with the fullness of his right malar region and a mass emanating from the nasal vestibule completely obstructing the right nasal cavity. Nasal endoscopy of the right nostril demonstrated an exophytic, fleshy mass arising from the anterior septum that extended posteriorly causing obstruction of the osteo-meatal complex (OMC). Endoscopy on the contralateral nostril demonstrated leftward deviation of the septum from the mass effect of the lesion. Examination of his neck revealed a firm, fixed, 2 x 1.5 cm mass in level IIB. Computed tomography (CT) imaging of the face and sinuses demonstrated an erosive mass originating from the right cartilaginous septum with erosion and obstruction of the right OMC (Figure ) as well as acute appearing right-sided ethmoid and maxillary disease. On both physical examination and imaging, there was no ostensible extension to or involvement of other intranasal structures other than the septum.
The patient was ultimately taken to the operating room for nasal endoscopy and excision of the right-sided nasal mass. Intra-operatively, a 5 x 4 cm mass as previously described was visualized which originated from the anterior and midportion of the septum. Due to an inability to access the posterior margin of the lesion, excision was only feasible through the contralateral nostril. A left-sided hemi-transfixion incision was made and a mucoperichondrial flap was extended backward past the bony-cartilaginous junction. The mass was noted to have eroded through the septum but was not involving the vomer or perpendicular plate of the ethmoid. After disarticulating the bony-cartilaginous junction and freeing the septum from pre-maxillary crest the lesion was removed in its entirety from the right nasal cavity. Pathologic examination of the specimen demonstrated a lesion with both epithelial and sarcomatous components (Figure ) which stained positively for cytokeratin 5/6 (CK 5/6), Cam 5.2, P40, and epithelial membrane antigen (EMA). The final pathologic diagnosis was carcinosarcoma. The patient opted against an elective neck dissection and instead chose to pursue chemoradiation therapy for the right-sided neck mass.
Ultimately, he completed three cycles of radiation (70 Gy/35 fractions) with concurrent high dose Cisplatin (100mg/m2) therapy. Due to underlying kidney function, his third dose of chemotherapy was reduced to 40mg/m2. Six weeks following completion of chemoradiation therapy the patient was seen in the clinic and noted to have clinical resolution of the right-sided nasal mass. Apart from some mild xerostomia, the patient denied any symptoms of nasal obstruction or dysphagia. He was scheduled to have a repeat PET scan in four weeks to re-evaluate for signs of residual disease or recurrence.


History of presenting illness
A 36-year-old Hispanic male with no past medical history presented to the emergency department (ED) with shortness of breath (SOB), initially with exertion and then also at rest. For three days prior to the arrival, the patient reported decreased oral intake and dry cough, but otherwise, the review of systems was negative. On arrival, vital signs were 103/66 mmHg, 120 beats per minute, initially saturating 77% on room air, but improved on 10-L non-rebreather mask.
On examination, he was tall, thin, in acute respiratory distress using accessory muscles to breathe, and with decreased breath sounds throughout all lung fields. Initial labs were remarkable for hyponatremia (128 mEq/L), a corrected anion gap of 13, with arterial blood gas indicative of primary metabolic acidosis with mixed respiratory alkalosis, acute kidney injury (Cr of 1.10 mg/dL), normocytic anemia (Hbg of 11.7 gm/dL, mean corpuscular volume [MCV] of 84 fL), and elevated inflammatory markers (D-dimer of 2.04 mcg/mL FEU, ferritin >1,000 ng/mL, lactate dehydrogenase of 814 units/L, creatinine kinase of 140 unit/L, and C-reactive protein [CRP] of 108 mg/L). Electrocardiogram revealed sinus tachycardia at a rate of 110, without ST or T wave abnormalities. Chest x-ray (Figure ) demonstrated hazy pan-lobar infiltrates concerning atypical pneumonia. The patient underwent computerized tomography (CT) angiogram (Figure ) to rule out pulmonary embolism, which revealed extensive interstitial infiltrates with consolidation, especially in the posterior right upper lobe and right lower lobe.
Initial hospital course
Admission labs for respiratory viral panel, influenza, procalcitonin, and COVID PCR were all negative. The patient was treated with convalescent plasma, Remdesevir, Decadron 6 mg IV daily, and vitamin C and zinc supplementation. On day 2, a repeat COVID-19 PCR was negative, and the patient remained dependent on a 4-L nasal cannula. The hyponatremia and tachycardia resolved with adequate oral hydration. Sputum cultures grew Gram-positive cocci in clusters, and the patient was started on Doxycycline 100 mg twice daily, intravenous (IV) Vancomycin 1 gram twice daily, and intravenous Zosyn 3.375 mg thrice daily for broad-spectrum coverage. At this stage, the patient’s imaging and clinical signs were concerning for Pneumocystis jirovecii (PCP). The patient reported unprotected receptive same-sex intercourse but denied a history of illicit drug use or transfusions in the past. The patient then revealed that he was diagnosed with HIV seven years ago. HIV was positive, and IV Bactrim 360 mg thrice daily and oral Prednisone 40 mg twice daily were started for PCP treatment. Bactrim was changed to Atovaquone oral 750 mg twice daily because of acute renal failure. Sputum cultures were positive for methicillin-susceptible Staphylococcus aureus (MSSA) pneumonia, and ceftriaxone 1 gram IV daily was continued. Azithromycin was initiated for Mycobacterium avium complex (MAC) prophylaxis. It was discontinued when the CD4 count returned as 145/mcL, with a viral load of 5,882,600 copies/mL.
Events following the diagnosis of HIV
By hospital day 4, the patient became more emotionally labile, appeared very anxious, and was tachycardic again. Depression screening was positive; however, the patient refused medical therapy at that time. He remained dependent on a 2-L nasal cannula at rest but became hypoxic (80%) on ambulation. Acid-fast bacilli were negative. Rapid plasma reagin (RPR) was positive. Fluorescent treponemal antibodies (FTAs) were sent, which returned positive. Syphilis was treated with intramuscular (IM) Benzathine Penicillin G. The patient never underwent bronchoscopy as there was enough clinical evidence to suggest PCP. By hospital day 7, a rapid response was called for an unwitnessed fall. The patient was actively hallucinating and agitated, stating that “a car hit me and that’s why I fell.” A CT of the brain without contrast was negative for acute pathology, and he was transferred to the Neurology floor for further monitoring. Overnight, the patient continued to be agitated and was noted to have seizure-like activity in the bed. In the early morning, the patient was still experiencing visual and auditory hallucinations, was combative with house staff, and was requiring four-point restraints and intramuscular medications.
Workup for altered mental status
The main concern at this stage was a Jarisch Herxheimer reaction; however, other differentials at that time included neurosyphilis, metabolic encephalopathy secondary to hyponatremia, toxic encephalopathy from worsening PCP infection versus other viral or bacterial encephalitides, given HIV status. Magnetic resonance imaging (MRI) was performed, showing diffuse atrophy with non-specific enhancements (Figure ). He underwent an electroencephalogram (EEG), which revealed moderate diffuse encephalopathy without active seizures. Thyroid function tests were within normal limits, and a urine drug screen was negative. His transient altered mental status resolved within approximately 12 hours, and the patient was taken off of restraints. He was unable to recall any of the events over the last day and a half. The patient underwent a lumbar puncture (colorless, clear, RBC 91 mm3, WBC 9 mm3, non-xanthochrome, Glu 62 mg/dL, protein 36 mg/dL), and cerebrospinal fluid (CSF) was negative for toxoplasmosis, cryptococcus, CSF acid-fast bacilli, and CSF fungal culture. Silver stain cytology from an induced sputum culture was significant for bland appearing squamous cells and scattered pulmonary macrophages, without evidence of malignancy or PCP. The remainder of the workup resulted in a positive serum EBV and a positive CSF CMV, with a viral load of 12,400. The working diagnosis was CMV encephalitis in the setting of HIV-AIDS with a CD4 count of 145. The patient was started on IV foscarnet 6,500 mg twice daily and ganciclovir 365 mg twice daily. He completed a 21-day course of steroids with a taper as well as treatment for PCP. He also received IV penicillin G of four million units six times a day for two weeks. He clinically improved with decreasing oxygen requirements and was able to ambulate on room air. The patient was medically optimized for discharge with a plan for outpatient anti-retroviral treatment (Bictegravir 50 mg/Emtricitabine 200 mg/Tenofovir 25 mg) and further monitoring of his HIV-AIDS, suspected neurosyphilis, EBV, and CMV.


A 55-year-old male presented with a 1-month history of perianal swelling with increasing discomfort. Other than malaise, he remained systemically well. He reported 3 months of intermittent abdominal discomfort, thought to be related to constipation, which had resolved by the time of his presentation. He had no prior history of perianal abscess and had a medical history that was significant only for conservatively managed diverticulitis, with a recent colonoscopy confirming mild disease. On peri-anal examination, there was fullness and tenderness over the right ischiorectal space. The tenderness extended from 9 to 11 o’clock ~4 cm from the anal verge. No external opening was obvious, and there were no masses on per rectal exam. His abdomen was soft and non-tender.
Bloods upon presentation revealed a mild leucocytosis (white cell count of 12.5 × 109/l). An external computed tomography (CT) scan performed 3 weeks prior showed sigmoid diverticulitis for which the patient had not been treated. A tiny pocket (<1 cm) of extra-luminal air was noted, but there was no abscess or collection. When reviewing these external images, there was suspicion of a right peri-anal abscess.
The patient was commenced on intravenous antibiotics and underwent EUA and drainage of perianal abscess. An ischiorectal cavity was found with small amount of purulent material. No fistulae into the rectum were identified. Further imaging was considered at thistime.
Magnetic resonance imaging (MRI) identified a fistulous tract extending from the sigmoid colon, around the anterior aspect of the anal canal, with small collections in the ischiorectal and ischioanal fat. CT fistulogram showed a long fistulous tract extending from the right peri-anal region to a sigmoid diverticulum above the recto-sigmoid junction ( and ). The patient underwent a second EUA at which a large tract was identified at 9 o’clock, running parallel to the anus and rectum, with no apparent connection to the anus but draining enteric content. The superior extent of the tract was not felt. Colonoscopy showed a benign-appearing, intrinsic moderate sigmoid stenosis measuring 2 cm in length, which was traversed with difficulty.
The patient underwent an elective laparoscopic Hartman’s procedure, with prophylactic ureteric stenting. Intra-operatively, significant inflammation at Denovillier’s fascia was found. The recto-sigmoid junction was diseased with chronic diverticulitis and numerous indurated appendages were attached to the pelvic sidewall. The rectum was predominantly healthy. A fistulous opening was laparoscopically visualized at 11 o’clock, originating at the junction of the TME plane (). This opening was dealt with by performing a sigmoid colectomy. The tract through the levator was curetted and managed with placement of a low pelvic drain. Given the proximity of the fistulous opening and inflammation, a decision was made not to re-anastomose immediately and a colostomy was formed.
Histopathology showed benign diverticular disease. The patient recovered well post-operatively and was discharged on Day 5. He has since been followed up in the outpatients’ clinic and is well. He will be considered for reversal of Hartmanns’ following review of MRI and rectal gastrograffin enema to ensure all peri-anal tracts are addressed prior.


We demonstrate this technique in a 72-year-old woman who was referred for evaluation of iron deficiency anemia. EGD was performed for evaluation and revealed a 3-cm × 3-cm flat polyp (Paris classification 0-IIa) in the second portion of the duodenum, sparing the ampulla. Capsule endoscopy and colonoscopy were subsequently performed and revealed no other polyps or etiology for anemia. The decision was made to proceed with EMR. The polyp was lifted using a mixture of 6% hetastarch and methylene blue. Complete piecemeal EMR was performed using snare cautery.
After resection, post-EMR defect margins were prophylactically treated with snare tip soft coagulation to help prevent recurrence., To reduce the risk of delayed AEs, closure of the EMR defect with endoscopic clips was attempted. Because of the large size of the resection bed, complete apposition of the 2 edges of the mucosal defect using standard endoscopic clips was not feasible. The decision was made to proceed with rubber band–assisted closure. As described, a small rubber band was attached to the first clip. The clip was then placed on the proximal edge of the lesion at the area of maximal width, fixing the rubber band in place. A second clip was used to grasp the rubber band and was then attached to the opposite edge of the defect, approximating both edges. This allowed for subsequent closure of the remaining mucosal defect by easily adding additional clips at the now approximated edges.
A total of 8 endoclips were used, achieving excellent closure. The patient was discharged home the same day. There were no AEs, including bleeding or delayed perforation. Final pathology revealed a tubulovillous adenoma with no high-grade dysplasia. Surveillance EGD 6 months later revealed no evidence of recurrent adenomatous tissue.


A 64-year-old man underwent the right upper lobectomy for lung cancer of adenocarcinoma (2.0 cm, pT1bN0M0, pStage IA2). The patient had no postoperative complications and was discharged on postoperative day 9. Nine years after the initial surgery, postoperative follow-up CT showed a left endobronchial nodule near the peripheral tracheal bifurcation (Fig. a). Bronchoscopy confirmed a protruding lesion emanating from the posterior wall of the left main bronchus (Fig. b). After a diagnosis of adenocarcinoma by tumor resection using a bronchoscopic snare was made, we performed a combination of EBRT and EBBT for the small residual disease as a definitive treatment. The patient had achieved a complete local response without adverse events at the time of the bronchoscopic evaluation (Fig. c). Three years after irradiation, CT revealed a new partly solid nodule at the left lower lobe. The patient then underwent partial wedge resection and is still alive at 90 months since the irradiation.


A 69-year-old man underwent the right lower lobectomy for lung cancer of squamous cell carcinoma (4.0 cm, pT2aN0M0, pStage IB). Two weeks after the surgery, we performed a right-sided open-window thoracostomy due to a postoperative bronchopleural fistula. Three months after open-window thoracostomy, he was discharged after undergoing thoracoplasty with omental plombage. One year and 6 months after discharge, postoperative follow-up CT showed a right endobronchial nodule at the truncus intermedius (Fig. a). Fluorodeoxyglucose-positron emission tomography (FDG-PET) revealed an uptake at the lesion (maximum standardized uptake value [SUVmax] 3.8) (Fig. b). After a diagnosis of squamous cell carcinoma was made by a bronchoscopic biopsy (Fig. c), we performed a combination of EBRT and EBBT for the endobronchial metastasis as a definitive treatment. The patient had achieved a complete local response without adverse events at the time of the bronchoscopic evaluation (Fig. d). The patient has remained disease-free for 36 months since the irradiation.


A 74-year-old man underwent the left lower lobectomy for lung cancer of squamous cell carcinoma (5.7 cm, pT2bN0M0, pStage IIA). The patient had no postoperative complications and was discharged at postoperative day 6. Two years after discharge, postoperative follow-up CT showed a left endobronchial nodule near the peripheral tracheal bifurcation (Fig. a). FDG-PET revealed an uptake at the lesion (SUVmax 7.4) (Fig. b). After a diagnosis of squamous cell carcinoma was made by a bronchoscopic biopsy (Fig. c), we performed a combination of EBRT and EBBT for the endobronchial metastasis as a definitive treatment. The patient had achieved a complete local response without adverse events at the time of the bronchoscopic evaluation (Fig. d). The patient has remained disease-free for 29 months since the irradiation.


A 71-year-old female with no significant past medical history had presented four and a half years ago with a weight loss of about 50 pounds over six months prior to presentation. She complained of occasional shortness of breath but denied any cough. Physical examination revealed enlarged right axillary and supraclavicular lymph nodes.
Mammography was performed, revealing multiple enlarged right axillary lymph nodes, but no suspicious lesions were seen in either breast. An ultrasound-guided core biopsy of the right axillary lymph node was performed. The histopathology report showed poorly differentiated metastatic adenocarcinoma. The biopsy was cytokeratin 7 (CK7) and thyroid transcription factor-1 (TTF-1) positive and negative for CK20 and mammaglobin, respectively. Epidermal growth factor receptor (EGFR), ROS1, and anaplastic lymphoma kinase (ALK) were negative, and PD1 and PDL1 expressions were less than 1%.
A computed tomogram (CT) of the chest with contrast enhancement was done. There were multiple irregular nodular opacities in bilateral lungs, with the largest measuring 10 mm, and extensive bilateral mediastinal lymphadenopathy and supraclavicular lymphadenopathy, with the largest measuring 1.8 cm (Figures ). Magnetic resonance imaging (MRI) brain and bone scans were negative for any metastases. However, a positron emission tomography (PET) scan revealed hypermetabolic nodules in the lung and multiple suspicious nodes in the neck, chest, and abdomen, suggesting advanced stage IV lung cancer.
She was initially treated with carboplatin, pemetrexed, and paclitaxel for a total of four cycles. She responded well to the treatment with a decrease in the size of pulmonary tumor nodules (from 11.12 to 7.97 mm) noted on the follow-up CT scan (Figures ). She went on to complete eight cycles of maintenance pemetrexed, and on follow-up, a CT scan revealed the right upper lobe lung nodule to have increased in size from the previous 1 x 0.7 cm to 1.5 x 0.8 cm (Figure ). At this time, she was started on nivolumab (3 mg/kg/dose). Six months following commencement of nivolumab, complete resolution of lung lesions was seen on CT chest (Figures ). The lung lesions remain unremarkable since then (Figure ). Her performance status was stable at ECOG-PS-0 over the four years of treatment, with weight gain from improvement in her appetite. She had resolution of all her respiratory symptoms and B symptoms.
After being on treatment for almost four years, the patient developed a pruritic, hyperpigmented rash on the upper and lower extremities and trunk. The rash was associated with dermographism and minimal erythema, suggesting grade II-III maculopapular rash, a well-known side effect often seen in patients being treated with checkpoint inhibitors. At this time, she received a treatment break from nivolumab while she was treated with steroids (1 mg/kg/day of prednisone) and hydroxyzine.
On the resolution of her rash, she was restarted on nivolumab. The patient presented to ER and was subsequently admitted for significant posterior epistaxis and melena along with a drop in her hemoglobin. A CT head scan was performed as part of the workup for severe posterior epistaxis, which showed a 10 mm enhancing lesion in the posterior left frontal lobe, suspicious for metastatic disease. MRI brain confirmed a 0.9 cm enhancing lesion at the posterior left frontal lobe (Figure ). For the incidental metastatic lesion in her brain, she received stereotactic radiosurgery, given her solitary lesion. The timeline of the events is shown in Figure .


This is a 57-year-old male patient from eastern Morocco, followed up for 10 years for ankylosing spondylitis and admitted to the emergency room for an occlusive syndrome and abdominal pain. The symptomatology goes back two years with the onset of intermittent postprandial abdominal pain in the right iliac fossa which worsened on the day of his admission to the hospital. The clinical examination of our patient revealed tenderness in the right iliac fossa with palpation of a mobile mass measuring about 4 cm and free hernial orifices. The standard biological assessment carried out in the emergency room had objectified an inflammatory syndrome with a CRP increased to 60 mg/L and the CT scan had objectified a cockade image next to the last ileal handle. This image, which is probably related to an ileo-ileal invagination, is also the site of a circumferential thickening, regular symmetrical, measuring 14 mm in maximum thickness with respect for the adjacent fat and without individualization of peri-lesional lymphadenopathy (Figure ).
After multidisciplinary discussion and discussion with the patient, we opted for surgical exploration performed under general anesthesia which had demonstrated an intussusception 50 cm from the last intestinal loop on an intraluminal process with mesenteric lymphadenopathy. Bowel resection with lymphadenectomy involving intussusception with manual anastomosis was performed (Figures , ).
The pathological study noted the presence of an inflammatory pseudo-polyp integrating into chronic inflammatory bowel disease Crohn's type (Figures , ). The patient's postoperative progress course was uneventful, our patient was satisfied with the overall care and the discharge was carried out for five days under specific medical treatment for Crohn's disease. Follow-up after two years was without abnormalities with control of rheumatological and digestive manifestations.


Case 1: A 60-year-old female with weak dorsiflexion of the feet and numbness for one year, occasionally with tingling, type 2 diabetes for five years, a maximum fasting blood glucose level of 15 mmol/L, and glycosylated hemoglobin of 6.9%. The diagnosis of DPN was based on numbness and tingling, slow conduction velocity (40.0 m/s) in the tibial nerves, and a waveform that vanished in the bilateral peroneal nerves as assessed by EMG examination. In the past year, the patient had experienced paresthesia and dyskinesia of the lower limbs. After treatment with insulin, her symptoms were somewhat relieved; subsequently, her glycemia was controlled with oral hypoglycemic drugs. The extensor digitorum brevis (EDB) muscle had significantly atrophied by 0.32 cm2 (), and the strength of the extensor of the thumb was grade 0/5 with steppage gait ().
After hospitalization, mecobalamin was started via ultrasound-guided injection of an appropriate dose (1 mg in 10 ml 0.9% NaCl). After therapy, the patient improved gradually. After one course of treatment, the foot strength returned to grade 2/5, with the calf circumference increasing from 25 to 28 cm (left) and 26 to 24 cm (right). The EMG results showed an insignificant change of 37.9 m/s in the bilateral peroneal nerve conduction velocity (). The cross-sectional area of the EDB was 0.43 cm2 after two courses of treatment (). The other changes are shown in and .


Case 2: A 56-year-old male with type 2 diabetes for six years accompanied by renal function impairment. The diagnosis of DPN was based on characteristic sock-like numbness, inflexible movement of the lower limbs, no waveform in the tibial nerves, neurogenic damage to the left anterior tibial muscle upon electromyographic examination, and exclusion of other peripheral neuropathies. He had experienced paresthesia of the distal extremities within the previous two years. After treatment with mecobalamin and epalrestat based on strict control of blood glucose, these symptoms gradually worsened, with frequent nocturnal tingling affecting sleep. The foot strength was grade –5/5 with hypalgesia ().
After admission, mecobalamin was injected via ultrasound guidance at an appropriate dosage at the malleolus medialis of the posterior tibial nerves. Fortunately, the patient improved gradually after the therapy. After two courses, the foot strength returned to grade 5/5, the legs became more flexible, the walking distance increased, and there was no numbness or pain. An EMG examination showed no significant change in the bilateral peroneal nerves (). The other changes are shown in and .


Case 3: A 52-year-old male with type 2 diabetes mellitus for 11 years and retinopathy stage III diagnosed with DPN due to slow conduction velocity of the tibial and peroneal nerves and no tibial nerve waveform found with EMG. Mecobalamin and vitamin B1 were taken orally for nearly one year, but areflexia, distal numbness of the limbs, and weakness had occurred when squatting within the last six months ().
After two courses of treatment, the neurological examination showed that the muscle strength of the lower extremities was grade 5/5. Flexibility and numbness of the lower limbs improved, but no EMG results were obtained after treatment (). Moreover, after ultrasound-guided injection of saline and mecobalamin, the symptom and ultrasound image scores were improved (), and it was found that the EDB and muscles of the first interstitium (MIL) were larger than those before treatment ().


Case 4: A 76-year-old male with a history of type 2 diabetes for over 10 years diagnosed with DPN for 4 years. He had paresthesia and weakness in his lower limbs that was not relieved after treatment with mecobalamin, vitamin B1, and Maizhiling for more than two years. The EMG bilateral fibular motor nerve conduction velocity was 27.9 m/s (right, 52% ↓) and 36.2 m/s (left). The EMG showed that the conduction velocity of the bilateral tibial nerve waveforms had disappeared. The fibular sensory nerve values were 77.1 m/s (right) and 60.5 m/s (left) (). After one course of therapy, the patient’s walking distance increased, though with persistent numbness. The muscle strength of the lower limbs was not ameliorated at grade –5/5. The other relevant change scores, muscle cross-sectional areas, and thickness values are shown in .


Case 5: A 44-year-old male with type 2 diabetes for 13 years, renal failure and retinal complications, persistent numbness of the distal limbs, paresthesia, and weakness of the lower limbs after walking 100 m for nearly 5 years as a result of poor glycemic control, and 11.9% glycosylated hemoglobin. The patient had been treated with painkillers during this period. The waveform of the bilateral peroneal motor nerves had disappeared, and the conduction velocity of the tibial motor nerves was 31.8 m/s (24% ↓). Moreover, the waveforms of the bilateral tibial and peroneal sensory nerves were not revealed by EMG examination ().
After a course of treatment, the distal muscle strength of the lower limbs increased from grade –4/5 to +4/5, and the numbness was relieved gradually. Nevertheless, one month after follow-up, the symptoms appeared again. There was little change in the EMG results (). The other improvement indicators are shown in and .


We present the case of a 59 years-old self-employed male with a 10-year history of high blood pressure (HBP), medicated with two anti-hypertensive drugs with irregular compliance and poor blood pressure control. Significantly, his mother started presenting signs and symptoms of dementia early onset (50 years old) and died from chronic depression and cognitive deterioration, with repeated hospital admissions at the Psychiatric ward. Furthermore, he had one brother diagnosed with schizophrenia and two other brothers with a history of alcohol abuse. He also had two daughters from which one suffered from severe depression.
This patient was referred to a history of psychomotor slowing, sporadic episodes of dysphagia, irritability, emotional lability, anxiety, decreased hearing, vertigo and paraesthesia, and pain in both lower limbs for the past year. He was taken to the ED due to an episode compatible with a generalized tonic-clonic seizure disorder and sphincter incontinence (faecal and urinary). Upon admission to the ED, he presented an altered level of consciousness, with 9 points on the Glasgow Coma Scale (GCS), conjugated deviation of the gaze to the right, flaccid plegia of the four limbs, and indifferent right plantar skin reflex, which was normal at the left foot and HBP. The medical team interpreted his condition in the context of the post-critical period. From the complementary study, the arterial blood gases showed moderate mixed acidaemia (pH 7.13, pCO2 83.3mmHg, HCO3-28.0mmol/L), respiratory predominance, hyperlacticaemia (lactate 6.2mmol/L) and hypokalaemia. Cranial computed tomography (CT) with angiography showed cerebral atrophy inconsistent with the patient's age and leukoaraiosis, not documenting acute ischemic or haemorrhagic lesions or presence of thrombi or other changes in cerebral arterial vascularization.
During his stay at the ED, the patient suffered a second convulsive seizure, which was controlled with diazepam. He was started on levetiracetam 1g. Despite an initial improvement in consciousness, the patient progressed to a third seizure, with maintained GCS below 8. He was then submitted to orotracheal intubation and mechanical ventilation for airway protection, under continuous sedation with propofol and midazolam. Lumbar puncture was performed, with a cytochemical and bacteriological unchanged cerebrospinal fluid. This was tested for neurotropic viruses without relevant findings. He was transferred to the Intensive Care Unit (ICU).
During his stay at the ICU, he had no recurrence of convulsive crises when weaning from sedation, having completed ventilatory weaning and subsequent extubating uneventfully. The patient remained hemodynamically stable, though he needed three anti-hypertensive drugs to control his HBP.
He was transferred to the Medicine ward, maintaining clinical stability, with a slight slowing of speech and slight distal atrophy of the upper limbs, despite maintaining muscle strength. He was submitted to a neuropsychological assessment that revealed articulatory effort with anomalous pauses and slowed recall, with difficulty in executive tasks, as well as a decrease in the speed of information processing.
Magnetic resonance imaging (MRI) of the brain was performed, which identified in the T2 FLAIR sequences (Figure , ) multiple areas of hyperintensity periventricular and subcortical frontoparietal white matter without restriction to diffusion, coexisting with other lacunar nucleus-capsular and bilateral thalamic sequelae lesions.
The Electroencephalogram (EEG) showed electrogenesis of a well-structured base overlaid with left temporal slowing without apparent paroxysms indicating left temporal regional dysfunction, not detecting associated epileptiform activity in this study; Transcranial Doppler echo documented increased pulsatility indices translating arterial inelasticity; Doppler echocardiography of the neck vessels showed diffuse carotid atheromatous without hemodynamic repercussions; Transthoracic echocardiogram and 24-hour Holter did not show relevant changes.
In the analytical study, hypercholesterolemia and hypertriglyceridemia were highlighted. The prothrombotic study and the study of reversible causes of dementia did not reveal any changes.
Due to the difficulty to control hypertension, the study of causes of secondary HBP was started, and the main causes were excluded. The renal echography did not show renal artery stenosis or renal parenchyma alterations. Given the history of cognitive decline with mood alterations with one year of evolution and the alterations described in the MRI, the diagnosis of epilepsy of vascular etiology and important ischemic cerebrovascular disease (CVD) was admitted. However, the MRI changes are excessive for the patient's age, and possible genetic causes were investigated, namely the search for genes NOTCH3 (CADASIL), HTRA1 and Mitochondrial Encephalopathy Lactic Acidosis Stroke-like episodes (MELAS), which were excluded, and FD.
During admission, antiepileptic therapy was progressively adjusted without recurrent seizures. He repeated EEG, which did not document epileptiform activity. He remained neurologically stable, without focal neurological deficits, calm and oriented in time, space, and person, although with slowed speech. He was discharged and continued the etiological investigation at the Internal Medicine and Neurology outpatient clinics.
The study of determining the enzymatic activity of alpha-galactosidase A in dried blood on filter paper revealed a partial deficiency (5.25 pmol/h/puncture, reference levels 8.75 - 15.6 pmol/h/puncture) not diagnostic for FD. Thus, a sample was sent to confirm the result in plasma and total leukocytes. This test revealed an enzyme deficiency of alpha-galactosidase A in leukocytes (6.9 nmol/h/mg protein, reference levels 36 - 80 nmol/h/mg protein) and a non-significant increase in globotriaosylsphingosine (2, 1 nmol/L reference levels 0 - 1,3 nmol/L). The presence, in hemizygosity, of the genetic variant c.427G>A (p.A143T) was also identified.
A diagnosis of non-classical FD was admitted, and a study of other manifestations of FD and family studies and genetic counselling was initiated and a study of the manifestations in other organs.


The patient was a 39-year-old Japanese female, gravida 1 para 1. She wanted to have a second child. For the first pregnancy, the patient underwent ART treatment due to severe oligoasthenozoospermia of her husband. She received intracytoplasmic sperm injection (ICSI) followed by embryo cryopreservation. A successful pregnancy was established by vitrified-warmed embryo transfer, and the child was delivered vaginally. The pregnancy was uneventful and no problems were noted in the patient's medical history. The patient decided to undergo ICSI treatment at the same clinic at which she became pregnant previously. Follicle-stimulating hormone and human menopausal gonadotropin were used for controlled ovarian stimulation under a gonadotropin-releasing hormone (GnRH) agonist long protocol. Recombinant human chorionic gonadotropin (250 µg) (Ovidorel, Merck Biopharma, Tokyo, Japan) was administered 36 h before oocyte retrieval to trigger oocyte maturation. Oocyte aspiration was performed under intravenous anesthesia with propofol and pentazocine. Atropine sulfate (0.5 mg) was premeditated, and pentazocine (15 mg) was administered intravenously. Subsequently, propofol (50 mg) was administered rapidly, with additional 10-20 mg doses until loss of consciousness. The patient did not respond to verbal commands and had lost spontaneous movements. After thorough vaginal lavage with saline, the follicles in the ovaries were punctured through the vaginal wall using a 17-gauge oocyte retrieval needle under transvaginal ultrasound guidance. The patient suddenly coughed and violently moved her body whilst the puncture needle was inside the ovary. After deepening the anesthesia by increasing the dose of propofol, the coughing subsided and no body movements were observed; therefore, oocyte retrieval was continued and 11 oocytes were retrieved. The patient had no symptoms after the oocyte retrieval and went home after 2 h of bed rest. Five hours following oocyte retrieval, she returned to the clinic with severe abdominal pain. Transvaginal ultrasonography revealed echogenic findings in the Douglas pouch. Douglas’ pouch puncture was performed, and 300 mL of blood was aspirated. Bleeding from the right ovary due to oocyte aspiration was suspected, and transvaginal compression was attempted. However, even after compression of the right ovary, blood accumulated in the abdominal cavity. Although her hemoglobin and hematocrit levels before oocyte retrieval were 13.4 g/dL and 40.6%, respectively, after compression of the ovary, the hemoglobin and hematocrit levels had decreased to 10.8 g/dL and 40.0%, respectively. Based on a transvaginal ultrasound and blood examination findings, it was determined that the patient had persistent bleeding from the right ovary into the abdominal cavity, and the patient was transferred to our hospital.
The patient’s characteristics were height: 161 cm, weight: 57 kg, and body mass index (BMI): 22 kg/m2. On arrival at our hospital, her blood pressure was 133/89 mmHg, pulse rate was 85/min, and shock index was 0.63. Her abdomen was flat, with tenderness and rebound pain. Internal examination was not performed because of severe pain. Transvaginal ultrasonography revealed an echogenic free space of 12.5 mm in the Douglas pouch and an enlarged right ovary with a size of 65 mm (Figure , ). These findings suggested hemoperitoneum due to bleeding from the right ovary. Contrast-enhanced computed tomography revealed hematoma formation in the right ovary with a small amount of extravasation (Figure , ). The diagnosis of hemoperitoneum from the right ovary due to oocyte retrieval was made. Since the vital signs were maintained and the pain was controlled, we managed the patient conservatively. After 2 h, her blood pressure was 150/82 mmHg and pulse rate was 101/min, the size of the echo-free space in the Douglas pouch and the size of the ovary were enlarged to 29 and 80 mm, respectively. Emergency laparoscopy was performed to ascertain the location of the bleed and to stop the bleeding.
Laparoscopic surgery was performed using four trocar ports with the patient under general anesthesia. A 12-mm trocar was inserted at the umbilicus under direct vision, and CO2 gas was insufflated to an intra-abdominal pressure of less than 10 mmHg. Three 5-mm trocars were placed in the lower abdomen on the right and left sides and in the middle. Laparoscopic findings revealed massive hemoperitoneum without intra-abdominal adhesions (Figure ). When the clot was removed, bleeding was confirmed in the right ovary. The right ovary was enlarged to the size of a fist, and hematoma was also observed inside the ovary (Figure ). When the hematoma was removed and the right ovary was examined in detail, the cortical region of the ovary was torn, and continuous bleeding was observed (Figure ). The partially torn ovarian tissue was excised, and the bleeding was coagulated and stopped using a bipolar device (Figure ). There were no abnormal findings in the left ovary. A drain was placed in the Douglas pouch, and the surgery was completed. The operative time was 57 min, and the estimated amount of blood lost was 200 mL. Postoperatively, there was no progression of anemia, and no blood transfusion was required. The patient had a favorable postoperative course and was discharged on the fourth following surgery. Histopathological examination revealed a corpus luteal hemorrhage in the excised ovarian tissue.


A 19-year-old pregnant woman developed acute psychiatric symptoms and oral-face-brachial dystonia at the 8th weeks of her third pregnancy. Physical examination of the nervous system revealed blurred consciousness, restlessness, slow reaction, poor memory and orientation, involuntary movement of the oral and facial arms, and high muscle tension of the limbs. Other physical examinations showed no positive signs. Barthel scale score was 40 points. What’s interesting is that when she was at the 10th weeks of her first pregnancy, this patient encountered severely neuropsychiatric symptoms similar to this time, but no seizures. Her blood culture during hospitalization turned out to be Escherichia coli. Despite continuous treatment, her clinical response did not improve significantly until the pregnancy was terminated at the 15th weeks of gestation. The patient fully recovered after taking olanzapine for 3 months. During the second pregnancy, she was absolutely normal and had given birth to a healthy boy.
Lumbar puncture examination was completed upon admission. Cerebrospinal fluid pressure was 150 cm H2O. CSF analysis showed white cells 47 × 106/L (normal value < 8 × 106/L), mononuclear cells account for 95%. The levels of protein, glucose and chloride were normal. No abnormalities were found in bacterial culture, fungi, acid-fast bacilli and cryptococcus. Gynecological Doppler showed the following: intrauterine single live fetus, breast, pelvic cavity, ovary, fallopian tube no abnormality. Admission routine tests, thyroid function, tumor biomarkers, and autoantibody profiles were normal. Brain magnetic resonance imaging illustrated Flair/DWI sequences hyperintense signal in the right hippocampus (Fig. ). EEG patterns revealed bilateral diffuse and persistent theta-delta slow-wave. The cerebrospinal fluid and serum were sent to Beijing Hearst Medical Laboratory for autoimmune encephalitis-related antibodies. The detection results showed anti-NMDAR-IgG 1:32 in CSF (Fig. ) and 1:1000 in serum. The paraneoplasm-related antibody amphiphysin in serum was positive, while that one in CSF was negative, thus confirming the diagnosis of anti-NMDAR encephalitis. First-line immunotherapy is recommended according to the management guidelines for autoimmune encephalitis. The patient received a course of intravenous immunoglobulin (0.4 mg/kg/day) and intravenous pulse methylprednisolone (1000 mg/day) for 5 days, and methylprednisolone is gradually reduced to oral dose. Considering the possible harmful effects of some anti-epileptic agent on the fetus, we choose the lamotrigine to control episodic dystonia. After received immunotherapy, the patient’s mental state was slightly improved, but there were still have oral-face-brachial dystonia and obvious cognitive impairment, and the patient was unable to take care of herself in daily life. She often refused to eat and did not sleep at night. However, the patient revisited the head MRI again; we found that the abnormal signal disappeared in the right hippocampus (Fig. ). Barthel scale score was 70 points. After her husband weighed the pros and cons, she induced abortion to terminate the pregnancy at 15th weeks. The presence of a tumor in her body has been the focus of our attention since the antibody amphiphysin in serum was positive. According to the general examination results, no tumor was found, especially teratoma. Prednisone acetate, lamotrigine and olanzapine were continued orally after discharge. However, the patient refused to receive second-line immunosuppressive therapy due to economic reasons. Follow-up for 3 months, the patient’s mental state was basically normal, without epileptic seizure, the basic diary life activities are basically self-care, but there are still obvious dyscalculia and memory disorders. Barthel scale score was 85 points. MMSE scale score is 14 points (her education background is primary school education). Follow-up for 1 year, the patient was recovered without any sequelae. The MMSE scale score is 20 points.
Two years later, at the 10th weeks of her 4th pregnancy, she developed similar psychiatric symptoms and epileptic symptoms. Barthel scale score was 40 points. After admission, she completed related laboratory tests. Brain MRI was normal. Transvaginal ultrasonography showed no teratoma or mass. EEG showed overall slow wave activity. CSF analysis showed white cells 56 × 106/L, mononuclear cells account for 96%. The level of protein, glucose and chloride were normal. Herpes simplex and varicella-zoster virus PCR and fungal and acid-fast bacillus smear and cultures were negative. Since anti-NMDAR encephalitis had been diagnosed previously in this patient with similar symptoms, we suspected the relapse of anti-NMDAR encephalitis. CSF and serum samples were sent for anti-NMDAR antibody analysis. It was detected that the anti-NMDAR-IgG was 1:32 in CSF and 1:320 in serum (Fig. ). At the same time, the anti-AMPAP-IgG was found to be 1:3.2 in CSF and 1:10 in serum. No abnormalities were found in systemic tumor screening. The patient was treated with a first-line regimen of immunoglobulin (0.4 mg/kg/day) and intravenous pulse methylprednisolone (1000 mg/day) for 5 days. Levetiracetam was chosen to control epilepsy because it had less effect on the fetus. Despite continuous treatment, her clinical response did not improve significantly until the pregnancy was terminated at the 15th weeks of gestation. Unfortunately, she still could not afford second-line immunotherapy. At the time of discharge, the patient’s mental behavior was slightly improved, epilepsy occasionally occurred, and cognitive function was significantly impaired, especially memory and orientation. She continued to take hormones, levetiracetam, and olanzapine outside the hospital. Follow-up for 3 months, she basically recovered and only had poor memory and mild cognitive impairment. Barthel scale score was 80 points. The MMSE scale score was 14 points. Written informed consent of the patient is required for the publication of case reports and associated images.


A 46-year-old woman presented to her clinician in February 2018 with diffuse discomfort and pain on the left side of her face. Her past medical history was unremarkable. Within the past five years, she had lived in Denmark but travelled to Spain, Greece, and Sri Lanka. The pain had started at the cheekbone, radiating intermittently out towards the nose, jaw, and forehead. A week later, the pain and discomfort regressed, leaving a small nodule above the left eyelid, with intermittent redness (). The clinician suggested idiopathic recurrent periorbital redness. No further work-up was performed, and the condition was left untreated. By mid-March, intense headaches emerged, and the patient was referred to the Emergency Department for evaluation. Physical examination and laboratory results (complete blood cell count, basic metabolic panel, lipid panel, liver panel, blood cultures and infection panel) were unremarkable, and the patient was discharged. No treatment was initiated. By early June, the occasional swelling, redness, and pain reappeared, this time on the right side of the face. Symptoms resolved spontaneously one week later. Five months later, a small 1.5 × 1 cm well-defined, firm nodule developed in the mid-forehead (). A course of oral antibiotics (penicillin V 1.5 mill. IU equiv. 660 mg three times per day) was administered on suspicion of an abscess. There was no clinical improvement. Three weeks later, the nodule had increased in size to approximately 3 × 3 cm and had a vesicle-like texture. The patient was then referred to an otolaryngologist, but rhino-laryngoscopy was unremarkable. An infected atheroma was suggested, and a new course of oral antibiotics (clarithromycin 500 mg once daily) was administered. The nodule now had the appearance of a pimple. The pain, redness and swelling migrated to the medial and lower aspect of the left eye. High-resolution ultrasound imaging was then performed which revealed a hypoechoic clarification with a nematode-like structure (). The patient was then referred to the Department of Infectious Diseases for further evaluation. Dirofilariasis was suspected based on the findings of additional ultrasound imaging coupled with an extensive medical and travel history and the report of migrating swellings. Ivermectin 12 mg was administered as a single dose. One week later, all symptoms had subdued, leaving a small, erupted nodule. At home, the patient removed nematode fragments measuring approximately 7–8 cm in total (). Seven months after the initial complaints, remnants of inflamed deeper tissues around the eye were removed by plastic surgeons. On examination, the face was homogenous in colour, texture, and temperature. Two pinpoint defects were observed in the frontal area. One defect was erupted and slightly indurated and located medial to the left supraciliary arch by the eye. The other defect was located as the base of the nose. Under local anaesthesia, an 8-mm incision was made above the tip of the erupted defect, and remnants were sent for microbiological examination (). The patient made a full recovery. DNA was extracted using the DNAeasy Blood & Tissue Kit Qiagen, Hilden, Germany), and PCR used the primers FIL 18S (5′-CAAAGTCGTAACAAGGTTTCCG-3′) and FIL_5.8S_R (5′-GCGTCTGCAATTCGCACT-3′) targeting the internal transcribed space 1 region and 5.8 ribosomal RNA gene. Sanger sequencing using the PCR primers as sequencing primers produced a 485 bp-long DNA sequence that was identical to Dirofilaria sp. ‘hongkongensis’ strain [,] (JX290194 in the NCBI Database); however, sequence coverage was only 48%. Only one reference in the NCBI Database provided 100% coverage, namely KM374817 (Dirofilaria sp. ‘Thailand’ clone 7D2), which exhibited 96.52% similarity. Three reference sequences of D. repens provided 98% coverage, but only 94.58–94.82% similarity (AB973229, MH059516, and MW349621). We deposited the DNA sequence generated in the present study in the NCBI Database under the accession number (MZ736411).


An 11-year-old male patient with no significant past medical history or known genetic syndromes presented to the emergency department three days after onset of left frontal headache and associated diplopia. The patient did not have nausea, emesis, paresis, or paresthesia. Physical examination was significant for diminished visual acuity, bilateral papilledema, and anisocoria in the left eye. He also had right pronator drift. He showed no other neurologic deficit. A T1-weighted MRI with contrast showed a heterogeneously enhancing left anterior temporal extraaxial tumor with mass effect and significant surrounding vasogenic edema suggestive of an invasive meningioma, based on its location and appearance (Figure ).
Surgical treatment was discussed and determined to be the best option to attenuate symptoms by decompression and obtain diagnosis to optimize long-term outcomes. The patient underwent surgical resection of their tumor through a left pterional craniotomy. Ultrasonic aspiration was used to debulk the tumor centrally followed by circumferential dissection through a plane. The gliotic brain was noted at the periphery of the tumor. No obvious interdigitations of tumor into the brain were grossly noted. Gross total resection was achieved. However, histopathologic examination found meningioma with invading cerebral tissue superficially (Figure ).
Histologic sections using glial fibrillary acidic protein (GFAP) immunostaining demonstrated a moderate cellularity meningothelial meningioma with increased mitotic activity. There was also suggestion of early focal necrosis, and high Ki-67 labeling indices were found supporting that this portion of the mass was a WHO grade 2 meningioma with atypical features. In addition, some flanking areas demonstrated distinct disturbances in cerebral parenchyma underlying the meningioma, and a strip of vertically oriented proliferating vessels were seen in vascular columns. This area was also flanked by meningothelial cells that were entrapping and distorting the cortical grey matter between them. This indicated meningioangiomatosis in addition to the mentioned meningioma tissue.
There were no postoperative complications and the patient’s presenting symptoms were completely resolved following surgery. The patient’s physical examination improved post-operatively and he was discharged without any sequelae of neurologic deficits. Upon a three-month follow-up, the patient continued to remain asymptomatic and without signs of recurrence on surveillance imaging. There was no plan for adjuvant therapy given no evidence of residual on imaging (Figure ).


A 72-year-old right-hand dominant female tripped over a stick and fell on a sidewalk. She landed on the left side of the body resulting in immediate pain and swelling of the left elbow. She presented to the emergency department immediately and then to our clinic three days post-injury. Clinical examination revealed swelling accompanied by diffuse ecchymosis of the dorsal side of the left elbow and proximal forearm. The range of motion (ROM) at the elbow was limited due to pain. She could not actively extend the elbow against gravity. The results of the neurovascular examination were normal. Anteroposterior (Figure ) and lateral (Figure ) radiographs of the left elbow demonstrated a displaced long oblique fracture of the olecranon with a short proximal fragment and an additional intra-articular butterfly fragment. Also, thinning of cortices and generalized increased bone radiolucency with the altered trabecular pattern were evident in the radiographs.
The patient was a non-smoker and an active community ambulator. Her medical problems were hypothyroidism and type II diabetes mellitus, controlled on regular oral medications. Being medically well and active, she was recommended ORIF, which was performed as an outpatient procedure on day six post-injury.
After successful general anesthesia, she was placed in a semi-lateral position using a beanbag on a standard operating table with her left upper extremity resting over the body. A single dose of 2 g of cefazolin was given intravenously as surgical prophylaxis. A pneumatic arm tourniquet was applied but not inflated. After sterile preparation and draping, a 10-cm midline posterior incision was made centering the fracture site with a smooth lateral curve around the tip of the elbow. Full-thickness flaps were created on either side. The ulnar nerve was identified and protected throughout the operation. The hematoma was evacuated, and fracture fragments were freshened (Figure ). Subtle comminution of articular and dorsal cortical margins was noted. The intraarticular butterfly fragment was found to be partially attached to the distal fragment. Direct reduction of the main fracture fragments was achieved by a pointed reduction clamp. Multiple 0.045-inch Kirschner wires (K-wires) were utilized for provisional fracture fixation. One of them was utilized as a joystick to anatomically reduce the butterfly fragment. The fracture reduction and articular congruity were verified by multiplanar fluoroscopic images. A pre-contoured low-profile proximal olecranon locking compression plate (DePuy Synthes, PA, USA) was placed along the dorsal surface. The triceps attachment was split in the midline to accommodate the head of the plate close to the bone (Figure ). Plate fixation was achieved with two 3.5-mm cortical screws into the ulnar shaft while three 2.7-mm (two cortical and one locking) screws were utilized proximally across the fracture line. Anatomic reduction, stability, and hardware position were verified by fluoroscopy (Figure ).
The ROM was tested to check for any hardware impingement. The ulnar nerve was found to be stable in the cubital tunnel and therefore no transposition was attempted. The triceps split was meticulously repaired, followed by standard wound closure in a layered fashion. A well-padded long-arm posterior splint was applied over sterile dressings keeping the elbow in 70-degrees of flexion. The sutures were removed on the 10th postoperative day and the arm was placed in a sling. Outpatient physical therapy (PT) was initiated allowing active elbow flexion and gravity-assisted extension along with a weight-bearing restriction for up to six weeks postoperatively. The sling was then discontinued to allow active extension and begin isometric strengthening exercises followed by graduated resistance training as tolerated. At three months, she demonstrated 10-to-130-degrees of active elbow motion with no pain at the fracture site. Radiographs of the same visit showed healing of the fracture with a stable hardware position (Figures , ).
She was, therefore, cleared to return all her previous activities with no restrictions. She was also discharged from PT with advice on regular home exercises.
She returned to the clinic two months later, approximately five months post-surgery, reporting intermittent pain and swelling of the proximal forearm overlying the distal portion of the plate. The follow-up radiographs did not show any hardware complications or stress fractures. After reviewing the treatment options, she had elected to pursue hardware removal. A computed tomography scan, performed before signing the patient up for this second surgery, had demonstrated no residual fracture lines confirming fracture union and stable position of hardware (Figures -).
However, her surgery was delayed because of the onset of the third wave of coronavirus disease 2019 (COVID-19), causing all elective surgeries at our institution to be rescheduled. She subsequently reported gradual improvement in her symptoms of hardware irritation and finally elected against second surgery. At the recent six-month follow-up, she had regained full elbow ROM except for terminal 5-degrees of extension (Figures -).
She had no pain in the elbow or proximal forearm, although the plate was still palpable over the ulnar shaft. Triceps strength was found to be equal and symmetric bilaterally. She returned to all her previous activities with no limitations and therefore cleared from our orthopedic trauma service with advice to return for hardware removal as needed.


A 79-year-old woman with a history of transurethral resection of bladder tumor (TURBT) 2 years ago presented to the emergency department with sudden diffuse abdominal pain acute urinary retention of 24 h. The patient denied any history of trauma. Upon arrival at our hospital, vital signs were as follows: blood pressure, 117/65 mmHg; heart rate, 130/min; respiration rate, 28/min; and body temperature, 36.8°C. Physical examination revealed a distended abdomen with diffuse suprapubic tenderness. Laboratory investigations showed an elevated white blood cell (WBC) count (11.96 × 109/L), serum creatinine (420 μmol/L), and urea (5.4 mmol/L). A Foley catheter was inserted and drained 250 mL of blood-stained urine. A CT scan () demonstrated both blood clots in the bladder and a small amount of fluid collection in the abdominopelvic cavity with a suspicious bladder wall defect in the bladder dome. Cystography showed intra-peritoneal contrast leakage and confirmed a defect at the dome of the urinary bladder. The patient's symptoms strongly suggested peritonitis from a ruptured bladder. As a result, emergency physicians and the urologist planned to repair the ruptured bladder by surgery. As the patient had a short course of disease and no history of intraperitoneal surgery, we chose laparoscopic bladder repair instead of laparotomy. An indwelling catheter was inserted for 14 days to allow the bladder defect to heal. Another cystogram was performed prior to catheter removal with no abnormal findings. The patient was discharged with a regular follow-up in the outpatient clinic.


A 63-year-old woman with a history of diabetes, diabetic nephropathy, and neurogenic bladder visited the emergency department with complaints of recurrent lower abdominal pain and fever for 3 days. Vital signs were as follows: blood pressure, 120/70 mmHg; heart rate, 110/min; respiration rate, 25/min; and body temperature, 36.9°C. Physical examinations showed tenderness throughout the abdomen by palpation. Her laboratory investigations showed a white blood WBC count of 9.95 × 109/L, serum albumin of 28.3 g/L, and creatinine of 424.6 μmol/L. A CT scan () demonstrated free fluid and a cyst-like mass between the bladder and uterus. The bladder water injection experiment was negative. And the drained fluid from the abdominal puncture demonstrated a creatinine level of 501.50 μmol/L, which was similar to the plasma creatinine level. Peritoneal puncture fluid examination showed that the Rivalta test was (+), the number of nucleated cells was 76,000/UL, and neutrophils were 90%. Escherichia coli was cultured in the peritoneal drainage fluid, the same as in a urine culture. The initial diagnosis was urinary tract infection, chronic renal failure, neurogenic bladder and pelvic effusion, and infection. The patient was treated with antibiotics, indwelling catheterization, and abdominal puncture drainage. The patient's level of serum creatinine gradually decreased to 194 μmol/L on the 7th day. However, there was low urine output and high peritoneal drainage. After multidisciplinary consultation and discussion, we suspected bladder rupture. A bladder rupture was confirmed by a methylene blue test and cystoscope that demonstrated a defect at the posterior lateral bladder wall. Laparotomy was performed, and a perivesical multilocular abscess was found during the operation. Multiple abscesses were drained, and repair of the bladder wall defect was performed in two layers. The patient made an uneventful recovery and was discharged after 14 days with a normal serum creatinine level and regular outpatient follow-up.


A 73-year-old male presented to our emergency department with acute decompensated heart failure. He suffered hypertension for almost 15 years and atrial fibrillation for 7 years. Electrocardiogram showed atrial fibrillation with tachycardia. Chest X-ray showed mediastinal widening along with mild congestion of both lungs and mild bilateral pleural effusions. Echocardiography showed a severely dilated ascending aorta (9 cm) with normal aortic root (the sinus of Valsalva = 3.7 cm × 3.8 cm × 3.5 cm and sinotubular junction = 3.5 cm;
;
[available in the online version]). There was moderate-to-severe degenerative aortic regurgitation, and the ejection fraction was calculated as 50% (
; available in the online version). Computed tomography (CT) angiography showed giant calcified AscAA (measuring 10 cm × 9.7 cm) without evidence of dissection. The aneurysm was causing compression and narrowing of the superior vena cava, main pulmonary trunk, and right pulmonary artery (
and
). Coronary angiogram was performed due to risk factors of coronary disease and inability to assess coronaries on CT scan due to atrial fibrillation. It showed normal coronaries and the large calcified AscAA (
;
; available in the online version).
After initial stabilization, the patient underwent successful replacement of the giant AscAA and hemiarch replacement with a vascular graft (size 32, Vascutek) and aortic valve replacement with a Magna Ease tissue valve (21 mm) under deep hypothermic circulatory arrest with antegrade cerebral perfusion through the right axillary artery (
). The overall postoperative course was uneventful except for high bilateral serous pleural drainage which settled spontaneously over the next 10 days. Biopsy of the resected ascending aorta showed fibroconnective tissue with myxoid degeneration and calcification. On follow-up, the patient was asymptomatic with a normally functioning aortic prosthesis on echocardiography (
; available in the online version). Follow-up cardiac CT scan revealed a well-seated vascular graft (
).


A 15-year-old female presented for the radiological investigation to assess the response to her treatment. She was diagnosed with CRMO at the age of 13 with pain in the right and then bilateral wrists and back. Her initial X-ray was unremarkable and MRI revealed multiple patchy abnormal bone marrow signals involving the distal metaphysis at the distal end of the tibia, distal metaphysis of the fibula, the middle part of the talus bone, most of the calcaneal and navicular bone, and proximal part of the first metatarsal bone (Figure ).
Investigations including biopsy and genetic testing excluded malignancy and genetic syndromes. She was instituted on naproxen for effective analgesia. A repeated MRI three months later showed persistent active disease that warranted the institution of pamidronate. Follow-up imaging due to elevated cardiopulmonary resuscitation (CPR) and erythrocyte sedimentation rate (ESR) revealed the absence of any improvement that confirmed the inefficacy of pamidronate. The patient was then started on canakinumab (interleukin-1 blocker) 150 mg subcutaneously every eight weeks. Despite decreasing dose interval, the disease showed no improvement on imaging and she continued to have elevated acute phase reactants. Ultimately, infliximab 5 mg/kg every eight weeks and methotrexate 10 mg weekly instituted. Fortunately, she showed excellent clinical response and improvement in the laboratory and radiological investigations and has had no relapse of the disease till date.


An 11-year-old girl presented to the emergency department (ED) with intermittent right hip pain for the last two weeks. Her pain showed exacerbation during the night and worsened gradually with time. Physical examination was unremarkable; however, the range of motion was reduced. Laboratory investigation was significant for increased C-reactive protein (CRP). X-ray showed enlarged and sclerotic bilateral iliac bones more on the right side (Figure ).
On MRI contrast, there was heterogeneous intensity expansion of the right iliac bone (Figure ). T2-weighted images showed non-homogeneous high intensity lesions in the affected areas (Figure ).
The adjacent part of the iliacus and gluteal muscles showed altered intensity in the pre-contrast sections (Figure ), while increased enhancement was seen in the postcontrast sections (Figure ). The mass could be seen extending to the acetabular roof.
These findings raised the suspicion Ewing sarcoma on top of the differentials. Biopsy from the right iliac bone showed multiple fragments of cortical bone as well as cancellous bony fragments. There was reactive new bone formation with numerous osteoblasts and associated with loose fibrous stroma in between and aggregation of chronic inflammatory cells particularly plasma cells. There was no evidence of granulomas or malignancy. Therefore, she was instituted on NSAIDs and paracetamol with continuous surveillance. MRI was done after nine months which showed improved right iliac lesions concomitant with her clinical improvement.


We report the case of a 26-year-old female patient from Fujian, China, who came to our hospital for “living together for 3 years after marriage, no contraception without pregnancy” G0P0. She was born of a non-consanguineous marriage. The age of menarche was 12 years, and she had a menstrual cycle lasting 30 days; her menstrual period lasted for 7 days, and the amount of menstruation was low. The patient was 149-cm tall, weighed 62 kg, and had a body mass index of 27.9 kg/m2. Tanner staging was breast 4 and pubic hair 4; she had a poorly developed left labia minora and a smooth vagina. Her bone age was approximately 18 years old, and her height for bone age was <3rd percentile. Biochemical examination: triglycerides 1.99 mmol/L, total cholesterol 5.44 mmol/L, fasting blood glucose 4.19 mmol/L, and serum insulin 9.59 mu/L; the patient's intelligence was normal, and there was no abnormality in the liver, gallbladder, pancreas, spleen, and kidney on ultrasonography. On the 3rd day of menstruation evaluation, her basic hormone levels were as follows: follicle-stimulating hormone, 10.16 mIU/mL (reference range: 1.5–10 mIU/mL before ovulation; 8–20 mIU/mL ovulation period; and 2–10 mIU/mL after ovulation), luteinizing hormone, 5.47 mIU/mL (non-ovulation period: 5–25 mIU/mL; ovulation period: 30–100 mIU/mL; and after ovulation: 4–10 mIU/mL), estrogen, <20 pg/mL (reference range: 48–521 pmol/L before ovulation; 70–1835 pmol/L ovulation period; and 272–793 pmol/L after ovulation), progesterone, 0.21 ng/mL (reference range: usually >15 ug/L), prolactin, 16.08 ng/mL (non-lactation, normal value is 0.08–0.92 nmol/L), testosterone 0.53 ng/mL (follicular phase <1.4 nmol/L; ovulation period <2.1 nmol/L; luteal phase <1.7 nmol/L; and postmenopausal <1.2 nmol/L), and anti-Mullerian hormone, 0.37 ng/mL (reference range: 2–8 ng/mL). The average follicle count was 4, with a size of 6.6 mm, 4 mm, 3.5 mm, and 3 mm; uterus size, 38 × 29 × 28 mm; right ovary size, 18 × 11 mm; and left ovary size, 21 × 11 mm. On the 10th day of menstruation, vaginal ultrasound evaluation showed a right ovary follicle (ROF) 9 mm and a left ovary follicle (LOF), 4 mm; and mean endometrial thickness, 6.6 mm, with unclear morphology and several echo-free zones in almost the whole endometrial section; the maximum was 13 × 9 mm. The endometrial thickness near the uterus bottom was 27 mm, with an unclear morphology. Considering the special conditions of the patient's endometrium, we continued to monitor follicular and intimal development. Vaginal ultrasound evaluation on the 16th day of menstruation showed a ROF, 19.2 mm; LOF, 3 mm; and average thickness of the intima, 8.8 mm; an endometrial 3D color Doppler evidenced multiple cystic echoes in the middle and lower endometrium (Fig. ).
The dominant follicle on the right side disappeared on the 18th day of the cycle, and the endometrial thickness was 9.5 mm. We administered luteal progesterone (Abbott Biologicals BV) 1 tablet orally twice a day for 14 days. The patient returned for ultrasound on the 16th day of the second menstrual period. Measurements showed a ROF, 17.9 mm × 1, LOF, 3 mm × 1, and average intimal thickness, 6.8 mm, 5.1 mm at the uterus bottom, with the same morphology as in the previous test with luteinizing hormone 7.59 mIU/mL, estrogen 107 pg/mL, and progesterone 0.32 ng/mL. The patient was hospitalized for “hysteroscopy + treatment.” During surgery, the uterine cavity was normal, the endometrium was flat, and the uterine cavity adhesions were excluded during surgery. Postoperative pathology results were as follows: a small amount of broken endometrial tissue and proliferative endometrium (Fig. ).
Cytogenetic examination revealed a karyotype 45, X, del (X) del (p11, 2) (Fig. ). The patient was treated with 1 cycle of preimplantation genetic diagnosis-assisted pregnancy therapy. Although 4 eggs were obtained from the patient, no embryos were available. This study fully complied with the tenets of the Declaration of Helsinki and was approved by the Ethics Board of the Women's and Children's Hospital affiliated to Xiamen University, China. Informed consent was obtained from the subject's parents before testing.


A 52-year-old man with a history of alcohol-induced acute pancreatitis and diabetes mellitus was transferred to our hospital for treatment of sepsis and multiorgan failure associated with emphysematous pancreatitis.
A day earlier, the patient was admitted to an outside hospital with fever and severe abdominal pain. Based on an abdominal computed tomography (CT) scan and laboratory findings, the patient was diagnosed with sepsis and multiorgan failure associated with emphysematous pancreatitis and subsequently transferred to our hospital for treatment.
The patient had a history of alcohol-induced acute pancreatitis event 2 years ago. He was also taking medications for diabetes and hypertension.
The patient was an alcohol abuser, but not a smoker. There was no significant medical history in the family.
On arrival, the patient was receiving inotropic agents and had a body temperature of 36.5°C, heart rate of 120 beats/min, and blood pressure of 80/50 mm Hg. The patient's mental status was confused. Physical examination revealed a rigid and distended abdomen, severe tenderness with muscle guarding upon palpation, and tympanic sounds with percussion. The examination was otherwise unremarkable.
The results of the complete blood count test were as follows: white blood cell count, 8.1 × 103/L; red blood cell count, 3.22 × 106/L; hemoglobin, 9.1 g/dL; platelet count, 263 × 103/L and prothrombin time (INR), 1.49 (reference range 0.8–1.12). Blood chemistry testing revealed the following data: serum blood urea nitrogen, 42.0 mg/dL (reference range 6–20 mg/dL); serum creatinine, 3.46 mg/dL (reference range 0.5–1.2 mg/dL); high-sensitivity C-reactive protein, 36.12 mg/dL (reference range 0–0.3 mg/dL); serum glucose, 378 mg/dL (reference range 70–99 mg/dL); serum ketone body, 266.30 nmol/mL (reference range 0–120 nmol/mL); serum aspartate aminotransferase, 33 IU/L (reference range 8–40 IU/L); serum alanine aminotransferase, 12 IU/L (reference range 5–41 IU/L); serum amylase, 57 IU/L (reference range 41–134 IU/L); serum sodium, 125 mEq/L (reference range 136–145 mEq/L); and serum potassium, 3.9 mEq/L (reference range 3.5–5.1 mEq/L).
An axial CT scan revealed extensive gas bubbles in and around the pancreatic necrosis (Fig. A) and in the mesenteric root and left anterior pararenal space. A coronal CT scan also revealed scattered gas bubbles along with the mesenteric root and fat (Fig. B). A sagittal CT scan showed better visualization of the extensive gas in the left anterior pararenal space (Fig. C).
A Gastrografin swallow study conducted to rule out perforations did not demonstrate any leakage. Upper endoscopy also revealed no evidence of gastroduodenal lesions, such as ulcers or perforations.
Culture of the pus obtained from the catheter drainage grew Escherichia coli. An antibiotic susceptibility test demonstrated that the microorganism was sensitive to aztreonam, cefepime, cefotaxime, cefoxitin, ceftazidime, cefuroxime, chloramphenicol, colistin, ertapenem, and fosfomycin but resistant to ampicillin, ciprofloxacin, gentamicin, piperacillin, and tetracycline.


An 81-year-old female patient was admitted to the hospital with a complaint of epigastric pain. She was receiving medication for hypertension and had a surgical history of open cholecystectomy. An abdominopelvic computed tomography (CT) scan revealed intestinal obstruction caused by hepatic flexure colon cancer and stricture of the distal common bile duct (CBD) with upstream bile duct dilatation (Fig. ). Magnetic resonance cholangiopancreatography was performed to discriminate distal CBD malignancy before surgery, and distal CBD stricture was considered as a benign lesion. A colonoscopic stent was inserted before surgery because of cancer obstruction. Curative resection was performed in June 2020. Laparoscopic right hemicolectomy was initially planned, however, the operation was converted to open surgery due to intraperitoneal adhesion. On postoperative day 2, laboratory values showed an increase of serum C-reactive protein (23.37 mg/dL). Her blood pressure was 90/70 mmHg and her heart rate was 103/min. Peritoneal fluid analysis showed that amylase/lipase was normal (15/8 unit/L), but total bilirubin was highly elevated (31.77 mg/dL) at more than 5 times higher than the serum level. Abdominopelvic CT showed a fluid collection in the perihepatic and perisplenic space (Fig. ). A percutaneous drain was inserted for intraabdominal fluid collection, and 600 mL of turbid brownish fluid was initially drained. However, the nature of the drain changed into a bile color after 3 days, with an amount of 580 mL/day. With suspicion of anastomotic leakage, we performed an emergency laparotomy. The anastomosis was intact without leakage; however, bile leakage was observed on the dilated intrahepatic bile duct exposed to the liver surface (Fig. , arrow) where adhesiolysis was conducted during the initial surgery. After suture ligation of the liver, we confirmed that there was no further bile leakage. The patient showed satisfactory recovery and was discharged 15 days after reoperation.


A 78-year-old female patient was admitted for ascending colon cancer surgery. She was receiving medication for hypertension and had a surgical history of cholecystectomy and open choledocholithotomy for CBD stone. Abdominopelvic CT showed ascending colon cancer with clinical stage T3N1 and distal CBD stone with upstream bile duct dilatation (Fig. ). However, she had no symptoms associated with bile duct dilatation, and serum bilirubin level was normal (0.74 mg/dL). Laparoscopic right hemicolectomy was performed on March 2021. There were severe adhesions because of the previous operation, and laparoscopic adhesiolysis was performed between liver surface and omentum (Fig. ). There was a large volume of intraoperative bleeding (500 mL) due to the tearing of the middle colic vein. On postoperative day 2, 185 mL of bile fluid without foul odor was drained through the Jackson–Pratt drain. The patient complained of diffuse abdominal pain and had tenderness on her right upper abdomen. Her body temperature was elevated to 38.3°C and heart rate was 116 beats/min. Peritoneal fluid laboratory tests showed an increase of total bilirubin (30.43 mg/dL). On abdominopelvic CT, the anastomosis was intact, but fluid collection around the liver was observed (Fig. ). Considering the possibility of CBD or duodenum injury and anastomotic leakage, the patient underwent emergency surgery. The anastomosis was intact without leakage, and there was no injury to the duodenum or CBD. However, a pinpoint opening of the intrahepatic bile duct was observed at the edge of the liver surface where adhesiolysis was performed during initial surgery due to omental adhesion (Fig. ). There was bile leakage through the injured bile duct (Fig. , arrow). Suture ligation and clipping were performed, and the operation was finished after confirming no further bile leakage. The patient recovered without additional complications and was discharged in good condition 9 days after reoperation. She will receive ERCP for distal CBD stone via the gastroenterology outpatient clinic.


A 71-year-old female with a past medical history of hypothyroidism presented to the emergency department with pain in her left leg that began after she stepped off a one-foot curb. She described a low-energy mechanism of injury. Radiographs in the emergency department demonstrated a non-displaced, proximal-third left tibia fracture. Additional history included a 20-pound weight loss over the preceding several months. Labs on presentation were unremarkable, with a calcium level of 9.2 mg/dl (reference: 8.4-10.2 mg/dl). She was considered likely to have osteoporosis and was managed conservatively with immobilization of the affected extremity and referred to physical therapy. Despite these measures, her pain worsened, and she became increasingly immobile, eventually requiring the use of a wheelchair. She also noted large erythematous cutaneous nodules developing over her anterior leg in proximity of the original fracture location (Figure ).
Five months after her original injury, repeat radiographs were obtained and showed a nondisplaced pathologic fracture involving the proximal tibial diaphysis with an adjacent soft tissue mass (Figure ). Notable lab values included a hemoglobin of 8.3 g/dl (reference: 12.0-16.0 g/dl), lactate dehydrogenase of 978 international units/liter (IU/l) (reference: 135-225 IU/l), and a C-reactive protein 86.5 mg/l (reference: 0.0-5.0 mg/l).
CT of the chest, abdomen, and pelvis showed multiple inguinal and retroperitoneal lymph nodes and enlargement of the bilateral kidneys and adrenal glands. Core needle biopsy of the tibial mass revealed aggressive large B-cell lymphoma. Cells were CD20-positive and had a KI-67 proliferation rate of 70%. Immunohistochemical studies showed cells were reactive for CD10 and Bcl-6. C-myc and BCl-2 were overexpressed. Positron emission tomography scan showed widespread cancerous involvement of the axial and appendicular skeletons, adrenal glands, and kidneys (Figure ). Lumbar puncture was negative for cerebral spinal fluid involvement.
The patient received six cycles of dose-adjusted rituximab, etoposide phosphate, prednisone, vincristine sulfate, cyclophosphamide, and doxorubicin hydrochloride. Her tibial fracture was treated with internal fixation and placement of an intramedullary rod. Six months after diagnosis, the patient is in clinical remission and doing well. She is now ambulating without difficulty.