A 50-year-old woman came with chief complaints of pain and swelling in the left knee. She had a recent history of twisting injury while walking. Physical examination revealed tenderness along the lateral joint line and McMurray’s test was positive for lateral meniscus. Flexion was terminally restricted and painful. Radiographs showed evidence of lateral compartment osteoarthritic changes. Tear of lateral meniscus () along with synovitis () and degenerative changes in the cartilage were evident on magnetic resonance imaging (MRI) of the left knee. Arthroscopic partial meniscectomy was planned on the basis of her clinical and radiological presentation.
Arthroscopic findings revealed hypertrophied and pigmented synovium (). There were small chondral defects of size 3 mm to 5 mm, Grade 2+ more over the lateral condyle than the medial condyle. There were pigmented loose bodies with size varying from 0.5 mm to 5 mm. Grade 3 changes were observed in the cartilage with kissing lesions and greyish-blackish discoloration. Both the menisci were discolored with tear in the lateral meniscus (). Although the integrity of all the ligaments was maintained, there was evident discoloration and thinning out.
Partial lateral meniscectomy was performed with removal of loose bodies. Arthroscopic debridement was done to remove the hypertrophied synovium and specimen was sent for histopathological examination. With the suspect of ochronotic arthropathy due to the discoloration observed in arthroscopic intervention, further examination and investigation were planned.
Urine was normal in color but turned dark brown when tested with sodium hydroxide (NaOH). Urine showed high levels of HGA. Histopathological reports revealed brownish pigmentation along with degenerative changes. Detailed examination of the skin, sclera, eye, and ear showed no abnormalities.
Patient achieved immediate pain relief after the arthroscopic intervention. Postoperatively, physical therapy rehabilitation program, emphasizing on full weight- bearing walking, was started along with achieving pain-free range of motion followed by strength training. Patient had no complaints in the subsequent follow-ups at week 2, week 4, and week 8.


A 47-year-old healthy male patient presented to our emergency department complaining of severe upper abdominal pain of 4 days duration. The pain lasted for 4 days, started abruptly, and was described as diffuse, and radiating to the back. He also suffered from nausea, recurrent vomiting, and reduced appetite. Three days prior to his admission, he was diagnosed with COVID-19 infection by the reverse-transcription polymerase chain reaction (RT-PCR) assay method for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via throat swab. On physical examination upon his admission, the patient’s vital signs were within normal limits. An abdominal examination revealed upper abdominal diffuse tenderness with guarding. No abdominal mass was palpated. Digital rectal examination was normal.
Complete blood count showed increased white blood cells of 16,000 × 103/µL, with 12% bands. Liver and kidney function tests were within normal limits. Serum amylase level was 2,708 U/L (normal range 25 - 125 U/L). Amylase level was also highly elevated in urine specimen. An upright abdominal X-ray and chest X-ray postero-anterior view were normal. A contrast-enhanced computed tomography (CECT) scan of the abdomen and pelvis revealed edema of the pancreas, mainly at the head and body, with inflammatory changes in the pancreas and peripancreatic tissue, as well as ill-defined peripancreatic fluid (). Multiple subpleural nodules were seen on the lower lobes of bilateral lungs, suggestive of COVID-19 infection. The CT scan findings were consistent with acute pancreatitis grade D according to the CT severity index (CTSI) score.
The patient was admitted with a diagnosis of acute pancreatitis for conservative management by nil per os (NPO) and analgesics. A detailed workup failed to uncover the etiology for the acute pancreatitis. An abdominal ultrasound (USG) for hepatobiliary system was normal and serum calcium, triglycerides and IgG4 levels were within normal limits. The patient negated any history of alcohol usage, recent binge drinking or a recent uptake of new medications. Following conservative management, the patient improved and was discharged on day 4 of his admission. A repeat RT-PCR for SARS-COV-2 via throat swab 10 days following discharge was negative.
Two weeks following his discharge, the patient was re-admitted due to upper abdominal pain and fever. A repeat abdominopelvic CT scan revealed edematous pancreas, surrounded by a multilocular fluid collection measuring 21 × 19 cm, with a small amount of free intra-abdominal fluid (). The patient was once again treated conservatively and discharged home when oral intake was resumed on his third day of admission.
On an outpatient clinic follow-up, 3 weeks later, the patient complained of abdominal distension along with significant increase of abdominal girth, with no nausea, vomiting or abdominal pain. An abdominopelvic CT scan showed a well-circumscribed fluid collection in the lesser sac measuring 22 × 12 cm, causing extrinsic pressure effect on the stomach and duodenum (). These findings were compatible with pancreatic pseudocyst development.
Due to the aforementioned findings, the patient was treated by NPO, total parenteral nutrition (TPN) and endoscopic cyst-gastrostomy, by which approximately 4 L of turbid fluid was aspirated (), and “Hotaxios Boston Lams” stent was inserted (), after which the patient’s abdominal distension decreased significantly, and he was discharged with a scheduled repeat CT scan within 3 weeks.
A repeated CT scan of the upper abdomen demonstrated significant improvement in the pancreatic pseudocyst size (4 × 2.5 cm). Five weeks following the endoscopic stent insertion, the patient underwent a scheduled repeat upper endoscopy that revealed an exceedingly small cyst lumen, and the stent was extracted.
On an outpatient clinic follow-up 2 weeks later, the patient was doing well with no gastrointestinal symptoms.


A 31-year-old Caucasian man presented to our clinic with a 4-month history of a solitary mass on the left mandibular area believed to be an abscess. It was slightly tender and exuded pus from several openings within the mass. He had a history of being HIV positive for 7 years. His HIV was well controlled on once daily oral Biktarvy containing bictegravir, emtricitabine, tenofovir, and alafenamide, and he had a normal CD4+ count and an undetectable viral load. Clinical examination showed a 5 by 5 cm erythematous mass with a rough surface and a few draining sinuses over the right mandibular area (). A previous X-ray showed no evidence of periostitis or bone destruction and he had previously seen a dentist and a dental sinus was ruled out. The differential diagnosis when seen included infectious causes such as actinomycosis, a deep fungus, tuberculosis (TB), and atypical mycobacteria. Two 4-mm punch biopsies were done, one for histology and one for cultures. Skin biopsy showed a squamous-lined cystic structure at the deep biopsy edge compatible with a sinus tract (). Periodic acid-Schiff (PAS), Grocott’s methenamine silver (GMS), Ziehl-Neelsen (ZN), and Fite stains were all negative. Cultures sent for aerobic and anaerobic cultures grew a few Staphylococcus aureus but were negative for Actinomyces species. Tissue culture for deep fungus, TB, and atypical mycobacteria were all negative. He was treated with oral doxycycline 100 mg PO BID for 2 months, and when reassessed, the morphology of the lesion had markedly changed () to a flesh-colored indurated plaque with marked cribriform scarring. A full skin examination at this time showed no lesions in the axillae, groin, and buttocks except for a 5-mm depressed scar in the left lower abdomen which the patient attributed to an “ingrown hair.”
At this time, the clinical appearance suggested HS localized to the face. An incisional biopsy from the plaque including an area of cribriform scarring was submitted for pathology and showed an acute folliculitis with deep dermal fibrosis and a lymphoplasmacytic infiltrate. All repeated cultures were negative. He was put on a course of oral isotretinoin and the plaque was injected with intralesional triamcinolone acetonide 10 mg/cc and he has a good response to this treatment.


We saw a 22-year-old man who had been complaining of dreamlike states for 6 months, associated with philosophical questions about the sense of existence. He described these derealization states as frightening, and as being accompanied by avolition, a depressed mood, and concentration deficits. The patient was admitted to a psychiatric hospital, and a mild-to-moderate depression in the context of an adolescent crisis was suspected. A pharmacological treatment with lorazepam 0.5 mg twice daily and bupropion initially 150 mg titrated up to 300 mg was initiated. The patient improved under the pharmacological treatment. On admission, no apparent focal neurological deficit was detected. As part of a further clinical diagnostic work-up, a routine magnetic resonance imaging (MRI) of the head was performed, which revealed a partially contrast enhancing space-occupying compressive lesion at the roof of the fourth ventricle, with a nodular hypervascular component [ and ]. This was thought to be an accidental finding. Furthermore, a cerebellar tonsil herniation through the foramen magnum with discrete compression of the medulla oblongata was apparent. The patient was promptly transferred to the neurosurgical unit, and a suboccipital craniotomy with tumor resection was successfully performed. Histopathological examination revealed both a rosette-forming glioneuronal tumor and a papillary glioneuronal tumor, corresponding to a World Health Organization Grade I (benign) tumor. Postoperatively, depression and derealization almost completely resolved, and the postoperative MRI displayed complete tumor resection and decompression of the foramen magnum [ and ]. By means of a stationary rehabilitation program, the neurocognitive deficits and apathy improved as well.


A 20-year-old man was transferred to our clinic for the treatment of life-threatening CCF. The patient had suffered a car accident a month earlier and has been in coma and on ventilator since. He had skull base fractures on both sides in the basal temporal region, fracture of petrous part of the right temporal bone, fractures of the right zygomatic bone, right part of the maxilla, and blood collections in the maxillary, ethmoidal and sphenoidal sinus. CT of the head had visualised a CCF on the right side. Since the crash, the patient has had several episodes of profuse bleeding from both ears and the nose. They were managed conservatively with placement of temporary tamponade. He required more than 10 hemotransfusions during the hospital stay.
On presentation, the patient was in severe general condition, intubated but with normal vital signs (HR 84 bpm, blood pressure 123/77 mm Hg). He had a quite tense right eye proptosis. The left eye was spontaneously opened. Glasgow-Liege Coma Scale (GLCS) Score was 11. The left corneal and glabellar (frontalorbicular) reflex were absent. The direct pupillary reaction to light was preserved as well as oculocephalic reflexes. A quadriparesis with spastic paralysis of the left arm, anisoreflexia and bilateral negative Babinski’s signs were evident. On pain stimulation, there was minimal flexor response in the right limbs. The head was deviated to the right side, with spontaneous mild movements. Verbal contact was missing.


An 84-year-old man with metastatic cutaneous melanoma of the forearm treated with ICIs: nivolumab, cabiralizumab, and APX005M, developed worsening bilateral mucopurulent discharge over 2 days. He was prescribed ciprofloxacin eye drops in both eyes (OU) and later referred for worsening pain and blurred vision OU. The best-corrected vision was 20/400 right eye (OD) and 20/70 left eye (OS). The baseline vision was 20/70 OD due to a prior central retinal vein occlusion and 20/30 OS. Examination revealed periorbital erythema, eyelid edema, circumferential hemorrhagic chemosis, and copious mucopurulent discharge OU []. Extraocular motility was severely limited OU. Fundus examination revealed dense vitritis OD and was normal OS. B-scan ultrasound confirmed vitritis OD []. Magnetic resonance imaging orbits with contrast showed bilateral postseptal fat stranding consistent with postseptal cellulitis. Gram stain of the mucopurulent discharge showed Gram-negative diplococci. The patient was admitted and treated empirically for Neisseria gonorrhoeae with a 2-week course of intravenous ceftriaxone and systemic azithromycin. Later, cultures confirmed Neisseria gonorrhoeae []. Urine testing for chlamydia and gonorrhea was negative. Within 24 h of systemic treatment, vitritis OD resolved []. Six days after treatment, visual acuity returned to baseline, ocular motility was full, and chemosis completely resolved.


A 7.5-year-old intact male Japanese macaque, weighing 8.3 kg, presented at TAEC for the evaluation of vision loss. In June 2017, the owner noticed that its right eye appeared partially cloudy white (Figure ). By September 2018, the owner confirmed that the right eye was completely cloudy white (Figure ). However, at that point, there was no change in its behavior. In January 2020, its left eye also became cloudy (Figure ) and the owner confirmed that its behavior had become abnormal. At presentation, it showed no menace response. The patient had difficulty navigating and eating. Although this macaque was a member of a circus group, it was unable to perform due to vision loss. The veterinary doctor reported that the physical examination performed prior to the TAEC visit showed no obvious abnormalities other than visual impairment.
Ophthalmic examination revealed a negative menace response in both eyes (OU), positive dazzle reflex OU, positive direct and indirect pupillary light reflex in the right eye (OD), and weak direct and indirect pupillary light reflex in the left eye (OS). Relative afferent pupillary defect (Marcus Gunn pupil) was negative. The anterior segment OU was observed using Slit-Lamp Biomicroscope (BQ-900 LED; Haag-Streit AG). No corneal abnormalities were found, but the lens was strongly opacified OU (Figure ). No obvious anterior chamber flare was seen OU. The measured intraocular pressure using the TONOVET-Plus tonometer (Icare Finland) was 28 mmHg for OD and 21 mmHg for OS.
Ocular ultrasonography was performed under general anesthesia using the ARIETTA 60 device (Aloka Corporation) with a high-frequency linear probe (5–18 MHz, L64 linear probe, Aloka Corporation) revealing globe axial lengths measuring 20.3 mm (OD) and 19.8 mm (OS), anterior chamber depths of 3.8 mm (OD) and 3.5 mm (OS), and lens thicknesses of 3.4 mm (OD) and 4.6 mm (OS), with thinning and sub-luxation of the lens OD (Figure ). However, there was no obvious lens dislocation or thinning OS (Figure ). There were no posterior segment abnormalities OU. Based on ultrasonography results, we calculated the power of the IOL to be used intraoperatively.
Electroretinography (ERG; LE-100; Tomey) was performed under general anesthesia after dilation of the pupil using a solution of 0.5% tropicamide and 0.5% phenylephrine (Mydrin-P, Santen Pharmaceutical). ERG was performed immediately before cataract surgery without dark adaptation to check for obvious retinal degeneration. Single flash ERG (Figure ) and 30 Hz flicker ERG (Figure ) were performed with light intensities of 20,000 cd/m2 × 10 ms and 3,000 cd/m2 × 1 ms, respectively. Flicker ERG was recorded with a 25 cd/m2 background stimulus. Due to the lack of dark adaptation, it was difficult to make a direct comparison with the ERG results in another reported non-human primate study. However, no obvious findings were suggesting retinal degeneration. The amplitude of the a-wave of the Single flash ERG was 250 μV OD and 122 μV OS. The amplitude of the b-wave of the single flash ERG was 173 μV OD and 109 μV OS. The amplitude of the 30 Hz flicker ERG was 68 μV OD and 75 μV OS.
Blood tests performed before the surgery showed an increase in white blood cell count (32,700/μl), but all other items were within the normal range. Since there were no obvious symptoms of bacterial infection, the cause of the elevated white blood cell count could be lens-induced uveitis or stress.
General anesthesia was performed by a board-certified veterinary anesthesiologist (Veterinary Anesthesiology Consultant). The patient was restrained by its trainer; then, a mixture of ketamine 5 mg/kg (Ketalar, Daiichi Sankyo) and medetomidine 0.03 mg/kg (Atipame, Kyoritsu Seiyaku, Co) was injected intramuscularly into the back of the thigh as pre-anesthetic medication. The patient became heavily sedated within 5 min of injection. While the patient was receiving oxygen supplementation with a facemask, a 24-gauge intravenous catheter (Surflo F&F, Terumo) was placed into the saphenous vein. After ERG and ocular ultrasonography were performed as previously described, midazolam 0.2 mg/kg (Dormicum Injection, Maruishi Pharmaceutical Co) was administered intravenously and endotracheal intubation was performed with an endotracheal tube (3-Fr, Fuji Systems). After confirmation of bilateral airflow with chest auscultation and seal with inflation of endotracheal tube cuff, anesthesia was maintained using isoflurane (Animal isoflurane, MSD Animal Health). The patient was mechanically ventilated (Fabius Plus, Dräger Japan) to keep end-tidal carbon dioxide concentration (EtCO2) around 40 mmHg inside the surgical room. A TOF Watch (MSD) was used to monitor perioperative neuromuscular blockade with train-of-four (TOF). Intravenous rocuronium 0.6 mg/kg/h (ESLAX, MSD) was administered continuously for paralysis of the extraocular muscles. The patient was administered lactated Ringer's solution at 2 ml/kg/h intravenously and kept warm using a heating pad throughout the surgery. Oscillometric blood pressure, electrocardiography, SpO2, body temperature, pulse rate, respiratory rate, and EtCO2 were monitored under anesthesia (Fabius Plus, Dräger Japan). Forty-five minutes after the start of anesthesia induction, the patient became severely hypotensive (mean arterial pressure less than 60 mmHg) most likely due to the vasodilatory effect of medetomidine. At this time, the patient was moved to the operating room after preoperative ERG and ultrasonography. A fluid bolus (5 ml/kg IV), a bolus of atropine 0.01 mg/kg IV (ATROPINE, NIPRO), continuous rate infusion (CRI) of dopamine (Dopamine Hydrochloride, KYOWA CritiCare Co) up to 12 mg/kg/min and intermittent IV ephedrine 0.1 mg/kg (Ephedrin “NAGAI,” Nichi-iko Pharmaceutical) boluses were used to support the blood pressure. In addition, propofol (PropoFlo, Zoetis Japan) CRI at 75–100 mcg/kg/min and intermittent IV boluses of fentanyl (Fentanyl, Terumo) at 3 mcg/kg were administered to reduce the amount of isoflurane. We confirmed an increase in blood pressure 35 min after starting treatment for hypotension. The following additional drugs were administered during the perioperative period: cefazolin IV 20 mg/kg (Cefamezinα, LTL Pharma) and prednisolone IV 1 mg/kg (Predonine, Shionogi). Sugammadex (BRIDION, MSD) were administered intravenously (4 mg/kg) when the surgery was completed. Isoflurane was discontinued once the TOF of >90% was confirmed. The CRIs were discontinued, and buprenorphine (Lepetan, Otsuka Pharmaceutical) at 0.01 mg/kg was administered intravenously for postoperative analgesia. The patient vomited a small amount of liquid after extubation, but the recovery was uneventful otherwise.
We usually prescribe antibiotics and anti-inflammatory agents a few days before cataract surgery and instill mydriatics a few times a couple of hours preoperatively. However, the owner said it was impossible to give eye drops to this patient, initially. Therefore, antibiotics (gatifloxacin, Gatiflo, Senju), anti-inflammatory agents (difluprednate, STEROP, Senju), and mydriatic eye drop (Mydrin-P, Santen Pharmaceutical) were administered several times within a short period after the introduction of anesthesia. The patient was placed in the supine position. Both eyes were washed with diluted PA-IODO Ophthalmic and Eye washing Solution (Nitten Pharmaceutical Co., Ltd). We then draped the surgical field and started the operation.
OD: Consistent with the prior ocular ultrasonographic findings, the zonule of Zinn was noted to be torn from 2 to 6 o'clock (Figure ). A 2-step corneal incision was performed at the 11 o'clock position using a slit knife (MSL 20, MANI Inc). Three side ports were created using a 20-gauge V-lance (MVR 20SK, MANI Inc) at 1, 7, and 9 o'clock positions over the limbus. Small amounts of Viscoat (Alcon Japan Ltd) and Healon (AMO Japan) were injected through the side port, ensuring they did not pass into the vitreous. Trypan blue staining of the anterior lens capsule was followed by continuous curvilinear capsulorhexis (CCC) using cystotome initially attempted from the main port. However, the anterior lens capsule was extremely hard, and CCC could not be performed. Even after using Scissors YAE Multi-Purpose 23 G (Inami), it was impossible to incise the anterior lens capsule. The anterior lens capsule was finally punctured using intraocular lens (IOL) scissors. We were planning to perform a 5-mm-diameter capsulorhexis, considering the size of the IOL. However, the finished capsulorhexis measured about a quarter of what was expected (Figure ). As the lens was completely liquefied, it was aspirated via a bimanual I/A handpiece using the phaco-machine (WhiteStar Signature, AMO Japan). Oxiglutatione ocular irrigating solution 0.0184% KIT (Senju) with 1 mg epinephrine (Bosmin Injection, Daiichi Sankyo) and 500 IU heparin (Heparin Sodium, Mochida) were used as the irrigating solution. Following lens aspiration, the CCC was widened and a 26D foldable IOL (Avansee, Kowa) was inserted. The lens capsule was contracted, with the diameter of the lens capsule almost identical to the IOL. The lens capsule was polished using the bimanual I/A handpiece connected to the phaco-machine. However, polish failed because the capsule itself had become cloudy and hardened. Since the zonule of Zinn was partially torn, we considered the use of a capsular tension ring (CTR). However, we only had a canine version of the CTR and felt it was too large for a macaque; therefore, we did not use it. Since the tear of Zinn's zonule was within 120°, it was judged that the IOL could be inserted safely. The IOL was slowly expanded and placed in the correct position, holding the lens capsule with a Forceps Micro Capsulorhexis IKEDA BEAK23G (Inami) to prevent the lens capsule from falling into the vitreous. After aspiration of the viscoelastic substances, the corneal incision site was sutured using 10–0 nylon suture material (Mani, Tochigi) in a double continuous sawtooth suture pattern. Postoperative eye drops were expected to be difficult due to the patient's disposition. Therefore, immediately after the surgery, subconjunctival dexamethasone (DECADRON, Aspen Japan) and tobramycin (TOBRACIN, Towa Pharmaceutical Co) were injected. Skiascopy was used to confirm that OD reached emmetropia.
OS: A 3-step scleral incision was performed at the 11 o'clock position using a 22.5-degree straight knife (MST22, MANI Inc), crescent knife (MCU26, MANI Inc), and slit knife. One side port was created using a 20-gauge V-lance at the 1 o'clock positions over the limbus. Even though mydriatics were topically instilled, poor mydriasis was observed (Figure ). After using viscoelastic substances to dilate the pupil, we were able to obtain sufficient mydriasis to perform the surgery. Viscoat and Healon were injected to maintain the anterior chamber while protecting the corneal endothelial cells. Following trypan blue staining of the anterior lens capsule, CCC was performed from the main port while expanding the pupil using viscoelastic substances. Although the anterior lens capsule of the OS was softer than that of OD, it was still very hard. Thus, CCC was performed mainly using YAE Multi-Purpose 23 G Scissors (Figure ). Since the lens was mostly liquefied, it was removed with minimal phacoemulsification. Oxiglutatione ocular irrigating solution 0.0184% KIT (Senju) with 1 mg epinephrine (Bosmin Injection, Daiichi Sankyo) and 500 IU heparin (Heparin Sodium, Mochida) were used as the irrigating solution. After phacoemulsification, prolapse of the iris from the main port was seen. This was considered to be an intraoperative floppy iris syndrome (IFIS)-like phenomenon (Figure ). Subsequently, another side port was created to reduce the anterior chamber pressure and return the prolapsed iris. After returning the iris, the lens capsule was polished with the bimanual I/A handpiece using the phaco-machine. A 26D foldable IOL was inserted and oriented in the correct position. After aspirating viscoelastic substances, the corneal incision site was sutured with 10–0 nylon suture material in a double continuous sawtooth suture pattern. Immediately after the surgery, dexamethasone and tobramycin were injected sub-conjunctively. Skiascopy was used to confirm that OS reached emmetropia.
The patient was able to eat and walk straight unassisted the very next day after surgery. On examination on the third day after the surgery, intraocular inflammation was observed. Inflammation was particularly severe OS, with fibrin deposition observed (Figure ). The degree of intraocular inflammation was determined based on the degree of anterior chamber flare. Based on previous reports, the degree of anterior chamber flare seen in this patient was considered to be moderately increased. Therefore, the following eye drops were initiated on the third day: atropine (Nitten ATROPINE, Nitten Pharmaceutical Co, Ltd) every 24 h and difluprednate (STEROP, Senju) every 12 h OS, and difluprednate every 12 h OD. Frequent anti-inflammatory eye drops were recommended for the left eye, but as the patient was uncooperative, twice-daily drops were prescribed. In addition, prednisolone (PREDONINE, Shionogi) was administered systemically. The systemic prednisolone was then tapered over 4 weeks. Four weeks after surgery, minimal anterior chamber flare was observed in both eyes. Therefore, only diclofenac sodium eye drop (DICLOD, Wakamoto Pharmaceutical Co) was used every 12 h for both eyes. The patient started performing in shows again 1.5 months after the surgery.
Ophthalmic examination of both the eyes 26 weeks after the surgery showed no inflammation, with a clear visual axis (Figure ). Despite IOP concerns initially, follow-up measurements were normal. Fundus imaging (VX-10, KOWA) and optical coherence tomography (OCT; Spectralis, Heidelberg Engineering) showed no abnormalities (Figure ). The postoperative vision was maintained.


A 65-year-old male, farmer by occupation, suffered a blunt trauma to his left upper cheek area and leg with the concrete of the roof of a building in Nepal earthquake on April 25, 2015, following which a progressively increasing nodular mass was noticed by him over the left upper cheek. One year later, he presented with pain in this mass. Six months before his presentation, the skin overlying this nodule ulcerated accompanied by blood-stained discharge from multiple overlying sinus tracts, five in number []. Redness and purulent discharge started in the left eye (LE) at this time. He was a chronic smoker for the past 40 years and reported difficulty in chewing food. At presentation, best-corrected visual acuity (VA) was 6/60 and 6/9 in the right eye (RE) and LE, respectively. RE was left aphakic following a planned intracapsular cataract surgery performed 10 years back during which no intraocular lens (IOL) implantation was done. LE was pseudophakic with a posterior chamber IOL in situ. RE had a divergent squint of 25 prism diopters. LE had epiphora and conjunctival congestion. The fundus examination of both eyes was normal and so was the intraocular pressure. A well-circumscribed mass measuring 35 mm × 30 mm × 40 mm was seen at the left zygomatic area extending from the lateral canthus posteriorly up to 4 mm in front of the tragus. The mass was tender, hard in consistency, immobile, and nonpulsatile with erythema of the surrounding skin. However, temperature overlying the lesion was not raised with the absence of overlying prominent vessels. LE was displaced upward and inward.
Hemoglobin was 10.8 g/dl with an erythrocyte sedimentation rate of 51 mm/h. A possibility of a cold abscess with atypical tubercular/actinomycotic maxillary osteomyelitis was presumed as there were multiple sinus tracts over the ulceroproliferative mass with a relatively longer duration of symptoms, an indolent course of the disease apart from an unconvincing history of trauma. However, the possibility of a posttraumatic osteomyelitis with underlying fungal etiology could not be ruled out.
Radiographs of the orbit and paranasal sinus (PNS) showed a homogenous opacity with sclerotic changes in the region of the left maxillary sinus, zygomatic bone with apparent nonvisualization of part of the lateral wall of the orbit, and zygomatic arch due to infective changes suggestive of chronic osteomyelitis with left maxillary sinusitis. The rest of the visualized bones, joint spaces, and nasal septum were normal.
Pus from the sinus grew methicillin-resistant Staphylococcus aureus on culture. Ziehl–Neelsen staining for acid-fast bacillus (AFB) was negative. There was no evidence of a fungal growth on culture studies. Fine-needle aspiration cytology from the enlarged preauricular and submandibular lymph node (LN) demonstrated reactive lymphadenitis.
Further, a proliferative growth was observed by a maxillofacial surgeon in the left upper alveolar retromolar region in relation to the mandible []. The growth was extending up to the midline and communicating with the external growth. This prompted a computed tomography (CT) scan of PNS that revealed a large ill-defined heterogeneously enhancing soft-tissue infiltrating, bone-eroding mass lesion (85 mm × 70 mm) destroying the entire lateral wall and lateral half of the floor of the orbit with extensions into the maxillary sinus and left extraconal space suggestive of a malignant pathology [Figure -]. The greater wing of the sphenoid, zygomatic arch, squamous part of the temporal bone, walls of the maxillary sinus, lamina papyracea, coronoid process of the mandible, orbital floor, and inferior orbital fissure were involved [Figure -]. A diagnostic workup to rule out a focus of malignancy elsewhere in the body was unremarkable. Possibility of left maxillary sinus carcinoma in stage four could not be denied.
Intravenous vancomycin administration based on the antibiotic sensitivity testing yielded an insignificant response. Sputum testing for AFB was unremarkable. Topical antibiotics were continued in LE along with daily cleaning of the wound with betadine solution [].
Meanwhile, a histopathological examination (HPE) of the sinus edge biopsy specimen revealed chronic inflammatory cell infiltrate without any granulomas or evidence of malignancy. Biopsy taken from the left retromolar region demonstrated proliferation of large cells with abundant coarsely granular eosinophilic cytoplasm [Figure -] that stained positive with periodic acid–Schiff []. Nuclei were hyperchromatic and eccentrically located with inconspicuous nucleoli [Figure -]. Immunohistochemistry (IHC) revealed CD68 [] and S100 [] positivity in the large cells suggesting a diagnosis of GCT. Neuron-specific enolase (NSE) staining was weakly positive []. The immunohistochemical staining for p53 [], epithelial membrane antigen, cytokeratins (CKs) and Ki 67 [] was negative. The patient was not inclined for a surgical debulking of the tumor. As the growth had caused extensive local bony destruction and extended into the surrounding structures, an oncology reference was sought and he was advised treatment with radiotherapy. However, the patient was lost to follow-up after that.


A 49-year-old man presented to the emergency department for evaluation of worsening shortness of breath. Seven weeks before the presentation he was seen by a rheumatologist for bilateral hand pain and swelling associated with morning stiffness thought to be related to systemic lupus erythematous (SLE).
Medical history is significant for SLE, Raynaud’s phenomenon, and erectile dysfunction diagnosed 1 year ago. Medications include prednisone, pantoprazole, and methotrexate.
External records revealed positive ANA-titer >1:1280, positive Anti-Smith, Scl-70, and RNP antibodies. However, his DS DNA, SSA/SSB, anticentromere, anti-histone, anti-CCP, and RF were all negative. CT of the chest, abdomen, and pelvis were unremarkable 1 year ago. An echocardiogram at that time showed EF of 55–60% with normal diastolic function. Of note 3 weeks before presentation, his creatinine and GFR were within normal limits.
In the emergency department, blood pressure was 166/119 mmHg, heart rate 130. He was breathing at 23 breaths per minute and saturating at 86% on room air. Physical examination was remarkable for moderate respiratory distress, with bibasilar crackles in the lungs and 1+ bilateral pedal edema. Motor strength 4/5 in all his extremities. Hands examination revealed clubbing, see .
Laboratory analysis revealed hemoglobin 9.0, sodium 132, creatinine 3.96, GFR 20, BNP 4172. ABG: pH: 7.52, pCO2: 29.4, pO2: 58 HCO3: 23.8. Urinalysis showed 6 RBC. Chest X-ray demonstrated bilateral opacities, see .
He was admitted to the ICU for closer monitoring of his acute hypoxemic respiratory failure. Further workup in the hospital revealed elevated dsDNA, with normal C3/C4 complements and cryoglobulin. HIV and ANCA tests were negative.
Echocardiogram showed LVEF is 25% with grade III diastolic dysfunction, moderate mitral regurgitation, and severe pulmonary hypertension with RA pressure 8 mmHg and RVSP (TR) 71.0 mmHg.
CT scan of the chest revealed bilateral ground-glass opacities as shown below in .
Given his clinical picture with worsening renal failure, a diagnosis of lupus nephritis vs scleroderma renal crisis was considered. Nephrology and rheumatology teams were consulted, and a kidney biopsy was obtained. Also, RNA polymerase 3 antibodies were ordered at this time.


A 66-year-old female with a past medical history of essential hypertension, chronic obstructive pulmonary disease with 40 smoking years, hypothyroidism was diagnosed with metastatic renal cell carcinoma six months before the presentation. At that time, the patient had CT brain, CT chest abdomen, and pelvis which showed multiple lesions in the brain and lung. She received five cycles of Nivolumab and Ipilimumab. The last cycle was one month before the presentation.
The patient presented to the hospital with worsening shortness of breath and progressive malaise. On physical examination, the blood pressure 135/80 mmHg, heart rate 150 beats per minute, afebrile, and saturating 93% on 5 Liters of oxygen using a nasal cannula. The laboratory workup is summarized in .
In the emergency department, she developed tachycardia and hypotension. The heart rate was 149 bpm with telemetry showing ventricular tachycardia (). She was cardioverted and was started on amiodarone. The patient underwent heart catheterization to rule out ischemic causes. The coronary angiography revealed non-obstructive coronary artery disease (Supplemental material 1, 2), left ventricular ejection fraction of 15–20%, right ventricle appears to have 20% of normal function, and cardiogenic shock indicated by hypotensive pressures below 100 and thermodilution cardiac output of 2.23, thermodilution cardiac index 1.18. The patient underwent placement of an Intra-aortic balloon pump for cardiogenic shock and a temporary pacemaker to maximize the efficiency of the balloon pump. The echocardiogram showed an ejection fraction of 25–30% with decreased left ventricular (LV) cavity size (LV compressed by enlarged RV, with LV systolic diameter 2.7 cm, LV diastolic diameter 3.5 cm and LV posterior wall diastolic thickness 1.3 cm) and severely reduced RV systolic function with RV internal diameter 4.4 cm (Supplemental material 3).
The patient was intubated and transferred to the intensive care unit. She was persistently in cardiogenic shock, requiring norepinephrine, dopamine, dobutamine, and a balloon pump. A multidisciplinary team including intensivists, cardiologists, and oncologists was involved in the patient care. This new onset of non-ischemic cardiomyopathy was attributed to the use of nivolumab and ipilimumab. After discussing the prognosis with the patient’s husband who is the next of kin, the goal of care was tailored towards comfort measures and the patient expired on the fourth day of admission.


The second case, a 32 year old, G3P2L2, with two previous CS received oral mifepristone and misoprostol for pregnancy termination which failed and subsequently was consulted on persistent-mild vaginal bleeding. Ultrasound revealed a live 11-week scar ectopic pregnancy with increased vascularity in the anterior uterine wall on Doppler. MRI confirmed an exophytic variant with thinning of anterior myometrium (<2 mm) (). Serum hCG level was 67.574 IU/L. Feticide with intra-sac KCL was achieved followed by giving combined local and systemic methotrexate at a dose of 50 mg/m2. Serum hCG levels were monitored and an additional dose of intramuscular methotrexate was given (50 mg/m2) as the fall between day 4 and 7 was less than 15%. Subsequently, >70% decline in hCG levels from the baseline value was achieved as depicted in , prompting the staff to begin discharge activities. However, she had been readmitted 2 days later with acute abdominal pain and was managed surgically. Hysteroscopy (Showing an empty uterine cavity) was followed by laparoscopic excision of caesarean scar ectopic pregnancy. Dilute vasopressin was infiltrated into scar for hemostasis, bladder was separated from the lower uterine segment carefully, and sac was enucleated after incision was made over the thinned myometrium. The incision was freshened and repaired with barbed sutures ().
In the third case, a 33 year old, G4P1L1A2, who had a prior CS, 2D ultrasound suggested a live 8-week scar ectopic pregnancy. A 3D USG confirmed its endophytic type (). With hCG levels of 117.048 IU/L, intra-sac KCL for feticide and intravenous methotrexate 1 mg/kg was given at four doses (Day 1, 3, 5, 7) alternating with intravenous leucovorin 0.1 mg/kg (Day 2, 4, 6, 8). Following this procedure, >15% fall was noted between day 4 and 7 and she did not require further methotrexate doses (). However, despite good response, the patient opted for surgery after two weeks to shorten the follow up. Laparoscopic excision of scar followed by repair was done ().


The fourth case, a 40 year old third gravida with two previous CS, was diagnosed with endophytic type of CSEP and crown rump length (CRL) was measured to be 6 weeks of gestation (). She had already received two doses of systemic methotrexate in a local clinic, but hCG had failed to show a significant decline from initial level of 21000 IU/L. She was treated with TVS guided intra-sac methotrexate which achieved a good response with hCG levels normalized in 6 weeks. The trend of her serum hCG decline following intra-sac methotrexate is depicted in .


A 71-year-old woman presented to our hospital with progressive dizziness, headache, and weakness for > 1 year.
She also complained of blurry vision, tinnitus, acid reflux, belching, anorexia, and lower back pain. She did not have fever, and her skin and sclera were normal.
The patient had a history of gastric ulcer in the antrum, which was diagnosed 1 year prior to presentation. She received regular treatment for gastric ulcer and recovered well.
There was no personal history of tobacco or alcohol consumption or any other family medical history.
The patient’s height and weight were 155 cm and 42 kg, respectively. Physical examination revealed that the tongue was swollen and smooth. There were no positive signs in the chest or abdominal area.
Laboratory examination indicated a significantly decreased erythrocyte count (1.01 × 1012/L), hemoglobin level (45 g/L), leukocyte count (0.52 × 109/L), and platelet count (54 × 109/L). The mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration were 124.3 fL (normal range, 82.0–100.0 fL), 44.6 pg (normal range, 27.0–34.0 pg), and 359 g/L (normal range, 316.0–354.0 g/L), respectively. Routine urinalysis and liver and renal function tests were normal. The markers of myocardial injury were within normal limits. The serum levels of folic acid and vitamin B12 were 28.43 nmol/L (normal range, 7.0–54.10 nmol/L) and < 37 pmol/L (normal range, 133.0–675.00 pmol/L), respectively, while the serum ferritin level was normal. A bone marrow biopsy revealed a decrease in the number of red blood cells and an increase in their volume. Both APCAs and AIFAs were positive. The gastrin level was 266 pg/mL, which was higher than the normal level (13.0–115.0 pg/mL). The pepsinogen (PG) I and PG II levels were 12.8 (> 40.0) and 6.7 (< 27.0) ng/mL, respectively.
Endoscopic findings: Endoscopy revealed normal mucosa in the gastric antrum. However, the mucosa in the gastric fundus and body was atrophic. Narrow band imaging (NBI) showed atrophic changes without regular arrangement of collecting venules (RACVs) in the gastric fundus and body. Moreover, enlarged tubular structures and pseudopyloric changes were observed in the gastric fundus and body (Figure ).
Pathological findings: Histology revealed decreased density of glands and lymphocyte infiltration in both the epithelium and lamina propria of the gastric fundus and body. However, the mucosa in the gastric antrum did not show atrophic changes. Immunohistochemical results showed negative H+-K+ ATPase antibody staining and positive CgA staining in most of the gastric mucosa. PG I staining was positive in a small number of glands in the gastric fundus and body (Figure ).


An 84-year-old male was admitted to our department due to dizziness and gait disturbance lasting more than 1 mo.
The patient had a history of hypertension for more than 10 years. Except for age, gender and hypertension, the patient had no other predisposing factors for stroke such as trauma, obesity, diabetes, dyslipidemia, heart disease, atrial fibrillation, smoking, alcohol consumption, drug abuse, asymptomatic carotid stenosis and sleep apnea syndrome.
There was no previous stroke or transient ischemic attack in his history.
There was no obvious abnormality in his personal and family history.
The blood pressure of the right upper limb was 128/78 mmHg, while that of the left was 113/66 mmHg. The neurological examination revealed the ataxia of right limb, but had no visual field defects and typical clinical symptoms of Wallenberg’s syndrome such as nystagmus, dysphagia, intersectional paresthesia and Horner’s sign.
Magnetic resonance (MR) diffusion-weighted imaging and non-contrast computed tomography of the brain revealed subacute infarctions in cerebellar hemisphere, occipital lobe and medulla oblongata after admission (Figure ). MR perfusion-weighted imaging also showed that there was no significant difference in relative cerebral blood flow, relative cerebral blood volume, the mean transit time and the time to peak between bilateral cerebellar hemispheres except the infarct core (Figure ).
Before admission, computed tomography angiography (CTA) of the head and neck had been performed in another hospital, showing total occlusion of the right vertebral artery (VA) and severe stenosis at the proximal LSA and the origin of the left VA. CTA also revealed the bilateral posterior communicating arteries were not opening which means the incomplete Willis circle (Figure ).


We report an 80-year-old female patient with paroxysmal pain in the right maxillary region for > 20 years, which was aggravated for six months.
Twenty years ago, without obvious inducement, the patient developed right facial pain, which was located in the maxillary region. The pain was paroxysmal, which could be induced when brushing her teeth and eating. During the past six months, the pain was aggravated and seriously affected her quality of life.
The patient had a history of RH for > 10 years, with the highest BP of 200/120 mmHg. We found that she did not take her medication according to the instructions and only took amlodipine besylate 5 mg/d, and the efficiency of this treatment was unsatisfactory. She also had a history of diabetes for more than 10 years.
No relevant personal or family history.
Physical examination was normal.
Laboratory examinations were normal.
Imaging examinations were normal.


A 22-year-old male patient, married since 6 months, was brought to psychiatry OPD by mother and brother, who are reliable and adequate informants with a history of alcohol consumption since 2 years. It began with one occasional pint of beer under peer pressure which gradually changed to whiskey. Soon, because of financial issues, he started consuming country-made liquor. Initially, it was 1–2 pouches of country liquor which gradually increased to 2–3 pouches (180 ml) in the past 1 year and was now round the clock. Five months back, he started experiencing episodes of convulsions. First episode happened around 8–10 days after his marriage when he was at home surrounded by family and friends. The patient was consuming alcohol at that time. The episode was associated with involuntary movements of the body, tonic–clonic in nature followed by uprolling of eyes, frothing at the mouth, and loss of consciousness but not associated with tongue bite or incontinence. He started having frequent fights and quarrels with family members. Due to these reasons, his wife left him around 1 month back. He claimed that to stop the thoughts of his wife he started drinking more. After another such episode, he was again admitted to a private hospital for de-addiction for 3–4 days but started drinking again immediately after discharge. The patient had nearly 7–8 episodes of seizure in the last 5 months. The last episode happened 1 day before admission. The episode was preceded by tingling and numbness of limbs and was associated with frothing of mouth and tongue bite with urinary incontinence and fall. Because of the above complaints, he was brought to psychiatric OPD and was admitted. There was no significant past of family history. General physical examination and examination of cardiovascular system, respiratory system, and abdomen were within normal limits (WNL). On central nervous system (CNS) examination: Higher function tests, sensory, motor, and cerebellar examination were normal. Frontal and Temporal lobe tests were WNL. Parietal lobe tests were altered in the patient as described below.
Such constructional tasks are extremely useful for detecting organic brain disease. The scores were altered for diamond, cube, pipe, triangles for his age group, indicating some parietal lobe damage [].
In drawings to command, the patient is required to draw three pictures, according to verbal commands. The common commands are to draw a house a flower pot and a clock. The clock setting task can often bring out interesting errors, not only in pure constructional ability but also in the conceptualization of time and its abstract relation to the placement of the hands. Following are the results of the patient which revealed moderately distorted or rotated two-dimensional drawings or a loss of all three-dimensionality with moderate distortions or rotations on three-dimensional designs indicating moderate constructional apraxia [].
Mental status examination revealed a young distressed adult male, well kempt and groomed, sitting on chair, with a respectful attitude towards examiner with normal psychomotor activity with a craving for alcohol and an intact judgment.
The magnetic resonance imaging plain and contrast showed a well defined lesion in the right parietal region appearing hypodense []. Findings were suggestive of neoplastic etiology-high-grade glioma. Neurosurgery opinion was taken, and after excision craniotomy, he was diagnosed with tuberculosis (TB) brain and is currently under treatment for the same. Tablet lorazepam gradually tapered off and stopped with parenteral thiamine substitution. He was started on tablet levetiracetam (500 mg) BD, pregabalin (75 mg) + nortriptyline (10 mg) HS. Motivation enhancement therapy was done on this patient, and he is currently abstinent and on regular follow-up with brief interventions for maintenance of abstinence.


An 18-year-old girl was brought to the psychiatry outpatient department (OPD) of a tertiary care hospital with a 10-day history of tremulousness, drooling of saliva, difficulty in walking, maintaining abnormal posture, disturbed sleep, and appetite as she could not swallow fluids properly or eat. The patient was apparently all right 6 months back when her parents started noticing that she was getting irritable on trivial matters and would start crying even on minimal provocation. One day following an altercation with parents, the patient stormed off and allegedly consumed half a cup of floor disinfectant. She was then rushed to the hospital for management. Following this incident, the patient started keeping to herself and would not interact with her family. Her symptoms gradually worsened so much so that her parents found her crying most of the day. She would get anxious and breathless even if approached by her mother for a regular conversation. Since 10 days, the patient would tell her mother that she was unable to write anything in college due to tremors in her hands and stopped going to college altogether. Her mother initially thought that she was making excuses to not study but noticed her hands used to tremble and she was not able to hold anything for long. Family members noticed progressive slowing in her activities along with frequent staring episodes. She would respond to her name only after being called 4–5 times. Gradually, her upper limbs started becoming stiff and the tremulousness worsened. She was unable to eat as she could not close her mouth and had drooling of saliva. Her forearms remained flexed in uncomfortable positions for long periods without discomfort. She was unable to sleep due to these symptoms. She was then taken to an Ayurvedic doctor; however, after treatment for a week, her symptoms worsened and her food intake drastically reduced. She was then brought to the medicine OPD and was referred to the psychiatry OPD to rule out dissociative disorder.
On initial assessment, she was unable to talk. Her body was rigid and akinetic []. Her limbs could be placed in odd postures which she could sustain for a considerable period of time []. She also demonstrated waxy flexibility, staring, and negativism. Bush Francis Catatonia Rating Scale (BFCRS) score was 26. Testing for comprehension revealed no facial reactions to questions. She could only respond in signals or with incomprehensible sounds and would start crying without provocation. Further assessment of higher mental functions was not possible. Pupils were equal in size with fluctuating light reflex. Deep tendon reflexes were uniformly brisk and plantar reflexes were bilaterally flexor. Conjuctiva showed a brownish ring around the corneal margin which was confirmed to be Kayser–Fleischer ring on slit lamp examination [].
Routine hemogram, platelet count, SGOT, SGPT, blood urea, serum creatinine, fasting blood sugar, and urine microscopy were within normal limits. Ultrasonography abdomen and pelvis showed hepatic and splenic parenchymal abnormalities mostly due to metabolic disorder. Magnetic resonance imaging (MRI) brain showed symmetric signal abnormalities in bilateral caudate and lentiform nuclei, bilateral thalami, dorsal pons, and splenium of corpus callosum – findings suggestive of metabolic/toxic encephalopathy []. Axial T2 weighted MRI of the brain at the level of the midbrain showed the “face of the giant panda” sign []. Serum ceruloplasmin was 0.05 mg/dL (20–35 mg/dL) and 24-h urinary copper was 212.1 mcg/24 h (15–60 mcg/24 h). Neurophysician diagnosed her to be suffering from WD. Her catatonia improved with injection lorazepam 2 mg IV stat. She was then started on lorazepam 2 mg QID, D-penicillamine 250 mg TDS, zinc acetate 50 mg BD along with trihexyphenidyl 2 mg TDS. Due to pancytopenia, D-penicillamine was replaced by trientine 250 mg BD. Zolpidem 5 mg was added for sleep disturbance. BFCRS score reduced gradually. Her interaction, behavioral disturbances, and food intake improved slightly with gradual improvement in posturing. She is continuing her chelation therapy and is currently maintaining well with near-total improvement.


A 77-year-old Japanese woman underwent upper lobectomy of the left lung for lung adenocarcinoma (cT1N0M0 stage IA) in 2004. In 2009, she received chemoradiotherapy (carboplatin + docetaxel, 70 Gy in 28 fractions) because of postoperative recurrence. In 2012, positron emission tomography scans showed an increasing consolidation in the right middle lobe, which indicated a recurrence of lung cancer (Fig. ). Genetic analysis showed that the surgically resected specimen had an EGFR L858R mutation, and she was treated with gefitinib (250 mg/day) and achieved a partial response.
In 2017, during treatment with gefitinib without recurrence of lung cancer, CT scans showed a mass in the stomach (Fig. ), which was diagnosed as a gastrointestinal stromal tumor (GIST). The patient underwent proximal gastrectomy. In March 2019, multiple low-density areas appeared and were diagnosed as liver metastases of GIST by liver biopsy (Fig. ). She was subsequently referred to our hospital for chemotherapy.
In April 2019, imatinib (300 mg/day) was started for multiple liver metastases of GIST while remaining on gefitinib (250 mg/day) for lung cancer. In July 2019, gefitinib was replaced with erlotinib (100 mg/day) because she presented with grade 3 (Common Terminology Criteria for Adverse Events version 5.0) diarrhea following an interaction between gefitinib and imatinib. In January 2020, CT scans showed increased right lung consolidation and pleural effusion, although multiple liver metastases of GIST continued to shrink (Fig. ), and the patient's carcinoembryonic antigen level increased. She had progressive lung cancer, although multiple liver metastases of GIST were controlled. Erlotinib was discontinued, and gefitinib was re-started because the patient refused to receive cytotoxic agents. She continued gefitinib and imatinib treatment without any side effects. However, lung cancer has progressed, and fatigue and anorexia have worsened.
We suspected the appearance of EGFR T790M mutation and submitted a plasma EGFR mutation test (Cobas® EGFR mutation test version 2.0) in March. Both EGFR L858R, which was originally positive, and T790M mutations were negative. To eliminate the possibility of false-negative results, we submitted pleural fluid that was pathologically diagnosed as adenocarcinoma cells for an EGFR mutation test (peptide nucleic acid-locked nucleic acid polymerase chain reaction [PCR] clamp). However, EGFR mutations were not detected. Subsequently, we prepared a cell block from the pleural fluid specimens (Fig. ) and submitted it for an EGFR mutation test (Cobas® EGFR mutation test version 2.0), but the results were similar (Table ).
The patient's performance status decreased, and she and her family wanted the best supportive care. Therefore, she discontinued both gefitinib and imatinib and died approximately 1 month later.


A 60-year-old African American female with a history of morbid obesity (body mass index: 39.06 kg/m2), hypertension, chronic hypoxemic/hypercapnic respiratory failure, chronic obstructive pulmonary disease, PH on triple therapy of ambrisentan, tadalafil, and treprostinil for 2 years (likely Group 1, 2, and 3), heart failure with preserved ejection fraction on torsemide and spironolactone was evaluated in our clinic in 2018. Examination was significant for lower extremity edema and loud S2. She exhibited severe limitation on 6 min walk test and needed 6 L/min of oxygen supplementation for 298 m walk distance. Her ventilation-perfusion scan was consistent with mild-to-moderate chronic obstructive pulmonary disease. Her sleep study showed severe obstructive sleep apnea (OSA) with apnea-hypopnea index 7/h of sleep and total respiratory disturbance index of 40.9 obstructive events/hour of sleep. Transthoracic echocardiogram revealed abnormal left ventricular diastolic filling, left atrial index 49.3, ejection fraction 60%–65%, and moderately enlarged right ventricle. Despite attempts at weight reduction, her body mass index and mean PAP did not decrease and she continued to deteriorate further. Subsequently, despite high risk attributed to PH, gastric sleeve surgery was done to achieve long-term weight loss and subsequent improvement in OSA and PH. During the hospital course, we used continuous pump treprostinil, milrinone, and inhaled nitric oxide to stabilize mean PAP and right ventricular systolic pressures. General anesthesia was used during surgery and she was weaned off inhaled nitric oxide and milrinone within 24 h. She was discharged on postoperative day 2 on ambrisentan, tadalafil, and treprostinil.
She experienced dramatic weight loss and functional improvement over the next 6 months. During her clinic visit, she denied any lower extremity edema and was able to exercise 30 min a day without any limitations. Within 6 months, she was able to be weaned off daytime oxygen and was placed on continuous positive airway pressure of 10 cm H2O for OSA. We have compiled her pre- and post-surgery pulmonary function test and right heart catheterization data for comparison as shown in .


An 8-year-old girl presented with a grade 2 car-tire injury (). The wound appeared to be clean, and progressive granulation was observed with dressing changes. On PTD 40, the granulation tissue was excised and debridement was performed. Artificial dermis with an STSG was used to cover the raw surface. During the 5-year follow-up period, no secondary deformity was evident and a good surgical outcome was obtained.


A 10-year-old girl sustained a car-tire injury on the medial side of the left ankle and foot (). Shortly after the injury, the defect was determined to be of grade 3 severity with a region that was mainly grade 2. After the defect had been dressed for 2 weeks, the central area had become necrotic and was surrounded with granulation tissue. The area of the defect was excised, and artificial dermis with an STSG was used to cover the raw surface on PTD 15. One year after surgery, hypertrophic scarring and scar contracture were identified in the margin area in the proximal region of the dorsum of the foot. Re-excision was performed, and the entire hypertrophic scar, together with 3 mm of the normal surrounding skin, was removed. No secondary deformity was evident during the 2-year follow-up period.


A 6-year-old boy presented with a grade 3 car-tire defect on the medial side of the foot, which was surrounded by a grade 2 defect (). On PTD 21, the patient underwent wound debridement, and the defect was covered using STSG. A hypertrophic scar and scar contracture on the dorsum of the foot were evident in the area of the grade 3 defect 2 months after surgery. The hypertrophic scar and scar contracture band were excised, and the defect was covered using FTSG. No secondary deformity was evident during the 10-year follow-up period and a good cosmetic result was achieved.


A 39-year-old, human immunodeficiency virus (HIV) reactive male patient was referred from the ART center for evaluation of generalized skin lesions present for 4 years.
Clinical examination revealed multiple, hypopigmented to skin-colored, well-circumscribed, wrinkled, centrally depressed, 0.5–2.5 cm flesh-colored, oval-to-round atrophic sac-like lesions which protruded on forward bending. Hundreds of lesions were present over the trunk, abdomen, chest, and proximal extremities bilaterally symmetrical with sparing of the scalp, palms, soles, face, and mucous membranes [Figures and ]. Lesions were asymptomatic in nature, were present for 4 years.
The patient gave a history of asymptomatic genital ulcer which healed on its own before 4 years followed within a month by the development of generalized papular, erythematous, inflammatory skin lesions; which were diagnosed as secondary syphilis on the basis of mucocutaneous features and positive serology for syphilis (rapid plasma regain test - RPR1: 64). The patient was treated with single dose of injection benzathine penicillin 2.4 mega units at that time by a private practitioner as the patient was HIV nonreactive at that time. His inflammatory skin lesions healed with atrophic scars and atrophic skin lesions were status quo since then. The patient sought no further treatment for skin lesions. The patient had no history of varicella, insect bites, prurigo nodularis, Lyme disease, or molluscum contagiosum or any other skin lesions. The patient was recently diagnosed as HIV reactive; 1 month before presentation to us. He was on standard tenofovir, lamivudine, efavirenz regimen, and prophylactic oral sulfamethoxazole-trimethoprim for 1 month. His CD4 count was 65 cells/mm3 (9%) at the time of presentation. No lymphadenopathy, oral or genital lesions were observed. Other hematological investigations were within the reference range except low total WBC count with lymphocytes 11%. Serum treponema pallidum hemagglutination assay was positive. The serum RPR test was 1:2.
An atrophic macule from the lower back was biopsied. H and E section showed mildly effaced epidermis with mild interstitial edema and perivascular lymphocytic infiltrate with loss of elastic fibers in the papillary and mid-reticular dermis []. Masson-trichrome stain confirmed fragmented elastic fibers and loss of elastic fibers at places in the dermis [].


This is a 5-year-old Saudi girl who presented with generalized weakness, easy fatigability, pallor, and poor oral intake, O2 saturation 97%, and the patient was hemodynamically stable. She was admitted to the neonatal intensive care unit (NICU) at birth when her first blood count showed hemoglobin (Hb) of 4 gm/dL for which she received a blood transfusion. Initial investigation included a normal flow cytometry, that ruled out malignancy or immunologic disorders, and molecular genetics that confirmed a diagnosis of α-thalassemia trait which had no clinical implications. Further investigations were planned but the patient was lost to follow-up. For 5 years till the current presentation, the child did not follow up at any medical center, and the parents clarified that the child had a normal life with no reported manifestations of medical concern. Both parents are consanguineous with no medical history of concern. She had no history of recurrent infection, no history of blood transfusions, hypertension, diabetes, or other conditions of medical concerns, no history of previous surgeries, and no history of drug allergies. Developmental history was compatible with her age and vaccination was up to date. On examination, she looked pale, fatigued, and not dysmorphic; cardiac examination showed a hemic systolic murmur at the apex; there was no organomegaly, no dermatologic manifestations, no signs of skin inflammation or vasculitis; and neurologic examination and other systems review were unremarkable. Subsequently, she was admitted to the hospital for further investigation and supportive treatment. Her initial blood works showed Hb of 3.8 gm/dL, reticulocytopenia, slightly elevated serum bilirubin, and glucose-6-phosphate dehydrogenase (G6PD) deficiency. She had a positive direct antiglobulin test (DAT++) and was given packed red blood cells (PRBCs) with good improvement (). The initial impression was autoimmune hemolytic anemia with reticulocytopenia, so the child started on trials of intravenous immunoglobulin (IVIG) 1 gm/kg/day for 2 days and prednisolone 2 mg/kg/day for 1 month and tapering over 2 weeks with no apparent response. Bone marrow aspirate and biopsy were performed and showed reduced erythropoiesis that is consistent with PRCA. Parvovirus and Epstein-Barr virus (EBV) DNA by polymerase chain reaction (PCR) were not detected. The patient was kept under close follow-up at the clinic while preparing for the bone marrow transplantation process. She has a human leukocyte antigen (HLA)-matched sibling donor. Meanwhile, whole exome sequencing (WES) was requested aiming at a final solid diagnosis. During that time, the patient required weekly blood transfusion, as the HB level was dropping so fast reaching down to 2 gm/dL in some reports. Sequence analysis using the Blueprint Genetics (BpG) Whole Exome Plus identified CECR1 c.714_738dup, p. (Ala247Glnfs*16) a homozygous variant and a heterozygous missense variant G6PD c.563C>T, p. (Ser188Ph). Following the diagnosis, we aimed to start the patient on anti-tumor necrosis factor agents; however, the parents refused this type of therapy, so we are currently preparing the patient for bone marrow transplantation; she is clinically well, with reduced blood transfusion requirements (every 3-4 weeks).


The second case is a 10-year-old Saudi boy, known to have Hodgkin’s lymphoma (HL), who ended chemoradiotherapy 6 years ago. He presented with fever, decreased activity, and poor oral intake; oxygen saturation was 98% room air, blood pressure was normal (120/80), and there was mild tachycardia (115 beats/min). Both parents are consanguineous with no medical history of concern. He had no history of hypertension, diabetes, or other conditions of medical concerns, no history of previous surgeries, and no history of drug allergies. His developmental history was up to his age, and his vaccination was up to date. On examination, he looked ill, fatigued, and not dysmorphic; the cardiac examination was normal, there was no organomegaly nor lymphadenopathy, ENT examination was unremarkable, the neurologic examination was normal, there were no dermatologic manifestations, and there were no signs of skin inflammation or vasculitis. He was admitted to the hospital for further investigation and supportive treatment. His initial blood works showed Hb of 10 gm/dL, white blood cells 7000, and the absolute neutrophil count (ANC) was 0.5. Liver enzymes and electrolytes were within the normal range. The initial impression was infection-induced bone marrow suppression, and the child was treated as a case of fever in immunocompromised patient using intravenous antibiotics. The episodes of fever and neutropenia recurred more than once, so the patient was further investigated for the cause of neutropenia. Other investigations including peripheral blood film, antinuclear antibody, anti-ds DNA antibodies, immunoglobulin level, and virology screening (HIV, EBV, CMV, hepatitis) were reported as normal (). Furthermore, we requested bone marrow aspirate and biopsy that showed no apparent malignancy nor clonal proliferation. Moreover, a molecular panel study for congenital neutropenia was also reported as normal. WES was requested as a possible diagnostic tool and showed a homozygous ADA2 mutation c.1447_1451del, p. (Ser483Profs*5). The patient is under close follow-up at the clinic while preparing to start anti-tumor necrosis factor (TNF) agents.


A 67-year-old woman with AF underwent pulmonary veins radiofrequency ablation in March 2017. Four months after index procedure, she was admitted with progressive dyspnoea and PVS was diagnosed using computed tomography (CT). Percutaneous treatment with BA and stent implantation was performed. Balloon-expandable cobalt-chromium stents Omnilink Elite® 10 mm × 19 mm on left superior pulmonary vein (LSPV), 8 mm × 19 mm on left inferior pulmonary vein (LIPV), and 7 mm × 16 mm on right inferior pulmonary vein (RIPV) were used.
Twenty months later, she started again with progressive dyspnoea and cough. The CT confirmed severe ISR of all treated veins, and new severe stenosis in right superior pulmonary vein (RSPV). A new percutaneous approach was decided by our Heart Team. Through the right femoral vein and transseptal access (AgilisTM sheath and BRK-1TM needle, St. Jude Medical, MN, USA) with SafeSept® wire (PressureProducts, CA, USA), a significant increased pressure gradient (20–30 mmHg on average) between pulmonary veins and left atrium was demonstrated. Intravascular ultrasound (OpticrossTM, Boston Scientific, MA, USA) showed severe ISR of RIPV [minimum stenotic area (MSA) 4.72 mm2], LSPV (MSA 21.4 mm2), LIPV (MSA 5.72 mm2), and severe de novo stenosis in RSPV was proved (Figure , Videos 1–3, and ).
With CT measures and IVUS assessment, drug-coated balloon (DCB) angioplasty was performed successfully (Table ) with no residual gradient and good luminal result (RIPV MSA after treatment 62.3 mm2, LSPV MSA after treatment 21.7 mm2, and LIPV MSA after treatment 18.1 mm2).
Clopidogrel 75 mg and edoxaban 60 mg daily for 3 months was used empirically. At 1-year follow-up, she has not presented new symptoms and until nowadays the patient remains in sinusal rhythm.


A 7-year-old boy presented with persistent erection of the penis with mild pain in the lower abdomen for 5 days. There was no definite history of trauma. Clinical examination revealed a swelling of 2 cm × 1 cm in the base of the penis with priapism. Complete blood picture and peripheral smears normal. There was no past history or family history of sickle cell disease/trait. Ultrasound showed a well-defined anechoic area in the right corpora cavernosa. On color Doppler, entire anechoic area showed increased color flow with arterial and venous spectral waveform. Magnetic resonance imaging showed a fairly well-defined area appearing hyperintense on T1 and hypointense on T2 with blooming on hemo (SWI - Susceptability weighted imaging sequence) measuring 17 mm × 7 mm × 9 mm (Antero-posterior × transverse × craino-caudal) noted in the midshaft of the right corpora cavernosa. No evidence of diffusion restriction was seen intact tunica albuginea. There was no evidence of soft tissue edema/inflammatory changes.
This was suggestive of AV fistula. The patient was suggested digital subtraction angiography (DSA) for further evaluation to rule out AV fistula or aneurysm.
DSA of the left pudendal artery confirmed pseudoaneurysm []. Left pudendal artery was embolized with poly vinyl alcohol particles (semipermanent embolic agent). Right pudendal artery injection was done and partially embolized with coils and gelfoam to prevent collateral filling of the aneurysm []. The swelling and priapism settled in 3 days. Postoperatively, he was well and pain free. At 1-year follow-up, he is completely normal with normal erection. He has been counseled regarding long-term follow-up.


A 57-year-old man presented with cervical spine pain and inability to stand following a serious fall from a height of 2 m.
The patient had no prior history with regard to the lesion.
The patient had no specific history of past illness.
The patient had no known personal or family medical history.
Physical examination revealed cervical spine tenderness and neurological deficits. He had grade 2/5 muscle strength in his right upper extremity and grade 0/5 muscle strength in his other extremities. He also had dysesthesia below bilateral C5 dermatomes.
All ordered laboratory tests (complete blood count, basic metabolic panel, lipid panel, liver panel, coagulation tests, urinalysis, and stool analysis) were normal.
No obvious vertebral fracture or dislocation was found at the time on standard lateral X-ray, CT, and MRI (Figure and ). No other injuries or comorbidities were found.


We present a 30-year-old male with selective anti-polysaccharide antibody deficiency (SPAD) and peripheral blood CD5+/CD19+ B-cell predominance (97%, control 52.5 ± 17.3%) diagnosed at 5 years old.
 His past medical history was significant for persistent childhood sinopulmonary infections, severe hemorrhagic varicella at 2 years old, ulcerative colitis in early adolescence, and ongoing autoimmune hepatitis. His initial immunological evaluation revealed seronegativity of 12 Streptococcus pneumoniae subtypes, Neisseria meningitidis A and C, Haemophilus influenza b, human parainfluenza viruses 1 to 3, influenza A and B, poliovirus 1 to 3, and respiratory syncytial virus.
 Post-vaccination antibody titers demonstrated negative pneumococcal valent conjugate serology but clinically adequate (≥.01 IU/mL) response to protein antigens tetanus and diphtheria anti-toxoids. Other immune laboratory assessments included persistently stable hypogammaglobulinemia. Blood leukocytes and mitogen- and antigen-induced lymphocyte proliferation panel were within normal limits. Serologic evidence of human immunodeficiency virus, EBV, and cytomegalovirus was absent. Immunological re-evaluation at 28 years old confirmed CD5 + B-cell predominance and revealed a MAGT1 mutation (c.923-1_934del) and reduced CD16 + CD56 + natural killer- and/or CD8 + T-cell receptor, Group 2, Member D (NKG2D) expression consistent with the XMEN genotype and phenotype.
The patient presented for a routine office visit with no acute symptoms. He denied recent history of COVID-19. COVID-19 vaccination and associated serology antibody testing was recommended. Anti-SARS-CoV-2 immunoglobulin (Ig)M and IgG antibodies before and after the first BNT162b2 (Pfizer/BioNTech) mRNA COVID-19 vaccine doses, as well as nucleocapsid antibody, were negative (). S protein total antibody was reactive after the second dose.


The manuscript was prepared and revised according to the CARE Checklist (2016), and the reporting of this study conforms to the CARE guidelines.
A 60-year-old male patient visited our outpatient clinic for treatment of unilateral SSNHL accompanied by vertigo. He had first presented with SSNHL of the right ear 2 months previously and visited another ear, nose, and throat clinic. He had been prescribed high-dose prednisolone and treated for 2 weeks, but his hearing did not fully recover and he visited our clinic.
The patient had a previous medical history of type 2 diabetes mellitus and hypertension. Seven years before the examination, he suffered from myocardial infarction and had coronary stents inserted. He was medicated for diabetes mellitus and hypertension, but this was poorly controlled because of poor drug compliance. He had a history of 10 pack-years of smoking since the age of 20 years. He drank alcohol eight times a month every month for 40 years. There was neither a history of a previous diagnosis of malignancy nor clinical evidence of a current malignant tumor.
The patient reported unilateral hearing loss of the right ear, with positional vertigo and intermittent headaches. Otoscopic findings were normal. No other neurological symptoms were observed.
An audiogram showed deafness of the right ear at all frequencies and high-frequency sensorineural hearing loss of the left ear (). Under videonystagmography, there was no definite nystagmus at rest or after a head-shake test. The video head impulse test was performed and showed decreased gain and covert saccade in the right posterior canal test, and decreased gain in the left posterior canal test. An overt saccade was observed on the left lateral canal test ().
Gadolinium contrast-enhanced MRI of the head revealed bilateral IAC enhancement, with an 11 × 6-mm lesion on the right and a 9 × 6-mm lesion with cystic change on the left (). Additionally, multiple, variable-sized, nodular and peripheral-enhancing lesions in the cerebrum and the right cerebellum were observed.
Laboratory tests for cancer markers showed elevated carcinoembryonic antigen (172.0 ng/mL; normal range: 0–3.8 ng/mL) and cytokeratin 19 fragment (4.7 ng/mL; normal range: 0–3.3 ng/mL) concentrations. Esophagogastroduodenoscopy and colonoscopy showed no abnormal findings. A positron emission tomography-computed tomographic scan showed multiple instances of lymph node uptake in the mediastinum and left pulmonary hilum, and a suspicious primary tumor on the left upper lobe (1.8-cm lobulated nodule). Adenocarcinoma was diagnosed on the basis of a fluoroscopy-guided percutaneous needle biopsy of the left upper lobe nodule. Anaplastic lymphoma kinase and programmed death-ligand 1 mutations were negative and epidermal growth factor receptor mutation (exons 18 and 20) was positive. On the basis of the biopsy findings of the left upper lobe nodule and the imaging findings from a gadolinium contrast-enhanced MRI of the head, the patient was diagnosed with primary pulmonary adenocarcinoma (epidermal growth factor receptor-positive) with bilateral IAC metastases and brain metastases.
We initiated treatment after we obtained the patient’s consent to treat with oral administration of afatinib and whole-brain radiation therapy to control the brain metastases. The patient reported a decreased incidence of headache and vertigo following the administration of afatinib. No adverse or unanticipated events of any type were reported during the first 2 months of afatinib treatment. In a 2-month follow-up after the brain MRI, multiple, variable-sized, nodular and peripheral-enhancing lesions in the cerebrum and the right cerebellum were markedly decreased. The enhancement of both IAC lesions was attenuated, and the size of the bilateral IAC lesions was also decreased, with an 8 × 6-mm lesion on the right and a 7 × 5-mm lesion on the left.


A 35-year-old man was admitted to Clinic of Cardiology at University Hospital in an extremely severe state conditioned by loss of consciousness and cardiogenic shock. The patient was transferred to the hospital from gym hall, where he suddenly developed retrosternal chest pain, excessive sweating, and severe breathlessness. Ventricular fibrillation and asystole were recorded in the Emergency Department of University Hospital. Cardiopulmonary resuscitation was successful with restoration of sinus rhythm. The patient was placed on mechanical ventilation following the return of spontaneous circulation 1 h after the successful cardiopulmonary resuscitation. An electrocardiogram recorded after the restoration of sinus rhythm revealed ST-segment elevation in leads I, aVL, and V2–V4 (Figure
). Subsequently urgent coronary angiography was performed for evaluation of the cause of cardiac arrest and revealed 90% stenosis, dissection, and subtotal thrombosis of the proximal portion of the left anterior descending artery (LAD) and 70% stenosis of middle portion of LAD (Figure
). Two everolimus-eluting stents (3.0 × 28 and 2.75 × 23 mm, Xience Prime) were successfully deployed at the culprit sites. After the procedure, the patient was transferred to the intensive cardiac care unit (ICCU).
On echocardiography, septoapical and apicolateral segments were akinetic, and left ventricular ejection fraction (EF) was estimated 25–30%. Admission blood tests demonstrated high level of cardiac troponin 3.64 ng/mL (normal <0.014 ng/mL). Blood tests showed biological inflammatory syndrome: leucocytes 20.6 × 109 L (normal 4–10 × 109/L), C-reactive protein 21.8 mg/dL (normal <0.5 mg/dL), and fibrinogen 9.0 g/L (normal 2–4 g/L). Respiratory acidosis was present (pH 7.09) at admission. Although the patient had no symptoms of COVID-19 viral infection, a nasopharyngeal swab was performed as a regular hospital standard operation procedure. Polymerase chain reaction (PCR) test for COVID 19 was negative. However, antibody test revealed high level of only SARS-CoV-2 immunoglobulin M (2.044 AU/mL), which provides strong evidence of recent infection. Chest computed tomography (CT) scan showed bilateral areas of ground-glass interstitial opacities in all pulmonary lobes on both sides (Figure
). Despite the positive immunoglobulin M test, detailed history taken after extubation of the patient did not reveal any acute respiratory disease symptoms before STEMI.
The coronary obstructions were successfully recanalized by deployment of two everolimus-eluting stents. The condition of the patient was significantly improved after successful angioplasty. Initially, the patient was hypoxic; oxygen saturation was 85% with 4–6 L/min oxygen supply. Patient's initial treatment included aspirin, clopidogrel, heparin, high-dose atorvastatin, metoprolol with additional amiodaron, and inotrope support with dopamine, which was interrupted after 4 days, when haemodynamic state improved.
Taking into consideration positive immunoglobulin M test and typical radiological pattern for COVID-19 pneumonia, decision to manage of patient as having a recent coronavirus disease, complicated by pneumonia and STEMI, was made.
In addition to the treatment of myocardial infarction, intravenous dexamethasone at 8 mg daily dose, umifenovir, and zinc were administered. Moxifloxacin was prescribed later for the prevention of secondary in-hospital pneumonia.
Extubation was performed after 24 h of the treatment. On Day 7 of admission, the consciousness and mental state of the patient were completely restored.
Second CT, performed on Day 8 of hospitalization, revealed a radiological pattern of pneumonia in the absorption phase. Before discharge, the left ventricular EF was estimated 25% with left ventricular apical aneurysm. The patient was discharged on the 12th day with complete neurological recovery and stable cardiovascular state. After 8 weeks, cardiac magnetic resonance imaging revealed septoapical and anteroapical aneurysm with segmental dilation and EF of 52% (Figure
).
Treadmill stress test with modified Bruce protocol, performed after 8 weeks, revealed high tolerance to physical exertion, without any ischaemic electrocardiogram changes and symptoms.


A 33-year-old man developed severe persistent retrosternal chest pain radiating to both arms during training in a gym hall. The complaints were accompanied by nausea, vomiting, and excessive sweating. The patient had a history of transient ischaemic attack 3 years ago. No remarkable abnormalities of neurological status were found on admission. Electrocardiogram performed on arrival showed 3 mm ST-segment elevation in anterolateral leads with reciprocal changes in the inferior leads (Figure
). Echocardiography performed in the ICCU revealed hypokinesis of septoapical, midseptal, basal–septal, and apicolateral segments of the left ventricle; left ventricular EF was estimated 30–35%. Urgent coronary angiography within 1 h from hospital admission revealed total occlusion of the proximal portion of LAD (Figure
). Drug-eluting stent (Xience Prime, 3.0 × 18 mm) was deployed at the culprit site. The patient was transferred to the ICCU. Three hours later, the patient experienced sustained ventricular tachycardia and loss of consciousness, absence of palpable carotid pulse, and spontaneous respiration with ventricular fibrillation detected on monitor. Subsequent resuscitation was successful with restoration of spontaneous circulation and sinus rhythm.
After the angioplasty, PCR performed on a nasopharyngeal swab was performed and showed a positive COVID-19 result. Blood tests showed leucocytosis (19.66 × 109 L), high level of C-reactive protein 4.956 mg/dL (normal <0.5 mg/dL), and fibrinogen 5.45 g/L (normal 2–5 g/L). High-sensitivity cardiac troponin was 7.1 ng/mL (normal <0.014 ng/mL).
Chest CT scan revealed widespread bilateral areas of ground-glass lesions and subpleural consolidations (Figure
); 24 h Holter monitoring was performed before discharge to detect ventricular activity, which revealed only non-frequent supraventricular activity. Cardiac magnetic resonance imaging performed before the discharge showed left ventricular apical aneurysm and late gadolinium enhancement in left ventricular anteroapical, septoapical, midseptal, and basal–septal segments, and EF was estimated 42% (Figure
).
In addition to guideline-based pharmacological therapy of myocardial infarction, amiodaron and inotrope therapy with dopamine was administered for haemodynamic support. Dopamine was stopped on the third day, after stabilization of blood pressure. Patient was transferred to COVID-19 specialized clinic (St Gregory Illuminator Hospital) after confirmation of positive PCR test at stable haemodynamic state according to the local healthcare regulatory protocols. Additional COVID-19 treatment, including dexamethasone 12 mg daily and ceftriaxone 2.0 mg daily doses, was provided. PCR test was repeated after 15 days and came back negative.
Follow-up visits to our outpatient unit after 8 weeks and 6 months from discharge showed stable condition without any symptoms of angina, heart failure and improved EF 34% by echocardiography.


A 62-year old woman presented in August 2017 with the complaints of difficulty in swallowing and pain in the right upper chest wall radiating down the medial aspect of the right arm and forearm for the past 1 year. She underwent right-side thoracotomy for gross tumor resection of pleural leiomyosarcoma a decade ago and referred to our pain clinic for palliative care.
On physical examination in our pain clinic, dysesthesia along the medial aspect of right arm and forearm but no weakness of the right upper limb was noted. The diagnosis of C8 and T1 axonal neuropathy was made clinically and confirmed with nerve conduction study. Magnetic resonance imaging chest showed tumour recurrence encasing oesophagus, trachea, neural foramina of C7 and T1 encasing C8 and T1 nerve roots []. She was already receiving pharmacological treatment for pain with oral gabapentin 1200 mg, amitryptyline 50 mg and tapentadol 300 mg per day and still continued to have severe pain (visual analogue scale 8/10).
The patient was explained about various modalities such as surgical rhizotomy, chemical neurolysis, or RFA and she opted for diagnostic stellate ganglionic block followed by PRF treatment. After obtaining informed consent, the patient was shifted to the operation room (OR) and positioned supine with continuous monitoring of all vital parameters. Using fluoroscopy, under local infiltration with 2% lignocaine, 23 G spinal needle (quincke) was placed at the junction between C7 vertebral body and transverse process and 8 ml of 2% lignocaine (preservative-free) was injected after ensuring linear spread of iohexol contrast. While 1 to 2 ml of local anaesthetic is sufficient to block the face, head and neck under fluoroscopy, or ultrasound guidance, 10 ml might be required to cover the upper limb also.[ We have used 8 ml in this case and ensured its adequate spread by fluoroscopy. Two hours after the successful diagnostic SG block, the patient was taken to OR again and PRF of right-sided SG was performed using 21G RF cannula with 5 mm active tip for 3 cycles of each 60 s at three locations as described in the previous literature[ (junction of vertebral body and transverse process, medial aspect of transverse process, caudally at anterolateral aspect of vertebral body) for a total duration 9 min with a set temperature of 42 degree Celsius. The sensory stimulation at 50 Hz and motor stimulation at 2 Hz done for a precise target needle placement and to rule out the close proximity of the needle tip to the cervical nerve root []. After the procedure, the right upper limb became hyperemic and warm which was 2.1°C more than the contralateral limb. The patient was discharged on the same day with oral gabapentin 300 mg a day for a month. Subsequently, the patient has undergone palliative radiotherapy. The patient was in continuous follow-up after the procedure for 3 years and the pain score remained 1/10 without any medications.


A 68-year-old woman presented with severe corneal edema of the right eye one day after trabeculectomy for primary open angle glaucoma. Her past medical history was unremarkable, and past surgical history was significant for uneventful trabeculectomy in the left eye one year earlier.
Preoperative data included a best corrected visual acuity (BCVA) of 20/200 in both eyes. Intraocular pressure (IOP) was 18 mmHg in the right eye with antiglaucoma medications and 10 mmHg in the left eye without medication. Central corneal thickness (CCT) was 553 µm and 560 µm in the right and left eyes, respectively. Both eyes had moderate nuclear sclerosis. Fundus examination was significant for glaucomatous optic disc cupping with cup/disc ratio of 0.75 in the right and 0.9 in the left eye.
At presentation, visual acuity had decreased to counting fingers at 0.5 meter in the right eye. Slit lamp examination revealed elevated bleb, severe corneal stromal edema, and IOP of 6 mmHg []. The patient was first managed conservatively with intensive steroids and hyperosmotics with probable diagnosis of DMD. The diagnosis of DMD was confirmed using anterior segment optical coherence tomography (AS-OCT) (anterior module, Topcon 3D OCT-1000, Topcon Inc., Tokyo, Japan), and the patient underwent air descemetopexy on postoperative day (POD) 3. This was unsuccessful, and the patient also developed choroidal effusion which made the situation worse due to shallow AC. AS-OCT revealed scrolled DMD touching the lens and a CCT of 1204 µm []. The patient underwent the 2nd reparative surgery including choroidal tap and intracameral air injection on POD 6.
The patient responded dramatically to this intervention, and the cornea was completely clear on day 7. The patient was on antibiotics, frequent steroids, and cycloplegics. However, she returned to the clinic 5 days later with decreased vision and the same scenario including shallow AC, DMD, and choroidal effusion and an elevated bleb.
As there seemed to be a vicious cycle of hypotony and choroidal effusion, the patient underwent the 3rd surgery aimed at breaking the cycle and preventing recurrent choroidal detachment. This surgery consisted of transconjunctival suturing of the scleral flap using three 10-0 nylon sutures, choroidal tap, and AC reforming using 0.3 ml of 20% sulfur hexafluoride (SF6). During injection, the tip of the injection cannula was placed on the iris in order to prevent further damage to the scrolled DM.
The eye responded dramatically to this procedure and cornea became clear the next day after the intervention. DM remained attached post operatively and gas bubble resorbed from AC within 6 days. Sutures were removed after 2 weeks, and needling bleb revision was done 1 week later. After 3 months, IOP was 13 mmHg without medication; and endothelial cell counts were 1170 and 1720 in the right and left eyes, respectively. Lens opacity gradually increased, and the patient underwent uneventful cataract surgery 4 months after trabeculectomy.


A 44-year-old man with an 8-year history of ITP presented with a history of 7 days of diarrhea, fever, vomiting, and asthenia. Initial evaluation revealed the presence of dyspnea, temperature of 38.9 °C, and emesis (six episodes/day), but was normotensive (125/82 mmHg). The patient had been treated for ITP for 5 years with prednisone (50 mg/daily, orally). Approximately 1 month before presentation he began treatment with rituximab (375 mg/m2 weekly intravenous × 4 weeks). Review of systems revealed no other significant factors. Pulse oximetry and analysis of arterial blood gasses revealed hypoxemia (PO2 77 %). The patient had mild elevations of C-reactive protein (CRP; 12 mg/dL; normal range 0.5–10 mg/L), erythrocyte sedimentation rate (ESR) of 7 mm/h (normal range <5 mm/h), white blood cells (14,850 per µL; normal range 4500–11,000 per µL), and markedly decreased platelets (14,000/mL; normal range 150,000–400,000/mL). Chest X-ray and high-resolution computed tomography revealed diffuse bilateral lung infiltrates, while pulmonary-function tests demonstrated a restrictive pattern and a diffusion deficit that was consistent with interstitial disease. Bronchoscopy revealed no endobronchial disease, and a broncho-alveolar lavage fluid analysis excluded the presence of bacterial, viral, and fungal infections. Cyto-immunological analysis revealed increased cellularity (253 × 106/L) with a decreased percentage of macrophages (62 %) and an increased percentage of eosinophils (18 %).
A diagnosis of ILD probably related to rituximab was postulated (Naranjo probability scale [] score of 6). Rituximab and prednisone were discontinued. Treatment with fluticasone + salmeterol (inhaler), methylprednisolone (1 g/day for 3 days and 500 mg/day for 2 days), and omeprazole (40 mg/day) was started with improvement of symptoms at 15 days and normalization of CRP (6.3 mg/L) and ESR (2.4 mm/h) at 30 days. Chest X-ray at 4 months revealed only minimal peripheral irregularities in apices. At 7 months, the patient had complete remission of both radiologic signs and clinical symptoms. The patient provided written informed consent for the publication of this case report.


A 70-year-old African American female with atrial fibrillation was referred to haematology in 2010 for evaluation of a mildly prolonged PT with persistent vaginal bleeding. Laboratory test results revealed a decreased FVIIc of 33 % (reference 50–150 %), and FVII deficiency was diagnosed. The patient underwent endometrial cryotherapy, and after 4 months without recurrent vaginal bleeding, haematology cleared the patient to start warfarin therapy, with an INR goal of 2.0–3.0. Haematology recommended discontinuing warfarin if FVIIc decreased to 10 % or less. The patient’s baseline INR was 1.4, and warfarin was conservatively started at 2 mg daily. The INR remained at 1.4 for the first 4 weeks of therapy, despite gradual dose increases. Nearly 6 weeks into therapy, the patient made a dosing error, which caused her INR to increase to 2.5. She developed recurrent vaginal bleeding, and her FVIIc was found to be 10 %, which prompted warfarin discontinuation. She was switched to aspirin 81 mg daily.
In 2014, she was evaluated by a different haematologist. Her FVIIc was 44 %, with a baseline INR of 1.2. It was decided to re-attempt warfarin therapy with a lower INR goal of 1.5–2.0, as the risks of stroke without anticoagulation seemed to outweigh the risks of bleeding with anticoagulation. The patient’s risk factors for stroke had not changed since her initial warfarin course. Haematology recommended discontinuing warfarin if FVIIc decreased to <15% or if the patient developed any clinical signs of bleeding. A total weekly dose of 40 mg was found to maintain her INR in the range of 1.6–1.8. The FVIIc varied between 24 and 28 % during the first 6 months of warfarin therapy. During the seventh month, the patient’s FVIIc decreased to 15 %, with a corresponding increase in her INR to 2.4, despite no change in her weekly dose. The patient denied any signs of bleeding during this second treatment course. Her weekly doses, INR results and FVIIc results are shown in Table .


The patient (female, 87 years old) was hospitalized on June 16, 2014, because of yellow purulent sputum and cough with dyspnea lasting 5 days. The chest film suggested right lower lung infection and a small amount of pleural effusion on the right side. She had a history of chronic renal insufficiency, blood urea nitrogen was 16.1 mmol/L, and creatinine was 334 µmol/L at the time of admission. There was no bleeding history. The pneumonia was successively treated with mezlocillin and piperacillin/tazobactam, but symptoms did not improve. The antibiotic was upgraded to cefoperazone/sulbactam 4.5 g twice daily intravenous infusion from June 23. The symptoms improved daily. At 4:00, June 30, the patient felt a sudden onset of left lower abdominal pain, associated with subcutaneous mass. This mass was round, 6 × 6 cm in size, and hard to touch. The patient experienced tenderness with no obvious wave motion. Abdominal computed tomography (CT) showed possible hematoma at the lower left abdominal wall (Fig. a). Abdominal B ultrasound revealed mixed masses (100 × 36 mm, smooth border, unhomogenous echo) at the left lower abdominal wall (Fig. b). The patient had not defecated in the past 48 h, and incarceration of a ventral hernia was considered. Fasting, rehydration, spasmolysis, and acesodyne were implemented, but these measures did not ease the symptoms. At 17:00, June 30, the patient vomited a coffee-colored liquid, about 200 mL. Occult bloods test of vomit were positive. On July 1, the patient’s condition had not improved, there was no anal flatus or defecation, the abdomen was soft, and the mass still had apparent tenderness. No skin ecchymosis was observed nearby. The blood coagulation showed on July 1: prothrombin time (PT) 80 s, partial thromboplastin time (PTT) 57.1 s, PT international normalized ratio (INR) 7.9, fibrinogen 4.8 g, and thrombin time 15.7 s. At 15:30, the mass was detected under ultrasound guiding. The puncture drew 30 mL dark red liquid. Cefoperazone/sulbactam-induced abnormal coagulation and hematoma were considered. The drug was withdrawn and vitamin K1 40 mg was given to correct the coagulation disorder immediately. On July 2, abdominal pain significantly reduced and the anal exhaust restored. Blood coagulation function improved visibly (PT 13.4 s, PTT 27.3 s, PT INR 1.2, fibrinogen 5.45 g, and thrombin time 15.2 s). On July 3, the coagulation function of the patient returned to normal (PT 11.9 s, PTT 22.9 s, PT INR 1.06, fibrinogen 5.45 g, and thrombin time 15.7 s). The symptoms had not recurred; the mass at lower left abdomen became smaller, which was confirmed by ultrasound (Fig. c). No other treatment was started and stopped at the same time. The patient was discharged on July 15, at which time she showed no symptoms.