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A 72-year-old female patient presented to the emergency department (ED) after a primary care physician referral for tachycardia, who saw her with complaints of epigastric discomfort, vomiting, and loss of appetite for the past 2 days. An electrocardiogram (ECG) at the clinic revealed a narrow complex tachycardia of 169 beats/min. She was admitted for ischemic stroke 6 months earlier and was on aspirin. During that admission, PSVT developed but was successfully treated with intravenous (IV) adenosine. She was reviewed by the cardiologist, and 2D echocardiography was performed, which did not reveal any underlying structural heart abnormalities. In addition, an electrophysiological study confirmed the underlying etiology of PSVT as AVNRT.\nOn arrival, she was alert with a temperature of 37.3°C; heart rate of 170 beats/min; respiratory rate of 25 cycles/min; blood pressure of 112/81 mm/Hg; and oxygen saturation of 97% on room air. Her physical examination was normal. The ECG revealed a narrow complex tachycardia suggestive of AVNRT due to the presence of retrograde conduction of P waves in leads I and aVR (). Previous ECG documented in electronic health records did not show any signs of pre-excitation for AVRT from an accessory pathway or prolonged QTc syndrome. She was observed on continuous cardiac rhythm monitoring throughout her ED stay.\nVagal maneuver (Valsalva) was attempted without success. A carotid sinus massage was not performed as the patient had a stroke history. IV adenosine at 6 mg was given for pharmacological conversion. Shortly after IV adenosine administration, the patient became unresponsive and developed a generalized tonic-clonic (GTC) seizure. Pulse was absent, and the cardiac monitor revealed ventricular fibrillation (VF). Cardiopulmonary resuscitation was immediately started together with the preparation for defibrillation. However, just before defibrillation, the seizure spontaneously aborted and she had a palpable pulse with a return of spontaneous circulation (ROSC). The whole episode of seizure and VF lasted for approximately 8–10 s. The cardiac monitor revealed a normal sinus rhythm conversion and the patient spontaneously regained consciousness. Repeat vital signs were stable with a heart rate of 72 beats/min; blood pressure of 102/62 mm/Hg, and oxygen saturation of 99% on room air.\nA rhythm strip () review recorded during the IV adenosine administration revealed an initial suppression of the AV conduction lasting for approximately 6 s interspersed, with non-conducted P waves and ventricular escape beats (), in which the last escape beat triggered the onset of VF (), which lasted for approximately 8 s. The VF duration corresponded to the GTC seizure duration, indicating a convulsive syncope secondary to VF resulting in seizure. The patient does not have any history of epilepsy. This was followed by spontaneous VF termination and continued AV conduction suppression with a period of aberrantly conducted supraventricular impulses () before sinus rhythm reversion (). A repeat ECG post adenosine administration did not reveal any pre-excitation features ().\nBlood investigations were done in the ED upon patient arrival before adenosine administration. These included a complete blood count with hematocrit level, serum electrolytes, and thyroid function test, which all revealed normal results. Coupled with her normal physical examination without signs of dehydration and ECG that was not suggestive of sinus tachycardia, the possibility of dehydration as a contributory factor to the tachycardia was ruled out. The patient was admitted to the High Dependency Unit (HDU) under cardiology. During admission, her serial cardiac enzymes were normal. Her symptoms of epigastric discomfort and vomiting were attributed to gastritis. She had another episode of SVT in the HDU, which was successfully converted with IV diltiazem. Myocardial perfusion imaging was negative for ischemia, and the transthoracic echocardiography revealed a normal ejection fraction without regional wall motion abnormalities. An electrophysiological study was not performed during this admission due to her advanced age and other co-morbidities. She was discharged stable after a few days and was started on long-term oral diltiazem.

A 56-year-old woman presented to the emergency room with mild left leg numbness of sudden onset. The symptoms had a rapidly improving course over a period of one week. She had hypertension and diabetes mellitus as stroke risk factors. In addition, she had experienced hypertensive intracerebral hemorrhage in the left thalamus five years earlier. She had regularly received antihypertensive medications, oral hypoglycemic agents and aspirin during the past one year. On initial neurological examination, she was alert and had no dysarthria, facial palsy, or language dysfunction. A motor function test revealed mild left leg weakness (MRC grade IV). A tingling sense and numbness in the left hand below the wrist were observed. Deep tendon reflexes and cerebellar function tests were also normal. Her initial National Institutes of Health Stroke Scale (NIIHSS) score was one. The result of her chest x-ray and electrocardiogram showed a normal configuration. A brain magnetic resonance imaging (MRI) scan taken 3 hours 46 minutes after the onset and diffusion-weighted imaging (DWI) showed an acute lacunar infarct in the right thalamus, which may be correlated with small vessel disease, without perfusion defects (). Antiplatelet agents with 75 mg/day of clopidogrel and 200 mg/day of cilostazol were administered for prevention of recurrent ischemic attacks. A brain magnetic resonance angiogram (MRA) showed a saccular aneurysm which was incorporated with the vessel in the left middle cerebral artery (MCA) bifurcation. A diagnostic transfemoral angiography (TFCA) revealed a 6.4 × 6.0 mm aneurysm with a wide neck (4.2 mm) located at the left MCA bifurcation in the antero-inferior direction (). Coiling rather than clipping was considered because of acute thalamic infarction, patient's age, and preponderance of the patient. Because of no recurrent ischemic attack or neurologic deficits, treatment timing was considered beyond acute period (minimum 2 weeks after initial attack). Therefore, coil embolization using a multiple catheter technique was performed at hospital day 15. The partial embolization was performed without difficulty because dense packing of the aneurysm was intentionally avoided to prevent protrusion of the Guglielmi Detachable Coils into the parent vessels or occlusion of the parent artery. Consequently, post-procedual imaging could detect some contrast filling in the aneurysmal sac (). The patient was discharged without recurrent or residual neurological deficits and maintained dual antiplatelet agents.\nAfter 14 days of coil embolization, clopidogrel was stopped and 200 mg/day cilostazol was maintained because the patient had no recurrent neurological symptoms. After five more days of single antiplatelet therapy, she visited the emergency room 6 hours after the initial ictus of a language disturbance and right hand clumsiness. A neurological examination showed sensory dominant mixed type aphasia and right arm weakness (MRC grade IV). DWI revealed acute infarction in the territory of the inferior division of the left MCA which was the location of the distal part of the coil embolization (), and then TFCA was performed without additional images and showed a filling defect as a thrombus in the proximal MCA just distal to the aneurysmal neck (). Therefore, we performed intra-arterial thrombolytic therapy using 100,000 units of urokinase (for thrombolysis) and 500 mcg abciximab (for inhibiting platelet aggregation) without intravenous tissue plasminogen activator. Immediate post-thrombolysis angiography showed a resolved thrombus and good blood flow to the left MCA branches (). Language disturbance and motor weakness were not observed. Seven days after the thrombolysis, TFCA revealed still complete recanalization of the thrombosed parent artery. Dual antiplatelet agents were maintained, and she had no recurrent neurological symptoms 12 month after the intra-arterial thrombolytic therapy.

Our patient was an 18-year-old female, who presented with gradual thinning of both the upper limbs (Left>Right) and weakness of both the lower limbs (Left>Right), since one and half years in the form of difficulty in walking and two episodes of fall.\nOn examination, there was severe wasting of both the upper limbs left side being more affected than the right. Power in left lower limb was 4/5 and right was 5/5 with spasticity, and in the upper limb was 3/5 on left side and 4/5 on right side with weakness of hand grip. Patient was able to walk only with the help of a walker. Plantar were bilateral extensors with exaggerated ankle and knee jerks and ill sustained clonus of left patella and ankle. Upper limb reflexes were absent. There were no sensory changes in upper as well as lower limb, and in rest of the body, the skin over the neck and back was normal with no evidence of any sinus, hairy patch, or any cutaneous mark.\nMRI of the cervical spine with contrast study showed widening of the cervical spinal cord from C3 to D2 []. An intramedullary space occupying lesion was present, which was hypo intense on T1W images, hyper intense on T2W images, and with peripheral ring enhancement on contrast study [Figures –]. Also, “whorls” were seen within the lesion on T2 weighted images []. There was associated excavation of the bony spinal canal and the cervical vertebral bodies.\nPatient was operated under general anesthesia in prone position. Injection of methyl-prednisolone was given intraoperatively and continued in the postoperative period for 23 hours at a dose of 30 mg/kg bolus over 1 hour followed by 5.4 mg/kg/hr for 23 hours. A midline incision extending from just below the external occipital protuberance to D3 was made. Para spinal muscles were retracted laterally by subperiostially dissection. Partial C2 and C3 to D3 laminectomy were done. After laminectomy, the cervical dura was found to be bulging and enlarged. Dura was opened in the midline and retracted by stay sutures. The cord was enlarged. A small midline myelotomy was made initially. White shiny debris with hair was removed. The myelotomy was subsequently extended rostrally and caudally. Whitish grumous contents mixed with hair was removed and the cyst decompressed. Only some part of the cyst wall, which was not adhered densely to the cord, was removed. In major part of the cyst, the wall was densely adherent to the cord and attempt to remove them would have lead to damage to the cord. Hence, it was left behind.\nThe myelotomy was left open. Dura was closed with vicry 4-0. Muscles and skin were subsequently closed with absorbable stitches. Recovery from anesthesia was uneventful.

A 55-year-old woman with a history of multiple sclerosis (MS), gastric bypass, bipolar disorder and myoclonic jerks treated with topiramate presented to an outside hospital with complaints of generalised weakness. She was found to be markedly hypokalemic at <1.5 mEq/L. The patient had a history of MS flares with similar presentations, last of which was 1 year prior. However, recent follow-up MRI had not shown any new MS-related demyelinated brain lesions. The patient did not have any vomiting or diarrhoea to explain hypokalemia and had reported that she was recently told to decrease topiramate dose due to side effects, rendering topiramate the likely culprit for her severe hypokalemia despite being on potassium supplementation. In addition to metabolic work up for her weakness, hypokalemic periodic paralysis and MS flare were also on the differential for this presentation.\nThe patient’s potassium was aggressively repleted at the outside hospital both orally and intravenously. She had also received 3 L of intravenous normal saline for hypotension. In review of transfer records, her sodium on day of admission was 137 mEq/L, but rose to 164 mEq/L on day 3 of admission, a change of 27 mEq/L in 72 hours. She was also making around 2.5–3 L of urine per day during this time, thus raising concern for diabetes insipidus (DI) due to a remote history of lithium use for bipolar disorder. The patient never had issues with hypernatremia or polyuria in the past. Her measured urine osmolality was 400 mOsm/kg, see for details.\nThe patient then developed acute onset encephalopathy and left hemiparesis on day 3. The unilateral upper and lower extremity weakness necessitated ruling out stroke as cause of symptoms and then she was transferred to our hospital for neurological evaluation and higher level of care due to concern for exacerbation of MS versus neurologic vascular event. Neurology did not feel that her presentation was consistent with MS flare or a vascular event. She had an unremarkable lumbar puncture and cerebral imaging.\nNephrology was consulted due to refractory hypokalemia. Review of outside hospital records revealed admission sodium of 137 mEq/L and normal anion gap metabolic acidosis. She had normal renal function, a urine potassium-to-creatine ratio of 100 mmol/g and a transtubular potassium gradient of 16 indicating renal potassium wasting. Urine output after resuscitation with intravenous normal saline was >3 L/day. Her presentation was consistent with renal tubular acidosis (RTA) induced by topiramate. It was concluded that hypernatremia developed due to hypokalemia-induced renal concentrating defect that leads to polyuria rather than lithium-induced DI. The patient was also noted to be hypophosphatemic and folate deficient in the setting of prior gastric bypass predisposing her to ODS. It was highly suspected that the altered mental status was due to ODS rather than MS or stroke given that her acute hypernatremia of 164 mEq/L was slowly corrected over several days rather than rapidly. Repeat MRI of the brain was pursued and showed a pontine lesion consistent with demyelination ().\nThereafter, aggressive free water supplementation was implemented to quickly decrease her sodium down to normal range. Her mental status gradually improved after that. She also had resolution of her left arm weakness and was discharged to a short-term physical rehabilitation programme.

We present a 60-year-old male with no significant medical history who presented to the emergency room with a rapidly growing lump in the right axilla for three weeks. Associated symptoms included jaw pain and swelling, bifrontal headache, weight-loss, and double vision for a one-week duration. Of note, he recently underwent dental surgery two weeks before presentation for a periodontal abscess associated with cervical lymphadenopathy and was now concerned about the possibility of disease progression.\nOn examination, the male patient was alert, oriented and was slightly cachectic appearing. On neurological examination, the patient’s extraocular movements in the left eye were completely intact however the right eye had ptosis and complete monocular ophthalmoplegia. Patient’s strength, sensation, and reflexes in upper and lower extremity was unremarkable. Neck examination was unremarkable with no palpable masses, S1/S2 was present with no additional heart sounds. Lungs were clear to auscultation, and an 8 cm hard, fixed and painless mass in the right axillary region was palpated. Remained of the examination was unremarkable.\nPatient’s complete blood count was unremarkable with no leukocytosis, and the comprehensive metabolic panel was only significant for hyperglycemia and mild transaminitis. In the emergency room, a CT of the chest was ordered that showed the large axillary mass as well as multiple liver hypodensities, suspicious of metastatic disease.\nAt this point, the axillary mass was highly suspicious for malignancy however, we could not explain the neurologic finding as a connective entity thus the patient was admitted for further workup of both the mass and eye findings. Biopsies were scheduled of both the axillary and liver mass. Both sampled returned as high-grade lymphoma and a bone marrow biopsy was scheduled for further differentiation. The bone marrow biopsy showed similar results with flow cytometry confirming the diagnosis of large b-cell lymphoma. In regards to the ophthalmoplegia, further imaging was ordered to rule out other etiologies that included CT Brain and MRI Brain. Both CT and MRI were unremarkable so an additional MRI of the eye orbit was ordered that was unexceptional as well. We performed lumbar puncture for further evaluation that demonstrated elevated protein with numerous atypical lymphocytes. Cytology of the cerebrospinal fluid confirmed CNS involvement with lymphoma as seen in , that lead to the diagnosis of LC secondary to Large B-Cell Lymphoma.\nBecause of the significant disease burden, the patient was started on R-CHOP therapy that includes: Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone. The patient was also started on intrathecal methotrexate treatments for the LC and discharged after the initial treatments. The patient was followed outpatient where he has a significant reduction of the size of his axillary lymph node and continued outpatient chemotherapy with intrathecal treatments with methotrexate. On re-examination during his admissions for intrathecal treatments, re-examination showed slight improvement of extra-ocular movements as the patient was able to abduct his eye approximately 4mm after the multiple treatments however complete resolution was not achieved. After four months, the patient’s lymphoma became to treatment however after extensive discussion, the patient opted to defer any further treatment and decided to transfer to hospice care.

A 52-year-old Chinese gentleman with a significant medical history of gout, hypertension, dyslipidaemia, asthma, ischaemic heart disease (IHD) and chronic kidney disease (CKD) with a baseline creatinine of 130 μmol/L presented to us with a swollen and painful left ankle of 2 days’ duration. The diagnosis of flare of gout of the left ankle was made. He had already been admitted twice within the past 2 months for the same diagnosis. The current flare of gout happened while he was still taking prednisolone 20 mg once daily and colchicine 500 microgram twice daily. Due to his underlying conditions of IHD and CKD, non-steroidal anti-inflammatory drugs were not used. His prednisolone dose was increased to 30 mg daily. The rheumatologist injected 20 mg of intra-articular triamcinolone into his ankle on day 2 of admission. Left ankle joint fluid aspiration under ultrasound guidance was simultaneously performed, but this was unsuccessful as only minimal fluid was present. A magnetic resonance imaging (MRI) scan of the left foot was performed as his gouty arthritis was frequent and recalcitrant. The MRI showed changes consistent with gout (Table ).\nThe ankle pain did not improve much; however, the C-reactive protein (CRP) showed significant improvement (Table ). Paracetamol and 400 mg of tramadol daily in divided doses provided minimal pain relief. The pain service team reviewed him and added oxycodone for pain control. Unfortunately, on day 20 of admission, he developed right neck, upper pectoral and sternoclavicular joint (SCJ) tenderness and swelling. A fever followed 2 days later. The CRP was remarkably raised (Table ).\nAn ultrasonography (US) of the neck showed right internal jugular vein (IJV) thrombosis and right pectoralis muscle abscess. A computed tomography (CT) scan of the thorax showed right pectoralis muscle and right supraclavicular abscesses likely related to right SCJ septic arthritis, as well as thrombosis of the distal third of the right IJV (Figures –). The first three sets of blood cultures grew methicillin-sensitive Staphylococcus aureus (MSSA). The transthoracic echocardiogram showed no evidence of infective endocarditis. The patient did not have any skin lesions or notable entry points for the MSSA. Blood cultures were repeated every 48 hours until they were negative. He was initially planned for a trans-oesophageal echocardiogram (TOE). However, in view of subsequent negative blood cultures and the fact that he had no further fever spikes after commencing treatment, infectious disease specialists opined that a TOE was not necessary.\nIn view of the septic arthritis with concomitant bacteremia, he was treated with 6 weeks of intravenous cloxacillin. Cloxacillin was chosen based on culture and susceptibility results. In view of the proximity of the IJV thrombosis to the superior vena cava (SVC), and thus the concern that he might develop pulmonary embolism, he was anticoagulated, initially with enoxaparin (low-molecular weight heparin), followed by 3 months of rivaroxaban. The duration and choice of anticoagulation is based on the American College of Chest Physicians (ACCP)'s guidelines on upper extremity DVT (refer to ). The patient was transitioned to rivaroxaban as it afforded him more convenient outpatient therapy.\nCardiothoracic and orthopedic surgery opinions were sought. No surgical intervention was deemed necessary. A follow-up CT of the thorax after 6 weeks of antibiotics showed resolution of the pectoral abscess with persistent IJV thrombosis. His CRP normalized.

A 44-year-old man presented to our hospital complaining of productive cough and fever for 5 consecutive days. He also reported suffering from chronic worsening dyspnoea, orthopnoea, and abdominal discomfort for ∼18 months. He underwent mitral valve replacement due to rheumatic valve disease (severe regurgitation and mild stenosis) with a mechanical prosthesis 7 years before. His medical history additionally consisted of moderate asthma and atrial fibrillation. After initial surgery, the patient remained asymptomatic for 6 years. He had serial echocardiograms showing mild ventricular dysfunction without significant valve prosthesis dysfunction or thrombosis that could explain the worsening symptoms. Cardiovascular physical examination revealed elevated jugular venous pulse, irregular cardiac rhythm with S3, a lower left parasternal heave and a pathologic pulsation in the left second intercostal space. Hepatomegaly and diffuse bilateral pulmonary rales and wheezes were also discovered. Due to pulmonary consolidations on superior and inferior right lobes on chest X-Ray () and elevated inflammatory markers, the initial diagnosis was acute decompensated heart failure triggered by community-acquired pneumonia, and treatment was initiated with intravenous loop diuretics and antibiotics. Other relevant laboratory tests showed leucocytosis, mild anaemia (HgB 112 g/L), mild hypoxaemia, and a supratherapheutic international normalized ratio (5.94).\nFurther evaluations by chest computed tomography (CT) and echocardiogram were performed because of persistent respiratory symptoms, elevated inflammatory markers and worsening cardiovascular symptoms.\nEchocardiogram showed left ventricular dilation and mild dysfunction with ejection fraction (EF) of 43%, right ventricular dilation and dysfunction, mild pericardial effusion, normally functioning mechanical mitral prosthesis and an intriguing anechoic structure adjacent to the left ventricle posterior lateral wall, near the mitral prosthesis with possible left ventricle communication (). Thorax CT confirmed pneumonia with concomitant pulmonary congestion. Furthermore, it revealed two massive multilobulated formations, located in superior and inferior aspects of mediastinum, with partially calcified walls (, ). Cardiac magnetic resonance imaging (CMRI) was performed for better assessment of these structures, showing one trilobed formation, located at left ventricle inferior wall, causing diaphragm compression, and one bilobed formation, located at left ventricle anterior wall and extending to the lateral wall. (). Both structures communicated with the left ventricle through perivalvular, contrast-filled necks. The absence of ventricular muscle layer and passive filling during ventricular systole characterized these structures as PSAs (, Video S1). On coronary CT angiography, we also identified a circumflex branch occluded which was confirmed by coronary angiography (, ).\nOwing to the massive size of PSAs and the presentation with new-onset severe heart failure, an operative approach was chosen. During the procedure, after initiation of CPB, mechanical mitral prosthesis was explanted permitting posterior ventricular wall exploration. It was impossible to find the PSA neck. The option was to perform an incision of the PSA external wall, and a tear was found on the posterior AVG, below the insertion site of mitral prosthesis, communicating the PSA with the left ventricle. This communication was closed with bovine pericardium patch using single pledgeted sutures and a new mechanical prosthetic valve number 25 was implanted with interrupted stiches. After weaning from CPB and protamine reversal, patient presented diffuse bleeding on the site of dissection from PSA wall, left ventricle, and diaphragm. Surgeons did not find bleeding on suture lines, nor any bleeding with possible surgical approach. Therefore, they packed the chest with compresses as a life saving measure before closing the sternum. After 48 h, patient’s chest was reopened in order to remove the towels. Further, post-operative course was uneventful.\nPrior to discharge, patient was re-evaluated with CMRI. The absence of contrast filling of the inferior wall PSA confirmed its successful closure. However, a contrast-filled peri-mitral valve neck on left ventricular basal anterior segment was noted, communicating it with the PSA located at the anterior wall, and a structure suggestive of small thrombus (), (, Video S2). Due to multiple previous interventions, a conservative approach was chosen and patient was discharged without any further complications.\nThe patient is being followed-up since hospital discharge. On echocardiographic assessment, 5 months after surgery, despite an improvement in left ventricular function with EF of 51% and normal right ventricular function, we identified a moderate paravalvular leak from the mitral prosthesis on anterior topography, which might be related to mitral annulus instability from both procedures. His last outpatient appointment happened 1 year and 2 months after surgery: he remains asymptomatic without signs of heart failure and is being managed conservatively.

An 84-year-old Japanese male patient with chest pain at rest and syncope 2 months ago who was admitted to the hospital for further evaluation. He had a history of smoking more than 50 years but quit smoking 5 years ago. Rosuvastatin calcium 2.5 mg was administered at a neighbourhood hospital due to dyslipidaemia. His blood pressure was 121/50 mmHg, and his pulse rate was 68/min. There were no abnormal findings regarding auscultation and physical examinations. After routine electrocardiogram and cardiac ultrasonography examinations, we performed computed tomography coronary angiography (CTCAG). After an hour-long administration of 20 mg metoprolol and 5 mg nitroglycerine tape before examination by CTCAG, he complained of typical chest pain and prodrome before syncope. During the attack, bradycardia and inverted T waves in the V5, V6 leads were observed, as shown in . We did not measure the Troponin because his chest pain disappeared within a few minutes. CTCAG revealed severe stenosis (70% <) at the proximal left anterior descending (LAD) artery according to the coronary artery disease reporting and data system (CAD-RADS), as shown in . Hybrid images of CTCAG and thallium-adenosine myocardial scintigraphy revealed no ischaemia in the LAD coronary artery territory, as shown in . We performed coronary angiography. However, LAD artery has a 50% stenosis. We did not measure coronary fractional flow reserve because LAD artery has just 31% stenosis by the analysis of Quantitative Coronary Angiography (, File S1). We administered intracoronary injection of 64 µg ER into the LCA, but no provoked spasm was observed, as shown in . Although we added another 40 µg ER into the LCA, no provoked spasm was recognized ( and Video 1A). After the administration of 80 µg ER into the right coronary artery (RCA), no provoked spasm was found. We administered 20/50/100 µg intracoronary ACh into the LCA without a pacemaker for 30 s. Neither bradycardia nor cardiac arrest has occurred during or after the administration of ACh. As shown in and Video 1B, intracoronary administration of 100 µg ACh into the LCA disclosed diffuse spasm at the distal LAD artery accompanied by usual chest pain and slight ST elevation (0.5 mm) on V2–V4 anterior leads. After the administration of nitroglycerine, no stenosis was observed in the distal LAD artery ( and Video 1C). We diagnosed the patient with CSA. A calcium channel antagonist (4 mg benidipine) and nicorandil (10 mg) were started. Since then, the patient has never complained of chest pain or syncope for more than 6 months.

An 18-year-old male presented with multiple swellings [first swelling appeared at the age of 5 years] involving the entire neck [] with history of dyspnea, change in voice, and 4 episodes of hemoptysis. The amount of blood was around 10 - 15 ml, and color was bright red. From the past 1 year, he had the complain of dyspnea on moderate exertion, which aggravated on neck flexion and also developed change in the voice. No other significant history was present.\nOn examination, he looked well, not in distress or sweating. His body weight 35 kg, heart rate was 92 beats/ min, and blood pressure 100/70 mmHg. Local neck examination showed multiple nodular swellings with enlarged thyroid more on the right side moving with swallowing, firm in consistency, nodular surface, not tender with normal overlying skin, swelling seen extending from 1 cm above thyroid notch up to suprasternal notch, lower margin of the swelling could not be make out, swelling on right side extends 2 cm beyond posterior border of sternocleidomastoid muscle []. Larynx and trachea displaced towards left side, right carotid vessel displaced anteriorly, bruit heard and thrill felt, left carotid thrill also felt; engorged right external jugular vein was seen.\nCardiovascular and abdominal system examination was normal. Chest examination revealed bilateral decreased air entry more at basal region. Chest x-ray showed thin miliary nodules in both lung fields with basal predominance, suggestive of metastasis [].\nX-ray soft tissue neck-AP and lateral view [] showed calcified mass lesion in neck compressing trachea with retrosternal extension into superior mediastinum. Trachea was shifted to left side.\nLaboratory investigations were within normal range.\nFine needle biopsy showed papillary carcinoma thyroid. The patient was scheduled to undergo total thyroidectomy under general anesthesia. During surgery, it was found that tumor was unresectable due to an extensive involvement of major blood vessels of the neck, therefore, case was closed. We shifted the patient to ICU, ventilated him overnight and successfully extubated him on next day.

A 33-year-old non-diabetic, normotensive male presented to us with a sudden onset, painless diminution of vision in his left eye. He denied any suggestive systemic history or recent onset of fever preceding his ocular symptoms. There was also no history of similar ocular complaints, such as redness, ocular pain or diminution of vision in the past. He had a history of contact with patients of pulmonary tuberculosis. His grandfather, grandmother, and uncle had pulmonary tuberculosis. On examination, best corrected visual acuity (BCVA) in the right eye was 6/6 and counting finger at a 1-metre distance in his left eye. Slit-lamp examination of both the eyes revealed quiet anterior chamber, clear lens, and cells in anterior vitreous of the left eye. Examination of pupil revealed a relative afferent defect in the left eye. The intraocular pressure and eye movements were normal. Colour vision with Ishihara chart was 21/21 in the right eye and 0/21 in the left eye. Fundus examination of the right eye showed multiple small areas of healed choroiditis sparing the macula []. Fundus examination of the left eye revealed an oedematous optic disc with large areas of peripapillary haemorrhages with surrounding subretinal fluid with hard exudates over macula []. Fundus fluorescein angiography (FFA) of the right eye delineated the healed areas of choroiditis with staining of the lesions []. FFA of the left eye showed hypofluorescence of choroidal involvement in early frame followed by the hyperfluorescence of the lesions and leakage of the dye from optic disc [Fig. and ]. Magnetic resonance imaging (MRI) of the brain and orbit with contrast was essentially normal and revealed a small elevation at the left optic disc.\nExtensive investigations were carried out to find out the underlying etiology and other causes of optic neuropathy. In these studies, neuroimaging and serologies for syphilis, toxoplasma, and human immunodeficiency viruses found negative. Serum angiotensin-converting enzyme and serum lysozyme were within normal limit. Laboratory investigations revealed a positive tuberculin skin test (TST), a positive interferon gamma release assay (IGRA), and high-resolution computed tomography (HRCT) of the chest revealed multiple lymphadenopathy involving mediastinal, axillary lymph nodes with fibrotic strands in the lung parenchyma. Consultation from a pulmonologist was sought who started the patient on anti-tuberculosis treatment (ATT). The patient subsequently underwent pulse corticosteroid therapy with intravenous methylprednisolone (IVMP) for three days followed by tapering doses of oral prednisolone starting at 1.5 mg/Kg body weight/day. He was examined again after two weeks. He felt minimal visual improvement, and BCVA in his left eye was recorded as 3/60. Examination revealed quiet anterior chamber, and anterior vitreous but left relative afferent pupillary defect persisted. Fundus examination revealed marked resolution of optic nerve edema with resolving haemorrhage and subretinal fluid. He was advised to continue tapering oral steroid under ATT cover [].\nTwo months after the initial presentation, the patient was seen again and BCVA had improved to 6/24. Examination of the anterior segment of the left eye was unremarkable and no relative afferent pupillary defect noted. Fundus examined revealed resolved optic disc edema and resorption of subretinal fluid with hard exudates and few retinal pigment epithelium alterations in macula []. Visual field of the left eye by 24–2 Humphrey automated perimetry showed nasal peripheral and superotemporal defects. Colour vision with Ishihara chart was 21/21 in the right eye and in the left eye it improved to 20/21. He was advised to continue ATT and oral steroid in low maintenance dose. The patient is under follow-up with us for the last eight months and till now he did not develop any recurrence.

A 44-year-old woman was admitted to the hospital for evaluation of pulmonary nodule detected on computed tomography (CT). She had a history of total thyroidectomy for PTC, which was performed 8 years ago. The primary PTC measured 2.4×1.3 cm in dimension with invasion into adjacent muscle and had metastasized to several regional lymph nodes (pT4N1) (). After total thyroidectomy the patient had taken neck and chest CT scan at an interval of one year. The PTC recurred in the cervical lymph node after 2 years of total thyroidectomy. There was no evidence of lung metastasis. A follow-up CT scan taken after postoperative 6 years demonstrated the presence of two nodules in both the lower lobes of lungs. Both the nodules were 0.6 cm in the longest diameter. At the 2 years follow-up CT scan after detection of the pulmonary nodules, there was a slight increase in the size of right lobe nodule from 0.6 to 0.8 cm (). Consequently, the patient underwent wedge resections of both lobes. The resected right lower lobe measured 5.8×3.3 cm in dimension and it contained a small nodule measuring 0.8×0.5 cm in dimension. Microscopically, the main part of the nodule showed typical histologic features of nonmucinous AIS. Single layer of cuboidal cells grew along the thick-ened alveolar walls in a lepidic pattern. There was no stromal or vascular invasion. Within the AIS area, there was a 0.2×0.1 cm sized lesion, which exhibited papillary structures with typical nuclear features of PTC. The papillary carcinoma was composed of enlarged cells with clear nuclei and occasional intranuclear inclusions (). In addition, multiple microscopic foci of metastatic PTC were also observed in the surrounding normal lung tissue. Immunohistochemical staining for thyroid transcription factor-1 (TTF-1) and thyroglobulin was performed on both thyroid and lung tumor. Immunohistochemically, PTC of the thyroid gland was positive for both thyroglobulin and TTF-1. The tumor cells of the AIS of the lung showed immunoreactivity for TTF-1 antibody but were negative for thyroglobulin. The tumor cells in the papillary carcinoma in the AIS displayed diffuse positivity for thyroglobulin (). These findings were consistent with AIS involved with metastatic PTC. The nodule in the left lung was identified to be chondroid harmatoma. After 11 months of lung resection, no newly developed lesion was observed in the lung. The patient remains still alive.

A 42-year-old White female sought treatment at the Maxillofacial Trauma Clinic of the Hospital de Pronto Socorro de Maceió – Alagoas (AL – Brazil), complaining of a 10-day history of difficulty in opening her mouth, which prevented her from eating, as well as pus in her mouth, fever, and headache. The patient reported that her third left inferior molar (tooth 38) had been extracted 13 days earlier. The initial clinical examination revealed severe trismus, limited side-to-side head movement, intense halitosis, as well as a large quantity of purulent secretion, accompanied by volumetric changes and skin redness of the lower third of the face, neck, and of the upper thorax ( and ). The patient said that she was using antibiotics (amoxicillin at admission, and that she had also previously used azithromycin and metronidazole, for less than 3 days in both cases. An emergency CT scan showed disseminated infection, originating in the left submandibular space and extending from the pretracheal fascia space to the mediastinum (). On the basis of the clinical and CT findings, the patient was diagnosed with a dental infection that had spread to the neck and mediastinum.\nThe patient underwent surgery (neck incision and drainage) under general anesthesia. During the nasotracheal intubation procedure, the patient aspirated pus from the oral cavity, progressing to asphyxiation, necessitating emergency tracheostomy, hampered by the large amount of pus in the cervical region. Drainage was performed by cervical bilateral extension of the incision to tracheostomy. The patient was admitted to the ICU and was treated intravenously for nine days with ceftriaxone (1 g every 12 hours), metronidazole (500 mg every 8 hours) and gentamicin (80 mg every 8 hours). After discharge from the ICU, the patient was hospitalized for two days in the infirmary until the removal of the tracheostomy tube, after which she was discharged to outpatient follow-up. 
Fifty-four days later, the patient underwent repair of the tracheal fistula () and was discharged on post-procedure day 7.

A 74-year-old man was admitted to the cardiology department of our institution with a history of chest pain and dyspnea on exertion. His functional capacity was class II according to the New York Heart Association (NYHA) classification. He had a history of stent implantation in the proximal left anterior descending coronary artery (LAD) two years ago, in another facility. Physical examination was unremarkable except for the hypotension (90/50 mmHg) and bradycardia (57 beats per minute). A chest X-ray revealed moderate cardiomegaly. The patient's complete blood count, biochemical analyses, and the coagulation tests were normal. An electrocardiogram (ECG) showed sinus rhythm and nonspecific ST-T segment changes. Transthoracic echocardiography images revealed hyperdynamic left ventricular systolic function, grade I diastolic dysfunction, left ventricular regional wall motion abnormality (mild anterior wall hypokinesia), and mild tricuspid and mitral regurgitation. In order to investigate the etiology of the chest pain, dobutamine stress echocardiography was performed, revealing worsening hypokinesia of the anterior wall. Due to positive dobutamine stress echocardiography and recurring angina, coronary angiography was performed. It revealed nonsignificant atherosclerotic plaques in the circumflex artery and the right coronary artery, a patent stent in the proximal LAD, and myocardial bridges causing severe compression and near complete occlusion of the middle and distal LAD during systole, with pulsatile contrast hanging or a “milking effect.” Despite medical therapy with acetylsalicylic acid, a β-blocker, and a calcium antagonist, the patient continued to experience dyspnea and chest pain during exercise; therefore PCI for the treatment of the bridged segments in the LAD was planned. After administration of a 600 mg loading dose of clopidogrel and an intravenous bolus of 10.000 units heparin, left main coronary artery was cannulated with a 7F JL4 guiding catheter and a 0.014′′ floppy guide wire was advanced. The middle segment of the LAD which was almost totally compressed by the myocardial bridge was stented using a 2.75 × 18 mm drug eluting stent (DES) deployed at 16 atmospheres. There was no residual stenosis, dissection, or evidence of compression by the myocardial bridge at the end of this procedure. During stenting of the bridged segment in the distal portion of the LAD with a 2.75 × 14 mm DES at 18 atmospheres, CP occurred and angiographic images showed massive and pulsatile extravasation from the LAD into the pericardial space (). An immediate drop in blood pressure and heart rate was noted, and the patient complained of severe chest pain. Bigeminal ventricular premature complexes and slight ST segment depression in the anterior precordial leads were noted on the ECG. A stent-graft 19 mm in length connected with a 3 mm balloon was implanted immediately in the site of the rupture, with subsequent complete restitution of blood flow in the LAD and termination of extravasation into the pericardial space. The chest pain abated and the ECG was normalized. Protamine sulfate (50 mg) was administered intravenously to reverse the effect of heparin after intervention. Ibuprofen (800 mg 1 × 2 p.o.) was prescribed as an analgesic and anti-inflammatory medication. Transthoracic echocardiography in the catheter laboratory and one day after the PCI procedure showed minimal intrapericardial fluid but no progression was observed. The patient was followed up for 2 days in the coronary care unit and was discharged from the hospital 1 week later. At the follow-up visits at 30 days and 2 months, the patient's NYHA class was improved and chest pain was alleviated. The patient is currently on follow-up with medical treatment for 4 months and long-term dual antiplatelet therapy for at least 1 year has been planned.

A 58-year-old female patient visited a private dental facility in Kuala Lumpur for replacement of missing teeth and other prosthodontic treatment. Medical history of the patient revealed that the patient was unremarkable. Patient had her teeth extracted because of caries. An extraoral examination of the head and neck region showed no obvious abnormalities. Intraoral examination revealed a few missing teeth and retained root in the maxilla, and quite a few prosthodontic procedures were done in the mandible. Patient was interested to have dental implants done to replace the missing teeth. A dental panoramic image was taken for radiographic investigation. The Pax-i Digital Panoramic Unit (Vatech Imaging Systems, Korea) with the following parameters were used: tube voltage: 74 kVp, tube current: 10 mA, and scan time: 13 secs. The image revealed generalized bone loss and innumerable unusual multiple thread-like radioopacities over a wide area. These fragments were observed located bilaterally over the lower border of the orbits and middle and lower facial soft tissues. Radioopacities were very thin and tortuous and have short fragments.\nPatient was enquired about whether she had undergone any kind of surgery before on her face. The patient revealed she had undergone “gold thread therapy” for facial “rejuvenation” (on multiple occasions) during the last 10 years. She mentioned that during the face-lift procedure, very thin needle with the gold thread was inserted under her skin, forming a mesh beneath it. The entire procedure was done under local anaesthesia and took 30 minutes to 1 hour. She also mentioned that she was very satisfied with the results of the procedure. These gold threads were inserted by a foreign medical doctor. The doctor carried his own instruments and visited households where patrons needed this service. All treatment is considered private and confidential and was also illegal as the doctor is not registered with the Malaysian Medical Council. The patient ordered for the service through a cosmetic agent, and procedures were performed whenever the doctor was visiting Malaysia.\nThe patient is a grandma with children and grandchildren; however, she still looks like a youthful middle-aged woman with firm facial muscles. She appeared to be confident and had high self-esteem. She admitted she has got addicted with the procedure and is very satisfied with it. She did not seem mindful if the doctor is not registered with the national medical council nor his procedure is considered an illegal practice.

An 89-year-old male complaining of epigastric pain underwent upper gastrointestinal endoscopy. A shallow depressed lesion with redness was observed at the anterior wall of the upper gastric body, and IIc-type early gastric cancer was diagnosed. Biopsy revealed differentiated adenocarcinoma. There was no abnormality in laboratory data. Due to severe heart complications (pacemaker implanted), surgical resection of gastric cancer was not feasible. The ASA physical status classification system gave category 3. Due to his old age and complications, he and his family hoped for a periodic follow-up without intensive treatment. Endoscopic treatment was recommended, but was rejected by him and his family. Endoscopy was carried out every 6 months to 1 year as a follow-up.\nPacemaker implant for arrhythmia at 85 years old.\nNo abnormality other than mild anemia.\nIn 1999, at 89 years old, he complained of mild epigastric pain at the clinic visit, but there was no physical finding. Abdominal ultrasonography and abdominal computed tomography revealed liver cysts but no swollen lymph nodes. Due to severe heart disease, it was decided that he was unable to undergo surgery, and he had been followed up periodically since then. Laboratory data showed no abnormality.\nIn 1999, CA19-9 and CEA showed normal values of 3.2 and 9.19, respectively, but CA19-9 was slightly elevated since 2005 and it was 376.3 in 2007. He was confirmed dead due to heart failure in December 2007 at 97 years old.\nBetween 1999 and 2002, a shallow depressed lesion 2 cm in size was confirmed at the anterior wall of the upper gastric body. Invasion depth M was suspected. The morphology of the IIc lesion found in 1999 had remained constant until 2002. The lesion was a little smaller than 20 mm in size (Fig. a).\nFurthermore, 3 years later, endoscopy showed irregularity on the depressed surface with elevated boundaries, which suggested submucosal invasion (Fig. b).\nIn 2004, the ulcer area enlarged and elevated boundaries appeared. Invasion depth SM2 was suspected (Fig. c) []. Despite the elevated boundaries, the size of the tumor remained constant and a little larger than 20 mm.\nIn 2005, the ulcer became deeper and the boundaries were even higher. Invasion depth MP was suspected (Fig. d). The lesion slightly enlarged to 25 mm. In 2006, the size of the lesion and the ulcer area enlarged. Invasion depth MP–SS was suspected (Fig. e). The size increased to 40 mm. In 2007, the ulcer area and elevated boundaries enlarged even more. Invasion depth SS–SE was suspected (Fig. f). The size was about 60 mm.\nA biopsy specimen showed well to moderately differentiated adenocarcinoma in 2002 (Fig. a, b).\nImages exhibiting early cancer were observed between 1999 and 2002 and thereafter the ulcer was deeper with heightened boundaries, which suggested the tendency of deeper invasion. Morphological change after submucosal invasion was striking. Eventually, no metastasis was found by imaging examinations but an increase in CA19-9 suggested lymph node metastasis. However, gastric cancer did not become the direct cause of death.

A 59-year-old male with end-stage renal disease due to nephrosclerosis was evaluated for a living unrelated kidney transplantation. A first kidney transplantation had been performed in 1993 (HLA of the first donor ) and the kidney had functioned for 10 years. Graft failure was caused by chronic vascular rejection. The nonfunctioning kidney was removed shortly after its failure and the patient was treated again with hemodialysis. Blood group of the recipient was 0+, HLA type is shown in , and the most recent PRA level was 34%. The past medical history included hypertension, coronary heart disease, deep venous thrombosis, prolonged reversible ischemic neurologic deficit, and a central venous thrombosis of the right eye. Currently the patient was under anticoagulation with phenprocoumon. Pretransplant evaluation included negative studies for hepatitis B surface antigen, hepatitis B surface antibody, HIV antibody, hepatitis C antibody, CMV IgG, and CMV IgM. Induction and immunosuppression were started before surgery with basiliximab, tacrolimus, mycophenolate-mofetil, and prednisone. The patient received a living unrelated kidney graft from his wife. Pretransplant T lymphocyte crossmatch was negative, whereas the B-cell crossmatch was positive.\nA 53-year-old nonrelative female, blood type 0+, HLA shown in . There was no medical history or regular medication. Both kidneys had a normal anatomy with each a single artery and vein (). The creatinine clearance calculated by Cockroft and Gault was 80 mL/h. Since the left kidney had a partial function of 47% it was chosen for donation. Nephrectomy was uneventful. Perfusion was performed with HTK-solution and did not present any abnormalities.\nAfter a cold ischemia time of 143 min the transplantation was performed on the left iliac axis with vascular anastomosis between the renal artery and the common iliac artery and renal vein and external iliac vein. Bladder anastomosis was performed in a modified Lich-Gregoir technique. Immediately after restoration of blood flow urine production was observed. The kidney had a normal aspect with a good turgor. The transplantation was uneventful. During the first three hours following the surgery urine production continued with a volume of about 150 mL per hour. Then urine production suddenly decreased. General symptoms did not occur and the patient remained cardiorespiratory stable. An immediately performed duplex scan revealed a normal perfusion of the renal artery and vein, but there were signs of acute renal failure present (). Differential diagnostic included acute humoral rejection, acute tubular necrosis, and a thromboembolic event. During relaparotomy the transplanted kidney impressed edematous, flaccid, and cyanotic (). It had to be removed and the patient continued with hemodialysis. The postoperatively repeated T- and B-cell crossmatch resulted negative.\nIn the histologic examination of the explanted kidney there was no hint for thromboembolic events of larger vessels. However capillary lumina were partially occluded by erythrocytes, granulocytes, and thrombocytes and adherent leucocytes near to or in the subendothelial surface were present. Fluorescent study did not show any immunoglobulin or complement, while there was a diffuse attachment of C4d along the peritubular capillaries ().\nIn summary histologic examination of the graft was consistent with a hyperacute rejection.

A 15-year-old boy came to the department of radiodiagnosis at our institute with the requisition for computed tomography (CT). The patient had history of lower abdominal swelling for the past one year, associated with a dull dragging pain. He had no history of fever or trauma. Ultrasound examination, performed elsewhere, showed a large cystic anechoic lesion in lower abdominal cavity suggesting mesenteric cyst.\nOn clinical examination, there was a mildly tender, soft lump in the right iliac fossa and hypogastric region measuring approximately 3 × 3 cm in size. There was no associated rise of local temperature.\nMultislice contrast-enhanced CT scan was done on Philips Brilliance TMCT scanner. A large cystic lesion of thin fluid attenuation was seen in right iliac fossa and lumbar region extending up to the umbilical region (Figures and ). The lesion was extending into the right scrotal sac through the inguinal canal suggesting an abdominoscrotal hydrocele. Undescended right testis was seen, located within the inguinal canal in the region of superficial inguinal ring. A small hydrocele was also noted on the left side.\nOn further observation, duodenum and superior mesenteric vein (SMV) were seen wrapping around axis of superior mesenteric artery(SMA) in clockwise direction producing the characteristic whirl-like appearance ().\nNo obvious intestinal obstruction could be established. Furthermore, the jejunal loops were seen on right side of the abdominal cavity with reversal of the normal anatomic relation of the SMAand SMV that is; SMV was seen on left side while SMA on right side ().\nUltrasound examination was repeated for the status of undescended testis. A large anechoic cystic lesion, measuring approximately 6 × 3 × 4 cm in size, in right iliac fossa extending inferiorly into right scrotum through the inguinal canal (). Right testis was located within the inguinal canal. It was normal in size and echotexure with no evidence of neoplastic change.\nOn colour doppler examination, reversal of normal anatomic relation of SMV and SMA was seen (see Video 1 in Supplementary Materials available online at doi:10.1155/2012/354514). SMV and mesentery were seen twisting around SMA in clockwise direction producing the “Whirl pool” sign (see Video 2 in Supplementary Materials). Dilatation of SMV was also noted.\nThe patient was referred for surgery to the paediatric surgery department.

M.J. is a 59 year old woman who presented to the emergency room at a tertiary care center with a three day history of mental status changes. According to her accompanying spouse, three days prior she had eaten out and had one episode of diarrhea. Since then she had slowly become increasingly 'confused', as she described it. She had trouble finding the right words and had been using incorrect words in sentences. M.J. seemed untroubled by this change. These symptoms were accompanied by mild anorexia.\nM.J. had a no significant previous medical history. She had no recent illnesses. She had experienced two vaginal births, and in true family medicine fashion, one of the medical team taking care of the patient had delivered her grandson about one year ago.\nThe patient emigrated from Germany thirty years ago, and English was her second language. She resided in a medium-sized northern New England town with her husband. She operated a daycare out of her home, with approximately five pre-school aged children, none of whom had recently had any serious illnesses.\nOn initial presentation to the Emergency Department, M.J. had no elevation in temperature. She had a mild frontal headache. Her vital signs were otherwise within normal limits. Her physical exam showed her to be alert and oriented, but with mild dysnomia on questioning. She did not have meningeal signs, but appeared mildly dehydrated. An initial computed tomography scan of the head (with and without contrast) was unremarkable for mass or bleed. However, it showed a moderate left-sided sphenoid sinusitis. Her leukocyte count, electrolytes, liver transaminases, folate, B12 and thyroid stimulating hormone were within normal limits.\nShe was admitted with intravenous fluids and intravenous ceftriaxone as empiric antibiotic coverage. An otolaryngology consult was obtained to determine whether the mental status changes could be attributed to the sinus findings. Throughout the next day, the patient became increasingly aphasic. Magnetic resonance imaging (MRI) of the brain was ordered and a lumbar puncture was performed. The fluid showed a leukocyte count of 75 and an erythrocyte count of 5, with a lymphocytic predominance (75%). The MRI showed left temporal lobe enhancement. The cerebrospinal fluid (CSF) was sent for polymerase chain reaction (PCR) analysis, as well as for viral cultures. While this was pending, the patient was empirically started on intravenous acyclovir for presumed herpes encephalitis.\nThe patient required transfer to the intensive care unit soon thereafter for airway protection, where she continued her antiviral medication. PCR testing of the spinal fluid confirmed the presence of Herpes simplex virus type 1 (HSV-1). M.J. spent three weeks in acute rehabilitation after her hospitalization. She was treated with intravenous acyclovir for four weeks and oral valacyclovir for an additional three weeks. M.J. has required longer term speech therapy; however, she has returned to fully independent living.\nIn our patient's case, the diagnosis of HSV encephalitis was first raised by the cerebrospinal fluid findings, strongly indicated by the information added by the MRI, and confirmed by the PCR testing. HSV encephalitis is an uncommon illness, with about 2 cases per 250,000 per year [,]. Most are caused by HSV-1, with 10% having HSV-2 as the etiologic factor. An MRI is abnormal in the majority of PCR-positive cases []. PCR itself has a reported sensitivity of 98% and a specificity of 94% for the detection of HSV in the CSF []. In general, the treatment for HSV encephalitis is to initially treat with intravenous acyclovir for 21 days [,], with a further period of oral antiviral medication as clinically indicated. Untreated, this particular encephalitis has a high case-fatality rate, of around 70% []. Even if it is treated in a timely fashion, the prognosis is only fair: approximately 40–50% would be expected to make full neurological recovery [,].

A 52-year-old female from a remote village in southern India, who is a known case of uncontrolled type 2 diabetes and hypothyroidism for the past 5 years, presented with a 1-year history of pain over her left shoulder and 2 months of increasing swelling of the same shoulder after a trivial fall. She had undergone an arthroscopic rotator cuff repair for the same side in 2019, with metal and bioabsorbable suture anchors from elsewhere. After the surgery, she was doing well with her shoulder, except for the occasional pain, that aggravated to the present status in 2 years. Owing to the COVID-19 pandemic, she did not have regular post-operative follow-ups. In March 2021, she had a trivial fall over the same shoulder, and since then, she noticed an increasing swelling around the same shoulder, which grew from the size of a lemon to a half-cut watermelon spanning in between her neck and affected shoulder ().\nOwing to the raging COVID situations in India, she could not attend a specialist hospital and took treatment at a local bonesetter with herbal massages until she presented here. She also had a few courses of broad-spectrum antibiotics from local hospitals with no resolution of her symptoms. The swelling looked fiery red at the time of presentation and had a local rise in temperature, and her shoulder movements were painful. There was no distal neurovascular deficit. There was no history of fever, chills or rigour, loss of weight or loss of appetite, or evening rise of temperature, or involvement of any other joints. There was no past or contact history of Tuberculosis (TB) nor any history of recent COVID infection. The pre-operative evaluation revealed normal leukocyte and neutrophil counts but raised C-reactive protein (CRP) – 67.6 and a normal erythrocyte sedimentation rate (ESR) – 06 mm. Her Hba1c was 10 depicting her uncontrolled diabetic status. Her blood culture was negative. An X-ray revealed bony destruction at the lateral end of the clavicle with the metal anchor in situ in the shoulder (). Magnetic resonance imaging (MRI) revealed a large fluid collection with few septations in the subcutaneous tissue in the supraclavicular region communicating to the acromioclavicular (AC) joint, which was widened and eroded. Moderate glenohumeral joint effusion extending into the subacromial and subdeltoid spaces were also reported suggestive of corresponding bursitis (). Our differential diagnosis where pyogenic/tubercular/fungal septic arthritis, which are the usual afflictions.\nThe patient underwent swelling excision in toto and debridement of the left acromioclavicular and shoulder joint (, , and ). Surprisingly the whole sac of swelling was traced from the subcutaneous plane through the AC joint to the subacromial and subdeltoid bursae up to the humeral head entry site for the metal anchor. Around 500 mL of straw yellow pus was drained out of the excised sac and from the shoulder joint (). The deep-seated metal anchor in the humeral head was surrounded by a nidus of osteomyelitis sequestrum, which was debrided and retrieved along with the metal and bio absorbable anchors ().\nMultiple specimens of infected tissue and pus were sent for histopathology, aerobic and anaerobic bacterial cultures, acid-fast bacteria (AFB), gram staining, TB GeneXpert, and Fungal DNA-PCR. The bacterial and tubercular reports were all negative and eventually, the fungal DNA detection by PCR was positive for Debaryomyces subglobosus, an extremely rare fungi to infect the shoulder joint, even in immunocompromised patients. HPE was consistent with chronic granulomatous infection ( and ). The patient was started on Voriconazole [], the specific anti-fungal for the same and got a complete resolution of her symptoms within 6 weeks of initiation of treatment. The serum markers for infection, CRP and ESR, returned to normal within this period, and her surgical wound healed completely.\nHowever, her functional recovery was lagging behind, even at two months follow-up, owing to the chronicity of the infection and the residual damages it has already made to the rotator cuff muscles and the joint.

A 60-year-old man underwent right apical and posterior segmentectomies via VATS for early-stage lung cancer. The bronchus and pulmonary parenchyma were divided by endoscopic staples (Echelon®; Ethicon Endo-Surgery). The resected tumour was 1.5 cm in the longest diameter and pathologically diagnosed as Stage IA adenocarcinoma. The patient was discharged uneventfully on eighth day after surgery. Chest radiography revealed no significant findings, and laboratory data were within the normal ranges on the 14th day after discharge at a scheduled visit to the outpatient clinic. However, the patient was transported by ambulance to our hospital owing to a sudden onset of chest pain and dyspnoea on the 32nd day after discharge. He developed hypotension and tachycardia with systolic blood pressure of 50 mmHg and heart rate of 114 beats/min. The haemoglobin concentration level, which had been 12.3 mg/dl on the 14th day after discharge, decreased by 8.7 mg/dl. Chest radiography revealed a massive right pleural fluid, and enhanced computed tomography (CT) showed an extravasation of contrast media near the fifth thoracic vertebra (). The patient was diagnosed with haemothorax and an emergency operation was performed. Thoracoscopic examination revealed massive blood coagulation in the right thoracic cavity, with no adhesions. After removal of the coagulation, continuous active bleeding from the intercostal artery was found near the fifth thoracic vertebra in the vicinity of a stump of the bronchus divided by a staple (). A thoracotomy through the fifth intercostal space was therefore performed to achieve haemostasis, and the bleeding was stopped by suturing using a 4–0 nonabsorbable monofilament ligature. In addition, the bleeding point was covered with a collagen-fibrin patch (Tachosil®). The posterior part of the staple line of the lung parenchyma adjacent to the bleeding point under full inflation was partly exposed, whereas the bronchial stump was covered with lung. Therefore, the scratching created by the staples was assumed to cause haemothorax. The total amount of haematoma in the right thoracic cavity and the intraoperative blood loss was 3980 g. Postoperative CT confirmed that the stapler dividing the lung parenchyma directly faced the bleeding point beside the fifth vertebra (). The patient progressed satisfactorily after the reoperation and was discharged on ninth day after reoperation.

A 48-year-old white female patient was admitted for workup of chronic pericardial effusion, which was first detected during an episode of pneumonia 3 months earlier, but remained constant despite complete remission of pneumonia after antibiotic treatment. At the time of admission, the patient was in a stable haemodynamic condition, but suffered from progressive dyspnoea on exertion (New York Heart Association Class III).\nLung auscultation on admission revealed diminished breath sounds and dull percussion sounds of the basal right lung. The rest of the physical examination, especially cardiac auscultation was inconspicuous with a regular rate and rhythm, normal heart sounds, and no murmurs. Initial vital parameters and laboratory testing were also normal. Bedside echocardiography demonstrated a large pericardial effusion up to 35 mm with ‘swinging heart’ phenomenon (Figure ). Left and right ventricular systolic function as well as valvular function was normal. End-diastolic collapse of the right atrium and increased respiratory variation of mitral and tricuspid valve flow velocities have been noticed as indicators of a beginning haemodynamic relevance of the pericardial effusion, but diastolic right ventricle relaxation and vital parameters were not compromised. Because of the chronic setting of the large symptomatic pericardial effusion, pericardiocentesis was performed demonstrating a serous pericardial effusion with low cell count and no evidence of purulence or malignity. Besides the known pericardial effusion, computed tomography (CT) revealed an unclear mass in the pericardial space (Figure ). The mass was attached to the anterior wall of the left ventricle, measuring 20 × 22 × 8 mm, and demonstrated pronounced peripheral uptake of contrast media. For additional non-invasive tissue characterization cardiac magnetic resonance imaging (CMR) was performed using a 1.5-T Magnetom Aera (Siemens Medical System). Cine MR images confirmed residual, partially organized pericardial effusion without haemodynamic relevance, as well as the previously described mass (Figure and , Files S1–S3), demonstrating isointense signal on T1- and hyperintense signal on T2-weighted images (Figure ). Most common entities of tumours in this location are pericardial cysts and lipomas, which both could be ruled out by T1- and T2-weighted MR images, fat saturation, and perfusion studies (Figure ). After administration of gadolinium contrast, CMR first-pass perfusion depicted peripheral perfusion of the mass, suggesting a hypervascular tumour (Figure and , File S4). Late gadolinium enhancement showed intense inhomogeneous signal after 5 min indicating slow blood flow (Figure ). In regards to the marked arterial perfusion of the mass as well as its proximity to the left anterior descending artery (LAD) and its diagonal branches, coronary angiography was performed. Contrast injection led to a ‘tumour blush’, emphasizing the vascular characteristic of the tumour, and revealed feeding arteries from the LAD (Figure ).\nWith the diagnosis of chronic pericardial effusion, as well as an unclear hypervascular and hyperperfused tumour with peripheral contrast uptake on CT and CMR located within the pericardial space in close proximity to the LAD, a decision for open surgical exploration via anterolateral thoracotomy was made by our Heart Team. Intra-operative frozen section was indicative for a benign vascular tumour, most likely a haemangioma. Consequently, the tumour was removed completely and specimens were further evaluated. Histological workup revealed numerous, capillary-type small vessels within a fibro-oedematous background. Staining for CD31 and ETS-related gene (ERG) expression were positive, highlighting endothelial cells. Proliferation rate of less than 5% was assessed using Ki67-staining. Thus, the differential diagnosis of a malignant neoplasm including metastasis, which is much more common than primary pericardial tumours, could be excluded and the final diagnosis of a capillary-type haemangioma of the pericardium was made. After surgery, the patient rapidly improved and at follow-up 6 months after the initial presentation neither the tumour nor the pericardial effusion recurred.

An 82-year-old Caucasian man was admitted to our urology department for radical cystoprostatectomy because of prostate cancer.\nDuring the night of the fourth day post-surgery the patient suddenly developed painless severe tetraparesis (Medical Research Council grade 2/5 of proximal muscles on both arms and 0/5 of both legs) without involvement of cranial nerves or impaired consciousness. There were no signs of sensory deficits. He did not present with any cerebellar symptoms. Further clinical examination revealed brisk tendon reflexes and positive pyramidal signs on both sides. The clinical presentation was highly suggestive for spinal cord affection, for example by abrupt compression, subdural bleeding or ischemia. There was no trauma or fall shortly before the onset of the neurological deficits. For analgesic treatment, a peridural catheter had been implanted after surgery which had been removed without any complications the day before.\nFor an emergency magnetic resonance imaging (MRI) diagnostic, metal brackets in the subcutaneous tissue placed after surgery had to be removed at night. Surprisingly, spinal MRI did not reveal spinal cord compression or signs pointing towards spinal cord ischemia (Figure \nA). By contrast, cranial MRI imaging showed bilateral acute infarctions in the median precentral gyrus (Figure \nB and C; arrows), whereas the internal capsule was unaffected on both sides (Figure \nD). The T2-weighted images at the level of primary motor cortex did not yet present with abnormal signal, thus confirming acute ischemia consistent with the time course of symptom occurrence (Figure \nE). The precentral area of the primary motor cortex is supplied by the anterior cerebral artery (medial one third of the precentral gyrus) and the middle cerebral artery (lateral two thirds) on either side\n[].\nIn the following days, paresis in both arms resolved but the legs remained paraplegic. Further diagnostic workup including carotid duplex sonography, 24-hour electrocardiogram (ECG) and transesophageal echocardiography failed to identify the underlying cause of stroke. Hypercoaguability due to prostate cancer may have been contributed to cerebral ischemia. Routine coagulation parameters were normal, and more extensive coagulation diagnostics were not performed in the acute phase of the cerebral ischemia. Due to the simultaneous bilateral territorial infarctions in at least two independent vascular territories, the absence of macroangiopathy, and the preceding extensive surgery with narcosis we considered a cardiac embolic origin. Therefore the patient was placed on full anticoagulant dose of low-molecular weight heparin for embolic stroke prophylaxis. Early prophylactic treatment with antiplatelet drugs was not possible according to current guidelines because of extensive surgical intervention four days before stroke onset. In consent with the surgeons, we decided in this case to use low-molecular weight heparin as an early prophylactic treatment. After neurological rehabilitation we started a prophylactic treatment with acetylsalicylic acid because repeated 24-hour ECG could not identify a paroxysmal atrial fibrillation.

An 18-year-old female met with an accident while working on electric laundry machine. Patient was wearing a salwar kameez, with a dupatta hanging loosely around the neck with the two arms of dupatta in the front. While working on the electrically powered laundry machine, the dupatta got caught in the rotating parts of the machine pulling the head towards it causing sudden hyperflexion of spine with anterior movement of pelvis and the femur, the foot remained static with knee abutting against the edge of metal panel causing hyperextension at the knee []. This may have caused bilateral knee dislocation which could have reduced spontaneously resulting in multiligament injury.\nPatient was referred to us after 3 weeks. As per the notes of the private hospital, patient had presented with bleeding through nose and breathlessness with bilateral knee joint swelling and foot drop. There she was intubated for 4 days and bilateral above knee slab applied. She was operated for mandibular fracture with plating 1 week after the accident after which she was referred to us. Plain radiographs, CT scan, and MRI of both knees revealed right knee - schatzker type 4 tibia condyle fracture, lateral collateral ligament (LCL) avulsion fracture from the fibular head and anterior cruciate ligament (ACL) rupture (KD type V) [Figures and ]. The patient was operated on the right knee tibia condyle fracture. Open reduction with intraarticular reduction and buttress plating was done []. The LCL avulsion fracture was found to be united. While the left knee showed LCL avulsion fracture and posterior cruciate ligament (PCL) rupture (KD type III) [Figures and ]. EMG-NCV showed common peroneal nerve involvement. In the subsequent week left knee PCL reconstruction with hamstring tendon grafting was done []. Due to patient refusal, left knee posterior lateral corner (PLC) reconstruction and right knee ACL which was planned in the subsequent week could not be done. The patient has been followed for 18 months, on clinical examination, right knee IKDC score was 60.9, Lysholm score was 64, the left knee IKDC score was 69 and Lysholm score was 69.

A 56-year-old Israeli Jewish woman was admitted to our surgical ward for a splenectomy due to a solitary splenic mass. Six years prior to her admission she had undergone a total abdominal hysterectomy with bilateral salpingo-oophorectomy due to carcinoma in the right ovary. The histology examination revealed an endometrioid carcinoma, grade 3. Staging with International Federation of Gynecology and Obstetrics (FIGO) classification was 1A. Following the surgery, our patient received chemotherapy treatment with paclitaxel (Taxol®) and carboplatin.\nTumor marker cancer antigen (CA)-125 was evaluated every year following the operation. Subsequent to a rise in CA-125 from 18.1 to 132.6 units/ml (normal <35 units/ml), our patient was referred for an imaging and an endoscopic assessment.An abdominal computed tomography (CT) scan revealed a mass of 6×8cm at the anterior of the spleen (Figure ), with close proximity to the wall of the stomach. There was no other indication of a secondary tumor spreading in the abdomen. Her chest CT scan was normal. A gastroscopy demonstrated exterior pressure on the stomach body. All the specimens from gastric mucosa that were taken with the gastroscope and that were subjected to histologic testing were normal except a chronic inflammation in the gastroesophageal area. A colonoscopy also showed normal results. A bone isotopic scan revealed no abnormalities.\nOur patient was asymptomatic and her gynecologic and abdominal examinations were without any remarkable findings such as tenderness or splenomegaly.An open laparotomy through a left subcostal incision was performed to exclude a peritoneal carcinomatosis. The laparotomy did not reveal any abdominal pathology except in the spleen. Neither peritoneal washing for cytologic examination nor peritoneal biopsies were taken. A total splenectomy was then performed (Figures and ). No intraoperative evidence of tumoral spreading in the abdominal cavity was observed, other than in the spleen. Our pathologic laboratory received a 550gram spleen, 9×11×17cm in dimensions, with fat tissue adhered to the spleen. Inside the spleen, we observed a tumor consistent with a high-grade metastatic endometrioid carcinoma grade 3 (Figures and ). Inside the adherent fat tissue, we observed another tumor with a diameter of 5cm, with the same characteristics as the splenic tumor.\nThe postoperative period was uneventful. Our patient was discharged from our ward a few days post surgery and was examined again two weeks later in our clinic, without any signs of operation-induced complications such as intra-abdominal bleeding, intra-abdominal infection or surgical site infection. CA-125 levels dropped to 33.3 unit/ml. The patient returned to the gyneco-oncologic clinic, and received another course of chemotherapy, again with paclitaxel (Taxol®) and carboplatin.

A 48-year-old, gravida 1, para 0 female was referred to the University of Minnesota Maternal-Fetal Medicine Center due to vaginal bleeding and uterine fibroids. Ultrasound findings revealed a viable gestation at 14 + 1 weeks' and an adjacent thickened, nonhomogeneous placenta with a diffuse multicystic appearance (see ). The adjacent placental mass was consistent with a coexisting molar gestation, and it was noted to be overlying the cervix. In addition, there were multiple intramural uterine myomas visualized, the largest of which measured 10.3 cm × 9.3 cm × 7.3 cm and 7.0 cm × 7.1 cm × 6.2 cm. A serum quantitative hCG was 290,000 iu/L. The patient reported persistent vaginal bleeding starting early in the first trimester, not associated with cramping. Given the diagnosis of a presumed molar gestation, the patient was counseled on the risks of continuing the pregnancy. An amniocentesis was performed at 16 weeks' gestation which returned as a normal 46, XY karyotype. Amniotic fluid AFP was 1.38 multiples of the median. After identifying a viable fetus, the parents opted to continue the pregnancy. Further evaluation included normal thyroid function tests, and in agreement with the patient, we proceeded with imaging studies, as the presence of any metastases may have resulted in her decision to terminate the pregnancy. MRI of the brain, abdomen, and pelvis were negative for evidence of metastatic choriocarcinoma, and the molar pregnancy measured 7.0 cm × 8.3 cm × 6.9 cm. We thoroughly reviewed the extremely low teratogenic and stochastic risks of radiation from a chest CT (<1 rad) prior to obtaining a pulmonary CT scan that revealed small incidental nodules not concerning for metastases.\nAt 17 weeks, the patient was admitted to the hospital for observation due to an increase in vaginal bleeding. Her hemoglobin was stable at 11.6 g/dL, and the remainder of her laboratory analysis was reassuring. She was discharged to home on modified bedrest.\nA comprehensive ultrasound exam at 18 weeks' gestation demonstrated a normal live male fetus without evidence of anomalies. The coexisting molar pregnancy was confirmed to be covering the internal cervical os as a complete placenta previa. A repeat quantitative hCG was 208,900 iu/L.\nAt 20 weeks, the patient again presented to the hospital with a marked increase in vaginal bleeding and passage of large clots. Her labs remained stable with a hemoglobin of 11.0 g/dL, and her hCG had decreased to 159,690 iu/L. The decision was made to hospitalize the patient for the remainder of her pregnancy due to the persistent vaginal bleeding in a complete previa molar pregnancy. Her antenatal care included the maintenance of a current type and screen, monitoring hemoglobin levels, and serial hCG levels. The patient continued to have intermittent spotting throughout the duration of her pregnancy, but her hemoglobin remained in the normal range. Her hCG level declined progressively to a level of 44,506 at 32 weeks' gestation. Successive ultrasound examinations confirmed appropriate fetal growth, amniotic fluid, and umbilical artery doppler studies. The molar pregnancy remained a complete previa, and measured 10 cm × 16 cm × 8 cm at her 30 week ultrasound exam. The patient also met with the gynecologic oncology service, who counseled her on the risk for persistent gestational trophoblastic disease, and established a plan for repeat imaging should the hCG levels plateau or increase.\nHer pregnancy was further complicated by gestational diabetes requiring glyburide as well as mild preeclampsia which she developed at 28 weeks' gestation. Her blood glucose levels and blood pressures were followed closely, and serial HELLP labs were within normal limits. She did not develop symptoms associated with severe preeclampsia. She received betamethasone injections at 23 weeks followed by a rescue course at 28 weeks. Antenatal testing included twice weekly biophysical profiles initiated at 32 weeks and twice daily nonstress tests since admission. We did not initiate prophylactic anticoagulation during her prolonged hospitalization as this is not standard policy in our institution; in addition we thought it not wise in light of her persistent bleeding and risk of hemorrhage.\nA comprehensive delivery plan was established and discussed with the parents. A decision was made to proceed with planned cesarean section at 34 weeks' gestation. In view of the concern for excessive bleeding secondary to the presence of multiple uterine fibroids and the molar pregnancy presenting as a complete previa, prophylactic control of local vascular flow was established by placing bilateral internal iliac artery balloon catheters, performed by interventional radiology (IR). Additionally, bilateral ureteral stents were placed prior to initiating the procedure. Both procedures were performed in the operating room under spinal anesthesia; urology placed stents via cystoscopy and IR gained access to the common femoral arteries under direct ultrasound visualization, followed by placement of a 7 French vascular sheath guided over the aortic arch to the internal iliac arteries using fluoroscopy. A 14 mm × 2 cm balloon was then inserted on each side. Balloon inflation to 2 atmospheres demonstrated appropriate arterial occlusion.\nGeneral anesthesia was then administered and a classical cesarean section was performed via vertical skin incision. A viable male infant was delivered with a weight of 2310 g and apgars of 7 and 9 at 1 and 5 minutes, respectively. The placenta of the live fetus was extracted easily. The classic hydropic villi of the molar component appeared to be degenerating, and were very adherent to the endometrium, clinically consistent with a placenta accreta. At this point there was significant uterine bleeding, thus a cesarean hysterectomy was initated with the molar pregnancy in situ. The internal iliac arterial balloons were inflated and a total hysterectomy was performed without complications. There was minimal bleeding during the hysterectomy, and estimated blood loss was 1000 mL for all procedures combined. Total time of arterial balloon inflation was 30 minutes, as they were deflated following ligation of the uterine arteries. The patient's postoperative course was unremarkable and she was discharged home on postoperative day number 6. Pathological examination of the second twin/placental mass confirmed a molar pregnancy (see ). Given the markedly advanced degeneration of the molar tissue and familiarity with identifying molar tissue as invasive in regards to a neoplastic process only, the pathologist had difficulty confirming an accreta on examination.\nWeekly hCG levels were followed after delivery, and at 6 weeks postpartum, they had reached a plateau. An hCG tumor marker assay remained in the 40s. A computed tomography (CT) scan was obtained and demonstrated no evidence of disease. However, given 4 values of hCG levels at a plateau, it was decided to treat her persistent gestational trophoblastic disease. Work up for metastatic disease including repeat CT imaging at this point was negative. Methotrexate administration was administered at 50 mg/m2, and hCG levels fell to <3 IU/L after 4 weekly injections. Her hCG levels have remained within the normal level, continuing followup for one year.

A 15-year-old male was brought to the emergency department after sustaining a gunshot wound to the head. Non-contrast computed tomography (CT) scan of the head demonstrated a trajectory entering the right inferior temporal bone, entering the anterior portion of the middle cranial fossa, traversing the anterior right temporal lobe, entering the right orbital cavity, and exiting through the ethmoid sinus and ultimately the left orbital cavity. There was a right temporal tip contusion along the ballistics path, with associated extra-axial and subarachnoid hemorrhage (SAH). The Sylvian fissures were not involved in the ballistic trajectory [].\nThe patient was taken emergently to the operating room for a right-sided decompressive craniectomy and debridement of the right temporal region. The patient started to follow commands, was moving in all extremities, and was extubated by hospital day 3. He underwent repair of his ruptured left globe and persisted with complete vision loss in the right eye.\nInitial CT angiogram (CTA) within 24 h of his admission showed no vascular injury; however, a repeat CTA was performed 5 days later for vascular surveillance for TICA, which showed interval development of a right middle cerebral artery (MCA) bifurcation aneurysm. The same scanner produced both CTAs with 420 slices at 0.6 mm thickness, including three dimensional reconstructions. A subsequent diagnostic cerebral angiogram (DCA) confirmed the presence of a 4 × 3 mm right MCA bifurcation aneurysm, and also identified a 2 mm right internal carotid artery (ICA) terminus aneurysm, as well as severe vasospasm of the proximal ICA and MCA vessels [].\nThe patient was taken to surgery for clipping of the right MCA and right ICA terminus TICAs. Direct clipping of the lacerations in the vessels was successful, although bypass was prepared for, depending on the intraoperative findings []. Due to the severe vasospasm, patient was treated with intracisternal papaverine. Sixty milligrams of papaverine diluted in 2cc of saline is injected into the intracisternal space over the affected vessels. Papaverine is a vasodilator which relaxes the smooth muscles of vessels. Adventitial dissection was performed allowing for better penetration of papaverine and removal of any possible sites of constriction.[] The surgical cavity is then irrigated and final hemostasis obtained.\nThe end-tidal CO2 was kept constant and cerebral blood flow (CBF) measurements were then obtained before and after performing the therapeutic maneuvers using the Charbel Micro-Flowprobe® (Transonic). Measurements were taken at the distal ICA just before the ICA terminus as well as the A1 and M1 segment arteries just after the ICA terminus. This instrument relies on transit-time ultrasound volume flowmetry to obtain blood flow measurements in mL/min. The measurements demonstrated improvement in flow after the therapeutic maneuvers [].\nThe patient returned to the intensive care unit. Repeat catheter angiogram was performed on hospital day 10 and confirmed that the two previously treated aneurysms were excluded from the circulation. Previously-identified vasospasm of the right supraclinoid ICA, M1, and A1 segments was improved. Two-month follow-up DCA demonstrated substantial improvement in the distal ICA caliber and improvement in the M1 irregularity. Several distal dilated vessels in the anterior temporal region were identified as suspicious for pseudoaneurysms, but have largely resolved on the 2-month catheter angiogram. Two weeks after the initial presentation, the patient was neurologically intact, with the exception of bilateral blindness related to the ballistics path, and was discharged to inpatient rehabilitation center.

A 21-year-old man presented to our institution with sudden onset pain in the left trapezius and shoulder.\nAt the time of symptom onset he was engaged at work driving heavy machinery, but denied any recent history of injury or trauma. He had not been recently unwell and denied any constitutional symptoms such as weight loss or fever. Over the following five hours his pain began to also affect his right shoulder and there was associated generalised abdominal pain of increasing severity, most marked in the left and right upper quadrants.\nThe patient had no significant past medical history, specifically never having had an episode of pancreatitis before. He was not taking any regular prescription medications but upon closer questioning admitted to occasional recreational cocaine use, the most recent ingestion of which was within 24 h of hospital admission.\nThe patient had no significant family history of medical illness.\nClinical examination revealed a well-looking man in no obvious distress. Although he was mildly tachypnoeic (20 breaths/min) his other vital signs were normal (heart rate 78 beats/min, blood pressure 129/84 mmHg, temperature 36.9 ºC and oxygen saturations 99% on room air). His abdomen was not distended but there was generalised percussion tenderness most profound in the left and right upper quadrants. Examination of his shoulders revealed no focal tenderness and full active and passive ranges of motion with preserved motor and sensory function.\nInitial biochemical findings included a haemoglobin of 138 g/L, leucocyte count 4.74 × 109/L, platelets 197 × 109/L and international normalised ratio of 1.1. Plain chest X-ray was unremarkable. Repeat blood tests were performed after five hours due to the increasing severity of his symptoms which revealed a haemoglobin of 99 g/L, indicating a significant decrease from the initial value.\nThe combination of worsening abdominal pain and a falling haemoglobin prompted a computed tomography (CT) scan of his abdomen and pelvis which was conducted with both oral and IV contrast in the portal venous phase. It revealed a large amount of high-density fluid within the abdominal cavity, consistent with haemoperitoneum. Moderate splenomegaly (16.4 cm × 9.9 cm × 7.4 cm) and an overlying Grade 3 subcapsular splenic haematoma[] were also noted (Figure ).\nA repeat CT with IV contrast in the arterial phase (CT angiogram) was then performed to exclude the presence of active arterial bleeding. Although no active extravasation was observed on this study, an incidental splenic artery pseudo-aneurysm measuring 9.1 mm × 8.3 mm × 8.1 mm was discovered near the superolateral aspect of the spleen (Figures and ).\nIn the search for an underlying precipitant, viral serological testing was ordered despite the absence of typical prodromal symptoms. Both IgM and IgG antibodies against EBV viral capsid antigen were detected 24 h later.

A 23-year-old female presented with a six-month history of a progressively growing mass in the right anterior chest wall associated with slight pain. The mass was hard, fixed to the chest wall and moderately tender. It measured 6 × 5 cm in its largest dimensions. The overlying skin was normal. She had no pulmonary symptoms. The acid phosphatase levels was 10.2 IU/L. All other hematological and biochemical investigations were within normal limits.\nPatient underwent fine needle aspiration cytology. Cytological smears were cellular and comprising aggregates of uniform appearing spindled stromal cells and innumerable osteoclast type giant cells, having variable number of nuclei. The nuclei of the stromal cells resembled those observed in the osteoclast type giant cells. The stromal cells showed high nuclear to cytoplasmic ratio, with evenly distributed chromatin and inconspicuous to small nucleoli. No significant nuclear atypia was observed either in the giant cells or the background stromal cells. Mitotic figures were noted frequently []. In correlation with radiographic findings of an eccentric expanded lytic lesion with cortical erosion of anterior arc of fourth rib [], a diagnosis of aggressive giant cell tumor of rib was offered cytologically. In our case, the musculoskeletal radiologist had opined an aneurysmal bone cyst and Askin tumor of anterior chest wall.\nIn view of the cytomorphological diagnosis and radiological cortical destruction of anterior arc of fourth rib, patient was referred to a surgical oncology centre with a possibility of soft tissue extension being also considered. At the higher centre, complete resection of the tumor was performed. The histopathological features suggested aggressive GCT of the anterior arc of rib. The cytomorphological features were in conjunction with that of histomorphological features observed.\nPatient remained asymptomatic without evidence of recurrence at the end of one year following surgical intervention. At the last follow up her acid phosphatase levels had dropped to 6.1 IU/L.

A 66-year-old man with locally advanced pancreatic head adenocarcinoma diagnosed by fine-needle aspiration biopsy 6 mo ago was admitted to our institution. Tumor markers were measured, with CA 19-9 = 4801 IU/mL and CA 125 = 161 IU/mL. After diagnosis, a plastic stent was placed in ductus choledocus with ERCP. Immediately afterwards, chemoradiation was administered to the patients [5 cycles of chemotherapy consisting of Folfox + 5-FU + Oxaliplatin every 14 d, for 28 d RTA (28 fractions 50, 4 gray IMRT received)]. After admission to our hospital, computerized tomography (CT) examination was performed to the patient, and a malignant mass of 45 mm in diameter was observed at the pancreatic head level (Figure ). It was noted that the tumor had surrounded the superior mesenteric artery 360 degrees, the affected segment of SMA was 40 mm. The tumor had apparently reduced the SMA diameter by 3 mm (Figure ). Main pancreatic duct was markedly dilated, and the diameter was measured as approximately 7 mm. There was no metastasis and the tumor was stable after neoadjuvant chemotherapy.\nThe patient was referred to our hospital with a diagnosis of LAPC. Irreversible electroporation for pancreatic tumor and simultaneous gastrojejunostomy was planned. The abdomen was opened with a median incision above the umbilicus and abdominal exploration was performed. During the exploration, no distant metastases were identified anywhere in the abdomen. Intraoperative liver ultrasonography was used to detect possible metastasis to liver. The patient was under general anesthesia, surgery was performed in the supine position. The gastro-colic omentum was opened to reach and expose the pancreatic tumor. Electroporation was performed in accordance with the procedural instructions.\nIRE was performed using the Nanoknife System (Angiodynamics, Lanthan), as described in the previous manuscript on IRE for the pancreas. High definition intraoperative ultrasound imaging was used in all cases, which is required to demonstrate non-traumatic precise needle placement and also for continuous ablation assessment during IRE. In sum, 3 monopolar probes with 2-cm spacing will deliver an electroporation defect of approximately 3.5 cm axial, 2.5 cm anterior-posterior, and 2.5 cm cranial-caudal. This electroporation procedure is achieved through a maximum of 1.5 cm exposure, 1500 V/cm, and 100 s wavelength. The procedure was performed in 45 min. After IRE procedure a gastrojejunostomy completed. After completing gastrojejunostomy anastomosis, a color change was concurrently observed in the small intestine. Based on a suspicion of SMA occlusion, arterial pulse was checked in the small bowel mesentery. No pulse was obtained in this area. The abdomen of the patient was closed, and he was taken to the angiography unit because SMA occlusion developed in the tumor surrounded segment. In angiography images, it was observed that a short segment after the origin of SMA, right hepatic artery was arising. Even after 1 cm distal to right hepatic artery origin there was no blood flow in the SMA (Figure ). First of all, occluded segment was dilated with a 3 mm balloon. After dilatation a 4 mm and 3 cm length metallic stent was placed to this dilated segment (Figure ). There were no complications in the postoperative follow-up. The patient was discharged without any complication the sixth day postoperatively.

A 21-year-old primipara with 32 weeks pregnancy was referred to us from the gynecology department with upper abdominal pain and high-grade fever for 3 days associated with abdominal distension. On examination, the patient had a pulse of 124/minute and her blood pressure was 96/64 mmHg. Mild pallor was noted and there was no icterus, lymphadenopathy or pedal edema. On abdominal examination, the patient had generalized tenderness, guarding, rigidity and rebound tenderness. Bowel sounds were absent. The uterine fundal height corresponded to 32 weeks' gestation. Routine laboratory tests revealed hemoglobin of 12.1 g/dL, total leukocyte count of 14100 cells per mL. The blood sugar, kidney and liver function tests were normal. Abdominal sonography showed a viable fetus of 32 weeks gestation. There was a large collection of fluid in the right side of peritoneal cavity below the liver. Other viscera were normal. Ultrasound guided diagnostic aspiration of the collection revealed frank bile, the presence of which confirmed by biochemical analysis of the fluid. With the presumptive diagnosis of duodenal ulcer perforation peritonitis, the patient was taken up for an exploratory laparotomy. There was an 800 mL collection of bile in the subhepatic and right paracolic space. The stomach and intestines were normal. The gall bladder was distended and a 0.5 × 0.5 cm perforation in the lateral wall of the supraduodenal portion of the CBD was seen. There was no evidence of gall stones. The CBD perforation was closed over a T-tube. The midline incision was closed after inserting a drain in the subhepatic space. The patient went into spontaneous labor 48 hours later and a preterm baby was delivered. Subsequently, on 15th postoperative day, after a normal T-tube cholangiogram (figure ), the T-tube was removed and the patient was discharged the next day. The mother and child are doing well after a follow up period of one year.

A 38-year-old previously healthy African-American female presented with an enlarging inner left cheek mass with overlying ulcer of 2 months duration. A computed tomography scan with contrast demonstrated a large irregularly outlined peripherally enhancing mass located between the anterior margin of the ramus of the left mandible and maxilla protruding outward. An incisional biopsy was performed followed by a wide local excision 3 weeks later. The excision included a composite resection of left buccal mucosa, a left modified radical neck dissection, a left partial maxillectomy, a right anterior thigh flap placement, and a left parotidectomy. A whole-body computed tomography survey demonstrated a 5-mm lingular lung nodule and a 7-mm right hepatic hypodensity. These areas were determined to likely be incidental findings; however, further workup was suggested.\nThe patient had an unremarkable surgical recovery and was discharged from the hospital 1 week later. An incisional biopsy was performed followed by a wide local excision 3 weeks later. She recovered well postoperatively but refused to follow-up chemoradiation therapy.\nSix months later, she presented with altered mental status secondary to hypercalcemia from bony metastases. She was discharged to a hospice facility as per her family's request.\nThe excised specimen displayed a pedunculated, exophytic, ulcerated, dark purple mass, appearing to arise from the buccal mucosa. The mass measured 6.0 cm × 5.4 cm × 2.8 cm in greatest dimensions. The cut surface revealed a light tan interior with scattered areas of hemorrhage and necrosis and an infiltrative margin involving the underlying subcutaneous tissue but sparing the overlying skin and adjacent maxillary segment [].\nHistologic sections of the incisional biopsy specimen revealed a diffuse hypercellular pleomorphic ill-circumscribed lesion with extensive necrosis. The viable areas exhibited slit-like vascular space and micropapillary architectural patterns and focal small cellular nests with features of squamous differentiation. Immunohistochemistry (IHC) displayed positivity for vimentin, p53, AE1/AE3 and CAM 5.2 (focally positive). All tumor cells were negative for desmin and CD34.\nExamination of the excisional specimen revealed similar morphology with more developed pseudovascular cystic areas with stromal eosinophilia [Figures and ]. IHC displayed positivity for AE1/AE3 and lack of E-cadherin and CD34 expression [Figures and ]. Focal areas of conventional SCC architecture were present at radial edges of the tumor.\nMetastatic tumor was present in four of 35 examined left cervical lymph nodes with the largest metastases measuring 1.5 cm and displaying extracapsular extension. The stromal eosinophilia was also present within the metastatic foci.\nThe incisional biopsy and resection specimens were evaluated via standard grossing protocols. Subsequently, sections were fixed with buffered formalin, embedded in paraffin, cut 4 mm thick and stained with H&E.\nIHC stains were performed for CD34, vimentin, CAM 5.2, AE1/AE3, desmin and P53. Before immunostaining, the slides were deparaffinized, hydrated and then incubated with anti-CD34 (Ventana, Tucson, AZ, 10 mg/ml), anti-p53 (Ventana, 3 mg/ml), anti-CAM 5.2 (Cell, Rocklin, California, 32.5 mg/ml) and anti-AE1/AE3 (Ventana, 5 mg/ml). All slides were counterstained with H&E.

A 76-years-old lady with background history of cryptogenic Child's B liver cirrhosis presented with intermittent epigastric pain of 2 weeks duration associated with abdominal distension and nausea. On examination, vital signs were stable but marked pallor was noted in her conjunctiva. Physical examination was remarkable for abdominal distension with mild splenomegaly and ascites. Rectal examination revealed brown stools.\nLaboratory investigations revealed anaemia with haemoglobin of 6.8 g/dl. Liver function tests were unremarkable with the exception of low albumin of 33 g/l and mildly elevated aspartate transaminase of 46 U/l. Coagulation profile was mildly deranged with a prothrombin time of 11.3 s and a normal partial thromboplastin time. She was admitted under the gastroenterology service with the preliminary diagnosis of dyspepsia with anaemia for investigation. Two pints of packed cells were transfused.\nDuring the second day of admission, the patient passed out large amounts of melena and had an episode of haematemesis. She also developed tacchycardia with heart rate increasing to 110–120 b.p.m. Repeat blood investigations showed that haemoglobin had fallen from 6.8 to 5.3 g/dl despite blood transfusion. An emergency oesophagogastroduodenoscopy was performed. Findings were that of grade 1 oesophageal varices with no features of variceal bleed. There was a large clot in the fundus and cardia of the stomach. After attempted removal of the blood clots with flushing, the patient developed torrential bleeding necessitating intubation for airway protection. The bleeding eventually ceased spontaneously and the source of bleeding was identified to be originating from a large ulcer crater in the greater curve with an overlying clot (Fig. ). Endoscopic ultrasound was performed which showed a 10 cm mass lesion abutting the stomach wall and extending into the peritoneal cavity (Fig. ). The preliminary impression was that of a bleeding GI stromal tumour and care was transferred to the surgical team for consideration of surgical intervention.\nA computed tomography scan was performed which showed multifocal HCC with a large exophytic lesion invading into the greater curvature of the stomach (Figs. and ). Peritoneal metastases and ascites were present. The patient underwent an angioembolization of the hepatic tumour on the same evening. Angiography identified a replaced left hepatic artery as the dominant vessel supplying the lesion of concern in the left lateral hepatic segment (Fig. a). Gelfoam embolization was performed with no residual tumour enhancement thereafter (Fig. b).\nThe patient's bleeding ceased after intervention and her haemoglobin levels stabilized. Alpha-foetoprotein level was elevated at >60 500 μg/l. She was eventually discharged and will be reviewed by the medical oncologists for consideration of palliative chemotherapy.

A 29-year-old man with a history of exercise-induced asthma (not requiring treatment for 10 years) and obesity (body mass index 39) presented to the emergency room in respiratory distress with evidence of systemic inflammatory response syndrome. His history was pertinent for heavy e-cigarette use for the previous 2 years. Of note, he admitted that he previously smoked ~1–2 packs of cigarettes and 0.5 g of cannabis per day from ages 19 to 27 but quit both of those when he started vaping. He admitted to owning 12 different vaping pens, 8 of which were used for nicotine and 4 for THC. He used a variety of flavors and estimated that he went through a 30-ml bottle every 7–10 days. He also reported that 5 days prior to the onset of symptoms, he tried a new branded vaping product that contained THC. Two days prior to presentation, he experienced rigors with associated nausea and several episodes of emesis. Despite cessation from all vaping activities, he became increasingly dyspneic with shortness of breath with minor activity prompting him to seek emergent evaluation. Upon presentation, he demonstrated evidence of hypoxemic respiratory distress with severe tachypnea with increased work of breathing and mild accessory muscle use. He reported coughing bouts with deep inhalation and associated production of white frothy sputum. He denied hemoptysis, chest pain, recent illness, travel or sick contacts. His examination was significant for tachycardia, tachypnea and distant breathing sounds with fine crackles in bilateral lung fields. An electrocardiogram showed sinus tachycardia (heart rate 115) with no ST-segment changes. Chest radiograph showed diffuse pulmonary infiltrates bilaterally (). Laboratory evaluation demonstrated an elevated white blood cell count of 19.5 cells/μl (the cell differentials by percentage were all within normal range and there was no eosinophilia present). Troponin was negative, and both brain natriuretic peptide and D-dimer were not significantly elevated (82 pg/ml and 195 ng/ml, respectively).\nTherapy consisted of scheduled nebulized albuterol, methylprednisolone (30 mg intravenous [i.v.] given twice over 8 hours, and then changed to prednisone 40 mg b.i.d.) and empirical antibiotic treatment with azithromycin and ceftriaxone. The patient continued to have fevers (Tmax 101.6), worsening hypoxemia (requiring up to 12 l via high-flow nasal cannula) and leukocytosis.\nOn Day 2, the patient’s respiratory status worsened and an arterial blood gas (ABG) analysis revealed a pH of 7.48, pCO2 of 33 and a pO2 of only 48 while on 8 l O2 high-flow nasal cannula. He did meet the Berlin criteria for severe ARDS and therefore was transferred to the intensive care unit (ICU) for closer observation but never required invasive mechanical ventilation. A computerized tomography (CT) chest angiogram with i.v. contrast revealed findings significant for pneumonitis ().\nAt this point, a workup for an infectious source including blood cultures, urine legionella, antigen, urine antigen for Streptococcus pneumoniae, antibody screen for coccidiomycosis, human immunodeficiency virus and respiratory polymerase chain reaction panel was negative. Antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies, cytoplasmic & perinuclear and anti–double-stranded DNA antibody were also negative. An ABG showed respiratory alkalosis with hypoxemia. Acute phase reactants were elevated including: C-reactive protein of 243.93 mg/l, procalcitonin of 0.17 ng/ml and sedimentation rate of 35 mm/h. Antimicrobials were discontinued after 3 days of duration and supportive care continued including supplemental oxygen, steroids and albuterol nebulizer treatments. By the sixth day of his hospital stay, the patient’s symptoms had resolved and was able to ambulate without supplemental oxygen. He was discharged home with an inhaler and to complete a course of prednisone 40 mg daily for five more days. His vaping paraphernalia was submitted to the county health department and was subsequently found to indeed contain THC. His case was also reported to the Centers for Disease Control and Prevention. The patient followed up with his primary care provider within 2 weeks of discharge and no further treatment was indicated. Additionally, upon contacting the patient 8 months after his hospitalization, we were pleased to discover that he has quit using e-cigarettes and has not had any further episodes of respiratory distress or need for an inhaler.

A 47-year-old Iranian woman was referred to a psychiatric clinic complaining of distressing eyelid twitching called eyelid myokymia. She was taking TPM 50 mg HS for at least 16 months, to control her weight gain due to binge eating problem. She explained that the eyelid twitching started from lower right eyelid which was not so much disturbing at first but was aggravating with stress and fatigue and diminishing by rest, but in the previous month, there was no response to rest. She had searched through the Internet and found out that this was a benign, periodic, and self-limiting condition, but less response to resting made her get worried more and more in the last month.\nPhysical examination was normal except previously diagnosed mild hypertension, controlled with 25 mg/day losartan over a period of 2 years. MRI and laboratory tests revealed no abnormal findings. An ophthalmological consultation was carried out but reported no significant visual disturbance. The patient was reassured and asked to continue her medications and also advised to decrease work time and to rest more.\nOne month later, she came back with worsening of her eyelid twitching which was expanded to her upper eyelid and occasionally the same side eyebrow. Her self-esteem and social communication were severely affected because she believed that twitching can be observed by others. Physical examination was again normal and no new sign was detected. She was advised not to use TPM anymore, with possible diagnosis of TPM-induced myokymia.\nInitially because of its favorable effects on weight loss, she resisted discontinuing TPM, but actually worsening of symptoms made her respect the physician's decision. The patient's symptoms decreased gradually and disappeared completely two weeks after TPM discontinuation. TPM discontinuation resulted in increasing appetite and body weight over two months; consequently she became depressed and started using TPM again. Eyelid myokymia reappeared two weeks later.

A six-year-old female child presented with a three-week history of mild left flank pain and low-grade fever. Her medical history was unremarkable, with no history of previous urinary tract infections. A routine urinalysis was suggestive of UTI. She was transferred to our care after her symptoms failed to resolve with oral antibiotics.\nPhysical exam at presentation demonstrated a temperature of 38.3°C and a palpable left flank mass with overlying fluctuance. Laboratory evaluation demonstrated a hemoglobin of 8.5 g/dL and a white blood cell count of 18.6 × 103/μL with 84% segmented neutrophils. A voided urine culture was obtained which was later positive for E. coli. Abdominal CT demonstrated a chronically hydronephrotic left kidney with calcified debris within the collecting system and perinephric abscesses extending anterior and posterolateral to the kidney ().\nThe patient was admitted for IV antibiotics, percutaneous perirenal abscess drainage, and nephrostomy. 120 cc and 30 cc of purulent material were drained from the abscess and nephrostomy, respectively. Initial and subsequent cultures demonstrated E.coli. The patient responded well to drainage and was treated with an extended course of culture-specific antibiotics. A dimercaptosuccinic acid renal scan after one month of percutaneous drainage revealed that the left kidney had a differential function of 5%.\nA left retrograde pyelogram was performed at the time of definitive surgery in order to identify the distal extent of the calcified debris and to demonstrate areas of potential obstruction. Fluoroscopy demonstrated a narrowing at the ureteropelvic junction with migration of calcified debris into the proximal ureter (). These findings do not exclude vesicoureteral reflux as a potential cause of her chronic pyelonephritis.\nWe elected for a transperitoneal left LN secondary to broader visualization, superior angles, and similar outcomes data compared to a retroperitoneal approach []. Trocar placement was as follows. A 10 mm camera trocar was placed in the umbilicus. Two working trocars were placed in the left midclavicular line: an infraumbilical 12 mm trocar and a supraumbilical 5 mm trocar. An assistant 5 mm trocar was placed in the midline below the xiphoid process. A Harmonic Scalpel was the primary energy source for dissection. Retroperitoneal access was achieved distally near the iliac vessels by reflecting the colon medially. The retroperitoneum was expectantly inflamed, requiring methodical dissection. Inspection of the kidney revealed dense perinephric adhesions with prominent inflammation near the upper pole. The renal vessels were ligated en bloc with an endoscopic vascular stapler. An inadvertent capsulotomy was created at the upper pole resulting in leakage of inflammatory debris. A Covidien Endocatch bag was used to deliver the specimen through an enlarged incision at the site of the 12 mm trocar. The abdomen was irrigated with one liter of bacitracin, and the irrigant and debris were aspirated with an endoscopic sucker. The total operative time was 286 minutes. Estimated blood loss was 100 cc.\nThe postoperative course was complicated by an ileus (Clavien grade II) requiring nasogastric tube decompression. This resolved by postoperative day three and the patient was discharged home on postoperative day five.\nHistology demonstrated marked chronic interstitial nephritis, tubular atrophy, fibrosis, and pelvic and muscular wall hypertrophy. Collections of foamy histiocytes admixed with lymphocytes and plasma cells were noted under the urothelium ().

A 19-year-old girl was referred to our clinic complaining of progressive reduced vision in her left eye for the past several months. Her best corrected VA was 20/20 in the right eye and 20/400 for the left eye. Biomicroscopic examination of both eyes and fundus examination of right eye were completely normal. Fundoscopy of the left eye revealed a 2.0 × 1.5 mm sized, elevated and round circumscribed, orange tumoral mass which was located in the inferotemporal juxtapapillary region. The tumor was covering more than half of the optic nerve head and protruding mainly to the vitreous and a thick ERM obscuring the foveal zone was also noted []. No additional pathology was observed within the peripheral retina.\nFundus fluorescein angiography of the lesion showed signs of early filling with late leakage implying the presence of a vascularized lesion. Optical coherence tomography showed an elevated hyperreflective mass shadowing the inner structures. The ERM extended to the fovea causing diffuse retinal thickening and subretinal elevation adjacent to the optic disc []. Systemic workup of the patient and the ophthalmological screening did not reveal any relevant finding of VHL or any other disease. A diagnosis of isolated JRCH was made.\nA combined approach was adopted for treatment. In the initial step of treatment, 532 nm argon laser photocoagulation (ALP) was performed with a long exposure time (0.5–1 second) for a deeper penetration. Sufficient energy (150–300 mjoules) to obtain the paleness of the lesion was applied using small spot sizes (50–200 microns). Three consecutive sessions of ALP were applied 5 days apart. An injection of intravitreal bevacizumab was given within 5 days following the last laser session. Apparent regression of the tumor was observed within a few days [Fig. –]. As the final step of the treatment, 20-gauge PPV (OG) was performed on the first week following intravitreal injection. In surgery, upon lifting the hyaloid, the fibrotic glial capsule of the hemangioma was carefully displaced from the optic nerve with an end-gripping forceps. The external segments of the tumor were partially vitrectomized and the remaining lesion was undermined from its retinal stalk. Consequently, the epimacular membrane was carefully removed. Slight bleeding could easily be stopped by increasing the bottle height and the operation was ended following fluid air exchange. Postoperative improvement was excellent with complete visual recovery except a paracentral scotoma, which persisted most probably due to the loss of ellipsoid zone layer on the nasal side of the fovea [Fig. and ]. Best corrected VA is still 20/20 on both eyes. No growth or activity of the tumor was observed within our 7 years of follow-up to present.

A 53-year-old female was referred to our spine clinic with complaints of chronic neck pain and stiffness; the left arm pain which radiated down the radial aspect of her arm, forearm, and hand; fixed kyphotic posture of the neck; and difficulty swallowing. She reported sustaining a traumatic neck injury 6 years prior when she was an unrestrained front seat passenger in a stolen car. Apparently, she and the driver of the vehicle were under the influence of methamphetamines when they crashed the vehicle into a tree. Both fled from the scene and did not seek medical treatment for fear of legal consequences. She developed immediate neck pain and neck stiffness. Shortly after, she developed electric-like left arm pain which radiated down the radial aspect of the upper extremity. She was homeless, uninsured, and she feared criminal prosecution as she was injured in the act of committing a felony. She began self-medicating to control her neck pain, using heroin, street bought oral opiates, and alcohol. She purchased a soft cervical collar from a local pharmacy and wore it exclusively for several months. Approximately 6 months after the injury, she noted progressive flexed cervical posture with difficulty maintaining forward gaze. Less than1 year after the accident, she was incarcerated in a local correctional facility for repeated drug convictions. The duration of incarceration was for 10 months with an additional court-ordered 6-month inpatient drug rehabilitation program. During this incarceration, the patient was evaluated for a high degree of global neck pain and deformity. Although imaging was performed in this evaluation, this patient’s cervical subluxation was not diagnosed. On completion of her rehabilitation, she was able to acquire government-assisted health insurance. At that time, the patient sought care from a primary care physician regarding her neck pain and stiffness. Initial attempts at physical therapy were unsuccessful. Outpatient plain cervical radiograph revealed a deformity and the patient was then subsequently referred to our spine clinic. On examination, she had a fixed flexion posture of her neck with limited axial rotation. She had no upper motor neuron signs nor did her exhibit weakness in upper or lower extremities. Sensory examination was normal. She had a markedly positive Spurling’s maneuver which recreated electric-like pain radiating down the left radial arm, forearm, and hand.\nFull-length plain spine radiographs revealed regional kyphosis from C4 to C6 measuring 50°, but a normal SVA (). There was 3mm of anterolisthesis of C4 on C5, bony ankylosis of C5/6 at the disc level and posteriorly at the facets. Cervical CT confirmed the sagittal cervical malalignment and fusion of the C5/6 level. Cervical magnetic resonance imaging revealed multilevel cervical disc degeneration, focal kyphosis in the mid-cervicalspine, and mild-to-moderate central stenosis (worst at C4/5) and multilevel mild foraminal stenosis.\nThe patient was taken for elective circumferential surgery. Initial procedure was an anterior C5 and C6 corpectomy, anterior placement of an expandable titanium cage from C4-C7 and this construct was augmented by anterior plating from C4-C7. The posterior procedure comprised posterior cervical decompression from C4-7 along with lateral mass instrumentation and fusion.\nShe was hospitalized for 3 days and was subsequently transferred to inpatient rehabilitation for 10 days. After her rehab stays, she was discharged to her daughter’s home. She wore a hard collar for 6 weeks and she also stopped smoking. She noted immediate improvement in her cervical posture in that she could achieve a forward gaze. Her dysphagia improved and left cervical radiculopathy resolved within weeks. At 2-year post-operative follow-up, her overall neck pain was improved, but she still required low-dose narcotics (Norco 5 mg every 12 h) to control this pain to an acceptable degree. The patient gave written informed consent for print and electronic publication of this report, as well as for reprint in foreign editions of this journal. The authors have no financial, or other, conflicts of interest to disclose.

A 67-year-old woman presented to Gangnam Severance Hospital with left buttock and leg pain and intermittent neurogenic claudication lasting less than 5 minutes for 12 months. The pain radiated to the left S1 dermatome. The patient had undergone 6 nerve blocks and continuous medical therapy for more than 6 months, but her symptoms did not improve. Magnetic resonance imaging (MRI) showed degenerative spondylolisthesis and left extraforaminal disc at L4–5 with foraminal stenosis. The patient underwent MIS-TLIF of L4–5.\nThe patient began ambulating on postoperative day 2, however, complained of sudden onset right leg pain on postoperative day 6. The pain was an 8/10 on the VAS, and she developed subjective weakness at the right hip, knee, and ankle. CT scans revealed a bony fragment at the right L4 pedicle (). We wanted to avoid removing the previously inserted screws and rod, which would be necessary if entering through the previous incision to remove the bony fragment. Therefore, we planned to remove the inferior articular process through a new incision using a right-sided approach. After general anesthesia, the patient was placed in a prone position on a Jackson table. From the CT image, we decided the target point on anteroposterior and lateral x-ray. Orient it towards the target, along the medical pedicular line, we made two independent incision 2 cm apart (, ). Inferior incision for endoscope and superior incision for working channel (; ). The operator was positioned on the patient’s right side and the assistant on the left. Two approximately 1-cm stab incisions were made 2 cm apart (, ). The endoscope was inserted through the left (inferior) incision, and continuous irrigation was begun. We ensured that there was saline output though the right (superior) incision because without continuous irrigation, the operative field is not clear and bleeding control is difficult to achieve. The working channel was then used to insert the surgical instrument and endoscope to secure surgical visualization ().\nAfter confirming the anatomical landmark under endoscopy, we first identified the upper and lower lamina, and then followed the anatomical structures to visualize the interlaminar space and the pedicle. The previous TLIF resulted in a laminectomy and facetectomy after removing the surrounding soft tissue. We were able to identify the screw thread in our operative field, and a broken piece of the medial pedicle was found next to it. When the bony fragment was removed, there was an area of bone bleeding that was controlled using bone wax. We then cleaned the surrounding tissues and confirmed that there was a sufficient gap between the root and screw thread, placed a Hemovac drain, and finished the operation. The bony fragment was removed successfully (). The operation time was 67 minutes, and blood loss was 50 mL. The medial pedicle had fractured for unclear reasons after the patient began ambulating following the first operation. The patient continued to complain of back pain at the operation site immediately after the revision surgery. However, her leg pain and weakness improved immediately. The patient discharged on postoperative day 4 with back and leg pain that was a VAS 4/10. Postoperative CT demonstrated that the bony fragment had been completely removed (). The patient was also regularly followed in the outpatient clinic after discharge and patients did well without pain at 6 months from revision surgery. Follow-up will continue to confirm fusion.

A 7-year-old male child presented with swelling and pain in the outer aspect of the right heel for past 1 month. Mother of the child correlated the swelling with a history of trivial trauma. The swelling was gradually progressing. A history of incision and drainage of swelling by a local practitioner after 5 days of onset of swelling was noted. There was an associated history of high-grade fever of insidious onset, intermittent in nature with chills and without any diurnal variation. Constitutional symptoms such as significant weight loss, loss of appetite, and malaise were present for the past 2 weeks. He was unable to walk or weight bear due to pain in right lower limb for the past 1 week. The patient was febrile and having tachycardia at presentation. No lymphadenopathy was detected clinically.\nA swelling of 5*4*2 cm size which was tender was present over the posterolateral aspect of heel extending anteriorly covering lateral malleolus, posteriorly extending to the area of tendoachilles insertion to the calcaneus, superiorly 5 cm above whole of the lateral malleolus, and inferiorly 2 cm above the heel (). It had an irregular surface, well-defined round margins with loss of skin cover in more than 50% of the surface area with reddish brown color. There was active oozing of blood from the superior and inferior edge of the swelling. Temperature around swelling was raised. Lateral malleolus was not separately palpable from swelling. Tendoachilles could be separately palpable. Ankle motion was restricted and painful with no distal neuro deficits.\nX-ray showed large soft-tissue shadow over heel with loss of soft-tissue planes and a lytic lesion over the posterior aspect of the calcaneus with destruction of the posterior tuberosity of calcaneus (). Magnetic resonance imaging showed a lobulated well-defined mass of size 5*3.5*6 cm in the posterolateral aspect of the ankle with hyperintensity in T2 and T1 images (-). The mass invaded calcaneus posteriorly with encasement of tendoachilles. Peroneal tendons were free. Diagnosis of soft-tissue sarcoma was made.\nThe initial two core biopsies were non-confirmatory, one of which showed features of acute inflammation with no evidence of malignancy. Aerobic, non-aerobic, or fungal cultures were negative. The swelling increased in size and turned into a fungating mass with sloughs hanging from the surface within 2-week duration after the presentation (). An excisional biopsy of the swelling finally showed features suggestive of non-Hodgkin’s lymphoma. The tumor mass was found to be eroding into the posterior aspect of calcaneum with the involvement of the insertion site of tendoachilles (). The swelling was curetted out till the healthy-looking bone was noticed along with partial excision of the encased tendoachilles. Intraoperatively skin closure could not be achieved. The wound gradually decreased in size with 5 days of continuous vacuum-assisted closure therapy at 125 mmHg (), and it healed with secondary intention with regular dressing within 4 weeks. The range of motion of the ankle and subtalar joint was reduced compared to the unaffected side. Gradual range of motion exercises was started for ankle and foot. In microscopy, the tumor showed sheets of tumor cells intermediate to large cells with moderate amount of amphophilic to eosinophilic cytoplasm and the nuclei appeared to be vesicular with multiple conspicuous nucleoli with some cells showing eccentrically located nuclei and nuclear membrane irregularities (). Immunohistochemistry showed ALK, CD30, CD99, EMA, ki67, and leukocyte common antigen positivity (Figs. and ).\nStaging of the patient was done by ruling out any synchronous or metachronous disease elsewhere by doing CT scan of chest and abdomen and bilateral bone marrow biopsy. Hence, a diagnosis of PBL with a histological diagnosis of ALCL was made. Treatment was carried out as advised by the oncology team, with 3 cycles of chemotherapy (CHOP – cyclophosphamide, doxorubicin, vincristine, and prednisone) followed by 5 cycles of localized radiotherapy. Supportive treatment in terms of prevention of anemia and infection was given. He did not have any presentation of any diseased lymphadenopathy or organomegaly during the course of treatment. At the last follow-up at 12 months, the wound over the posterior aspect had healed with the patient being ambulatory.

A 63-year-old Caucasian male with no significant past medical history presented to the emergency department with complaints of bilateral lower-extremity muscle weakness and paresthesia. The patient first noticed a tingling sensation and bilateral lower-extremity myalgias approximately two weeks prior to presentation beginning the morning after engaging in a vigorous snow shoveling session. He initially attributed the symptoms to his shoveling; however, he reported no traumatic events while shoveling and did not experience any symptoms immediately afterward. Over the next few days, the patient’s symptoms began spreading to his back and upper extremities, yet he was unable to describe any specific pattern of spread. The patient initially saw his primary care physician who started him on gabapentin for his neuropathic symptoms and encouraged him to follow up with outpatient neurology. Due to extenuating circumstances regarding pandemic-associated restrictions, the patient was unable to secure an outpatient neurology appointment date for more than a month out, prompting him to visit the emergency room.\nUpon presentation, the patient reported occasional shock-like sensations in his fingertips, progressive difficulty with ambulation, and pain between his shoulder blades that had interfered with his ability to sleep. He was noted to have been very active leading up to his presentation and was unable to identify any precipitating factors for his illness aside from his shoveling. After extensive questioning for additional history, the patient reported a known COVID-19 exposure when his wife tested positive about four weeks prior to the onset of his current symptoms. He was never tested at that time but did experience fatigue, headaches, mild cough, and loss of taste. He completed a 14-day quarantine at home, and apart from the loss of taste, all his other symptoms had completely resolved. He saw no association between those symptoms and his current symptoms.\nOn examination, the patient was in no acute distress with no evidence of respiratory compromise. Muscle strength was 4/5 bilaterally in the lower extremities and 5/5 in the upper extremities. No sensory abnormalities were noted. Deep tendon reflexes were absent bilaterally in the lower extremities and 1+ in the upper extremities. Gait was grossly abnormal and unsteady. The physical examination was otherwise unremarkable. The patient denied any difficulty breathing or bladder/bowel incontinence. Vital signs were all within normal limits, and the patient remained hemodynamically stable throughout his hospital course. Initial laboratory workup was significant for an elevated creatinine kinase of 472 units/L. Results of a complete blood count, comprehensive metabolic panel, lactate, vitamin B12 level, and C-reactive protein were otherwise within normal limits. Chest x-ray revealed no acute cardiopulmonary process, and brain and complete spinal MRI results were notable for only mild lumbar spinal stenosis and age-related degenerative changes. Lumbar puncture was performed under fluoroscopic guidance, and cerebrospinal fluid (CSF) analysis revealed albuminocytologic dissociation (Table ).\nReverse transcription polymerase chain reaction (RT-PCR) test was positive for SARS-CoV-2 antigen despite the patient having no symptoms of active disease, which likely represented residual virus from infection during the previous month. The clinical picture and albuminocytologic dissociation in CSF analysis were at this point consistent with GBS, likely from the recent COVID-19 infection as no other possible etiologic causes could be identified. Electromyography analysis was inconclusive to distinguish between axonal loss and demyelination; however, findings were consistent with a diffuse, largely symmetrical sensorimotor peripheral neuropathy of moderate degree. A “sural sparing” pattern was identified in the left lower extremity, which can sometimes be seen in the acute inflammatory demyelinating polyneuropathy subtype of GBS (Table ) [].\nThe patient was started on a five-day course of 0.4 g/kg IVIG, as per neurology recommendations. He remained stable throughout treatment with excellent negative inspiratory forces. At the completion of treatment, he was medically cleared for a safe discharge to home, with recommendation to continue home physical therapy, and was instructed to follow up with neurology on an outpatient basis in 3-4 weeks.

A 38-year-old man was admitted to the ED with stable vital signs and normal level of consciousness after he had been near the site of a high-pressure tank explosion at work. The patient was thought to have miniscule particles of cement and other materials impacted in his skin, especially in the face. Skin damage was observed on the right side of the face and neck, and the center of the chest, where numerous cement particles were presumably impacted. Additionally, the patient presented with a foot fracture, resulting from tripping while stepping backwards at the time of explosion. Facial CT scans revealed the presence of minute FBs in the dermal layers. The ophthalmology department was consulted to eliminate the possibility of ocular FBs. A corneal abrasion was observed, but no FB. Local anesthesia was administered to reduce pain. Immediate treatment consisted of thoroughly brushing out and rinsing the wounds with 2 L of normal saline. Visible FBs in the dermis were also removed using a no. 11 surgical blade. After removal, bleeding persisted with considerable black colored pigmentation in the affected sites, suggesting possible persistent FBs, too small to be visible to the naked eye. For further removal, a slit-lamp microscope (Topcon Slit Lamp SL-3F; Topcon Medical Systems, Oakland, NJ, USA) and a 26-gauge needle were used in order to prevent traumatic tattoos. The patient sat in front of the slit-lamp microscope as we adjusted the focus setting to ×16 magnification. We increased the light intensity, and decreased the slit width. Next, we adjusted the screw of the chin rest bar for proper vertical alignment. For horizontal alignment, the face angle was adjusted to the right or left. We shone the light next to (but not directly on) the impacted area. With direct, localized light, it was too bright to see the FBs, which could be visualized as solid 3-demensional shapes defined by their shadow lines (, ). We used a 26-gauge needle to access the identified areas through a wound in the skin created by the initial penetration (). We confirmed the FBs by feeling them with the needle tip; larger FBs were removed through the formed passage of the wound, while the miniscule powder ones were carefully scratched off the skin surface. Approximately 50 FBs were removed each time, with 150 removed for the three procedures in total (). The removed particles were between 0.5 and 2.0 mm. The total procedure duration was approximately 15 minutes in total. After removal, an antibiotic ointment was applied, and a moistened dressing was given; the wound recovered with no sign of traumatic tattoo or secondary infection at the time of follow-up ().

A 53-year-old male presented to emergency department with complaints of acute onset, generalized rigidity and tremors of all limbs, difficulty speaking and swallowing along with slowness of movements, masked facies, and decreased blinking. He was recently discharged from medical ICU after being managed for episodes of vomiting and decreased food intake associated with confusion, lethargy, disorientation to time and place. Also he developed two episodes of generalized tonic clonic seizures. His serum Na+ was found to be very low (102 mEq/ml). He was also put on tab levetiracetam 1000 mg for seizure prophylaxis. At the time of discharge after 6 days of hospitalization his serum Na+ was 131 mEq/ml. His hyponatremia had been corrected rapidly (by 13 mEq/ml in initial 8 h). He had undergone neurosurgery for non-functional pituitary macroadenoma 10 years back. He was not taking any hormone supplements. It was hypothesized that he might have been having chronic hyponatremia due to hypopituitarism. Patient developed rigidity and associated symptoms after 6 days of sodium correction. He also underwent magnetic resonance imaging (MRI) of the brain which did not reveal any abnormality except for chronic ischemic changes in the bilateral centrum semiovale.\nDetailed assessment did not reveal psychiatric symptoms or any previous psychiatric illness nor was there any history of substance abuse. There was no family history of any psychiatric illness as well. From the history and review of medical records, a provisional diagnosis of CPEM was made. Neuroleptic malignant syndrome was ruled out as patient was not subjected to any antipsychotics in previous hospital as per records. Moreover, serum creatine phosphokinase (CPK) levels were normal. He was started on oral trihexyphenidyl (centrally acting anticholinergic) 1 mg TDS along with supportive treatment.\nMRI brain was repeated on day 4 of admission (after 5 days of onset of symptoms) which showed pontine hyperintensities and bilateral basal ganglia (caudate and putamen) hyperintensities on T2W1 and FLAIR sequences confirming the diagnosis of CPEM (secondary to rapid correction of hyponatremia) [Figures and ].\nPatient's symptoms started improving dramatically after the treatment was started. Hormone supplementation was started following reports of low Adrinocorticotrophic Hormone (ACTH), Thyroid Stimulating Hormone (TSH), Follicle Stimulating Hormone (FSH) and Leutinising Hormone (LH) levels. After 3 days of hospitalization, he developed behavioral symptoms for which psychiatric consultation was again taken. He was found to have disturbed sleep, irritability, suspiciousness toward a fellow patients in the ward and aggression toward treating resident doctors. He developed delusion of persecution and reference, claiming that a female patient on neighboring bed was passing insulting remarks to him indirectly when talking to others and was also teasing him through her gestures. He would appear restless and kept pacing in ward in anger. He was fully conscious and oriented with clear sensorium. No apparent mood symptoms could be noticed. He did not have any Schneiderian First rank symptoms. Possibility of any substance abuse in ward was ruled out. He was started on quetiapine 50 mg and dose was increased to 100 mg over a period of 3 days. He tolerated it well and his psychotic symptoms started improving over a period of 4 weeks. He was discharged from the ward after his extrapyramidal symptoms got completely resolved. During follow-up visits, trihexyphenidyl was tapered off over next 1 month and quetiapine was gradually tapered off over next 6 months without any new symptoms. The patient achieved complete remission and started attending office subsequently.

A 20-year-old smoker male experienced mild weakness and paresthesia of lower extremities for 3 days. There was no underlying diseases or history of trauma. He went to the clinic and took home some medicine. Three days later, the patient developed dyspnea, generalized seizures, and subsequent loss of consciousness. He was sent to the emergency department of the local hospital and intubated promptly. A few minutes later, the patient had a cardiac arrest. Immediate cardiopulmonary resuscitation was performed nine times until the presence of vital signs. Computed tomography (CT) scan of the brain was obtained and showed a hyperdense lesion in the dorsal region of the left-sided of the medulla oblongata, corresponding to medullary hemorrhage []. The patient was sent to the intensive care unit for close observation until clinical stable. Ten days later, the patient was sent to another larger local hospital. Following day, magnetic resonance imaging (MRI) of the brain revealed diffuse hyperintensity of the medulla oblongata on fluid-attenuated inversion recovery and T2-weighted sequences, corresponding to venous congestion or edema of the medulla. There were multiple dilated flow voids surrounding the medulla, more prominent on the left side, with venous varix embedded into the left-sided of the lower medulla. T1-weighted images demonstrate a round mixed iso and crescent hyperintense lesion in the dorsal region of the enlarged upper medulla, representing acute to subacute hematoma. The trajectory of hemorrhage projected superiorly from the left-sided of the lower medulla into the mid-dorsal region of the upper medulla []. Tracheostomy was performed due to prolonged intubation and recurrent pneumonia. The disabled patient gradually improved and could follow command in the next 2 weeks with quadriparesis status (power Grade 1–2/5). Two weeks later, the patient was transferred to Prasat Neurological Institute (PNI) for further investigation and proper management. The neurological examination revealed fully consciousness, evidence of spastic quadriparesis (power grade 2–3/5), hyperreflexia of upper and lower extremities, and the presence of Babinski's sign. Digital subtraction angiography (DSA) demonstrated DAVF of the foramen magnum supplied mainly by dural branches of bilateral hypertrophic posterior inferior cerebellar arteries (PICAs), slightly by the posterior meningeal branch of the left vertebral artery (VA), and the neuromeningeal trunk of the left ascending pharyngeal artery (APA) originating from the occipital artery. The venous drainage was split in two directions via the dilated lateral medullary veins and run superiorly along cerebellomedullary and cerebellopontine cisterns into both petrosal veins. On the left side, the left basal vein of Rosenthal receives venous blood from the anterior pontomesencephalic vein and the left lateral mesencephalic vein with subsequent drainage into the great vein of Galen. On another side, the right dilated superior hemispheric vein connects from the dilated right transverse pontine vein with further drainage into the right proximal transverse sinus through the tentorial sinus []. Transarterial embolization through the bilateral dural branches of the PICAs was successfully performed using N-butyl-2-cyanoacrylate (NBCA). Postembolization angiography confirmed complete obliteration of the fistulas []. MRI of the brain obtained 1 week after endovascular treatment revealed a large round mixed central isointense and peripheral hypointense mass with hyperintensity in a venous aneurysm, probably representing a thrombosed venous aneurysm with resolving hematoma. There was the disappearance of previously seen venous congestion of the medulla and multiple dilated flow-voids surrounding the medulla []. The patient gradually improved, and tracheostomy tube was removed before discharging home 2 weeks after treatment. Six months after endovascular treatment, the patient showed no residual neurological deficits. Routine annual follow-up was scheduled for him, but the patient was lost to follow-up without any reasons.\nSeven years later, the patient experienced occipital headache without the stiffness of the neck for 7 days. He went to the local hospital and was sent back to PNI again due to the previous history of DAVFs of the foramen magnum. There were no neurological deficits on neurological examination. Follow-up MRI of the brain showed multiple dilated flow-voids, more prominent on the right side, along both cerebellomedullary and cerebellopontine cisterns, representing recurrent DAVFs of the foramen magnum. There was the disappearance of a previously seen thrombosed venous aneurysm and complete resolution of the hematoma in the medulla with the small residual hypointense area of hemosiderin stain in the dorsal region of the medulla []. DSA with angiographic CT in three-dimensional reconstruction and maximum intensity projection (MIP) reformatted images of the craniocervical junction clearly demonstrated the exact location of the DAVFs at the posterior rim of the foramen magnum, mainly supplied by the hypertrophic jugular branch of the APA originating from the occipital artery. Without supplying from the right PICA, the left PICA and posterior meningeal branch of the left VA partially fed the fistulas. The venous drainage drained to both sides of the medulla and run superiorly along cerebellomedullary and cerebellopontine cisterns into both petrosal veins. On the left side, the fistulas drain superiorly into the great vein of Galen through the left dilated vein of cerebellomesencephalic fissure. On the right side, the fistulas still drained into the right proximal transverse sinus through the dilated superior hemispheric vein and tentorial sinus, respectively. Inferiorly, it also drains into anterior medullary vein connecting to anterior spinal vein []. Endovascular treatment was performed through the jugular branch of the left APA using NBCA []. DSA after embolization revealed residual fistulas. Due to incomplete obliteration of the fistulas, the patient then was informed about surgical option and accepted this option.\nFollowing suboccipital craniotomy without C1 laminectomy, resecting the dural leaflets and disconnecting leptomeningeal medullary draining veins were successfully performed using indocyanine green fluorescence imaging during operation []. In addition, watertight duraplasty was done with synthetic dural graft. The postoperative course was uneventful. Follow-up DSA, obtained 1 month after surgery, confirmed complete obliteration of the fistula []. The patient has remained clinically asymptomatic 2 years after the operation.

A 74-year-old lady with no medical comorbidities presented with reduced visual acuity. Vitreous cultures prior to antibiotic administration grew multisensitive Staphylococcus aureus. Three sets of blood cultures were taken prior to commencement of antibiotics and were negative. She received treatment with intravenous flucloxacillin initially; however, a repeat vitreous sample was clear and intravenous antibiotics were stopped. A course of oral antibiotics was completed. She was continued on a course of oral prednisone for endophthalmitis with continued ophthalmology outpatient followup and discharged from hospital after a weeklong admission. She presented three weeks later with a four-day history of insidious onset lumbar back pain. This was accompanied by rigors, fevers, and anorexia.\nInitial examination revealed boggy swelling over the lumbar spine with midline and paraspinal tenderness to palpation. She had symmetrical range of motion of the spine and a normal neurological exam.\nX-rays of the lumbar spine revealed an old L3 compression fracture and an L4/L5 spondylolisthesis. Initial blood tests showed a white cell count of 13, neutrophils of 12.7, and C reactive protein (CRP) of 329.\nThe triad of back pain, raised inflammatory markers, and possible recent Staphylococcus infection led to potential concern of an epidural abscess. MRI with gadolinium was requested.\nThe paraspinous region demonstrates at least two small collections (to the right of the L4 spinous process as depicted by the large arrow on both images of Figures and ). demonstrates the extension of the infection. Significant compression of the thecal sac and spinal cord is seen on , along with the collection opposite the L4 spinous process.\nSubsequent blood cultures grew multisensitive Staphylococcus aureus. She was taken to the operating theatre for posterior lumbar decompression of L2 to S1 with open washout and evacuation of an epidural abscess. Nonoperative management was not considered. The indication for surgery was significant sepsis coupled with the radiological extent of the abscess with anterior and posterior elements exerting significant mass effect upon the thecal sac.\nShe was commenced on intravenous flucloxacillin for a total of six weeks. Abscess cultures grew multisensitive Staphylococcus aureus as did prior vitreous cultures. A transesophageal echocardiogram ruled out endocarditis. Her postoperative course was complicated by syndrome of inappropriate antidiuretic hormone secretion (SIADH) and hyponatremia; postoperative anemia; and clostridium difficile diarrhea secondary to antibiotic administration. She was discharged home after a two-week admission. Upon discharge, weekly reviews were carried out in outpatients with repeated inflammatory markers. She had an excellent response to the therapy; her pain settled completely and inflammatory markers returned to normal limits within four weeks of intravenous treatment. A total of six-week intravenous antibiotics were completed.

This eighty-year-old gentleman presented to accident and emergency with right arm weakness. The patient reported a sudden onset of right neck pain at rest radiating to his right shoulder and back, leading to immediate numbness and tingling down his right arm and associated heaviness. There was no report of any preceding trauma or headache. He had a past history of hypertension, tablet controlled diabetes mellitus, previous transient ischaemic attacks, bilateral carotid endarterectomies and peripheral vascular disease. His medications included aspirin 75 mg once a day and dipyridamol sustained release 200 mg twice a day.\nNeurological examination revealed 3/5 power in his right upper limb with reduced sensation throughout. He had pain on right lateral neck movement but no stiffness. Cranial nerves and lower limbs were normal. He was haemodynamically stable with a systolic blood pressure of 140 mmHg. Electrocardiogram showed sinus rhythm with no acute features. Blood results were unremarkable. The main differential diagnoses were cerebral stroke, aortic dissection and cervical myelopathy. An urgent Computed Tomography (CT) aortic angiogram was normal. Cervical spine x-ray showed no fracture. CT head scan did not reveal any infarct or haemorrhage and his dual antiplatelets were continued. A non-urgent Magnet Resonance Imaging (MRI) of his cervical spine was arranged.\nThe patient underwent rehabilitation therapy. Symptom resolution occurred within 24 hrs of presentation. On day 6 of admission he was fit to be discharged home with follow-up in one month. The MRI neck report was still outstanding but as the patient was well, we did not wish to delay discharge. On review of the MRI the next day, it showed ‘a right sided shallow fluid collection projecting into the spinal canal from the posterolateral aspect of the canal between C4 and C7. Cause uncertain but includes haematoma or abscess’ (Figure ). There was also spondylosis with potential nerve impingement at C6/C7 bilaterally. The patient was contacted and advised to stop the dipyridamole. The images were linked to our nearest neurosurgical centre and discussed with the doctor on duty. It was agreed that due to his symptom resolution, conservative management was appropriate.\nA repeat MRI after a further 3 weeks showed the epidural haematoma to have resolved.

A 44 year old afro-Trinidadian female presented with a two week history of abdominal distension, weight loss, decreased appetite and low grade fever. She had a normal white cell count, a haemoglobin of 9.02 g/dL and a CA125 level of 909 U/ml. Ultrasound scan showed moderate ascites with a septated cystic left adnexal mass (Figure ). CT scan showed smooth peritoneal thickening (Figure ). There was no lymphadenopathy or peritoneal or hepatic deposits. Chest CT showed no lung parenchyma lesions. An ascitic tap was negative for malignant cells and a mantoux test was negative. Primary ovarian malignancy was suspected and the patient was referred to the gyne-oncology clinic. One week later her symptoms improved and the CA125 level fell to 303 U/ml. Due to this unexpected result, alternate diagnoses were considered. The patient declined to have a diagnostic laparotomy at this time as her symptoms had resolved. She agreed however to be monitored in the clinic but was counselled on the need for definitive diagnosis due to the possibility of ovarian carcinoma.\nA few months later she developed dyspnoea due to a large right pleural effusion. A chest tube was inserted and the pleural fluid was negative for malignant cells and acid-fast bacilli (AFB). Repeat CT showed multiple subcentimeter nodules as well as a ‘tree in bud’ appearance throughout the lung parenchyma (Figure ). The ascitic volume decreased but became denser. Bowel loops appeared matted with mesenteric stranding (Figure ). In view of the radiological findings tuberculosis was strongly suspected in spite of the negative skin and bacteriologic tests.\nThe patient then agreed to diagnostic laparotomy (laparoscopy services were not available).\nAt laparotomy the peritoneal cavity was difficult to enter with thick adhesions and miliary seedlings (Figure ). Frozen section facilities were not available however biopsies were taken for tissue diagnosis, leaving the uterus and ovaries intact. Histology revealed caseating granulomas with epithelioid and Langhan’s type giant cells. The Ziehl–Neelsen stain for AFB was negative. PCR testing was unavailable however the patient’s symptoms resolved and the CA125 levels normalized after 2 months of antituberculosis therapy. She is to continue her treatment for a total of 6 months.

A 74-year-old male, living alone in a rural area, with no particular history is brought back by his neighbors for headaches associated with impaired general condition and fluctuation of consciousness.\nA laborious anamnesis found an episode of head injury without loss of consciousness following a fall of his own height dating back 3 days. The headaches that appeared after the trauma were neglected by the patient. On the other hand, the family was alerted by the installation of intermittent confusion and weakness of the limbs.\nOn physical examination, the Glasgow coma score was 13 points of 15, and the patient had analgesic attitude of the head with neck pain to the gentle mobilization. The neurological examination showed spastic tetraparesis more pronounced in the lower limbs without achieving sensitivity or reflexes. The examination of the perineum was without abnormalities.\nBlood tests were also without anomalies.\nA radiograph of the cervical spine showed an abnormal gap between the vertebral spinous of the atlas and axis associated with a significant anterolisthesis [].\nA computed tomography scan eliminated a brain damage and showed a fracture at the junction of the body and the odontoid process corresponding to the type 2 of Anderson and D’Alonzo classification.[] This fracture was associated with anterior atlantoaxial dislocation of more than 5 mm corresponding to the type III of Fielding classification[] [].\nA progressive reduction of the dislocation with a cranial traction was initiated. This device was not well tolerated by the patient. So we decided to go for surgery.\nUnder general anesthesia, reduction and realignment of the odontoid process were obtained by external maneuvers. An instrumented arthrodesis atlanto-occipital posterior approach has been made and completed by the addition of cancellous grafts. The final fluoroscopic control was satisfactory [].\nSeveral postoperative ventilator weaning attempts have been initiated. The patient died five days after surgery following respiratory complications.

The first case involved a 31-year-old pregnant illegal immigrant from Mali with a history of a caesarean birth due to preeclampsia. At 20 weeks of gestation, she was admitted to our department for fever of 38.8°C of unknown origin. The pathology was initially attributed to a nonspecific viral illness. The genetic sonogram showed a fetus without signs of malformation, except for increased gallbladder volume (appropriate for gestational age) and polyhydramnios. Genetic analysis of the amniotic fluid extracted by amniocentesis showed the resulting karyotype was 46 XX.\nThe patient's symptoms exacerbated rapidly: her fever increased to 40°C and she presented general malaise, facial paresis, cardiac arrhythmia, respiratory distress, joint pain, and stiff neck. Laboratory tests showed slightly elevated erythrocyte sedimentation rate (ESR) and mild leukocytosis as well as lymphocytic pleocytosis with increased IgG and specific oligoclonal bands. Lumbar puncture was performed as the woman had retronucal pain and stiffness. Lymphocytic pleocytosis was detected in cerebrospinal fluid (CSF) with a high concentration of protein and glucose and specific oligoclonal bands. These results and the geographical origin of the patient suggested severe sepsis. Cell cultures such as BSK-Hrevealed infection by Borrelia spp., confirmed by polymerase chain reaction (PCR).\nThe patient was diagnosed with Lyme disease, stages 2 and 3. Intravenous ceftriaxone sodium was administered at doses of 500 mg/mL every 24 hours for 16 days, which effectively cured the infection.\nAt week 26 a distended gallbladder with echogenic content of lumpy consistency was observed (). In addition, the fetal growth percentile decreased to percentile 14.\nGestation continued with no significant events but fetal growth almost reached a plateau and gallbladder findings persisted. At week 36, urgent caesarean was required due to fetal distress after fetal growth stopped and pathological hemodynamic data were identified. The female newborn weighed 2090 g and had an Apgar score of 9/9 and umbilical cord pH was 7.25.\nIn the first hours after birth, the newborn experienced bilious vomiting, so, in addition to being breastfed, she received neonatal serotherapy for three days. The infant showed gradually increasing tolerance to oral feeding, beginning with artificial milk, although there was some sporadic vomiting due to reflux. Positive health developments and a ponderal growth in the 25th percentile allowed hospital discharge at 25 days of birth with a weight of 2,450 grams.\nCurrently, at two years and six months of age, the infant still suffers from cholelithiasis and has suffered several episodes of typical food intolerance. During this time she has been admitted twice to the hospital emergency department, once for viral meningitis without sequelae and on another occasion for dehydration after a period of acetonemic vomiting. Ponderal index percentile remains low. Cholecystectomy and other possibilities are being considered to treat the infant, depending on short term developments. The infant is currently being studied in the pediatric ward of the hospital.

A 73-year-old male was referred to our hospital for gradually progressing right lower abdominal pain. His past history included prostate carcinoma with bone metastasis at 60 years of age, and type 2 diabetes mellitus diagnosed at 62 years of age with poor control of the hemoglobin A1c (HbA1c) level measuring 8.0%. Family history revealed that his siblings had type 2 diabetes mellitus and his uncle had gastric cancer. He had a personal history of social alcohol drinking of less than 60 g per day, and smoking of 25 cigarettes per day for 25 years but had quit for over 20 years. Current medications included bicalutamide for prostate carcinoma, metformin, glimepiride and sitagliptin for type 2 diabetes mellitus, and ramelteon, suvorexant, and zolpidem for insomnia.\nThe vital signs of the patient were stable. Right lower abdominal tenderness was noted without abdominal guarding or rebound tenderness. Laboratory data revealed abnormal liver enzyme levels, and serologic tests were negative for hepatitis B and C (Table ). Esophagogastroduodenoscopy and total colonoscopy revealed no abnormalities except for cecal diverticulum. Ultrasonography revealed a 5.5-cm tumor near the ileocecal junction, while contrast-enhanced computed tomography (CT), and positron emission tomography-CT showed multiple nodules with cystic lesions in the peritoneum, suggesting peritoneal dissemination in addition to the main tumor (Fig. ).\nA diagnostic laparoscopy was performed, and a tumor extending from the right lateral abdominal wall with irregular focal protrusion was noted. Multiple brown-colored nodules on the greater omentum, one nodule on the small intestines, and one nodule on the anterior abdominal wall, sharing the same gross appearance, were also noted. Histological examination revealed tumor cells with a relatively abundant cytoplasm and a large area of hyperplasia in a palisading pattern (Fig. ). Small bile droplets were detected in the tumor cells by bile stain. Immunohistochemical staining showed that the tumor cells were positive for alpha methyl acyl coenzyme A racemase, cytokine (CK) 8, alpha-fetoprotein (AFP), and protein induced by vitamin K absence or antagonist-II (PIVKA-II), and weakly positive for anti-hepatocyte, CK 18, heat shock protein 70, and glypican 3 (Fig. ). According to the abovementioned results, HCC of the abdominal wall with peritoneal seeding was diagnosed. Because no lesion of the mother liver was discovered by abdominal sonography, CT, or magnetic resonance imaging, a diagnosis of ectopic HCC was determined. Additional laboratory tests showed an elevated serum AFP level and PIVKA-II level, and liver biopsy revealed slight inflammatory infiltrates in the portal area with mild to moderate fibrosis and slight fatty change in liver cells.\nThe patient received 400 mg of sorafenib per day for ectopic HCC. Two months later, CT imaging showed a significant increase in the tumor size, and blood tests showed increased levels of serum AFP and PIVKA-II. During the follow-up, the tumor response was classified as progressive disease according to response evaluation criteria in solid tumors (RECIST) version 1.1 and modified RECIST (mRECIST). However, the patient showed strong willingness to continue the treatment. Four months later, hematochezia and grade 3 anemia were noticed, according to the categorization of common terminology criteria for adverse events (CTCAE) version 5.0. Contrast-enhanced abdominal CT for evaluation of gastrointestinal bleeding showed tumor progression in the small intestines, which was considered the cause of bloody stools and progressive anemia. However, since the patient refused further survey of the lesions, conservative treatment with blood transfusion was performed. In addition, the bleeding complication was also considered one of the adverse effects of sorafenib, by which the blockade of vascular endothelial growth factor caused endothelial disruption and consequent bleeding events. As a result, the dosage of sorafenib was modified to 200 mg per day. In spite of that, sorafenib was eventually ceased 7 months after the start of treatment because of persistent diarrhea and progressive anemia. One month after the cessation of sorafenib, the serum PIVKA-II level increased abruptly (Fig. ).\nAfterward, the patient had persistent anemia with tarry stool and dizziness. In consequence, the cause of progressive anemia was suspected to be intestinal infiltration of ectopic HCC, rather than side effects of sorafenib. Because the patient refused further treatment for malignancy, he was transferred to hospice care and expired 1 year after diagnosis.

A 3-month-old girl was admitted to hospital for assessment and management of faltering growth. The child was born at 39 weeks' gestation by emergency caesarean section due to foetal distress following induction of labour for intrauterine growth restriction. There were no problems in the immediate postnatal period, and she did not need admission to special care. Birth weight was 2.4 kg (0.4th–2nd centile), and head circumference was 33 cm (9th centile). She was bottle fed, consuming around 4 to 5 oz., 3 to 4 hourly with 4 or 5 bowel movements per day. She showed poor weight gain. Her mother's previous two pregnancies had also resulted in small for gestational age babies (1.4 kg at 34 weeks and 2.3 kg at 41 weeks' gestation). Both family and social history were fully explored during the admission. There was a history of significant alcohol consumption in the mother for which she had undergone a detoxification course during pregnancy.\nOn admission the child weighed 3.4 kg with a length of 52.4 cm (both below 0.4th centile). She had microcephaly with a head circumference of 35 cm (less than 0.4th centile). On examination she had several distinctive features with a wide anterior fontanelle, large mouth and tongue, short anteverted nose, flat nasal bridge, long smooth philtrum, thin tented upper lip (), short neck, widely spaced nipples, mild camptodactyly of the left fifth finger and deep palmar crease on the right hand (), wide sandal gap on both feet (), and deep sacral crease. She also had a heart murmur which had been present since birth. A small atrial septal defect was noted on echocardiography. Her growth was falling further away from her centiles (), and she was extensively investigated.\nThe child was reviewed by the genetics team in view of her facial features. Chromosome tests including karyotype and FISH tests for William syndrome and DiGeorge syndrome were all normal. Skin biopsy (for evidence of chromosome mosaicism) and telomere studies were also normal.\nShe had a normal neurological examination including MRI brain and fundus. CSF analysis was normal including a normal lactate. Full blood count, coagulation profile, biochemistry profile including ammonia and lactate, liver function, bone profile, coeliac screen, inflammatory markers, thyroid function tests, sweat test, and kidney scan were all within normal limits. Metabolic investigations including tests for galactosemia (GALIPUT), fatty acid oxidation disorders, peroxisomal disorders, Smith-Lemli-Opitz syndrome (7-dehydrocholesterol levels), congenital disorders of glycosylation (sialylated transferrin), and maternal phenylketonuria did not reveal any abnormalities.

A 50 years old white man was sent to our outpatient clinic. He started to feel sick a month before with headache, muscle pain, appetite loss, yellow skin complexion and fatigue. His medical history was unremarkable except for two gout attacks years ago for which reason he was taking allopurinol for more than 5 years. He ceased taking it as soon as he felt sick. Alcohol consumption was three beers per day. Sexual history revealed intercourse with two women, homosexual contacts were negated. No intravenous or nasal drug use and no tattoos were reported. The clinical examination showed two red, erythrosquamous plaques of 10x10mm and 5x5mm in diameter in the décolleté and scleral icterus. Sonography of the liver revealed liver steatosis but no signs of fibrosis or cirrhosis. Liver enzymes were elevated above 50 times the upper limit of normal. HCV antibodies were positive. CMV, HIV and hepatitis A and B serology were negative, EBV serology consistent with past infection. The diagnosis of HCV genotype 1a was confirmed by HCV-RNA. Since a screening test for HCV was negative six months ago we considered this constellation despite a lacking transmission history as an acute HCV infection. For the following 12 weeks transaminases and HCV-RNA were monitored to follow a potential spontaneous HCV clearance (Fig. ). Because the patient remained viraemic we initiated a treatment for acute HCV with 180 μg peg-INF-α weekly and 1000 mg ribavirin daily. Two weeks after treatment initiation HCV-RNA was undetectable (Fig. ).\nAt treatment week 3 the patient developed itching red papules around 1 to 3 mm in diameter on the forearms and feet. Some of them were confluent to plaques and had a scaly aspect. Symptomatic treatment with cetirizine and hydrating lotion was started. Over the next weeks the exanthema was confluent and therapy with oral prednisone (0.7 mg/kg body weight) was added at treatment week 6 (Fig. ). After an initial improvement the exanthema worsened again. Serological tests for HIV and syphilis were repeatedly negative and ribavirin was stopped at week 9. At week 10 the whole therapy was ceased because of increasing severe erythrodermia (Fig. ). There were no oral lesions. One week after treatment cessation skin lesions aggravated further. A dermatologist was involved and a skin biopsy performed. The biopsy showed papillomatosis with vessel convolutes that reached the stratum corneum as well as neutrophiles in the dermis and parakeratosis consistent with psoriasis vulgaris (Fig. ). Systemic prednisone doses were further increased to 1 mg/kg body weight (70 mg) and complemented with local whole body clobetasol propionate applications. HCV-RNA was not detectable at end of treatment and during follow up consistent with a sustained virological response (Fig. ).\nOver the next weeks after HCV treatment cessation prednisone could be tapered and replaced by 50 mg acitretin per day. 6 months after treatment termination the patient still had some psoriatic lesions and acitretin was maintained.

A 52-year-old man was diagnosed in March 2010 with multiple sclerosis (MS) when he presented to a neurologist with episodes of fatigue, lower extremity paresthesias, and bowel and bladder incontinence. The diagnosis of MS was made based upon the McDonald criteria with multiple clinical events associated with characteristic imaging findings []. He received initial treatment with glatiramer 20 mg daily via subcutaneous injection (an immunomodulatory drug that activates regulatory T-lymphocyte suppressor cells) and dalfampridine 20 mg twice daily orally (a potassium channel blocker affecting nerve conduction). After a year of treatment, he then received interferon beta 44mcg three times weekly via subcutaneous injection. His MS, characterized as the relapsing-remitting subtype, was active as he had suffered flares associated with increased weakness once every few months, requiring hospitalization and subsequent rehabilitation. Nonetheless, he was fully ambulatory and independent with his activities of daily living.\nThe patient’s melanoma history began shortly after initiation of treatment for MS when the patient first noted a lump on his right lower back. Shave biopsy revealed invasive, ulcerated melanoma to a depth of at least 3.5 mm Breslow thickness. He then underwent a wide excision and sentinel lymph node biopsy. Sentinel lymph node biopsy revealed micrometastatic disease in one lymph node in the right axilla, and a separate lymph node with melanoma was involved in the right inguinal region. Molecular analysis showed no detectable BRAF V600 mutation. After extensive discussion of options, the patient elected a program of vigilant observation rather than complete lymph node dissection of the two involved lymph node basins. Interferon alpha was discussed, but due to the patient’s active multiple sclerosis, he was thought not to be a good candidate for aggressive adjuvant therapy.\nNine months after wide excision, patient’s cancer recurred as multiple skin nodules involving his right flank, as well as right groin and right axilla lymphadenopathy. Excisional biopsy of a right groin nodule revealed metastatic melanoma. He was treated initially with temozolomide 75 mg/m2 daily in an extended dosing regimen []. After one month, a computed tomography (CT) scan showed evidence of disease progression with worsening lymphadenopathy, as well as progressive subcutaneous lesions on his right flank.\nDue to limited treatment options and after carefully considering the risks and benefits of treatment, standard ipilimumab was initiated at 3 mg/kg every three weeks for four doses. During ipilimumab, he had no significant irAEs and no exacerbation of his MS. He continued to receive interferon beta treatment for his multiple sclerosis while receiving ipilimumab. Unfortunately, after completing ipilimumab, a positron emission tomography (PET) scan showed progressive disease with worsening widespread metastatic melanoma. Despite subsequent treatment with carboplatin and paclitaxel, he died due to melanoma progression in March 2013.

A 35-year-old, otherwise healthy female was assessed in June of 2017 for her isolated right olecranon injury. She described being bucked off a horse with a direct blow to her right elbow. Her physical exam revealed a closed injury, soft compartments, and intact neurovascular status. Initial X-rays demonstrated a simple transverse fracture pattern of her olecranon with no evidence of articular depression, osteopaenia, or substantial comminution (). She was splinted for comfort and consent was obtained for open reduction internal fixation of the right elbow.\nIn the operating room, she was positioned in lateral decubitus with the right side up and right elbow prepped and draped, and positioned on a sterile padded mayo stand. Alternatively, the patient may be positioned supine or prone with a radiolucent arm board. A tourniquet was applied to the proximal arm prior to prepping and draping, but was not inflated. A 7-cm longitudinal incision was made over the posterior aspect of the elbow. The incision may be curved medially or laterally around the olecranon, so as not to sit directly over the prominence of the olecranon process, and continued along the subcutaneous border of the proximal ulna. Sharp dissection was carried on through the skin and the subcutaneous tissue. The facia was incised midline, and the location of the ulnar nerve medially was identified and protected throughout the remainder of the case. The fracture site was identified and assessed. The broad insertion of the triceps on the proximal fragment was maintained, and control of the fragment was obtained using a sharp towel clip. The elbow joint and fracture surfaces were irrigated and anatomically reduced using sharp bone reduction clamps. The proximal tine was placed away from the olecranon tip as to avoid the start point for the screw. At this point, additional temporary K-wires can be used peripherally to help maintain the reduction as needed. Augmentation with unicortical mini fragment plate fixation may also be useful at this point, particularly as a buttress for sheer-type fracture planes.\nThe start point in our experience typically lies 2 mm radial to the midpoint on the medial-lateral plane and 2 mm dorsal to the apex of the olecranon in the dorsal-volar plane (). This allows the trajectory to include the natural varus of the proximal ulna of 17.5° (range 11–23°), and the anterior deviation of 4.5° (range 1–14°). The goal of the start point is to permit a screw trajectory in line with the intramedullary canal, while accommodating the proximal ulna dorsal angulation (PUDA), which is a slight ulnar inclination starting 47 mm from the apex of the olecranon, at an angle of 5.7°. An X-ray of an intact contralateral proximal ulna can be used to determine the optimal start point if needed by drawing a line corresponding to the screw trajectory, in line with the ulnar diaphysis, similar to the trajectory shown in . Dorsal start points may cause volar displacement of the proximal fragment as the screw engages the isthmus and volar start points may result in dorsal displacement, resulting in nonanatomic reduction. A triceps split was made with a scalpel and the 3.2-mm drill bit was used to obtain access to the intramedullary canal of the ulna, which was then overdrilled with a 4.5-mm drill bit. Position prior to drilling was confirmed fluoroscopically (). Once within the intramedullary canal, the drill can be used on oscillate or reverse to avoid breaching the cortex.\nA 6.5-mm tap was inserted by hand to determine the length at which good endosteal cortical bite was obtained. A bone clamp was placed on the ulnar shaft to gauge the torque generated by the hand tap. Ideally, this tap should be calibrated; however, a sterile tape can be used to mark the depth at which good cortical engagement is achieved, and the length measured afterward with a ruler. In this particular case, the length was 130 mm. A partially threaded, noncannulated screw from the pelvic set was utilised and inserted with a washer. Excellent bite and fracture compression was achieved. Care was taken to advance both the tap and the screw slowly as it engaged the isthmus, as rapid advancement could generate hoop stress high enough to create secondary fractures (particularly in osteoporotic bone). For fractures with minimal dorsal commination, this construct may still be supplemented with a tension-band wire, or low-profile mini-fragment plates.\nIn our experience, 6.5-mm solid partially threaded cancellous screws of the appropriate length are typically not available on most standard large fragment set; however, they can be found on most pelvis fixation implant sets or are available separately wrapped or as part of an extra-long screw caddy. Solid screws are preferred to their cannulated counterparts, which tend to be too stiff to accommodate the natural curvature of the proximal ulna.\nThe bone clamps were removed and final fluoroscopic X-rays were taken to confirm anatomic reduction of the proximal ulna throughout full range of motion with no gapping at the fracture site (). The incision was irrigated. The triceps split was repaired over the head of the screw using a #1 vicryl suture, and superficial tissues were closed with running 2-0 vicryl and interrupted 3-0 nylon, followed by placement of a sling to allow for early range of motion. Total operative time was 18 minutes and blood loss was negligible.

A 51-year-old female patient received a kidney from her sister after a double nephrectomy owing to renal tuberculosis 12 years previously. At that time, the transplanted ureter was anastomosed to the ileum in the left lower abdomen with an ileal conduit on the opposite side. Ureteroileal anastomosis was performed by using 2 sutures of 3-0 Vicryl. The patient experienced no problems for 12 years. At a routine checkup, she complained of abdominal pain, gross hematuria, and increased debris in the ileal conduit. Her serum creatinine was elevated to 1.7 mg/dL (normal, 0.6 to 1.1 mg/dL), and her transplanted kidney developed hydronephrosis with calcified debris observed by sonography (). Neither hydronephrosis nor calcified debris had been observed 6 months before in a routine outpatient checkup.\nProteus mirabilis and Pseudomonas aeruginosa were detected by urine culture. Abdominopelvic computed tomography revealed hydronephrosis with encrusted pyelitis and ureteritis in the transplanted kidney ().\nThe patient was treated by percutaneous nephrostomy and empirical antibiotics. Microorganisms in the urine showed no evidence of tuberculosis. A cystogram showed that the bladder was not refluxed but had a small capacity (50 mL).\nAfter 3 weeks, we operated to anastomose the transplanted renal pelvis to one end of the ileal conduit, performing augmentation cystoplasty with new ileum and to anastomosis the other end of the remnant ileum with the augmented bladder. Augmentation cystoplasty is a reconstructive technique for creating a compliant, large-capacity urinary storage unit to protect the upper urinary tract.\nThe operation was performed via a midline incision. Because it was difficult to approach the major calices of the transplanted kidney in the left pelvic rim, we anastomosed one end of the ileal conduit to the pelvis of the transplanted kidney in an end-to-end fashion. The ileal conduit was lengthened by 30 cm to extend from the pelvis to the augmented bladder chimney. The encrusted upper ureter of the transplanted kidney was retained. We observed that the encrusted ureteritis involved the entire upper ureter. Bladder atrophy was remarkable, with only the trigon portion remaining. After exposure of the urinary bladder, a transverse wide V-shaped cystostomy incision was created, with the apex approaching the anterior bladder neck and the base extending posteriorly past the midcoronal plane of the bladder dome. A 20 cm segment of new ileum at least 15 cm proximal to the ileocecal junction was used for ileocystoplasty. For the small bowel, a V-shaped plate was created by a side-to-side anastomosis with 2-0 Vicryl. A circumferential, continuous, full-thickness, single layer anastomosis of the bowel to the bladder was started posteriorly by using 2-0 braided absorbable sutures. Bladder drainage was maintained with a 24 French urethral catheter. The other end of the ileal conduit was anastomosed through small separate ileotomies (1.5 cm length) in the limb of the augmentation cystoplasty.\nAfter surgery, calcified debris was decreased and encrusted pyelitis was absent on sonography. The patient's creatinine level was also normalized on follow-up. A follow-up cystogram showed increased bladder capacity to approximately 300 mL with well-preserved end-to-end anastomosis of the ileo-pelvic portion with the other end of one chimney of augmentation cystoplasty with the elongated ileal conduit (, ).

We report the case of a 3-month-old male infant with bilateral corneal opacity since birth who was transferred from the pediatric unit for further ophthalmic care. Written informed consent was obtained from the patient’s parents to publish this report. Prenatal and natal history were unremarkable apart from the fact that the mother, aged 35 years at the time of childbirth, was HIV positive. There was no family history of similar ocular disorders or other congenital anomalies. Upon initial ophthalmic examination, a positive light pursuit was found. There was a homogeneous bilateral central corneal opacity without neovascularization. Ophthalmologic examination under general anesthesia revealed a deep anterior chamber with iris strands that crossed the anterior chamber from the iris. The lens was transparent on the edges and did not adhere to the cornea. The retina was difficult to evaluate because of central corneal opacity. The intraocular pressure measured with a Schiotz tonometer was respectively 18 mmHg and 20 mmHg in the right and left eye. Other malformed features found in the physical pediatric examination included: broadening of the nose base and microcephaly (), bilateral polydactyly with camptodactyly, clinodactyly of the supernumerary finger (), an umbilical hernia with hypochromic macules of the abdomen () and bilateral supernumerary toe with hypertrophy of the hallux (). There were no genital, vertebral, or cardiac anomalies on pediatric physical examination. Laboratory examination revealed that the child was also HIV positive. The diagnosis of Peters plus anomaly Type 1 was made. Management consisted of the administration of mydriatics, one drop two times per day, 3 days a week. One drop of dorzolamide in the evening was also prescribed. Immediate penetrating keratoplasty (PKP) in both the eyes was advised. After being informed that this intervention was not available in our country, the parents did not bring the child back for further consultation, and were lost to follow-up.

A 39-year-old male patient was admitted to the Neurology Department with the complaint of dysphasia with a sudden onset 2 years ago and sudden right limb weakness for 4 months, who had the habit of playing badminton and golf.\nTwo years ago, the patient experienced intermittent episodes of difficulty in speaking and language comprehension with resolution after about 2 h. Head magnetic resonance imaging (MRI) showed abnormal signal intensity in the left temporal lobe, indicating acute infarction, while head magnetic resonance angiography (MRA) was normal. The transesophageal echocardiogram (TEE) combined with color transcranial doppler (TCD) indicated paradoxical embolism from a patent foramen ovalis (PFO). He was diagnosed as cerebral infarction (left temporal lobe) with high possibility of cardiac embolism and PFO. Then, he underwent transcatheter PFO closure successfully. After that, he adhered to aspirin (100 mg once per day) and atorvastatin (10 mg once per day) therapy.\nFour months before admission, the patient experienced weakness of right limbs and inability to speak with a sudden onset, and recovered within seconds spontaneously. The next day, he was noted by his colleagues due to difficulty speaking accompanied by low spirits, and was sent to the local hospital, where he was diagnosed as acute cerebral infarction. At that time, his head MRI revealed acute infarction on diffusion-weighted imaging (DWI) sequences in the left anterior cerebral artery (ACA) and middle cerebral artery (MCA) territory. The digital subtraction angiography (DSA) revealed M1 segment occlusion of the left MCA. He underwent endovascular therapy (thrombectomy) of the left proximal MCA, and recovered with sequelae of mild dysarthria and poor short-term memory. He was then discharged with a prescribed regimen of aspirin (100 mg once per day) and atorvastatin (10 mg once per day).\nApproximately 2 months before his first visit to our department, although there were no new symptoms, a repeat head MRI showed hyperintensity on DWI and T2-weighted images, and hypointensity on T1-weighted images in the left frontal, temporal and parietal lobes with a normal MRA. A repeat MRI at our institution showed multiple lesions in the left MCA territory, indicating a convalescent ischemic stroke (). A carotid ultrasound in neutral head position showed increased intima-media thickness (IMT) with single plaque formation in bilateral carotid arteries, whereas in the rotated neck position revealed a heterogeneous echo outside the left carotid bifurcation. When the patient was in the right lateral decubitus position with neck rotating to the left, the carotid duplex scan demonstrated a compressed and narrow lumen at the distal end of the left common carotid artery (CCA), which was related to the hyoid bone, and the transcranial color-coded Doppler (TCCD) showed a significantly decreased flow velocity of the left MCA (). This phenomenon was not found in the rotation to right. And the compression of hyoid bone to carotid arteries in the right side was not recognized. He subsequently underwent a computed tomography angiography (CTA) of the neck and head, which revealed an enlarged left hyoid bone on close contact with carotid bifurcation, without evidence of artery stenosis (). Time of flight-magnetic resonance angiograph (TOF-MRA) showed abnormal signal in the left-internal carotid artery (ICA) lumen, which was more be likely caused by artifact, because the signals of right CCA and bilateral vertebral artery (VA) were also decreased at the same level, as well as the flow on the left ICA on carotid ultrasound on neutral head position was normal. High-resolution magnetic resonance imaging (HR-MRI) displayed no abnormality in the arterial wall. Subsequent DSA revealed no dissection, stenosis or pseudoaneurysm of the internal and external cranial arteries, and no arterial repair or reconstruction was necessary. Extensive workup for multiple causes of stroke in young adults was unrevealing, including complete blood count, erythrocyte sedimentation rate, liver and renal function tests, lipid profile, electrolytes, hemoglobin A1c and C-reactive protein. Thyroid function analysis, tumor markers test, antithrombin III activity, protein C and protein S levels, homocysteine and D-Dimer levels were within the normal limits. Serologic tests of human immunodeficiency virus, hepatitis B and C viruses, syphilis, anti-cardiolipin antibodies, beta-2-glycoprotein antibody, antinuclear antibody and rheumatoid factor were negative. A transthoracic echocardiogram did not demonstrate thrombus, right-to-left shunting post PFO closure or valvular disease, and 24-h Holter monitoring demonstrated episodic bradycardia without atrial fibrillation.\nBased on the imaging study as well as the lack of other findings, the working diagnosis was considered as the external compression of the left carotid artery by the hyoid bone, resulting in recurrent ischemic strokes. Given repeated recurrence under antiplatelet treatment, anticoagulation was added. The following 2-year follow-up showed no new neurologic events or any other complaints.

A 40-year-old Caucasian male, a past medical history of smoking, complaining from 5 years of occasional abdominal discomfort started having an acute, stinging pain in the right upper abdomen. A blood sample was taken that showed a smoldering increase of the transaminases and C-reactive protein of 22 mg/L. He was investigated in the outpatient setting with an abdominal ultrasonography that revealed a polycystic lesion of 9 cm of diameter in the right flank. He was than referred to our Hospital, where the physical examination was completely silent. A contrast enhanced CT scan of the abdomen revealed a polylobate hypodense formation, with multiple thin internal septa which are enriched after contrast (dimension 83 × 43 × 61 mm) (Figs and ). Radiologist posed differential diagnosis among peritoneal lymphangiomatosis, enteric duplication cyst and—even if less likely in a male without history of past abdominal surgery—benign multicystic peritoneal mesothelioma. After multidisciplinary discussion we proceeded to an exploratory laparoscopy that confirmed the presence of multiple cystic lesions of the peritoneum, some interesting the omentum, with a weak adherence with the ascending colon (Figs and ). We performed a complete excision of the neoformation, with free margin on omental fat. A small lesion of the colonic serosa was treated with a prophylactic continuous suture with Vycril 2-0. The postoperative course was uneventful ant the patient was discharged after 2 days without complications.\nOn gross examination a soft, yellowish tissue specimen was seen, measuring about 13 × 9 × 4 cm, composed of multiple cysts, up to 1 cm in diameter, containing a clear fluid. It was fixed in 10% formalin, embedded in paraffin, and the sections were evaluated by hematoxylin and eosin stain. Histologically, it consisted of cysts lined by a single layer of flattened to cuboidal mesothelial cells without atypia. Immunohistochemistry using an automated stainer (Ventana, Tucson, AZ) was performed and all tumor cells showed immunoreactivity for WT1 and Calretinin. Based on these findings, the final histological diagnosis was multicystic benign mesothelioma.\nAfter discussion with Referral Center was suggested an annual follow-up with MRI, and in case of relapse an approach with cytoreductive surgery and subsequent HIPEC.

A 59-year-old female with Sicca syndrome and rheumatoid arthritis presented to our department with blurred vision of the right eye for 5 days. She has been diagnosed with retinal vascular occlusion in the left eye 2 months ago. Her best-corrected visual acuity (BCVA) was 0.03 in the right eye and 0.2 in the left eye. Intraocular pressure was 15 mmHg in the right eye and 17 mmHg in the left eye. There were no keratic precipitates, neither flares nor inflammatory in the anterior chambers. There was also no vitritis in her both eyes. Bilateral disc hyperemia and serous retinal detachment at the posterior pole in her both eyes were noticed by fundus examination []. FAG revealed bilateral late dye leakage from the disc and posterior choroid []. Color sensation loss in both eyes was also noticed. OCT showed bilateral subretinal fluid and choroidal thickening, with right eye more copious than the left eye []. The patient denied ocular pain, headache, hearing impairment, or other neurological signs. Under the tentative diagnosis of VKH disease, she was admitted for intravenous methylprednisolone pulse therapy.\nHowever, positive rapid plasma reagin (RPR) (1:256) and treponema pallidum hemagglutination (TPHA) (1:2560) were reported during admission, while HIV test showed a negative result. Her diagnosis was revised as bilateral ocular syphilis with optic neuritis and serous retinal detachment. As she is allergic to penicillin, intravenous ceftriaxone and oral minocycline were given for 14 days, and the steroid was discontinued instantly. Two weeks after the treatment, her BCVA recovered to 0.5 in the right eye and 0.9 in the left eye. Serous retinal detachment and disc hyperemia in her both eyes improved gradually []. During the following 1 year, there was no recurrent intraocular inflammation even without systemic steroid or immunosuppressive therapy or antibiotics []. Her BCVA improved to 1.0 in both eyes and intraocular inflammation remained quiescence.

A 61-year-old male with no previous medical history, presented with right upper quadrant pain and mild elevation of total bilirubin to 2.9 and Ca 19-9 was elevated at 559 u/mL. All other laboratory values were within normal limits. Evaluation included a right upper quadrant ultrasound (U/S) and computed tomography (CT), which demonstrated left intrahepatic bile duct dilatation. No stones were noted in the biliary system or gallbladder. ERCP and MRCP demonstrated a mural nodule arising from confluence of the left hepatic duct and the common hepatic duct (). Brushings were nondiagnostic. During staging laparotomy, what initially appeared to be metastatic satellite lesions proved to be dilated intra-hepatic biliary system (, arrow head). The planned surgical resection was undertaken with curative intent: resection of the common bile duct with en bloc left hepatectomy, caudate resection, and regional lymphadenectomy. Reconstruction was performed with a Roux en Y hepaticojejunostomy to the secondary right hepatic bile ducts. Two exophytic polypoid tumor masses were identified within the left intrahepatic bile ducts, 2.5 and 2.9 centimeter in size (). Microscopic analysis demonstrated well-differentiated adenocarcinoma arising within a hepatobiliary cystadenoma (). Multifocal severe dysplasia was seen within the left intrahepatic biliary tree without evidence of invasive carcinoma. The remaining right biliary ducts and distal common bile duct were uninvolved. A 1 mm focus of metastatic disease was identified in the regional nodes (1/13).\nThis patient was taken to surgery for treatment of a suspected intrahepatic cholangiocarcinoma not hepatobiliary cystadenocarcinoma. Radical resection with regional lymphadenectomy was performed with curative intent and frozen section only obtained at the right biliary margin (negative for dysplasia and cancer). Microscopic analysis demonstrated well-differentiated adenocarcinoma arising within a biliary cystadenoma with multifocal severe dysplasia. The malignant polyps contained atypical glands infiltrating into underlying mesenchymal (ovarian-like) stroma. A 1 mm focus of metastatic disease was identified with the lymphadenectomy specimen (1/13). The remainder of the resected biliary system, right biliary duct, and distal common bile duct were uninvolved. Adjuvant chemotherapy and radiation therapy were discussed but not recommended. Prognosis and outcome in some clinical series seem favorable in comparison to the highly fatal cholangiocarcinoma diagnosis. At two years following surgery, he remains disease-free with a normal computed tomography and Ca 19-9 level.

SM, a 55-year-old female, in established renal failure secondary to adult polycystic kidney disease, received a living unrelated renal transplant through an exchange donor program. The kidney was implanted in the left iliac fossa. Her past medical history included a mechanical aortic valve replacement, cerebrovascular accident, and ascending thoracic aortic aneurysm treated by aortic root replacement and was maintained on long-term warfarin. One week prior to her transplantation, her warfarin was replaced with enoxaparin 60 mg daily.\nThe donor renal vein was thin walled and cut short requiring the recipient's long saphenous vein to be harvested and used as a cuff to lengthen it. The kidney had three arteries: a small upper polar artery which was ligated, a middle artery that was anastomosed end to side to the external iliac artery, and a medium sized lower polar artery that was anastomosed end to end to the inferior epigastric artery.\nPostoperatively, she was put on a heparin infusion at a rate of 15 units/kg/hour with a targeted activated plasma thromboplastin time (APTT) ratio of 1.5–2.0. Immunosuppression comprised induction with basiliximab and maintenance on tacrolimus, mycophenolate mofetil, and prednisolone.\nA routine ultrasound scan performed on the first postoperative day showed global perfusion of the kidney, but a deep fluid collection of about 5 cm diameter was seen at the lower pole. Given an APTT ratio of 3.5, the heparin dose was reduced to 11 units/kg/hour. On the second postoperative day, she developed frank haematuria and her haemoglobin (Hb) level dropped from a preoperative level of 10.8 g/dL to 8 g/dL. A CT scan was performed which confirmed a large retroperitoneal haematoma (15 cm in diameter) with layered density but no evidence of active bleeding (). At reexploration of the transplant, the haematoma was evacuated and the kidney was noted to be well perfused without any obvious active bleeding point. Heparin (7.5 units/kg/hour) was restarted on the next day (postoperative day three) maintaining the APTT ratio within the target range until postoperative day five when this was switched to enoxaparin 80 mg daily. The dose of enoxaparin was increased to 120 mg on day 7 as the transplant function improved.\nSM experienced several complications following transplantation including CMV viraemia, pulmonary oedema, late urine leak managed conservatively, and recurrent urinary sepsis treated with antibiotics. On postoperative day 27, she developed pedal oedema, pain in the right hip, and thigh especially on moving as well as a 3 cm swelling in the right groin. In addition, there was a significant amount of bruising in the right flank extending into the thigh and upper calf associated with paraesthesia, significant discomfort, and weakness in the right leg. She also became hypotensive (81/53 mmHg) and required resuscitation with three units of packed cells and protamine 50 mg as her Hb dropped to 4.8 g/dL and anti-Factor Xa level was 0.97. Enoxaparin was stopped. An abdominal and pelvic CT scan showed bilateral psoas haematomata (). A repeat CT scan performed on the 31st postoperative day found no change in the haematomata apart from an extension to other retroperitoneal sites.\nBy the 36th postoperative day, she was restarted on warfarin and a CT scan showed a mature haematoma (with gas locules) around the transplant kidney as well as the bilateral psoas haematomata. Linezolid was added to the antibiotic regimen and later switched to Teicoplanin based on a urine culture which grew enterococcus. Antibiotics were continued for four weeks in one form or another. Her mobility was severely impaired when she developed the psoas haematomata, effectively confining her to her bed in the initial period. Regular physiotherapy was carried out throughout and she made steady progress. On postoperative day 78, she was discharged to a local community hospital where her rehabilitation continued for a further 16 days. She then continued her convalescence at home. By eight months after her transplantation, she had returned to her pretransplant levels of fitness. At her last clinic visit (18 months after transplantation), she stated that she had returned to full fitness with regular outdoor activities and her transplant function was excellent with a creatinine of 97 μmol/L (MDRD 54 mL/min).

A nonsmoking, healthy, 35-year-old man complained of nasal stuffiness, crusting, and bleeding due to a nasal septal perforation. This had been caused by nasal insufflation of cocaine for one year ten years previously. He initially used only one dose (25 mg) weekly but this dose was taken five times the last week before the perforation occurred. Eight weeks later cautery with silver nitrate was applied once unilaterally to a bleeding point at the posterior edge of the perforation. He had been off the cocaine abuse for ten years at the time of surgery. This is confirmed by his employment as an officer in the merchant marine during these years. There was no history of nasal trauma, surgery, or long-term use of nasal sprays. The perforation measured 5 × 5 mm. There was crusting at the posterior end. No other nasal abnormality was observed, the mucoperichondrium looked healthy and the cartilage seemed strong at palpation. The surgical closure was performed by an experienced surgeon using an endonasal approach. The incision started as a hemitransfixion on the right side, continued along the nasal sill to the inferior concha and thereafter dorsally underneath the concha until the equivalent position of the posterior end of the perforation and then curved medially to the middle of the nasal floor. A lower mucoperiosteal/perichondrial flap was then created and the nasopalatine artery and nerve severed so the flap could be brought medially and upwards along the nasal septum to close the perforation. The same procedure without the hemitransfixion incision was performed on the left side. The mucoperichondrium above the perforation was left in place. A piece of cartilage and bone was then brought forwards into the perforation to obtain a three layered closure. The perforation and the incisions were carefully adapted with PDS sutures making sure the blood supply was not compromised. Silicone sheaths were placed endonasally for protection and slight compression. They were removed after nine days revealing a defect at the site of the perforation. The hemitransfixion incision had failed to close. Oral and topical antibiotics were given despite absence of infection. A reperforation occurred after two weeks and the hemitransfixion incision widened. The incision closed after a further two weeks; a cartilaginous saddle deformity was then apparent. The size of the perforation (3 × 3 mm) has remained unchanged one year later.

This 27-year-old pregnant woman, presented initially at 19 weeks gestation with intermittent headaches, nausea, and vomiting for two months duration. She was admitted to an outside hospital and was diagnosed with a prolactin secreting pituitary adenoma. At that time, the patient was noted to have normal visual acuity in both eyes with no evidence of field cut as well. The patient was treated with bromocriptine therapy given the diagnosis of prolactinoma. At 36-week-gestation, the patient presented to our hospital with severe onset headache and acute vision loss in the left eye. MRI of the brain revealed a suprasellar, hemorrhagic mass measuring approximately 2.1 × 1.3 cm in size with noted optic chiasm compression (). On neurological examination, the patient was noted to have decreased visual acuity in the left eye (20/200), with normal vision in the right eye. Visual field testing revealed a severe bitemporal visual field loss. All other cranial nerves remained intact. Given the significant, acute, neurologic deficit noted upon the examination, the decision was made to offer the patient minimally invasive surgical intervention. Prior to the planned surgery, a lengthy discussion with the anesthesia team was conducted with regards to risks to the unborn fetus. A multidisciplinary “team” approach was implemented to ensure the greatest degree of safety for the patient.\nThe patient was taken to the operating room to undergo an endoscopic endonasal transsphenoidal resection of the pituitary apoplexy. The patient's head was immobilized using a three-pin head fixation device. The operation was performed endoscopically through both nostrils. The left middle turbinate was fractured outward to widen the corridor to the sphenoethmoid recess in order to facilitate the identification of the sphenoid ostium. Bilateral anterior sphenoidectomies were performed extensively with Kerrison rongeurs. The intersinus septum of the sphenoid sinus and sinus mucosa were then removed (). The bone in the anterior wall of the sella was notably attenuated. The exposed dura mater was then incised and old blood products extruded under pressure once the dura was opened and an internal decompression of the tumor was performed (). The interface between the pseudocapsule of the tumor and normal pituitary gland was identified and dissected with a microdissector and a small ring curette. Once the remaining tumor had been identified in the corners, it was removed under direct endoscopic visualization. Care was taken not to tear the arachnoid membrane to reduce the risk of postoperative cerebrospinal fluid leakage. The entire procedure lasted less than two hours. The patient was transferred to the neurosurgical intensive care unit for postoperative care. On postoperative day one, the patient developed polyuria and increased serum sodium. The patient was treated with desmopressin and liberal intake of water for central diabetes insipidus. The patient's serum sodium stabilized after one day and the central diabetes insipidus remained only transiently. Upon examination, the patient demonstrated rapid visual acuity and visual field improvement. Finally, the patient was transferred to the labor and delivery unit where an elective Cesarean section was done one week after the endoscopic endonasal surgery was concluded. The newborn and the mother remained in stable condition. Postoperative MRI revealed complete excision of the tumor, with no further evidence of optic chiasm compression ().\nFrozen sections revealed mainly blood products with fragments of pituitary gland tissue. The histopathology was consistent with prolactinoma.

A 49-year-old Caucasian male with a history of recurrent pancreatitis complicated by a large peripancreatic fluid collection, presented with acute abdominal pain for one day. It was described as 8 out of 10, constant in the epigastrium and left upper quadrant, non-radiating, worse with movement, and partially relieved with analgesics. It was also associated with nausea and one episode of nonbloody, nonbilious emesis. He had 2–3 episodes of loose bowel movements; however, he denied melena or hematochezia. Social history was notable for one pack per day tobacco use, occasionally smoking of marijuana, and alcohol abuse. He had two previous episodes of acute pancreatitis in the past year. Physical examination showed unremarkable vitals, a soft non-distended abdomen with epigastric tenderness, and audible bowel sounds. Laboratory workup was only remarkable for a lipase of 425 U/L. Computed tomography (CT) scan of the abdomen () revealed peripancreatic fat stranding and multiple acute peripancreatic fluid collections, including a 5.6 × 5.1 cm collection between the spleen and the greater curvature of stomach, an 8.3 × 1.8 cm collection extending medially along pancreatic tail and wall of the stomach, and a 3.8 × 2.1 cm heterogeneous collection between the spleen and tail of the pancreas. Due to the nature and locations of the fluid collections found, an abdominal CT angiography () was done which showed a hyperdense component between the spleen and pancreatic tail with suspicion for either clot or pseudoaneurysm of the splenic artery. For further investigation of the hyperdense component, a catheter angiogram of the splenic artery was performed which demonstrated a rounded area of late arterial phase opacification, with staining consistent with a pseudoaneurysm of the splenic artery. A transcatheter embolization () was then successfully performed by placing the embolization coil both distally and proximally to the blood vessel supplying the pseudoaneurysm. Complete resolution of pseudoaneurysm was confirmed with a postembolization angiogram, after which the patient’s symptoms completely resolved.

A 38-year-old female patient with no cardiovascular morbidities presented to the emergency department with chief complaint of acute central chest pain that started 3 hours earlier and worsened in the last hour before coming to hospital. Patient had normal vital signs and unremarkable physical examination. Her 12-lead electrocardiogram (ECG) showed 0.5 mm ST segment depression in the left-sided limb and lateral precordial leads (I, aVL, V5, and V6). High-sensitive cardiac troponin I (hs-cTnI) was slightly positive at 0.12 ng/mL (normal range <0.04 ng/mL). She received a loading dose of dual antiplatelet (DAPT) agents and was planned for elective coronary angiography (CAG) during the same hospital admission. She was categorized as a case of non-ST elevation acute coronary syndrome. A bedside transthoracic echocardiography showed no regional wall motion abnormalities and an ejection fraction of 60% with no valvular abnormalities.\nCAG through the right femoral artery unexpectedly demonstrated a SCA branching from the right coronary sinus (RCS). There was no left coronary system arising from the corresponding left coronary sinus. The right coronary artery (RCA) was normal in course and anatomy with large caliber, dividing into posterior descending artery and right posterolateral branches. The left system originated separately from the RCS, giving rise to a small left circumflex artery and two left anterior descending arteries with no obstructive disease along their course (\n;\n[available in the online version])\nCoronary computed tomography angiography (CCTA) was done to further characterize the course of the anomalous SCA, as well as to delineate the type of surgery indicated. This confirmed our diagnosis and demonstrated a benign course of the first proximal LAD artery, but a malignant course was to be distal long LAD that was running between the aorta and the right ventricular outflow tract (\nand\n;\n[available in the online version]).\nAfter a heart team assessment, the patient was counselled to perform coronary artery bypass graft (CABG) surgery with reimplantation of the anomalous coronaries. However, she declined any surgical intervention, and she was treated conservatively with DAPT, B-blocker and statins followed by aspirin for life.\nOn frequent follow-up visits for the following 18 months, the patient was well, with no angina or effort intolerance.

A 20-year-old male patient came to Department of Oral Medicine and Radiology, Rajah Muthiah Dental College and Hospital with a complaint of swelling in the left lower jaw, since 6 months. Patient revealed that the swelling gradually increased in size to attain the present status. It has become symptomatic for the past 10 days with the onset of a mild, intermittent and nonradiating type of pain. His medical, dental, and family histories were not contributory.\nExtraoral examination revealed facial asymmetry due to a well-defined, swelling over the left body of the mandible []. It measures approximately 4 cm × 3 cm in size and is roughly oval in shape. It extended superiorly to the level of ala-tragal line and inferiorly extending 1 cm beyond lower border of the body of the mandible. Medially it extends 2 cm from the corner of the mouth and laterally to the posterior border of the ramus of the mandible. On palpation, the swelling was tender, hard in consistency, immobile and skin over the swelling is pinchable. Regional lymphadenopathy was not evident.\nIntra-oral examination revealed single well-defined swelling with bicortical expansion extending anteroposteriorly from 36 to retromolar area []. On palpation, the swelling was tender, hard in consistency and immobile. There was no pus discharge or any secondary changes. Third molars in all the four quadrants were clinically absent. Teeth in the region were normal and showed no evidence of displacement of 36 and 37.\nA painless, well defined, slow growing, bony hard swelling, with bicortical expansion located in the posterior aspect of the mandible, apparently not related to the neighboring teeth is suggestive of a bony neoplastic swelling and was provisionally diagnosed as ossifying fibroma (OF).\nInvestigations performed were intraoral radiographs, orthopantomogram and computed tomography (CT). Intraoral periapical radiograph in relation to 36 region showed a radiopaque mass surrounded by a radiolucent area []. Periodontal ligament (PDL) is seen to be continuous, and lamina dura was found intact. Root resorption or tooth displacement was not evident. An occlusal view revealed a uniform bicortical expansion which was further confirmed on CT examination [].\nPanoramic radiograph showed a well-defined radiopaque lesion measuring 4 cm × 3 cm in diameter surrounded by a radiolucent area []. There was inferior cortical bowing and thinning.\nThe CT scan in axial and coronal sections showed an oval hyperdense mass with central attenuation of 1358 HU [Figure and ]. Periphery was surrounded by a uniform hypodense area with 14 HU. In coronal sections, the mandibular canal was evident on the superiolateral aspect of the mass, suggesting a tumor of nonodontogenic origin [].\nSurgical excision of the mass was done under general anesthesia by placing submandibular incision. After excision, the bony wall of the cavity was curetted thoroughly to ensure that no remnants of the lesion were left out. The osseous specimen was submitted for histopathological examination.\nHistopathologically, the tissue section revealed stromal tissue containing acellular fibrous connective tissue with numerous spindle fibroblasts. It also showed globular masses of cementum-like calcifications. The final diagnosis was given as OF. The patient is under regular follow-up with no signs recurrence.

A 56-year-old woman, who works as a store seller, first experienced symptom onset 16 years previously in a first attack that altered tactile sensation in her legs. She was diagnosed with MS and treated accordingly at the Mexican Institute of Social Security and at the INR ().\nThe case was studied in the CAPD laboratory in 2011 and 2014. Our study protocol for patients with MS has not changed since the previous publication []; however, the method now includes recording of long latency auditory evoked potentials (LLAEPs).\nIn the interview conducted at 2011, she reported stable tinnitus and bad auditory discrimination since 2010; however, audiograms were normal for both ears. She had a phonemic discrimination deficit, poor sound localization, mixed dysarthria, walking instability with a tendency to fall, and memory disorder ().The first CAPD study found no significant alterations; she only had a slightly higher percentage of correct answers for DDR test for the right ear (). The study was repeated in 2014 with the same symptoms and persistent tinnitus. Three of four monaural tests showed a dominance of left ear processing, with a higher percentage of successes for the left ear, and a similar profile in the frequency pattern discrimination test. In contrast, the DDR test found a higher percentage of correct answers for the right ear relative to 2011 ().\nIn brainstem auditory evoked potentials (BAEPs) from the right ear, we observed a mild retardation in interwave interval I–III, and the left ear response presented bad morphology definition and retarded latencies. We also found a retardation of the left N2 wave in LLAEP (). In this case, the results suggest an alteration of the left auditory pathway, probably involving structures connecting temporo-frontal areas, the limbic system, and subcortical thalamic-reticular areas () [,-], with better function of the right ear in the DDR test, BAEP, and LLAEP.

A 63-year-old nonsmoking woman with metastatic colorectal cancer to the lungs and liver, diagnosed four years previously and treated at that time with surgery and 12 cycles of FOLFOX, presented to our clinic with oligoprogression of right paratracheal metastatic lymphadenopathy. We initially recommended optimization of her systemic therapy. She underwent treatment with three months of FOLFIRI-bevacizumab followed by a two-month treatment holiday, and presented to our clinic again with decreased right paratracheal lymphadenopathy and no new metastatic disease. Considering her limited disease burden and long progression-free interval, we offered definitive dose hypofractionated radiotherapy as consolidation, and treated her with 60 Gy in 15 fractions with highly conformal volumetric modulated arc therapy (VMAT) (Figures -). The patient tolerated the treatment well. However six months later she developed new metastatic disease in the lung and abdomen and recommenced FOLFIRI-bevacizumab for five months.\nSix months after finishing her post-radiotherapy course of FOLFIRI-bevacizumab, she presented to our clinic with productive cough with thick sputum with occasional blood streaks for which she tried oral antibiotics with no improvement. We performed a CT scan, which showed a tracheal diverticulum in the region we had previously treated with radiotherapy (Figure ). We performed bronchoscopy, which also revealed a large tracheal diverticulum (Figure ).\nWe prescribed hyperbaric oxygen, pentoxifylline and vitamin E, which unfortunately did not improve her tracheal diverticulum per bronchoscopy performed three months later. We consulted our thoracic surgery colleagues who performed a serratus muscle flap repair of the tracheal diverticulum to prevent progression to tracheovascular fistula, as we were concerned the defect was extending toward the superior vena cava. The patient tolerated surgery well without complications, and was discharged home in stable condition on postoperative day 11. She has done well since then and continues to undergo routine monitoring with bronchoscopy and computed tomography (CT) imaging. Her most recent bronchoscopy, 15 months postsurgery, shows continued resolution of the tracheal diverticulum (Figure ). In this case, due to expert surgical care we were able to avoid a potentially catastrophic complication.

A 29-year-old, right-handed white female was admitted to the epilepsy monitoring unit for video electroencephalography monitoring and medication adjustment in a large urban academic medical center. Her medical history was significant for medically refractory frontal lobe epilepsy with complex focal seizures with or without secondary generalization status post partial right frontal (2001) and right temporal resection (2008). Medication adjustment was warranted because of frequent daily seizures including clusters of 2 to 3 seizures despite adherence to phenytoin and clonazepam (CLZ). A complete list of home medications, social history, and admission vital signs and labs, are included in . Several AEDs and a modified Atkin's diet were previously discontinued because of inefficacy and/or intolerance ().\nPerampanel was added to her current home AED regimen of phenytoin and CLZ and, because of her prior history of paradoxical reactions, patient was initiated at 2 mg/d, a lower dose than recommended for an individual on concomitant strong CYP3A4 inducers., She denied all commonly reported AEs following initial administration other than nausea and drowsiness which resolved the next day. Her electroencephalogram remained unchanged. The day after initiation of PER 2 mg/d, she was discharged with instructions to increase by 2 mg/d every 2 weeks up to 6 mg/d until follow-up with her epileptologist (sooner for AEs or increased seizure frequency). Previous home doses of phenytoin and CLZ were continued. Upon admission and discharge (hospital day 2) complete blood count and complete metabolic panel were unremarkable and free phenytoin level was unchanged (2.1 mg/dL).\nShe tolerated the initial PER dose titration well. Three days after the dose increase to 6 mg/d, she experienced new-onset food aversion. Over the phone, the food aversion was described by her mother (primary caregiver) as the smell or sight of any food including fruits or vegetables resulting in nausea despite absence of any physical problem. No change in sense of taste was reported. This was a new presentation for her, not previously experienced. In addition, the patient became more irritable and anxious after the dose increase. No seizure frequency improvement was reported. The patient and her mother expressed interest in PER discontinuation. Two days after dose reduction to 4 mg/d, she was able to sit by the kitchen table during meal times but had some residual effect and was unable to eat a large amount of food, and this further improved when dose was decreased to 2 mg/d. When PER was discontinued, it took about 2 months before return to baseline appetite. During PER trial, the patient lost a total of 8.4 lb (body mass index = 18.5 kg/m2). Body mass index increased to 19.3 kg/m2 within approximately 2 months after PER discontinuation.

A 40-year-old male presented with complaints of bloody diarrhea of 3 months' duration. Five days after the onset of blood in stools, he noticed small vesicular lesions over the dorsum of the right foot, followed by the appearance of similar lesions on the left foot, buttocks, and hands. These lesions subsequently formed ulcers. The size of the largest lesion was 5.5×4.5 cm. The base of the penetrating ulcer exposed the deep fascia of the tendon of his foot, with complete denudation of the skin and subcutaneous tissue ().\nAt admission, the patient had a clinical Mayo score of 9. He had pallor, as well as ulcers over dorsum of both feet () and over the left buttock. Laboratory evaluation revealed a hemoglobin level of 8.6 g/dL, total leukocyte count of 10,800 cells/µL, total serum protein level of 5.2 g/dL, and a serum albumin level of 2.9 g/dL. Colonoscopic evaluation revealed diffuse loss of vascular pattern, multiple superficial ulcers, and oozing of blood involving the entire length of the colon. The extent of the disease was therefore classified as E3 as per the Montreal classification, and the colonoscopic severity was 7 as per ulcerative colitis endoscopic index of severity (UCEIS). A diagnosis of UC with acute exacerbation and PG was made.\nThe patient was started on intravenous hydrocortisone (100 mg every 8 hours), mesalamine, and azathioprine. Topical antibiotics and dressing were used to treat the skin lesions. The patient showed partial improvement of bowel symptoms; however, there was no improvement in the skin lesions, even after 1 week of intensive steroid therapy. Hence, he was started on intravenous infliximab at a dose of 5 mg/kg. Following infliximab administration, he showed signs of healing at the peripheral margin of the skin lesions, coupled with appearance of granulation tissue over the previously visible deep fascia of the foot within 1 week of receiving the first dose (). The transverse diameter of the lesion on the lateral malleolus of the right foot was decreased by approximately 1 cm within 1 week. Subsequently, he received the remaining two induction doses of infliximab at weeks 2 and 6. The skin lesions continued to heal, and he was discharged with a prescription of oral mesalamine and azathioprine. After 6 months, the skin lesions had healed completely, albeit with extensive scarring on the dorsum of the foot (). His bowel symptoms were also in remission at the time of the last follow-up.

Chief complaints: The recipient presented with an advanced liver cirrhosis and suffered from the typical symptoms, including ascites, renal impairment and feeling chronically tired and cold.\nHistory of present illness: The donor liver was offered from a 71-year-old male donor with brain death due to intracranial haemorrhage. The candidates underlying liver disease presented with the typical features of a slowly progressive liver disease over many years, despite alcohol abstinence.\nHistory of past illness: The past medical history of the donor included arterial hypertension and cholecystectomy due to cholecystitis with peritonitis more than 20 year prior to donation. The recipient’s history other than the liver disease was uneventful.\nPersonal and family history: The recipient’s history was uneventful.\nPhysical examination upon admission: The recipient presented with the typical symptoms of advances liver cirrhosis with several litres of ascites, requiring regular paracentesis, sarcopenia and encephalopathy.\nLaboratory examinations: The donor liver parameters were entirely normal. The recipient presented with a lab end stage liver disease (MELD) score of 22 points and the sodium was in the low normal range.\nPhysical examination upon admission: According to the national allocation system, our team was allowed to choose the recipient from the waiting list. We selected a 62-year-old patient with alcoholic liver cirrhosis and large amount of ascites, regular paracentesis and previous spontaneous bacterial peritonitis. Recipient selection (large volume ascites) was based on the expected large right lobe of 2.2 kg.\nLaboratory examinations: Despite such advanced liver disease, the candidate achieved only limited number of 22 and 54 points for the model of MELD and United Kingdom model for end stage liver disease score with, respectively (Table ). The standard recipients imaging, performed during transplant assessment revealed patent vessels and a replaced right hepatic artery (HA) from the supra-mesenteric artery.\nImaging examinations: Due to an aspiration pneumonia, a computer tomography (CT) of the donor’s chest was done and the upper abdomen was captured, where a very small left lateral liver segment with possible biliary dilatation was identified. The recipient’s ultrasound scan, done as per routine prior to admission on the waiting list showed ascites and the expected cirrhotic and shrunken liver with patent vessels. Interestingly, the intraoperatively identified portal vein thrombosis was not seen on the abdominal CT scan.\nFinal diagnosis: The donor liver with anatomical variation was accepted for liver transplantation for a recipient with advanced alcohol related liver disease within the fast track liver offering system.\nTreatment: Based on the long waiting time in blood group 0, we have decided to go ahead with the donation procedure and assess the donor and the liver. The procurement was done by a team from an experienced centre in the United Kingdom. A large right liver lobe (Riedel’s lobe) combined with an atrophic left lateral segment was identified. Only minimal liver tissue was evident on the left side of the falciform ligament (Figure ). The weight of this graft was 2.2 kg, with mild steatosis and normal vascular anatomy. Some adhesions from the previous cholecystectomy were found, however no other lesions or findings were evident. Importantly, the anatomical development was normal for all vascular and biliary structures on both liver sides with a however small left hepatic vein corresponding to the atrophic left lateral segment (LLS). This graft was declined by all other centres and became fast tracked.\nDuring transplantation surgery, 7 L of ascites were evacuated, severe portal hypertension, and advanced SBP were found. Additionally, a grade 2 portal vein thrombosis (PVT), requiring thrombectomy was identified. Due to the graft-recipient size relation with the thick right Riedel lobe and dominant right and middle hepatic vein, the decision was made to implant the graft with a modified piggyback technique, in contrast to the standard classic piggy-back technique (graft cava–to recipient orifice of left and middle hepatic vein), which is routinely performed in half of whole grafts at our centre (Figure -). To achieve optimal draining of the compact right liver lobe through the dominant right hepatic vein, a large teardrop shape incision was performed at both, donor and recipient vena cava. The satinksy clamp was rotated slightly to the right side of the recipient towards the graft. The recipient hepatic veins were not included in the anastomoses, due to their fragile texture. The portal vein anastomosis was done in a standard fashion (end-to-end) and the recipients replaced right HA demonstrated a good calibre and strong pulse, enabling us to use this vessel for the reconstruction with the common donor HA at the gastro-duodenal artery patch (Figure ).\nOutcome and follow-up: The reperfusion was uneventful, no reclamping was required and immediate graft function was evident through bile flow, decreasing lactate and minimal inotrope support at the end of surgery. The reconstruction of the common bile duct (CBD) was done over a recipient duct plastie, based on the size discrepancy with a large donor CBD. Vessel patency was confirmed through intraoperative ultrasound. The liver demonstrated good function and the recipient was extubated within the first day after transplantation with an overall short intensive care stay of 2 d. Acute kidney injury occurred without requirement of hemofiltration. The recipient was discharged within 12 d and required one short, local readmission for diarrhoea (Table ). Further follow up was uneventful with an asymptomatic patient more than 12 mo after liver transplantation.

We present the case of a 70-year-old man who underwent dipyridamole Rb-82 positron emitting tomography (PET) 3 days following percutaneous coronary intervention with right coronary artery (RCA) stenting []. There was complete occlusion of the proximal RCA, as well as multiple borderline lesions in the left anterior descending (LAD) and circumflex territories (LCx). Postthrombectomy and stenting [], angiography showed complete resolution of the proximal RCA lesion and no residual disease in the remainder of the RCA territory. No intervention was attempted for the lesions in the LAD and LCx territories.\nA follow-up dipyridamole Rb-82 PET MPI study was requested to assess the significance of the lesions in the LAD and LCx territories []. Perfusion images showed significantly decreased tracer uptake in the inferior wall, which normalized on the poststress images. No other significant perfusion defects were appreciated. Flow quantification revealed an impaired global myocardial flow reserve (MFR) of 1.37 with relatively homogeneous myocardial blood flow (MBF) in all territories at stress at a stress rate-pressure product (RPP) of 7850 mmHg × bpm. Hypokinesis of the inferior wall was present on both rest and poststress studies, in keeping with stunned myocardium. No misregistration errors, or other obvious source of artifact, were noted on either rest or poststress images. On the rest study, there was a clear defect in the inferior wall, which normalized on the stress acquisition following a dipyridamole infusion. On the same day, the patient underwent a repeat MPI study, using dobutamine as the stressing agent. This study again demonstrated a defect in the inferior wall which was present on both the rest and stress studies. Aminophylline was administered after the study dipyridamole study with no additional interventions performed in the time between the two studies.\nEight hours later, a repeat Rb-82 PET MPI study was performed using dobutamine as a stressing agent []. Stress RPP reached 14350 mmHg × bpm. The inferior wall defect was again seen on the rest study; however, the defect persisted on stress images. MFR to the inferior wall was again diminished on both sets of images (rest = 0.59, stress = 1.21), with a corresponding regional wall motion abnormality. The reason for the difference in findings between the two studies is unclear but is likely related to the differences in mechanism of action between the two stressing agents.

An 8-month-old baby boy weighing 5700 g presented with a history of absent anal opening and continuous dribbling of urine from the lower abdomen since birth. He underwent high sigmoid loop colostomy at day 3 of life for ARM. On presentation, his abdomen was not distended and a superior vesical fissure was seen in the lower abdominal wall. He was decompressing well from the colostomy. The perineum was poorly developed with flat gluteal folds and the sacrum was impalpable. External genitalia were normal male-like and bilateral testes were descended.\nA pressure augmented, distal colostogram showed anorectal atresia with a radiolucent separation, no identifiable rectourinary fistula, and sacral agenesis. The distal length of sigmoid colon seemed adequate to attempt a posterior sagittal anorectoplasty (PSARP). The preoperative echocardiography and renal ultrasound were normal. There was no associated limb anomaly.\nThe child was taken-up for PSARP with the provisional diagnosis of high ARM with sacral agenesis and superior vesical fissure.\nThe standard PSARP incision was given, and the muscles were cut and deepened in layers. The perirectal sheath was entered till the shiny rectal pouch serosal layer was reached. Stay sutures were taken on the rectal pouch, adequate lateral mobilization was done, and the pouch was opened in midline for submucosal dissection and anterior mobilization. Another compressible cystic structure was seen superolateral to the previous pouch. Both pouches were opened and were seen to be communicating with one another through a narrow opening, rest being separated by a thick septum. Both were mucosa lined []. The blind ending smaller pouch was completely excised and sent for histology. The second, proximal pouch was mobilized adequately, pulled down, and tapered, and anorectoplasty was completed.\nThe child was discharged on the 5th postoperative day on full oral feeds and no surgical site complications. The histopathology confirmed the distal excised pouch as a RD cyst. Three months later, he underwent colostomy closure and subsequently repair of the superior vesical fissure. At the last follow-up at 6 years of age, he is doing well on bowel management program for fecal incontinence and urotherapy and medical management for neurogenic bladder.

A 40-year-old man with a swelling in the right palatal region was referred to the department of oral pathology for evaluation and diagnosis. The painless mass was noticed 4 months ago by the patient.\nIntraoral examination exhibited a firm, exophytic, oval mass with an intact overlying mucosa in the region of the right hard palate measuring 3 × 4.5 cm in size []. There were no signs of ulceration, bleeding, discharge, or numbness in the area. The patient did not have the habit of chewing tobacco or betel nut. On general examination, he was found to be afebrile, with no palpable lymph nodes in the head and neck region. He did not mention any sudden weight loss in the recent past and the medical history was noncontributory.\nCT scan revealed a mass on the right side of the hard palate, with no involvement of the maxillary sinus []. A provisional diagnosis of benign tumor of salivary glands was given.\nAn excisional biopsy [] was performed under local anesthesia. and a bony crater-like defect was seen on the palatal bone after soft tissue removal. Histopathological examination of sections of the resected specimen revealed an intact stratified squamous epithelium with underlying vaguely follicular and diffuse proliferation of lymphoid cells [Figure and ]. The follicle-like structures were composed of central large cells (giving a ‘washed-out’ appearance) surrounded by a thin rim of small, round lymphocytes. The central large cells had abundant pinkish cytoplasm and convoluted nuclei with inconspicuous nucleoli []. Epimyoepithelial islands were also observed. On microscopic examination of hematoxylin and eosin (H and E)–stained sections, there was a conflict of opinion over the distinction between benign (reactive) lymphoid hyperplasia (pseudolymphoma) and non-Hodgkin lymphoma. Immunohistochemical investigations were performed to resolve the issue. The large lymphoid cells showed immunoreactivity for CD20 and the rim of small lymphocytes were positive for CD5 []. The large lymphoid cells were negative for CD5, Bcl-2, and CD10 [Figures –]. The Ki67 proliferative index was 1% [].\nThe patient was referred to a general physician for systemic evaluation and was found to be free of other systemic manifestations. There were no palpable lymph nodes found anywhere in the body. A final diagnosis of low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) was accorded based on the clinical, radiographic, histopathologic, and immunohistochemical investigations.

A 64-year-old man (height 169 cm, weight 70 kg) was presented for laminoplasty C3-7 due to incomplete cervical spinal cord injury. He started taking antihypertensive medication daily a year ago. Except that, the patient was in good health until he fell from a three-meter-high cliff. Four weeks ago, he had an emergency operation, anterior cervical discectomy and fusion (ACDF) C3-7, under general anesthesia, and no specific events happened during the perioperative period. Anesthesia was induced using a propofol and remifentanil, and the paralysis was facilitated with rocuronium. Endotracheal intubation was achieved using a light-wand and a reinforced endotracheal tube of the inner-diameter 7.5 mm was successfully placed. Anesthesia was maintained with sevoflurane and 50% oxygen in the air. A three-pin head holder was affixed to the patient's head. After the patient was turned prone, the surgeons slightly moved his neck to find an appropriate position and fixed the holder with the head in a neutral position. The total anesthetic and operation time was 405 min and 310 min, respectively, and the blood loss was estimated to be 700 ml. The patient was extubated after a full recovery of respiration and consciousness, and was transferred to the general ward.\nOn the first postoperative day, the patient began to complain of dysphagia and recurrent aspiration, and the symptoms have persisted for two days. A rigid fiberoptic laryngoscope showed the deviation of the tongue to the left on protrusion, the absent movement of the left vocal cord and the pooling of saliva in the left pyriform sinus. Neurologic examination revealed the palsy of the left hypoglossal and recurrent laryngeal nerves. Video fluoroscopic swallowing study (VFSS) showed the impairment of pharyngeal contraction on swallowing and left side deviation and atrophy of the tongue. There was no uvula deviation or abnormality of the soft palate elevation. On neurologic examination, there were palsy of the left hypoglossal and recurrent laryngeal nerve, and the remainder was normal. On a magnetic resonance imaging of the brain and neck, there was no evidence to suspect central neurologic or vascular involvement. These findings suggested a peripheral type of Tapia's syndrome. Conservative management included intravenous corticosteroid, electrical stimulation therapy aimed at a restoration of swallowing ability and the nasogastric tube feeding to reduce the risk of aspiration. VFSS-guided balloon dilation of the esophagus was also performed. Seven weeks after the operation, the patient's symptoms began to improve and he started a soft diet. He gradually recovered thereafter, and was discharged three months later.

A 68-year-old man had undergone low anterior resection and regional lymph node dissection for rectal cancer (Fig. ). The pathological examination showed the tumor to be a moderately differentiated adenocarcinoma with invasion to the subserosa (T3) and regional lymph node metastasis (N1). No distant metastases were found at the time of operation (M0), and the pathological staging of the tumor was stage IIIB, according to the seventh edition of the International Union Against Cancer TNM classification. He was treated with oral uracil and tegafur plus leucovorin for 5 cycles as adjuvant chemotherapy. Eight months after the initial surgery, follow-up computed tomography (CT) showed an enlarged retroperitoneal lymph node located below the aortic bifurcation, which would be considered one of the aortic bifurcation nodes (Fig. ), a tumor in the head of the pancreas (Fig. ), and dilation of the common bile duct and main pancreatic duct. Positron emission tomography (PET) showed abnormal uptakes of 18F-fluorodeoxyglucose (18FDG) in these two lesions (Fig. ). Biopsy of the narrowed section of the pancreatic duct showed an adenocarcinoma. However, it was difficult to identify whether the pancreatic tumor was primary or metastatic disease. Clinical examination was unremarkable. Blood tests showed continued elevation of serum bilirubin (>2.0 mg/dL). The serum carcinoembryonic antigen level was within normal limits (4.1 ng/mL), while the serum carbohydrate antigen 19-9 level was increased to 127 U/mL. Based on these findings, a diagnosis of retroperitoneal lymph node metastasis from the previously resected rectal cancer and primary pancreatic head cancer or pancreatic metastasis from rectal cancer was made. For these lesions, resection of the enlarged retroperitoneal lymph node and pancreaticoduodenectomy were performed. The pathological examination of the resected specimen showed that the histological type of both the retroperitoneal lymph node and the pancreatic head tumor was adenocarcinoma. Moreover, they were identical to the primary rectal cancer (Fig. –), and immunohistochemical study of the pancreatic tumor showed positive immunoreactivity for CDX-2 staining (Fig. ). Based on these findings, these lesions were diagnosed as metastases from the primary rectal cancer. These specimens had negative resection margins. The patient’s postoperative course was uneventful. After the second surgery, he was given 5-fluorouracil, leucovorin, and oxaliplatin (modified FOLFOX6) as adjuvant chemotherapy. However, the chemotherapy was discontinued after only 5 cycles due to an adverse event. He was then routinely followed up without any medication. Sixty-nine months after the metastasectomy, there has been no indication of recurrence.

Here, we present the case of a 44-year-old woman with a medical history of coronary disease with myocardial infarction and stent placement at 29 years old. The patient smoked for 10 years until 39 years old and she did not have a family history of heart or breast diseases. She presented with a 2-week history of left breast swelling with a painful and inflammatory mass in the upper-outer quadrant, measuring approximately 7 cm. Under medical evaluation, she received cefadroxil as a treatment. Breast ultrasound revealed inflammatory changes characterized by cutaneous thickening, increasing echogenicity of subcutaneous tissue, superficial laminar collection, and loss of fatty planes due to multiple anfractuous collections (). Blood laboratory analysis showed normal leukocyte count and a mild elevation of inflammatory markers (C-reactive protein and erythrocyte sedimentation rate).\nAfter 1 week of treatment, clinical worsening was noticed, with increasing redness and edema. A new ultrasound was performed showing no abscess formation and she underwent an ultrasound-guided core biopsy (). On histological examination, the breast tissue revealed an extensive, chronic-active inflammatory process which included granulation tissue with suppurative granulomas, some with lobulo-centric pattern, with an optically empty central vacuole and Gram-positive coccobacilli. These findings were present in an area with solid DCIS, nuclear grade 2. The diagnosis of GLM with coryneform bacteria associated with DCIS was established ( and ). Cefadroxil was maintained for 10 days followed by a 6-day course of azithromycin. Prednisone at 1 mg/kg was also started. An initial favorable response to corticosteroids was noticed, but a clinical worsening with increasing pain and fever presented when steroids doses were lowered. Multiple collections in the upper-outer quadrant and lower-outer quadrant developed during next months, requiring multiple antibiotics schemes and several collection drainages under local anesthetics. Cultures taken from the collections were all negative for aerobic germs.\nMammogram and breast ultrasound were performed after 4 months of treatment searching for images suggestive of DCIS involvement, but both studies revealed no microcalcifications or other suspicious images for malignancy ( and ()). During the next months, she presented clinical worsening with several inflammatory collections growing in the outer quadrants, and she underwent incisional surgery and drainage of the collections. The pathological and microbiological studies were repeated. The microscopic analysis of the breast tissue obtained revealed similar pathological findings to those described in the first biopsy. Therefore, the diagnosis was similar: GLM with coryneform bacteria associated with DCIS of nuclear grade 2, with intensely positive estrogen and progesterone receptors. With the Ziehl–Neelsen and periodic-acid Schiff (PAS) stains, no infectious agents were found. Aerobic, anaerobic, fungi, and mycobacteria cultures were negative.\nThe serology for rheumatologic conditions revealed no evidence of inflammatory diseases. Methotrexate was started with a mild and slow improvement of local inflammation, but with incomplete response.\nSubsequently, and given the progression of the disease, the patient underwent a lumpectomy. The study showed an extensive zone with DCIS with several surgical edges involved and also associated with GLM. With this information, the patient underwent a total mastectomy; we found, in both external quadrants, a wide region with DCIS, distant to more than 1 cm from all the surgical edges, also in coexistence with GLM ().

A 76-year-old man with longstanding dyspepsia, indigestion, tiredness, and rapid weight loss was referred for gastrointestinal evaluation. Blood tests showed macrocytic anemia with low concentrations of folate and vitamin B-12. The patient's hemoglobin concentration was 7.9 g/dL, albumin 32 g/L, and transglutaminase 212 mg/mL (normal range = 0–10 mg/mL). An urgent colonoscopy and duodenal biopsy were performed, which yielded macroscopically normal results. At this level his IgG and IgA concentrations against gliadin and transglutaminase were checked using FDA-approved kits. Both IgG and IgA against α-gliadin were very high; against transglutaminase, IgA but not IgG was 3.8-fold higher than the reference range. In view of the IgA positivity against gliadin and transglutaminase and diagnosis of celiac disease he was transfused with 2 units of packed cells and started on both a gluten-free diet and 20 mg of prednisone daily. Six months later he had gained about 12 pounds and showed few GI symptoms. Because of this improvement the patient became committed to the GFD. One year after the first performance of IgG and IgA antibody testing against gliadin and transglutaminase the repeat tests for these antibodies were negative, which is a further indication that disease management plus a GFD was instrumental in the treatment of this elderly patient with silent celiac disease.\nAccording to Catassi et al. [, ], celiac disease (CD) is one of the most common lifelong disorders in western countries. However, most cases of CD remain undiagnosed mostly due to the poor awareness of the primary care physician regarding this important affliction. Celiac disease is perceived as presenting GI symptoms accompanied by malabsorption. But many patients with celiac disease do not present GI symptoms. These individuals may have silent or atypical celiac disease, and the condition may present with iron deficiency, anemia, increased liver enzymes, osteoporosis, or neurological symptoms []. As used herein, the term “atypical celiac disease” refers to celiac disease in patients who have only subtle symptoms, and the term “silent celiac disease” refers to celiac disease in patients who are asymptomatic.\nThe increasing recognition of celiac disease is attributed to the use of new serological assays with higher sensitivity and specificity. Until recently celiac disease was incorrectly perceived as being uncommon and detected mainly during infancy or childhood. However, it is now recognized that most cases of CD occur in adults 40–60 years old. Patients in this age group may present their symptoms, lab test results, and other examination signs in atypical fashion. In fact, according to a very recent publication, less than one in seven patients is correctly diagnosed with CD [].\nConsequently, as this case shows, if an adult patient presents with symptoms and signs suggesting malabsorption, testing for IgA antibody against gliadin and transglutaminase should be considered. If the test results are positive, celiac diseases should then be made a part of the differential diagnosis, based on which a gluten-free diet should be recommended. If the gluten-free diet should produce an improvement in symptoms, the patient should commit to the diet regardless of age.

A 40-year-old female presented with suspicious increasing micro-calcifications in the right breast. A stereotactic biopsy of the most worrisome area in the right upper inner quadrant demonstrated ductal carcinoma in-situ with microinvasion. Because of the diffuse extent of the malignant appearing calcifications, a mastectomy was recommended. On the morning of surgery, a 0.4 mCi dose of filtered Tc-99 m sulfur colloid was injected subdermally at the biopsy site. Two sentinel lymph nodes were identified, one at level I and a second, that was very medial and interpreted as a possible internal mammary node (Figure ). In the operating room, 5 ml of isosulfan blue dye was injected subdermally near the biopsy site, and the procedure was started after 5 minutes of skin massage. The first sentinel lymph node was found at level I and was blue and radioactive. Continued dissection at level I did not demonstrate any other radioactive or blue-stained lymph nodes. However, using the lymphoscintigraphy as our guide, we performed a more thorough search for the second sentinel node in the internal mammary chain and under the most medial part of the clavicle. Radioactivity was detected in the latter location, suggesting a level III sentinel lymph node, i.e., medial to the pectoralis minor. Since it was not easily accessible through the small axillary incision, we proceeded with the mastectomy then dissected the remaining sentinel node through a trans-pectoral approach. The medial aspect of the pectoralis major was divided in the direction of its fibers, thus allowing access to the level III space medial to the pectoralis minor, where a blue and radioactive lymph node was identified and removed (Figure ). The patient had an unremarkable postoperative course and was discharged on the first post-operative day. Final pathology demonstrated multifocal micro-invasive comedo-DCIS in the upper inner, upper outer, and retro-areolar regions of the breast. Both sentinel lymph nodes were negative for metastatic disease based on routine histology as well as immunohistochemistry for cytokeratin.

A 48-year-old Caucasian man with past medical history of asthma, diverticulitis, benign prostatic hyperplasia, presbyopia, and obesity presented with a tender palpable left forearm mass. The pain started five years after the patient sustained a deep knife wound in this area that required stitches. Initially, without significant discomfort, the mass progressively grew for years. The pain worsened significantly in the last eight months prior to presentation as he began experiencing dysesthesias that radiated distally to his thumb, index, and middle fingers when the mass was lightly touched. The pain had become so bothersome to the patient that even the wind blowing across his forearm caused extreme discomfort. It affected his livelihood as a truck driver and was deterring him from playing golf.\nPlain radiograph revealed a 1.6 cm ovoid density within the lateral soft tissues of the left forearm (Figure ). Subsequently, a MRI of the left forearm was taken, which showed a 1.6 x 1.3 x 1.8 cm subcutaneous mass with low T1-weighted signal intensity that avidly enhanced with contrast and high-intensity signal on T2-weighted imaging (Figure ). The mass was closely associated with the neurovascular bundle following the course of the superficial branch of the radial nerve (Figure ). This led to the initial conclusion of the mass resembling an intrinsic nerve tumor such as schwannoma, neurofibroma, or a traumatic neuroma.\nOn physical examination, light touch of the mass elicited significant discomfort and dysesthesias in the distribution of superficial branch of radial nerve, but sensation to both light touch and pinprick was intact as well as the motor function of the entire hand. No atrophy of the hand muscles was observed. Considering the patient’s prior trauma to the forearm at the same location as the tumor and the imaging features, the presumptive diagnosis became neuroma, a reactive neoplasm that can arise from an injured nerve [].\nThe patient was taken to the operating room where general anesthesia was administered. The left forearm was prepped and draped in standard fashion. A 5 cm curvilinear incision was made over the palpable mass in the left forearm. The mass was seen just below the subcutaneous fatty tissue superficial to the fascia. A small nerve fiber was seen in the vicinity of the mass, appearing to be contiguous with the mass. Vessel loops were used to isolate the nerve fiber, and the nerve was directly stimulated. There was no movement in the hand with direct intraoperative stimulation. The mass was slowly dissected in a proximal to distal fashion off the nerve. The mass appeared to have a robust blood supply that was controlled with bipolar coagulation. The mass was grossly resected, and hemostasis was achieved. At the two-week follow-up, the patient reported significant improvement in his pain, mentioned mild tingling around the site of incision, and resolution of his pre-operative pain symptoms.\nHistologic examination demonstrated a well-circumscribed, encapsulated soft tissue nodule consisting of sheets, nests, and trabeculae of glomus cells interspersed with small hyalinized vessels (Figure ). Immunohistochemical stains showed the glomus cells were positive for calponin (Figure ) and smooth muscle actin, and negative for S100, chromogranin, synaptophysin, epithelial membrane antigen, and desmin. CD34 highlighted the vessels. The diagnosis of glomus tumor was rendered.

A 55-year-old female with no significant past medical history, except for anxiety, presented to the emergency room (ER) with chest pain. Initial workup in the ER indicated an abnormal electrocardiogram (EKG). The EKG displayed ST wave depressions in leads V3 and V4 (Figure ). As a part of chest pain workup, a computed tomography (CT) scan of the chest was done, which was negative for pulmonary embolism (PE).\nThe initial laboratory evaluations revealed mild leukocytosis with elevated acute phase reactants and mild transaminitis (Table ).\nWith the suspicion of pericarditis, the patient was admitted for further evaluation. A transthoracic echocardiogram (Echo), CT angiogram, and CT cardiac chest were performed during the course of admission. The Echo revealed pericardial effusion (Figure ) and an ejection fraction of 68% with normal right ventricular function. The CT angiogram and cardiac chest performed on day two of admission revealed a calcium score of 0 with minimal atherosclerotic plaque. Moreover, this time it was positive for a new PE in the right lower lobe.\nGiven the findings of pericarditis, leukocytosis, and transaminitis, further infectious and inflammatory workup was performed. The workup revealed positive antibodies for CMV infection (Table ). Autoimmune conditions were also ruled out given the patient developed a PE. A hypercoagulable panel was also ordered.\nThe CMV infection was confirmed with a CMV antigenemia test, which has a sensitivity of 91% and specificity of 98%, and DNA quantification (Table ).\nA duplex scan of the lower extremities did not reveal any DVT. The hypercoagulable workup was unremarkable. There were no other risk factors or history of any risk factors in the patient to have explained the PE either. There was no family history of any hypercoagulable disorder. It was concluded that the PE was a result of the underlying CMV infection.\nOur patient was hence diagnosed with acute CMV infection leading to pericarditis, complicated by PE. She was started on high-dose aspirin and valganciclovir to treat the active CMV infection and pericarditis. She was also started on rivaroxaban to treat the PE.\nHer symptoms improved since being discharged from the hospital and she did not present with any new complications at the one-month follow-up with her primary care physician and continues to follow up with the infectious disease department.

A 54-year-old female presented with a history suggestive of recurrent episodes of small-bowel obstruction over 2 months. She had undergone a Wertheim's hysterectomy followed by radiotherapy for carcinoma cervix 2 years prior. This was followed by the development of a lymphocele that had required repeated tapping and a second course of radiotherapy for a small vaginal vault recurrence.\nInitial diagnosis on admission was adhesive intestinal obstruction, and she was treated conservatively. An erect abdominal X-ray showed a large gastric bubble with few air–fluid levels present medially to it. All laboratory values were within normal limits. Following initial conservative management, a computed tomography (CT) enteroclysis was performed that showed gross dilatation of the stomach [] and the distal stomach and the transverse colon placed posteroinferior to the mesentery and most of the small bowel. Some small-bowel loops were seen between the lesser curvature of the stomach and the left lobe of the liver []. These imaging findings were suspicious of an internal herniation, but the precise type of herniation could be not be identified on the CT scan.\nShe was offered laparoscopic surgery. The first port was inserted by open laparoscopy well below the level of the umbilicus, and three additional 5-mm ports were placed. An abnormally dilated stomach was seen reaching up to the level of the umbilicus. Further exploration revealed a defect in the transverse mesocolon [] with significantly thinned out greater omentum. Roughly 20 cm of the proximal small bowel was seen protruding through the defect behind the stomach and re-emerging through a rent in the gastrohepatic omentum. This had distorted the anatomy and placed the duodenojejunal flexure directly behind the dilated stomach. The small-bowel loops were reduced from the mesocolic defect to correct the anatomy and bring the duodenojejunal flexure below the transverse colon. The mesocolic defect was closed by taking interrupted sutures of 2–0 polyester suture (Ethibond, Johnson and Johnson, India) between the edge of the defect and the first loop of the jejunum []. The left transverse mesocolon was sutured to the posterior peritoneum, and a posterior gastropexy was performed by suturing of the greater curvature to the posterior peritoneum to obliterate the lesser sac []. All the ports were closed in a standard fashion under vision. Post-operatively, the patient tolerated liquids on the 1st post-operative day and transitioned to regular diet at the time of discharge on the 3rd post-operative day. She has remained well some 26-month post-surgery.

A 58-year-old female with a history of chronic rheumatic heart disease and atrial fibrillation was admitted for cranioplasty. She previously underwent a decompressive craniectomy for the management of her massive right middle and anterior cerebral artery infarction 6 months before. The ischemic stroke rendered the patient severely disabled with left hemiplegia and hemisensory loss. The patient also experienced chronic headache and nonspecific dull aching pain over the left side of the body that required gabapentin for partial relief. There was a large right fronto-parietal-temporal scalp concavity coinciding with a craniectomy skull defect of 25 cm × 20 cm [Figure –].\nCranioplasty using the patient's autologous bone flap was performed uneventfully and there was no intraoperative breach of the dura. Blood loss was 150 ml and the operation lasted for 100 minutes. During scalp wound closure, a single subgaleal suction drain was placed with vacuum applied as a routine measure. The drain was a negative pressure closed system with an inner diameter of 3.33 mm (Fr 10) and according to the manufacturer supplied medical device specifications, exerted a negative pressure 75 mmHg (10kPa). Within 1 hour after extubation the patient developed status epilepticus with bilateral eye deviation to the left. Pupil size was 3 mm bilaterally and reactive to light. There was fast atrial fibrillation (160 beats/min) and hypotension of 85/40 mmHg. At that juncture, the subgaleal drain output was <20 ml. The patient was mechanically ventilated and her seizures were controlled after administrating intravenous midazolam and phenytoin. A computed tomography (CT) brain scan showed an interhemispheric acute subdural hematoma, intraventricular hemorrhage within the left occipital horn of the lateral ventricle with obliteration of the quadrigeminal and superior cerebellar cisterns. There was also upward displacement of the vermis at the level of the incisura and flattening of the posterior third ventricle [Figure –]. The patient was diagnosed with ATH and the subgaleal drain was immediately removed. She was sedated for 24 hours and a CT brain performed the next day showed resolution of the ATH [Figure , ]. The patient eventually recovered to her preoperative functional performance level with no further headaches and resolution of her limb numbness. There were no seizures and her phenytoin was weaned off a month after the cranioplasty.

A 50 year old male patient reported at the Department of Oral Pathology, Government Dental College, Calicut, with a painless slow growing swelling on left side of mandible at the angle – ramus region of 4 years duration. He gave a history of a similar swelling at the same location 12 years ago, which was diagnosed as dentigerous cyst associated with an impacted third molar. It was treated by cyst enucleation and removal of the impacted tooth. The patient remained symptom free for about 7 years after the procedure, following which he developed a painless swelling, which reached the present size.\nClinical examination showed the presence of a diffuse, nontender swelling of approximately 6 × 4 centimeters over the left angle–ramus region of mandible []. Intraorally the swelling extended from 34 to retromolar region, obliterating the buccal vestibule []. The mucosa overlying the swelling was intact with normal color and smooth texture. A panoramic radiograph was taken which showed a multilocular radiolucency, which extended from 34 region toward coronoid and condyle, involving both []. With these features a provisional diagnosis of ameloblastoma was made. The patient underwent an intraoral incision biopsy from the lesion.\nH and E stained sections of the biopsy specimen showed cystic spaces filled with eosinophilic material, surrounded by epidermoid cells and sheets of large polygonal cells with centrally placed nuclei, clear cytoplasm, and sharply defined cytoplasmic borders []. The intervening connective tissue stroma was scanty. The sections were stained with mucicarmine and Periodic acid Schiff's reagent (PAS) to assess the nature of clear cells. The eosinophilic material in cyst like spaces was PAS and mucicarmine positive. Mucus-secreting cells were visualized through mucicarmine staining []. The clear cells retained PAS positivity after diastase digestion [] with a focal positivity for mucicarmine []. Diagnosis of clear cell variant of intraosseous MEC was confirmed on this basis.

A 36-year-old married female [], resident of Pune, housewife by occupation referred by Department of Dermatology, Command Hospital Pune for the gingival lesion to division of Periodontics, Department of dental surgery, AFMC, Pune, with chief complaint of burning sensation of the oral cavity for the last 3 months. The patient was apparently asymptomatic before 3 months. She noticed ulcers in the mouth [] and felt severe burning sensation, specially aggravated on taking hot and spicy food. The vesicles on the gum ruptured to produce pain and severe itching in the mouth. She also noticed small eruptions over skin on face, back [Figures and ] extremities just 3 weeks before, for which she reported to the dermatologist.\nThe medical history and family history was clear and patient was not taking any other drugs and had no ocular or genital lesions. The patient had a proper oral hygiene habit without any deleterious habits.\nOn general physical examination, the patient was moderately built and nourished with vital signs within normal limits. She had numerous flaccid vesicles and ruptured bullae of varying diameter seen over the back and nose, which are mainly seen as ulcerated eroded surfaces. On extra oral examination no relevant findings were observed.\nOn intra-oral examination, denuded and spontaneously bleeding gingival zones were revealed. The clinical picture of persistent superficial ulcers with a positive Nikolsky's sign strongly suggested a vesicullobulous disorder. Based on the history, clinical signs, and symptoms of both intaoral and extraoral lesions, a provisional diagnosis of desquamative gingivitis was given.\nAfter routine hemogram, urine and blood sugar examination of patient was taken up for incisional perilesional biopsy with intact epithelium. The sample was sent for histopathological examination in normal saline to Department of Pathology.\nThe patient was taken back to Department of Dermatology for opinion and biopsy of skin was taken from back for histopathological examination and for the direct immunofluorescence assay in Michel's solution. On histopathological examination, acantholysis was revealed along areas of ulceration without dysplastic changes with polymorphonuclear leucocytes infiltration. Basal cells of epithelium remained attached to the basement membrane. Higher resolution showed perivesicular edema with loss of cohesiveness and hyperchromatic epithelial cells called “Tzank cells” [Figures and ], suggesting diagnosis of pemphigus vulgaris. The direct immunofluorescence showed intercellular deposition of C3, IgG, and IgM in stratum spinosum [Figures and ] confirming the diagnosis of pemphigus vulgaris.\nThe oral lesions were treated with 0.1% Triamcinolone acetonide ointment and skin lesion with topical application of 0.05% Clobetasol with Soframycin twice daily. Prednisolone 20_mg twice daily with multivitamins was administered systemically. The patient is under control and still under review [].

An 84-year-old female presented with progressive dysphagia to both solids and liquids and failure to thrive over several months. Her other medical problems included gastroesophageal reflux disease, hypertension, deep vein thrombosis, severe osteoarthritis of both hips, lower extremities contracture, and chronic low back pain. Initial laboratory work up was essentially unrevealing. Manometry study confirmed severe achalasia type 2. The decision was made to proceed with POEM procedure. During endoscopy, she was placed in supine position which was standard practice at our institution. Incision site was first injected with a premixed solution of saline and methylene blue (5 mL/500 mL) followed by careful dissection to the submucosal layer using a triangle-tip knife. A submucosal tunnel was being made from the incision site to 2 cm distal to the cardia, but after a complete submucosal tunneling process just before myotomy (Figure ), she developed severe hypotension and bradycardia. Consequently, the procedure was aborted. Chest X-ray revealed left apical pneumothorax, pneumomediastinum, pneumoperitoneum, and extensive subcutaneous emphysema. Her hypotension resolved with supportive care within minutes of aborting the procedure. A gastrografin swallow study was obtained which did not show any evidence of contrast leakage, but it demonstrated a grossly dilated esophagus consistent with achalasia, and postoperative edema with slow emptying at the gastroesophageal junction (Figure ). Thereafter, she underwent an upper endoscopy with Botulinum injection every 2-3 mo but eventually her symptoms stopped responding to botulinum treatment. Repeat POEM was thus performed 1 year later. She was placed in the same supine position due to her medical comorbidities. A severely dilated sigmoid esophagus was observed (Figure ). The GE junction was tight, and some pressure was required to traverse the endoscope, consistent with known achalasia. Due to great difficulty orienting the endoscope on a different plane, submucosal incision was made at the exact same site (Figure ) of the original tunnel, and surprisingly we did not encounter any submucosal fibrosis or technical challenges. The repeat tunneling at the same submucosal plane was successfully completed and felt similar to a native POEM (Figure ). A myotomy was quickly and uneventfully performed followed by mucosal closure with hemostatic clips (Figure ). The length of the myotomy was 8 cm, which is the standard at our institution. At 4-wk follow up her symptoms remarkably improved, as shown by a decreased Eckhardt score from 9 to 4. Her reflux symptoms also remained stable on the same dose of omeprazole.

A 12-year-old male child got admitted in our hospital with severe headache and projectile vomiting for 15 days. He did not have any history of fever, altered sensorium, suggestive history of focal neurological deficit or cranial nerve involvement. He did not have any significant past and family history. General physical examination did not reveal any abnormality like neurocutaneous markers and facial dysmorphism. His blood pressure was 98 (systolic)/62 (diastolic) mmHg and pulse rate was within 90–100 beats per minute. On central nervous system examination, he was conscious and oriented and the cranial nerves and papillary examination were within normal limit. This patient did not reveal any focal neurological deficit but had meningeal signs at admission. Fundoscopy did not reveal any abnormality and central venous pressure (CVP) or intracranial pressure (ICP) could not be measured. The routine investigations did not show any abnormalities (Hb% 12 gm%; leukocyte count 9400/mm3; platelets 254,000/mm3, urea 22 mg/dl; creatinine 0.5 mg/dl; sodium 139 meq/l; potassium 4 meq/l, normal coagulation profile). Peripheral blood smear was normal and sickling test was found to be negative. Lumbar puncture was done and cerebrospinal fluid (CSF) analysis revealed the presence of red blood cells with mild elevation of protein and CSF sugar was within normal range. As he was having severe headache with meningismus, a neuroimaging was planned and the noncontrast Computed tomography (CT) scan of head [] showed IVH of the right lateral ventricle. He was treated conservatively with intravenous bolus of isotonic electrolyte solution followed by N/2 in 5% dextrose solutions as maintenance fluid and oral glycerol was used as hyperosmolar solution to reduce the raised ICP. After admission, intake–output chart was maintained and he was passing urine adequately. Though the patient was kept nothing per oral for the first 24 hours after admission, he was advised to take orally when vomiting subsided. Magnetic Resonance (MR) imaging with angiography of brain, which was done 5 days after doing CT scan when the patient had developed sudden weakness of right side of the body though it was not associated with vomiting, altered sensorium and hypotension at that time, revealed the features of Moyamoya disease with lacunar infarcts (acute) in right and left posterior paraventricular white matter and centrum semiovale along with IVH [Figures and ]. Digital subtraction angiography (DSA) was not performed. Neurosurgical opinion was taken and the patient was planned to be treated with stenting of intracranial arteries. He neither suffered from hypotension, hypovolemia or dehydration nor did he receive injection Mannitol. Till the last follow-up, he was doing well and he has no neurological deficit at present.

A 5-year-old male child was brought to the casualty of our hospital with complaints of respiratory distress and endotracheal tube in situ; the child also had gangrene over the abdomen and upper and lower limbs.\nA previous history of the patient revealed that the child had a fever and swelling over the abdomen for 20 days. Fever was intermittently associated with chills and rigors. Swelling over the abdomen was gradual in onset and progressed leading to abdominal distension followed by edema of limbs. This was associated with blackish discoloration of abdomen including four limbs and was noticed for 5 days. It progressed to the formation of blebs and oozing of pus. There was no history of vomiting, loose stools, convulsions, or trauma. For these chief complaints, the patient was initially taken to multiple hospitals where he was diagnosed as dengue fever (immunoglobulin M positive) with anterior abdominal cellulitis and was treated with multiple antibiotics. The patient was referred to Indira Gandhi Hospital, Bengaluru, in view of vascular surgery requirement, from where he was again referred to our hospital and presented with the above complaints. On admission to our hospital, his heart rate was 176 bpm, respiratory rate 76 cpm, saturation of 44% with bag and tube ventilation with blood pressure 53/35 mmHg and prolonged clot formation time. The child was put on ventilator with maximum ventilator parameters. Complete hemogram revealed hemoglobin of 2.9 mg/dl and total leukocyte count of 29,580 cells/cu.mm with 54% neutrophils. The patient was afebrile on admission but in due course had high-grade fever intermittently. The patient was on treatment with multiple antibiotics such as meropenem, linezolid, and clindamycin. Despite treatment with antibiotics, the patient still continued to have high-grade fever. Hence, to rule out sepsis, two blood samples were collected 1 h apart from two different sites under aseptic precautions and were sent to the Department of Microbiology for culture and sensitivity. The samples were loaded to BacT/ALERT 3D 60 automated blood culture system, and both the bottles were flagged positively within 48 h of incubation. The samples were subcultured onto blood agar, chocolate agar, and MacConkey agar for isolation of the pathogen, and the plates were incubated at 37°C for 24 h. At the end of 24 h, small, convex, smooth, translucent, nonhemolytic colonies were seen on blood agar [], and chocolate agar and MacConkey agar showed no growth. Smear from the culture showed Gram-negative coccobacillary forms []. The isolate was positive for catalase, oxidase, and hydrolyzed urea rapidly within 2 h of incubation. The organism when subjected to VITEK 2 automated system identified the pathogen as B. melitensis. Considering this as critical alert and when called to inform the report to the clinician, we got to know that the patient had already expired. The patient serum sample was retrospectively subjected to standard agglutination test to know the significant titer, and the patient had a titer of 1:1280 suggestive of brucellosis []. According to the treating physician, the patient was infused with noradrenaline in view of shock and 1 pint of packed red blood cell, and platelet was transfused. Antibiotics were not changed due to unavailability of the reports. Gangrene was nonsalvageable which involved thrombosis of arteries and veins. The patient in due had an episode of bradycardia with desaturation, and in spite of best resuscitative measures with three doses of adrenaline, he could not be revived and succumbed to death.

A 71-year-old man visited our pain clinic presenting with a 3-year history of abdominal pain. The nature of pain was constant, superficial throbbing and lancinating and sometimes diffusely radiated with visual analogue scale (VAS) score 70-80 of 100. The location of the tumor was on the right lower quadrant of abdomen. The patient complained of tenderness on the area but the pain developed even spontaneously. It was more severe at night and early morning, thus resulting in sleep disturbance. There was no traumatic history including medical operation on the pain area. The patient had no specific medical history except pain killers due to the pain described above. Previous treatment included non-steroidal anti-inflammatory drugs (NSAIDs), opioids, local heating, bracing, epidural block, peripheral block and local anesthetic infiltrations, and had no effect. Imaging studies including X-ray, abdominal ultrasonography and magnetic resonance imaging (MRI) showed non-specific findings. He was taking anticonvulsant medications under the diagnosis of post herpetic neuralgia (PHN) at the hospital he had previously visited. Neurological examination and routine laboratory tests showed normal findings. No gastroenterological problem could be found as the cause of chronic abdominal pain after consultation to the department of internal medicine. Physical examination was characterized by exquisite pressure tenderness over the painful area on the right lower quadrant. A careful examination of ultrasonography over the painful area showed a 4.7 × 3.6 mm2 small nodular lesion with increased focal blood flow, and a well-circumferenced hypoechoic character. Suspicions of infected sebaceous cyst or epidermal cyst were made (). We did not think of this cyst as the origin of the patient's pain. Increasing anti-convulsant medication did not show any effect. NSAIDs showed some effectiveness but the patient failed to be free of pain. Local anesthetic injections around the cyst decreased his pain to some degrees (VAS score 60 of 100). Nevertheless, injections into the cyst developed more severe pain up to VAS score 100. In spite of repetitive treatment, his symptoms did not improve. With the possibility that this cyst could be the source of his pain, we transferred the patient to the department of surgery for a detailed evaluation. A general surgeon carefully followed up for about 5 months with conservative treatment including steroid and painkillers under the suspicion of thrombophlebitis. However, he did not seem to get any better, maintaining a VAS score of 80 out of 100. Finally the surgeon decided to proceed with diagnostic excision. It was confirmed as a 14 × 10 × 7 mm3 glomus tumor by histologic examination (). The excision was completely curative, and the patient was free of pain, with a VAS score of 0 out of 100 without any medication.

An almost three-year old girl, was admitted to the pediatric ward of Serdang Hospital (Malaysia) with a history of two days cough, runny nose and shortness of breath. Prior to the hospitalisation, she was given one dose of Salbutamol nebulizer in a private clinic for her respiratory problem. Her symptoms partially relieved. She had been diagnosed with bronchial asthma at the age of 18 months when she first presented with 2 episodes of wheezing and breathing difficulty following an upper respiratory infection which had responded well to the bronchodilator nebulization. Subsequent to the above episode, she continued to have intermittent symptoms such as nocturnal cough and occasional wheeze 2-3 times per week. However, she had not been given any prophylactic medications for asthma. The symptoms were triggered by changes in temperature, dust, common cold and cigarette smoke. Her father is a chronic smoker. There was no history of allergy but she has strong family history of asthma. There was no history of exercise-induced cough or wheeze. On admission, she was afebrile but tachypneic with respiratory rate of 50 breaths per minute with intercostal and subcostal recession. There was an audible wheeze. Her vital signs except the increased respiratory rate were within normal limits. There was no skin eczema. The patient’s throat was inflamed without tonsillar enlargement. Chest X-ray showed hyperinflation. No pneumonic changes were observed and cardiac size was normal. Generalized rhonchi on lungs auscultation could be heard.\nDuring hospitalization she did not required oxygen. She was diagnosed with acute exacerbation of bronchial asthma due to acute pharyngitis with underlying moderate persistent asthma. She was treated with regular Salbutamol nebulisation and a five day course of oral prednisolone. She was prescribed with asthma medications including Fluticasone MDI 250 mcg to be taken twice a day and Salbutamol MDI 200 mcg to be used when needed via aerochamber device. Tamiflu syrup was also prescribed for her flu-like symptoms. An asthma education was provided to the parents. She was hospitalized for 5 days. Her blood tests revealed Hb of 12.8 g/dl, total white count of 16.2 × 109/l with prodominantly neutrophil 70%, lymphocyte 21% and 7% of eosinophil. The platelet count was 390 × 109/l. Her blood urea and electrolytes were within the normal limit. The level of C-Reactive Protein was 15 mg/L.

Our patient was a 66-year-old man of Mongolian race who had previously exhibited coronary arteriosclerosis, spinal canal stenosis, transverse colon cancer, and alcoholic encephalopathy. He was presented to our institute for the removal of wires used for the closure of his chest during a coronary artery bypass graft. However, on admission, severe abdominal distention and emaciation were observed. Emaciation caused the wires to be conspicuous along the incision line. Blood tests revealed an inflammatory response, malnutrition, anemia, and coagulation disorder. Staff at the referral institute informed us that the patient had recently been exhibiting a tortured expression. An abdominal computed tomographic scan revealed rectal cancer with stenosis and invasion to the adjacent tissues (Fig. ). At the same time, multiple distant metastases in the lung, liver, and bone were detected. Palliative care was therefore offered. Based on an interview with the patient’s family, informed consent for best supportive care (BSC) was obtained. In regard to palliative support, placement of a metallic stent at the stenotic portion in the rectum was performed (Fig. ). The patient’s abdominal distention was relieved by this procedure. The patient’s waist size decreased from 100 cm to 80 cm. Although this led to improvement of tachycardia, latent torture was still suspected. Staff at the referral institute informed us that his expression was not as calm as observed previously. Therefore, we felt the need to assess cancer pain. We applied the Abbey Pain Scale, a useful tool for the assessment of pain in patients with communication difficulties. In the present case, the patient’s pain score was 5, indicating that his pain was mild. Initially, acetaminophen (200 mg three times per day) and an internal liquid of morphine (5 mg twice per day) were tentatively administered. This not only calmed the patient’s voice tone and wrinkles between his eyebrows but also stabilized his heart rate. Following this, his medication was switched to fentanyl patches, a barbiturate suppository, and a Voltaren suppository (Novartis, Basel, Switzerland), among other medications, to prevent misswallowing. Gradually, the patient’s Abbey Pain Scale score, in addition to his vital signs, showed stabilization. Fortunately, rescue agents were not required. After 2 weeks of medication, the patient was returned to the referral institute. He died 1 month later, following calm days.

A 17-year-old woman whose chief complaint was left wrist pain on the dorsal and ulnar side and anomalous appearance of the left wrist, presented at our institution. She was informed about deformity of her left forearm by a school physician when she was a junior high school student. However, she did not visit the hospital because her left wrist was asymptomatic. She had scoliosis (left thoracic–lumbar scoliotic curve extending from Th11 to L4 with apex at L1, measured as about 12° using Cobb method). No one in her family has this variant.\nAs a participant in a high school Japanese drum club, she often had wrist pain after playing the drums. Her wrist pain of the ulnar side had worsened gradually during activities of daily life, such as when opening a bottle lid. At first presentation, her wrist and hand translated the volar side relative to the longitudinal axis of the forearm; the ulnar head projected dorsally ( and ()). Clinical examination revealed that she had deep pain by pressure of the dorsally protruding ulnar head on the left side. However, she had not complained of any symptom in the right wrist. The posteroanterior and lateral radiograph of left wrist showed a 30° ulnar tilting angle, 5.7 mm lunate proximal subsidence and a distal radial notch and 50° palmar tilt angle (). On the right side were a 53° ulnar tilting angle, 2.0 mm lunate proximal subsidence and no distal radial notch and 80° palmar tilt angle ().\nLeft wrist extension and flexion were, respectively, 45° and 60°. Forearm pronation and supination were 90° and 90° (right side wrist extension and flexion were 60° and 60°, with forearm pronation and supination of 90° and 90°). Scores of QuickDASH of Japanese version and Hand 20 at the first visit were, respectively, 79.5 and 81. The Japanese version of QuickDASH has equivalent evaluation capacities to those of the original version. Hand 20, a self-administered comprehensive measure, comprises 20 questions with illustrations intended to identify upper extremity symptoms and capability to perform certain activities. The response to each question was rated using a 0–10 Numeric Rating Scale. The points are added up to produce a total score (minimum 0, maximum 100). A higher total score is related with worse upper extremity function. Suzuki et al. verified Hand 20 reliability and validity. Grip strength of the left side was 20.7 kg (right side, 29.3 kg).\nWe diagnosed the patient as having bilateral Madelung deformity and instructed her to stop heavy use of her left wrist such as hitting the Japanese drum, heaving and lifting heavy luggage, and push-ups. Moreover, we administered conservative treatment with a wrist brace. Her ulnar wrist pain worsened during activities of daily life. Therefore, we planned a corrective osteotomy.

A 50-year-old healthy female came with a complaint of gradual painless diminution of vision associated with a floater in her left eye from the last one month. On examination, her visual acuity was found to be CF 3/4M Vision in the Left Eye and CF — M in the left eye. Anterior segment examination was unremarkable with intraocular pressure 19 mmHg in the right eye and 9 mmHg in the left eye. Fundus examination revealed myopic tessellated fundus with macular degeneration with the presence of an oval greyish lesion inferior to the macula within the deep posterior staphyloma symmetrically in both eyes [Fig. and ]. The right eye also showed macular hole with retinal detachment. The left eye showed macular hole with Bullous Retinal Detachment extending from 11 to 7’o clock hr with choroidal detachment as evident on Bscan [Fig. , , and ].\nA spectral domain OCT was performed and confirmed the presence of macular hole with retinal detachment in both eyes along with the presence of deep macular staphyloma []. Interestingly, deep within the base of the staphyloma on SD–OCT, there was further deep excavation within the staphyloma with thin RPE and choroid which was bilaterally symmetrical suggestive of choroidal coloboma [Figs. , , and ]. This coloboma was corresponding to the oval dark grey excavation seen clinically inferior to the macula and was found to be symmetrical in both eyes. She underwent Encirclage with Pars Plana Vitrectomy with Silicon oil injection. The ILM peel was not done in this case as the posterior staphyloma was too deep and could not be reached.\nShe improved to 6/36 in the left eye three months post-surgery with maintenance till the last follow up six months later. After surgery, the thin retina was seen to be completely reattached along its contour without any gap even over the colobomatous area [Fig. and ]. There was no surgery done for the right eye as the patient complained of the visual loss from the last 30 yrs or so and was thus considered to be amblyopic and, hence, had nil visual prognosis.

A 15-year-old female patient reported to the Oral Medicine unit with complaint of bilateral swelling of the face for the past three years. The swelling started initially as smaller in size at nine years of age, which gradually increased in size to the present size. The patient agreed to participate and was explained the nature and objectives of this study, and informed consent was formally obtained. No reference to the patient's identity was made at any stage during data analysis or in the report. Family history did not reveal any previous records regarding cherubism in the other members of the family. On extra-oral examination, facial asymmetry was identified (Figure ). Diffuse, bilateral swelling was noticed over the face measuring about 4 cm × 4 cm in dimensions. Skin over the swelling was normal, freely movable, and intact. The right submandibular lymph node was enlarged, palpable, and non-tender (Figure ).\nThe teeth present were displaced from their normal position, with multiple missing teeth in mandible and maxilla. Expansion of the buccal and lingual cortical plate was noticed, and the overlying mucosa was normal. Laboratory investigations showed an elevated serum alkaline phosphatase value of 188 IU/L (normal, 0 to 150 IU). Serum calcium and phosphorus levels and other investigations were within normal limits. Panoramic radiograph revealed multiple radiolucencies involving the bilateral maxilla and mandible along with the coronoid process and unerupted and displaced permanent teeth (Figure ).\nComputed tomography showed a well-defined multilocular radiolucent lesion resulting in the thinning and expansion of the buccal and lingual cortical plates, involving the entire mandible, maxilla, and lifting of the floor of the orbit (Figure ).\nA three-phase bone scan was done with 10 mCi of 99MTc-MDP injected IV and blood-pool images were taken immediately. Static images were taken three hours later. Blood-pool images revealed increased vascularity in the region of the mandible and maxilla, suggestive of an infective or inflammatory pathology. A static whole body bone scan showed increased radiotracer uptake in the maxilla and mandible (Figure ). Physiological tracer uptake was seen in the upper end of the right and left humerus.

A 60-year-old male patient was referred to our outpatient clinic with an incidental mass in the right kidney, which was recently diagnosed during work-up of his microscopic hematuria. His previous medical history consisted of kidney stone lithotripsy, hypertension treated with a beta-blocker and diuretic, and two episodes of transient ischemic attack.\nAbdominal CT scan showed a rapidly enhancing, exophytic mass in the lower pole of the right kidney with a maximum diameter of 2.5 cm (Fig. A), which was radiologically suspect for RCC. The appendix was noticed in a retrocecal position, at a 1.4-cm distance from the renal mass (Fig. B, C). Based on his mild comorbidity and on the small size of the renal mass, minimally invasive CT-guided radiofrequency ablation of the renal mass was performed.\nOur technique of RFA in renal masses has extensively been described in previous articles [, ]. In short, after the patient received an antibiotic prophylaxis (1,500 mg cefuroxim) and epidural analgesic before the RFA procedure, he was placed in prone position on the CT table. A planning CT scan was performed to locate the renal mass. Under fluoroscopic CT guidance, a 17G cool-tip electrode (Valleylab, Covidien, Boulder, CO) was placed centrally into the mass. Subsequently a 20G needle was inserted lateral in the anterior pararenal space for injection of dextrose in water to hydrodissect the renal mass from the surrounding vital tissues, such as the colon and appendix. After the hydrodissection and the positions of the needles were checked with a CT scan of the area of interest, ablation was started. Final temperature after 15 min was >75°C with adequate roll-offs. The expected ablation zone was 3 cm. The electrode was removed under constant ablation to avoid any tumor spill. The RFA procedure was performed by a highly experienced interventional radiologist (W.P.) who at that time had already performed >180 percutaneous image-guided ablative procedures (including renal, liver, and lung).

A 75-year-old Chinese man who had been experiencing chest pain for 10 years presented at our institution. He was moderately active, doing odd jobs around the house, and accelerating angina over the past 2 years. The patient had been taking aspirin, nifedipine for high blood pressure and metformin for diabetes mellitus type 2 for almost 10 years. He smoked one pack of cigarettes per day for about 40 years before quitting the previous year. His past history was remarkable for chronic obstructive pulmonary disease.\nAt the time of admission, the physical examination showed heart rate (HR), 67 beats/min (bpm); blood pressure (BP), 156/89 mmHg; and blood glucose, 6.85 mmol/L. An electrocardiogram (ECG) showed a sinus rhythm with ST depression and T-wave inversion when chest pain occurred. A complete blood count and a basal metabolic profile were examined; the evaluation of kidney function, blood acid, base balance, and blood sugar levels showed that there were all within a normal range. The treadmill exercise test was positive, and showed ST depression on the ECG when chest pain or shortness of breath occurred. The patient’s response to clopidogrel therapy was determined by testing for CYP450 genetic polymorphism, which showed non-resistance to such therapy. Testing for CYP450 genetic polymorphism was to predict response to clopidogrel\n[].\nThe patient was prepared for coronary angiography (and stent placement if necessary). Before the procedure, the patient’s spontaneous baroreflex sensitivity (BRS), heart rate variability (HRV), and blood pressure variability (BPV) were measured (Table \n). Six hours before the patient underwent coronary angiography, he was given 300 mg aspirin and 300 mg clopidogrel. An initial dose of heparin (100U/kg) was intravenously given before the procedure; an additional dose of heparin at 500U would be given if the procedure lasted 1 hour. The activated clotting time was maintained at 325 s.\nThe coronary angiogram was done through the radial approach. The angiogramrevealed a proximal 90% diffuse stenosis with calcification in the middle segment of the left anterior descending artery (Figure \nA), and 95% stenosis with calcification in the left circumflex artery (Figure \nB). The right coronary artery was observed to have >80% diffuse stenosis with heavy calcification and occlusion in the middle segment (Figure \nC).\nTwo overlapping sirolimus-eluting stents (Cypher; Cordis, Miami, USA.), mounted on a balloon catheter, were inserted without a gap into the left anterior descending artery (stents were 36 mm in length and 3 mm in diameter) and the left circumflex artery (stents 14 mm in length and 3 mm in diameter), respectively (Figure \nA). The stents were advanced into the narrowed section of the arteries. When the stents were positioned, the balloon was inflated. To ensure full expansion of the stents, the stent balloon was gradually inflated to 14 atm in 10 to 40 seconds. Because of chronic total occlusion in the right coronary artery, we attempted to pass a wire through the lesion but failed. Considering that collateral circulation was already present, we abandoned the stent placement into the right coronary artery. After the stenting procedure, the thrombolysis in myocardial infarction (TIMI) grade was 3, and no cineangiographic characteristics of thrombus were present. The procedure was uneventful without a special condition for the patient.\nApproximately 20 minutes after the procedure (18:40), the patient developed nausea, vomiting, sweating and slow breathing associated with diaphoresis and pale complexion. His blood pressure was 87/52 mmHg and heart rate was 39 bpm. At that time, the patient was conscious and had no chest pain. No evidence of bleeding or hematoma was found. The ECG monitor showed no change in ST/T waves. The HRV and BRS were, however, found to be greatly elevated (Table \n) compared with the levels measured before stenting, suggesting VBA. After administration of 1.5 L intravenous saline with dopamine and atropine, the BP and HR slightly improved.\nHowever, at 22:50, the patient complained of precordial chest pain and diaphoresis, and presented drowsy, cold and clammy extremities. His peripheral pulses were not palpable, and blood pressure was not recordable. The ECG monitors showed ST elevation in leads V1, V2, V3 and V4; reciprocal ST depression in leads I, aVL and aVF; and sinus bradycardia with first-degree heart block. The cardiac troponin I (cTnI) testing value was 0.06 ng/mL (normal value 0.04 ng/mL). A diagnosis of myocardial infarction associated with first-degree heart block and cardiogenic shock was made.\nImmediately a repeat coronary angiogram was done through the femoral approach, and the left anterior descending and circumflex arteries, into which the stents had been placed, were reexamined. The angiogram revealed thrombotic occlusion of the planted stents (Figure \nB) in both the left anterior descending and circumflex arteries, with TIMI flow grades of 1 and 0, respectively. The thrombus burden was graded as G3 in the circumflex artery and as G4 in the left anterior descending artery. No evidence of artery dissection was found.\nAn intra-aortic balloon pump (IABP) was immediately inserted. The TIMI flow grade showed no improvement after runs of aspiration in the two arteries; at that time the patient was still in cardiogenic shock. An intracoronary balloon was placed at the location where the thrombi adhered in the left anterior descending and circumflex arteries. While continuing counterpulsation of the IABP, the thrombi in the stents disappeared shortly afterward (Figure \nC). The patient was given tirofiban, aspirin, clopidogrel and heparin; the balloon counterpulsation was maintained until the patient’s heart rate normalized and blood pressure stabilized. The patient was discharged with a normal echocardiographic evaluation, and was asymptomatic at follow-up.

A 28-year-old male was admitted to the emergency department (ED) with a 5 cm stab wound (SW) under his left nipple. Pre-hospital treatment included insertion of a left chest drain due to dyspnoea, but this was clamped during transport because of massive hemorrhage. On admission, he was self-ventilating, with palpable carotid pulses, but without a measurable blood pressure. He was agitated and pale with a Glasgow coma score of 12 since he could open his eyes, localize pain and speak. The blood pressure ranged from 80/60 to 100/60 mmHg after starting intravenous fluid therapy and he had a tachycardia of 100–120 beats per minute. When the clamp was removed from the chest drain, 650 ml of blood was rapidly drained. The chest x-ray showed persisting hemothorax and atelectasis and an additional drain was inserted. The arterial saturation varied from 86% to 98% and blood gas analysis showed a haemoglobin of 12.6 g/l, pH 7.17, base excess −9 and lactate 5.5 mmol/l. Focused Assessment with Sonography in Trauma (FAST) revealed no blood in the pericardium and upper abdomen. The neck veins were not distended and so the patient received transfusion of 1500 ml of crystalloid fluid and 250 ml of red cells. The blood pressure decreased as soon as the intravenous therapy was reduced, the tachycardia did not resolve and the patient was therefore transferred to the operating room.\nAfter intubation, the ECG showed ST elevation and a median sternotomy incision was rapidly performed. The pericardium was opened and although there was a clot ventral to the heart, there were no signs of cardiac tamponade. There was a 6 cm cut in the lateral pericardium corresponding to the stab wound in the chest and a 7 cm, almost transmural wound in the left ventricle, parallel to a major diagonal branch (Figure\n). The wound was not bleeding. A 5 cm stab wound in the left lung (Figure\n) was sutured and cardiopulmonary bypass (CPB) was established. The cardiac injury ended close to the origin of the left main stem and crossed the left atrium. The ventricular wound was repaired with single mattress sutures reinforced by strips of bovine pericardium (Figures \n,\n) without arresting the heart and without cross-clamping the aorta. The left atrium was sutured using 5/0 Prolene (Ethicon). Blood appeared in the tracheal tube and bronchoscopy revealed ongoing bleeding from the left lung which required resection of the lingula. Weaning from CPB was initially unsuccessful and we suspected that there had been injury to the left main stem either caused by the initial stab or by the hemostatic sutures. The left anterior descending artery was grafted using the internal mammary artery and a vein graft was anastomosed to the circumflex artery. The patient was thereafter successfully weaned from CPB.\nPost-operatively, the patient had signs of a stroke and a CT scan revealed a cerebral infarction. One week after surgery he was transferred to the neurological intensive care unit. After three weeks he was awake and self-ventilating. He was moved to his local hospital and was discharged after 6 weeks with only a minor deficit affecting the left upper extremity.

An 82-year-old man (64.5 kg, 175 cm) diagnosed with falcine meningioma was admitted for craniotomy. The patient presented left-sided weakness. Comorbidities included atrial fibrillation and Parkinson's disease. He had undergone prostate surgery under spinal anesthesia 1 year previously. Preoperative thoracic radiographs revealed several small nodular opacities in the upper lobe of the right lung. Low-dose thoracic computed tomography (CT) was performed to further evaluate the possibility of pulmonary tuberculosis, which revealed fibro-atelectatic changes, bronchiectasis, calcifications, and small nodules, considered to be sequelae to resolved pulmonary tuberculosis. The patient presented no respiratory symptoms, and pulse oximetry readings were 100% in room air. He was a non-smoker. Tracheobronchomegaly was not detected on the preoperative thoracic radiograph as the image was not clear enough to distinguish the trachea. Therefore, the anesthesia plan was to manage the patient as if he had chronic obstructive pulmonary disease, in terms of his pulmonary condition.\nAfter denitrogenation with 100% oxygen, anesthesia was induced via intravenous propofol and remifentanil infusion. After confirming the loss of consciousness and following sufficient manual ventilation, 50 mg of rocuronium was injected prior to intubation. A reinforced tracheal tube with an inner diameter of 7.5 mm was inserted and fixed at 23 cm from the incisors. An arterial catheter was placed in the left radial artery and central venous catheter in the right subclavian vein. Total intravenous anesthesia was maintained using a target-controlled infusion system.\nAfter the completion of central venous catheterization, tidal volume was considered insufficient and breathing sounds were reduced on auscultation in both lung fields. The ventilator circuit was checked for respiratory leakage, and no leak was found. The patient was reintubated with a new tracheal tube in case of tube malfunction; however, lack of airway control consistent with air leakage persisted. The extubated tube was examined, and no malfunction was identified.\nAt this stage, an airway deformity was suspected, and thoracic CT images were reviewed in the operating room. The patient's tracheal diameter appeared larger than normal. One anesthesiologist suggested MKS based on his experience of airway management in a patient with MKS in the past []. Because of possible damage to the tracheal wall due to additional expansion of the tracheal tube cuff, the oropharyngeal cavity was sealed with wet gauze packing, which allowed us to achieve an adequate tidal volume. The total operation time was 8 hours. Postoperatively, the patient was sedated with a benzodiazepine and transferred to the intensive care unit without tracheal extubation.\nThe transverse diameter of the patient's trachea was measured 2 cm above the aortic arch on a chest scanogram (similar to a simple chest X-ray) as 25.4 mm (). Transverse and sagittal diameters of the trachea at the same level were 26.8 and 32.0 mm, respectively, on the CT images (). These measurements were consistent with the diagnostic criteria for MKS. After surgery, a three-dimensional (3D) reconstruction of the preoperative chest CT was created, which confirmed the abnormal anatomical morphology of the trachea ( and ). The patient was extubated on the same day as surgery. Eight days post-surgery, he was discharged without acute complications.

A 54 year-old man with no past medical history was brought to hospital with cardiac sounding chest pain and an electrocardiogram revealing ST elevation in leads II, III and aVF. He was taken for immediate primary coronary intervention for an inferior segment elevation (ST) elevation myocardial infarction via right radial approach. During diagnostic imaging of his left mainstem artery, he suffered a Ventricular Fibrillation (VF) cardiac arrest on table. He had immediate CPR by hand and then the Lund University Cardiac Arrest System (LUCAS) device was used. He required a total of five shocks in order to restore spontaneous circulation. His total downtime was approximately 10 minutes. During CPR, coronary angiography continued and he was found to have a right coronary artery culprit lesion, which was successfully treated with primary percutaneous coronary intervention (drug-eluting stent). At the end of his procedure, arterial blood gases showed an Hb of 69 g/l, significantly lower than his admission Hb of 112 g/l. However, this was in the context of 3 l of IV fluid during the resuscitation and angiogram. Repeat formal laboratory blood tests were requested as well as cross-match.\nHe was then transferred to the intensive care unit for on-going post-resuscitation care. Within minutes of arrival to the intensive care unit, he became significantly more haemodynamically unstable, requiring large doses of vasopressor to maintain blood pressure. Repeat arterial blood gas testing revealed an Hb of 45 g/l, at which point a peri-arrest call was put out. Clinically, he had a clear chest, normal heart sounds but a distended abdomen. He received hypovolaemic shock treatment, with fluids and blood transfusion. A bedside FAST scan was conducted, in the setting of a patient with shock and acute abdominal distension after cardiopulmonary resuscitation. In the hepatorenal recess view, free fluid was observed in Morison’s space with a varying degree of echogenicity. This finding was highly suggestive of an acute intra-peritoneal bleed, and in the context of recent CPR, a liver laceration was suspected.\nHe was taken for immediate laparotomy, which revealed a grade III liver haematoma, according to the American Association for the Surgery of Trauma liver trauma classification (intra-parenchymal hematoma of more than 10 cm). A definitive primary hepatic surgical repair was performed, and the patient was transferred back to the intensive care unit for supportive care.\nDespite the history of a cardiac arrest and peri-arrest a few hours later, with haemorrhagic shock from liver trauma, he showed good neurological signs on sedation hold in the intensive care unit. His organ support was gradually weaned off, and he was discharged from the intensive care unit 5 days after initial admission and from hospital 4 days later. Echocardiography showed globally preserved systolic function with an ejection fraction of 59% and mild diastolic dysfunction. He made a full functional neurological recovery.

A 49-year-old woman visited the clinic due to a mass in her right thigh. The patient first noticed the mass four years prior to presentation. After needle biopsy was performed, she was referred to our hospital with a diagnosis of leiomyosarcoma.\nA physical examination confirmed the mass with a diameter of 4 cm on the lateral side of the right thigh. There was no adhesion with skin and no tenderness.\nMagnetic resonance imaging (MRI) identified a subcutaneous soft tissue mass, which exhibited low signal intensity on T1-weighted images and heterogeneous signal intensity on T2-weighted images. The tumor was enhanced by a gadolinium injection (). Computed tomography (CT) of the chest, abdomen, and pelvis did not demonstrate any distant metastasis. All routine blood laboratory data were normal. Wide tumor resection was performed. Adjuvant chemotherapy and radiotherapy were not administered because of the small (<5 cm) and superficial tumor.\nOne year and 3 months postoperatively, the patient developed lung nodules. The maximum size of the lung nodules was 5 mm. Therefore, excisional biopsy was performed. The histopathological diagnosis was consistent with lung metastasis of leiomyosarcoma. Positron emission tomography (PET)–CT revealed the high FDG uptake with a maximum standardized uptake value of 4.4 in the lung and the right mid-shaft of the femur. On MRI, the tumor size on the mid-shaft of the right femur was 2 cm (). The cortical bone was maintained, and therefore, the patient did not present any symptoms. We diagnosed the patient with lung and bone metastases. Therefore, systemic chemotherapy using doxorubicin and ifosfamide was administered. Next, we planned to treat the bone metastasis of the right femur. First, cryoablation under CT guidance was performed ( and ). Ablation needles were inserted into the proximal and distal side of the tumor. Cryoablation was performed using an argon gas–based system (CryoHit, Galil Medical) under CT-fluoroscopic guidance (Aquilion ONE, Canon Medical System, Ootawata Japan). After administration of local anesthesia with 1% lidocaine (Xylocaine, AstraZeneca International), after tract was holed by electric drill, 17-gauge cryoprobes (IceRod; Galil Medical, Japan) were placed into the tumor according to their size and shape. Cryoablation was then performed with two cycles of 15-min freeze and 5-min thaw. To monitor the size of the ice ball, CT scans were obtained at the end of each freezing cycle. After one week after cryoablation, curettage and fixation with plate and cementation were performed to prevent fracture. Tumor cells were not observed in the histopathological findings of the curettage tissue ( and ). After cryoablation, radiofrequency ablation was performed regularly for lung metastases. Four years after cryoablation, there was no recurrence and the patient could walk without any support.

A 31-year-old male with no significant past medical history who presented from an outlier hospital to our emergency department with an acute onset crushing substernal chest pressure and dyspnea with profuse sweating following 1-week-long febrile illness with malaise. He denied any intravenous drug use, and urine drug screen on admission was negative for illicit substance use. Initial physical exam revealed normal vital signs and clear lungs, but shortly thereafter, the patient rapidly developed dyspnea, tachypnea, and tachycardia. On vital signs patient was noted to be suddenly hypotensive and hypoxic. Neck exam exhibited elevated jugular venous distention and lungs on auscultation revealed significant crackles in bilateral lung fields. The initial electrocardiogram (ECG) showed diffuse ST depressions in all precordial leads, consistent with an acute coronary syndrome (). Thereafter, he underwent an emergent transthoracic echocardiogram showed ejection fraction (EF) of 45% with severe aortic insufficiency with emanating from a torn right coronary cusp, and cardiothoracic surgery consultation was procured (). Blood cultures came back positive for S. lugdunensis in both bottles.\nDiagnosis of cardiogenic shock and flash pulmonary edema was suspected, and patient underwent rapid sequence intubation. With the consent of his family, the patient then underwent emergent transesophageal echocardiogram while intubated. This revealed a large vegetation prolapsing into the left ventricular outflow tract, confirming the diagnosis of acute severe aortic insufficiency from endocarditis (). While deliberating with the family about emergent aortic valve replacement, the patient suffered cardiac arrest. Advanced cardiac life support (ACLS) protocol was followed for 13 min, return of spontaneous circulation was restored and the patient was sent for emergent mechanical aortic valve replacement surgery. The native valve specimen cultures grew S. lugdunensis. The patient had a remarkably uncomplicated postoperative course and was extubated postoperative day 4, and he was neurologically intact. He was discharged home on postoperative day 8 on intravenous nafcillin to complete a 6-week course and made a full recovery without disability.