A 57-year-old female referred to Imam Khomeini hospital with chief complaint of exertional dyspnea. She lived in the southern parts of Tehran. Her dyspnea which began about 4 months before her admission to hospital was gradually progressive and was accompanied by non-purulent cough. At the time of her admission she had some problems for performing activities of daily living. Dyspnea did not occur during resting and sleep and was not related to the time of eating. She didn't complain of orthopnea and paroxysmal nocturnal dyspnea (PND). The history of hemoptysis and exposure to tuberculous patients was negative.
In her past medical history, she was under treatment for hyperlipidemia (atorvastatine) and hypothyroidism (levothyroxine). She didn’t mention the history of any other respiratory or cardiovascular diseases. She didn’t have any hypersensitivity to drugs or nutritious substances and the history of seasonal allergy was negative as well.
Her family history was negative for respiratory and cardiovascular diseases. History of smoking, alcohol consumption and drug abuse was negative. She was a housewife without any specific occupational exposures. Her husband was a farmer who had been died due to cardiovascular diseases 9 years ago. She lives in the first floor of a 3-storey buildingin Tehran (She didn’t use to live in her husband's farm). Her house was not near any industrial plants.
In the physical examination, she was completely alert. Her vital signs included: Pulse rate: 78/min, respiratory rate: 20/min, temperature: 37.1°C, blood pressure: 110/75 mmHg. Her body mass index was 35.5 kg/m2. Lung field auscultation revealed inspiratory crackles in the bases of both lungs, especially right lung and to a lesser intensity in the mid-zones of both lungs.
In arterial blood gas analysis, O2 saturation was 78%, and other parameters were normal. The results of complete blood count included:
WBC: 10900/mm3
RBC: 6.66 × 106 ml/mm3
Hemoglobin: 18.6 g/dl
HCT: 58.9%
MCV: 88 fl
MCHC: 28 pg
Plt: 230000/mm3
MPV: 8.5 fl
RDW: 15.1%
Poly: 63.3%
Lymph: 28.3%
Mono: 4.6%
Eos: 3.3%
Baso: 0.5%
Anisocytosis: Slight
The result of spirometry showed a severe restrictive pattern (FVC = 1 L, 47.3% of predicted) which was approved by body plethysmography (TLC = 2.97 lit, 76% of predicted). Diffusing capacity (DLCO) was decreased (73.9%). She showed a significant response to bronchodilator administration hence a 21% and 17.7% increase in FVC and FEV1, respectively. The purified protein derivative (PPD) test for TB was negative.
Exercise stress test was performed but not completed because of her dyspnea. The result of transthoracic echocardiography was as following:
PAPs: 40 mmHg, LVEF = 55%, Normal RV size and systolic function, diastolic dysfunction grade 2, trivial MR, and mild TR
Chest X ray showed reticulo-nodular pattern in both lower lung fields (despite a normal chest X ray 6 months before). shows two chest X rays before and after onset of disease.
High-resolution computed tomography (HRCT) scan results in inspiration and expiration was as following: Generalized ground glass opacities in both lung fields and hypo-dense areas due to focal emphysema. Multiple lobular, patchily dispersed areas of air trapping throughout pulmonary fields, on expiratory views, mostly accompanied by mosaic perfusion on the corresponding inspiratory phase views. Interlobular septa were unremarkable. Neither bronchiectasis nor bronchiolectasis was noted, on either side. Interlobular and peribronchchovascular interstitium were ordinary depicted. The main pulmonary artery was dilated. Cardiomegaly was depicted [].
After observing the results of paraclinic tests, because of high suspicion of hypersensitivity pneumonitis, another history with details was obtained from her. She mentioned that her son keeps a considerable number of birds (doves) on the roof of the building and their cage was beside the desert cooler of the building. So she fulfilled the criteria of HP and after removing the exposure her symptoms subsided and her pulmonary function improved significantly hence FVC = 1.79l, 82% of predicted and FEV1 = 1.42l, 79% of predicted.
A written informed consent was obtained from patient to publish her case report with her radiographic images. This consent is available (in Persian) for the journal editorial.


A 7-year-old Chinese girl presented to our department with a 3-week history of low-grade fever and cough. Her previous history was unremarkable. Physical examination revealed a soft abdomen with a tender liver edge 3 cm below the right costal margin and a palpable spleen tip; the chest was found to be normal. Routine laboratory tests were normal except for hemoglobin 9.9 gr/dL (nv 11.5–14.5) and erythrocyte sedimentation rate (ESR) of 79 mm/h (nv < 38). Tuberculin skin test was positive with 20 mm induration. Quantiferon-TB Gold test was 59 IU/mL (nv < 0.34). HIV test was negative. Chest X-ray showed mild thickening along the right major fissure and bilateral hilar enlargement. Abdominal ultrasound (US) performed using a 3.5 mHz convex transducer (Acuson Sequoia 512, Siemens, Mountain View, CA, USA) revealed mild hepatomegaly, multiple hypoechoic nodules up to 13 mm in diameter scattered throughout the liver and spleen (Fig. ); slight wall thickening of the last ileal loop and ascending colon, and multiple enlarged mesenteric lymph nodes were also shown. Multidetector computed tomography (CT) of the abdomen was performed using 16-slice CT scan (LightSpeed, GE Healthcare, Milwaukee, WI, USA) with 5-mm slice thickness (reconstructed 2.5 mm) and low dose technique (80 kv, 50–90 mAs) after i.v. contrast medium administration. CT revealed multiple rounded, low-density lesions in the liver and spleen, ranging in size from 2 to 18 mm (Fig. ); peripancreatic, periportal, para-aortic, and paracaval lymph nodes up to 15 mm in diameter with no calcification, and diffuse small bowel wall thickening were also shown. CT of the chest demonstrated small opacities in the right lower lobe and multiple enlarged lymph nodes in the hilar, paraesophageal, and paratracheal regions (Fig. ). Direct smear microscopy for acid-fast bacilli in the sputum and gastric lavage was negative, but the culture for Mycobacterium tuberculosis was positive. Colonoscopy showed a nodular, ulcerated mass that partially obstructed the cecum. Intestinal biopsy and image-guided needle biopsy of the liver revealed granulomatous tissue with caseous necrosis. Both direct smear microscopy for acid-fast bacilli and culture for Mycobacterium tuberculosis of intestinal and liver biopsy specimens were negative.
Diagnosis of macronodular hepatosplenic TB with concomitant intestinal and lung involvement was made, and a three-drug anti-TB therapy consisting of isoniazid, rifampicin, and pyrazinamide was planned. After 9-month therapy, there was a marked improvement in the general condition, and the liver and spleen were no longer palpable. Abdominal US revealed reduction in size and peripheral calcification of the hepatosplenic lesions (Fig. ); abdominal lymph nodal groups were normal.


A 30-year-old male reported to dental O.P. with the complaint of asymmetric appearance of the face. The swelling had been present from childhood and had become evident after puberty. Patient had no history of significant medical problems, trauma or family history of any hereditary disease.
Clinical examination revealed a diffuse enlargement of the lower one-third of the right side of the face. The enlargement was also seen to involve the lower border of the right mandible []. Intra oral examination revealed a swelling involving both the buccal and lingual aspect of the right mandible. The enlargement was more prominent on the buccal side, extending from the distal aspect of 45 to the distal aspect of 47 obliterating the vestibule. On palpation, the enlargement was bony hard in consistency. No sign of inflammation of the overlying mucosa was seen. Intra oral examination revealed an impacted 38 and missing 48 []. Furthermore, observed was that the lesion had not caused any malocclusion [].
Orthopantamogram (OPG) revealed an increase in vertical height of the body of the right mandible of normal bone density. The ramus and condyle of the affected side were normal. An OPG taken at the age of 25 years (5 years back) and the current OPG showed the lesion was stable [].
Computed tomography (CT) axial image revealed a solitary well-defined homogenous mass seen on the right body of the mandible measuring around 2 cm × 3 cm with uniform radiopacity. Bony enlargement was seen on both buccal and lingual side, buccal aspect being more prominent than the contralateral side. The bony enlargement can be well-appreciated in three dimensional (3D) CT. Furthermore observed in the radiographs, the enlargement was restricted to the body and did not extend to the condyle, which later aided in the diagnosis [].
The histopathology showed compact bone and numerous, small marrow spaces. The compact bone exhibited reversal and resting lines with osteoblastic rimming. Osteocytes could also be seen entrapped within the bone [].
Based on the clinical, radiographic and histopathologic findings the diagnosis of hyperplasia of the right mandible was given.


A 50-year-old male patient presented with a history of moderate periodontitis with Grade 2 mobility of most of the mandibular [] teeth and his profession dictated for an immediate solution. Clinical and radiological evaluation revealed adequate alveolar bone support. Atraumatic extraction of 41 42 43 44 45 51 52 53 54 55 56 57 58 was carried out under local anesthesia [] using lignocaine with adrenalin. Atraumatic extraction using periotomes without excessive enlargement of the socket was done in order to preserve the alveolar bone which is very important to the success of immediate implant placement. The implant size is determined by the help of the root length and diameter also with conventional methods [Figures and ]. The sockets were debrided and 3i Biomet implants 4 mm × 11.5 mm were placed in the extracted sockets of 45 55 12 22 [Figures and ]. Stability was checked by osstell []. Patient was administered appropriate antibiotic and analgesic. A pre-fabricated mandibular provisional denture with a soft reline was placed [].


We report on the case of a 25-year-old Caucasian man who presented to the outpatient clinic complaining of right scrotal stiffness for 1 year and new left scrotal pain and tenderness. He had been diagnosed with sarcoidosis by a mediastinal lymph node biopsy owing to a hilar lymphadenopathy 2 years previously after presenting with an acute onset and progressive course of fatigue and cough. The physical examination revealed multiple, painless subcutaneous nodules on his arms and upper thighs in addition to large, bilateral epididymal masses. The consistency and size of the testes were normal and there were no signs of varicocele on the physical examination. Laboratory investigations revealed a normal blood sugar concentration and normal liver and kidney functions with a slightly elevated erythrocyte sedimentation rate (14 mm/h). Moreover, serum α-fetoprotein and β-human chorionic gonadotropin were within the normal range. The urine was negative for acid-fast bacilli by Ziehl-Neelsen stain, which was repeated three times. Biochemical analysis revealed normal serum testosterone (15.85 nmol/L; normal range, 10.07 to 38.76 nmol/L) and luteinizing hormone levels (3 IU/L; normal range, 0.9 to 7.0 IU/L) and elevated serum follicle-stimulating hormone levels (15.4 IU/L; normal range, 1.5 to 12.4 IU/L). Semen analysis showed severe oligospermia (2×106/mL, ).
T1-weighted post-contrast magnetic resonance imaging (MRI) revealed an enlarged and enhanced epididymis on both sides (). The sizes of the lesions in the right and left epididymis were 3.1 cm and 1.3 cm, respectively.
The patient underwent inguinal exploration to differentiate the scrotal malignancy. Exploration revealed enlargement of both epididymides with increased bilateral vascularity and firm consistency of the mass. The masses extended from the epididymis through the testis with thick adherent coverings. Incision of the tunica albuginea demonstrated normal seminiferous tubules with no mass in the testis. A biopsy sample was obtained from the epididymal mass for frozen section analysis. The sample revealed multiple noncaseating epithelioid granulomas (). Because the patient had been diagnosed with pulmonary sarcoidosis 2 years ago, malignancy of the testis and epididymis was ruled out easily and medical treatment considered.
The patient was given 40 mg of prednisone/d for 1.5 months. Subsequently, the dosage was reduced to 20 mg/d, which was administered for another 1.5 months. After the first 3 months, the prednisone dose was tapered every month and the patient received the drug as 10-mg, 5-mg, and 2.5-mg tablets during the fourth, fifth, and sixth months, respectively. As a result, the prednisone was gradually reduced to a maintenance dose of 2.5 mg/d at the end of 6 months (). The patient discontinued the medicine 1 month after the maintenance dose was achieved. During the follow-up period, the patient underwent physical examination with repeated semen and biochemical analysis every 3 months (). The results of the semen analysis at the end of therapy showed a dramatically increased sperm count of 34.7×106/mL with normal follicle-stimulating hormone and testosterone levels.


A 17-year-old boy underwent posterior instrumentation from L2-S1 vertebra and anteriorcolumn reconstruction for an unstable burst fracture of L4 vertebra. Intraoperatively, the left L4 nerve root was avulsed with a dural defect. A fat graft was used to seal the CSF leak at the time of wound closure. The patient had complete motor and sensory loss in left L4 root distribution which remained unchanged postoperatively. Postoperatively, the patient was put on routine antibiotics for gram positive and negative coverage and analgesics. He was catheterized and advised strict bed rest. On the 5th postoperative day, when the patient was mobilized, a fluctuant swelling of approximately 12 × 8 cm was noticed at the operated site. Since the patient remained asymptomatic and the wound healed uneventfully, he was discharged after suture removal and was observed closely. At 3 months followup, the swelling had resolved completely both clinically and radiologically [].


A 24-year-old male presented to us 4 months following a right L4-L5 fenestration and discectomy, with a fluctuant swelling of about 5 × 4 cms at the operated site. He had grade 4 power in right long toe extensors which remained the same after surgery. He was otherwise asymptomatic. He was advised exploration and repair, but he declined. He was followed-up and at 6 months postoperatively, the pseudomeningocele was found to have resolved completely both clinically and radiologically [].


A 61-year-old lady who underwent posterior instrumentation, debridement, and fusion of L5-S1 vertebra for tuberculous spondylodiscitis. She presented after 18 months postoperatively with fluctuant swelling of approximately 9 × 6 cm at the operated site. She did not have any neurological deficit she had taken antitubercular course for 9 months. She had noticed the swelling 2 months after surgery but did not seek any medical attention as it was completely asymptomatic. She had completed a 9-month course of anti tubercular regime. The diagnosis of a large pseudomeningocele was confirmed on a magnetic resonance imaging (MRI). She was advised exploration and repair but she declined. She returned for followup 3 years later and the lesion was found to have resolved completely both clinically and radiologically [].


A 26-year-old male, who underwent a left sided L4-L5 fenestration and discectomy, presented 10 days later with a fluctuant swelling over the back. His neurological status was normal. His radicular symptoms were relieved but had occasional postural headache. He was planned for surgical exploration and repair of the dural defect. During the waiting period for surgery, as he showed spontaneous regression, the surgery was deferred and it was decided to observe the patient closely. At 3 months, he showed complete resolution of the swelling which was further confirmed on the MRI [].


A 13 year old girl presented to us with diffuse hair loss over the scalp involving more than 50% of the scalp [] for the past 6 months. She had consulted many dermatologists in the past 6 months since the onset of her complains, but none of the treatment brought relief. Therefore, it was not only the disease entity that we needed to consider but also the financial and psychosocial impact on the patient. She had no associated hair loss over any other body site. There was no history suggestive of any associated complaints. Her nails were normal on examination. There was no history of similar complains in the family. After taking a prior informed consent, phenolisation was done over the bald patches with 88% phenol until a uniform ivory white frost appeared. Phenol was applied all over the bald patches, covering more than 50% of scalp surface; 1 ml of phenol was taken in a container and applied to the scalp by dipping a bud in phenol. We assume that out of 1 ml, some amount of phenol was left in the bud. Thus, the total application of phenol was below the safe limit. No neutralization was done. The patient did complain of burning sensation and was given 5 mg diazepam orally. She underwent 5 such sittings at an interval of 15 days each. She was also given dexamethasone pulse therapy for 4 months. Dexamethasone was given in the dose of 60 mg intravenously in 5% dextrose. She was given dexamethasone and phenolisation at an interval of 15 days. She began to show response to therapy after the 2nd sitting when vellus hair regrowth was evident diffusely all over the bald patches. After five sessions done with 88% phenolisation and 4 pulses of dexamethasone intravenous therapy, she showed marked improvement with well-marked hair growth over the patches. Phenolisation is painful and therefore she was given intravenous diazepam prior to the procedure. There were no reported side effects in the present case.


A 3-year-old female patient presented with a 5-day history of fever, sore throat, and cough, but no rash. Past medical history was unremarkable, as was family history. Immunizations were up to date for age. On admission to the ward, her vital signs were: temperature 39.5°C; pulse 130 beats per minute; blood pressure 100/70 mmHg, respiratory rate 50 per minute; oxygen saturation 90% on oxygen 2/L per minute via nasal cannula; weight 13.8 kg (50th percentile); and length 94 cm (48th percentile). Her skin had normal texture, with no rashes, hypopigmentation, or hyperpigmentation, her capillary refill was around 3 seconds, and the oral mucosa was mildly dry. The patient had decreased air entry and coarse crackles in the right lower and middle zones of the lung. The throat was erythematous and there was no cervical lymphadenopathy. The rest of the physical examination was unremarkable.
Initial laboratory results were: white blood cells 24,000/μL (neutrophils 60.2%, lymphocytes 35.4%, monocytes 4.3%, basophils 0.1%), hemoglobin 10.3 g/dL, and platelets 206,000/μL. C-reactive protein was 100 mg/L, erythrocyte sedimentation rate was 65 mm/hour, albumin was 18 g/L, creatinine was 66 μmol/L, aspartate aminotransferase was 100 U/L, and alanine aminotransferase was 60 U/L. Serum glucose, blood urea nitrogen, calcium, sodium, chloride, and potassium were normal. Venous blood gas was pH 7.2, pCO2 44 mmHg, pO2 29 mmHg, and HCO3 17 meq/L, with a base excess of 11. Anteroposterior chest radiographs showed a right middle and lower lobar consolidation with moderate pleural effusion.
The patient was started on intravenous normal saline 20 mL/kg due to dehydration. She was then transferred to the pediatric intensive care unit due to increased oxygen requirement. A chest tube was inserted and 200 mL of pus was drained. The pleural fluid culture yielded GAS. The patient was started on intravenous cefuroxime and clindamycin. Nasopharyngeal and throat swabs, blood culture, and a Mantoux skin test were all negative.
On the eighth hospital day, there was no clinical response to antibiotics, and fever persisted, with new onset of abdominal pain, diarrhea, and slight tachycardia at a heart rate of 150 beats per minute.
A repeat blood count showed a significant white cell count of 30,000/μL, hemoglobin 7.7 g/dL, platelets 600,000/μL, aspartate aminotransferase 180 U/L, alanine aminotransferase 120 U/L, and albumin 18 g/L, with a rise in erythrocyte sedimentation rate and C-reactive protein.
The differential diagnosis included bacterial resistance to antibiotics, nonbacterial etiologies such as a virus or aspiration of a foreign body, bronchiolitis obliterans, hypersensitivity pneumonitis, atypical Kawasaki disease, eosinophilic pneumonia, Wegener’s granulomatosis, pulmonary sequestration, and cystic adenomatoid malformation.
Since atypical Kawasaki disease was in the differential diagnosis, an echocardiogram was ordered which showed a prominent of left anterior descending artery (0.26 cm, z-score 3.2) and left main coronary artery (0.35 cm, z-score 3.2), with no vegetations or pericardial effusion. Our team decided to give one dose of intravenous immunoglobulin 2 g/kg, and high-dose aspirin (80 mg/kg/day) was started. The fever resolved in 24 hours and the patient’s general condition improved, but desquamation developed on the hands and feet. The diagnosis of atypical Kawasaki disease was confirmed.
The patient was discharged home in a stable condition on oral antibiotics for 2 weeks and on an antiplatelet dose of aspirin. She was seen in the outpatient clinic in good condition, and a repeat echocardiogram at 6 weeks was normal.


The patient was a 61-year-old male. He had no relevant medical or family history, but he was a heavy drinker who consumed >2 L of beer every day. He visited a nearby hospital for a chief complaint of general malaise and was diagnosed with multiple HCCs caused by alcohol-related cirrhosis. Approximately 1 month after the first visit, he was admitted to our hospital for rapid development of abdominal fullness. Physical findings at admission showed blood pressure 148/98 mmHg, pulse rate 64 bpm, ascites retention, and a palpable fist-sized tumor in the epigastric region. Blood tests upon admission showed Hb 10.4 g/dl (normal 14.0–17.0 g/dl), AST 55 U/l (normal 12–35 U/l), ALT 35 U/l (normal 6–31 U/l),γ-GTP 283 U/l (normal 9–58 U/l), T-Bil 4.9 mg/dl (normal 0.1–1.0 mg/dl) and PT % 68 % (normal ≥70 %), suggesting mild anemia and increased hepatobiliary enzymes. Hepatic function was evaluated as C (10 points) in the Child–Pugh classification. Tumor markers were high, as shown by the levels of AFP and PIVKA II of 27.4 ng/ml (normal 0.0–15.0 ng/ml) and 567 mAU/ml (normal <40 mAU/ml), respectively. HBV and HCV were negative and renal function was normal. Hemorrhagic ascites was found in abdominal paracentesis and the case was diagnosed as ruptured HCC.
Abdominal CECT showed a large HCC with a maximum diameter of 15 cm in S7/8 of the liver and multiple HCCs in both lobes (Fig. ). The attenuation value of the ascites was as high as 30 Hounsfield units, but no clear extravasation was found in the arterial and equilibrium phase, and thus the bleeding site could not be identified. Abdominal ultrasonography also showed multiple tumors in both lobes and ascites with high echo density (Fig. a). However, even with these data the bleeding site was unclear, and CEUS was performed for the large HCC in S7/8 as the region of interest. The ultrasound equipment used in this examination was SSA-790A (Toshiba Medical Systems, Tokyo, Japan) with a convex probe (PVT-375BT, 3.75-MHz center frequency). The imaging mode used was wideband harmonic imaging (pulse subtraction) with transmission/reception frequencies of 1.8 and 3.5 MHz, respectively. The mechanical index for acoustic output was set to 0.2; the dynamic range was set to 60–65 dB. A intravenous bolus injection of Sonazoid (0.5 ml) was administered via a left cubital venous line followed by 10 ml normal saline flush. Observation in the arterial phase showed no clear leakage of contrast agent from this tumor, but punctate high-intensity echoes of Sonazoid microbubbles were observed in ascites. In particular, extremely high-intensity echoes of Sonazoid microbubbles were present in ascites surrounding the tumor, close to the S5 gallbladder bed. The tumor was imaged again using the re-injection method [] with Sonazoid in the post-vascular phase and leakage of the contrast agent from the tumor into the abdominal cavity was observed, indicating that this was the site of bleeding (Fig. b).
Abdominal angiography was urgently performed. Imaging of the celiac artery and hepatic artery showed no clear extravasation. However, since the tumor on the gallbladder bed was suspected as the bleeding site based on CEUS, selective cannulation of the cystic artery was performed (Fig. a). The artery was imaged using carbon dioxide (CO2), which is a highly sensitive method for evaluation of blood flow []. Leakage of CO2 out of the vessel was apparent, confirming that the bleeding site was the tumor in S5, which was fed by the cystic artery (Fig. b). TAE was conducted using a gelatin sponge (Gelpart; Astellas Pharma, Tokyo, Japan) with a particle size of 1 mm, and the clinical course after TAE was favorable with arrest of bleeding.


A 39-year-old male patient, diagnosed with ulcerative colitis and sclerosing cholangitis
10 years ago, was admitted to the hospital for elective liver transplantation. The
patient was taking azathioprine 100mg/d, ursacol 1.2 g/d, prednisone 10mg/d, simvastatin
20 mg/d, spironolactone 100mg/d, folic acid and calcium carbonate. On admission his
general condition was good, and he had a healthy skin tone, was well hydrated,
feverless, jaundiced +++/IV, with stable vital signs. On physical examination, he had
target painless hepatomegaly, spider veins and lower limb edema. Twelve hours after
admission, the patient had high fever, tachycardia, myalgia in the calves and
anuria.
Ceftriaxone was empirically started. Within hours, lesions resembling purplish
erythematous plaques occurred on the lower limbs, with rapid growth and proximal
progression.
The patient reported a recent trip to the coastal area of the State of Paraná, one day
before the admission. Samples for leptospirosis, dengue, yellow fever, spotted fever and
meningococcemia were collected and were found to be negative.
The patient became unresponsive to volume, had dyspnea and respiratory distress. He was
transferred to the ICU and needed vasoactive drugs and mechanical ventilation. His
clinical condition progressively worsened associated with increased need for vasoactive
drugs. The skin lesions became confluent, forming blisters, and there was discharge of
sero-sanguineous fluids (). Therapy with
ceftriaxone was changed to meropenem and oxacillin. Blood cultures revealed growth of a
gram-negative bacillus, which was later identified as Vibrio
vulnificus. Approximately 32 hours after the onset of infection, the patient
died.


A 51-year-old white man from Brazil, suffering from idiopathic chronic renal failure, presented with a immunosuppressive agentes. 2-year history of asymptomatic cutaneous lesion on the left groin, noticed by his nephrologist during hospitalization due to sepsis caused by catheter infection.
The patient was frequently catheterized at this site since an unsuccessful kidney transplantation 2 years before.
The lesion was a yellow-erythematous-purple plaque measuring around 1 cm in diameter, on the left groin, near a femoral vein catheter ().
The lesion was sampled for histopathologic and culture studies. The culture results revealed the growth of Providentia spp and Candida albicans. Histopathologic analysis revealed a chronic inflammatory process characterized by sheets of closely packed macrophages containing PAS-positive inclusions (von Hansemann cells) and calcospherites known as Michaelis-Gutmann bodies, as demonstrated by Von Kossa stain, which shows the homogeneous bodies in black ( e ). Prussian blue staining demonstrated the presence of hemosiderin inside macrophages, which may explain the purple color of the lesion ().
The patient was treated with surgical excision in association with sulfametoxazol-trimetoprin antibiotic therapy. No evidence of recurrence was detected on 3-year follow-up, as shown in .


A 75-year-old woman had a large blue patch on the right shin for 3 years. She underwent a left total knee replacement 18 years ago and a right total knee replacement 14 years ago due to severe osteoarthritis of both knees. Each of the operations was carried out successfully without any serious adverse events. Eleven years after the right total knee replacement, she noticed a discoloration of her right shin, and the lesion continued to enlarge slowly over time. She was referred to a dermatology clinic where a large, well-demarcated bluish-gray patch was noted on her right shin. The surface of the skin was smooth with no palpable infiltration. For 1 year, she experienced pain when walking on the right shin. She had a 10×15 cm well-demarcated bluish-gray patch on the extensor surface of her right shin (). Routine laboratory tests, including complete blood count, liver function tests and urine analysis, yielded normal findings. Histopathologic findings from the skin lesion showed perivascular, fine black particles in the dermis (). The black particles were stained positive with both melanin and demelanin stains. Polarizing microscopy of the skin specimen revealed refractile foreign materials in the perivascular area of the dermis (). Further, energy-dispersive X-ray spectrophotometry revealed the presence of titanium and aluminium (). Metallic discoloration was diagnosed on the basis of clinical, histopathological, polarizing microscopy and energy dispersive X-ray spectrophotometer findings. The radiographs revealed loosened and dislocated tibial components of the right knee prostheses. Preoperative and intraoperative cultures were negative for bacteria. During surgical revision, marked loosening of the tibial component and wearing of polyethylene were found. Additionally, an intense black staining of a substantial amount of wear debris adjacent to the tibial components and tibial bone defect was observed (). The patient was treated by debridement, and the right tibial component was replaced. After the revision procedure, metallic discoloration disappeared and has not reoccurred over the past 4 years.


A 43-year-old woman, known to have asthma for 5 years, is presented to the Emergency Department (ED) in a gasping state. Her clinical assessments include: heart rate, 140 bpm; blood pressure, 70/42 mmHg; respiratory rate, 35 per min; and SpO2 78% on plethysmography. Initial resuscitation was done with intubation and fluid management. Her initial arterial blood gases showed severe respiratory and metabolic acidosis (pH 6.90; PaCO2 114 mmHg; PaO2 30.0 mmHg; and HCO3 13.4 mEq/L). After securing the airway, the clinical exam revealed, tachycardia, unstable hemodynamics, peripherally mottled skin, and silent chest with no air entry. The case was diagnosed as a severe life-threatening asthma leading to type II respiratory failure and shock. Initial laboratory exams showed hemoglobin, 13.4 g/dL; hematocrit 40.8%; leukocyte count 15.7 × 109/L and platelet 225 × 109/L. Chest X-ray revealed hyper-inflated lung fields. The patient was sedated with ketamine and relaxed with rocuronium infusion. She was placed on mechanical ventilation (Draeger C500) in assist control mode, respiratory rate 12 per min; tidal volume 7 mL/kg (according to ideal body weight); inspiratory flow rate 70 L/min; Positive end expiratory pressure (PEEP) 5 cm H2O; and 1.0 FiO2. Lung mechanics revealed high-peak airway and plateau pressure (80 and 30 cm H2O respectively). The Intrinsic-PEEP (PEEPi) measured at that time was non-significant. The treatment was started with bronchodilators (salbutamol and ipratropium), inhaled and intravenous corticosteroids, and bolus of magnesium sulfate (2 g).
Subsequently, the patient was treated with salbutamol infusion and intermittent doses of 0.5 mL (1:1000) subcutaneous adrenaline. Despite being on maximum support, the patient showed no significant improvement. Lung mechanics still displayed high peak and plateau pressures (75 and 35 cm H2O respectively). Bicarbonate infusion was started to maintain the pH near normal. The patient continued to have mixed acidosis with pH 7.01; PCO2, 71.8; PaO2 87; and HCO3 13.4. Urgent flexible bronchoscopy was performed for diagnostic purposes and removal of mucus plug as warranted. Bronchoscopy revealed hyperemic airways, purulent secretions in central airways. Lavage was done and mucus plugs were removed. The process of bronchoscopy was unremarkable.
Immediately after bronchoscopy, the patient's respiratory condition began to improve. Acidemia improved from 7.01 to 7.24, PCO2 decreased from 72 to 32 mmHg and PaO2 improved from 87.2 to 186 mmHg []. FiO2 was also reduced from 1.0 to 0.4. Peak and plateau airway pressures decreased to 25 and 18 cm H2O respectively. Patient's severe bronchospasm had remarkably improved.
At the same time, the patient was also treated for sepsis. The presence of Gram-positive cocci in blood was noted in gram stains and vancomycin was started. Hematological assessment showed elevated leukocyte (21.2 × 109/L), low platelet (98 × 109/L) count, and normal hemoglobin.
Furthermore, patient's sepsis worsened. Patient was resuscitated with fluids, vasopressor, and broad spectrum antibiotics. Despite improvement in respiratory status her course was complicated with septic shock and multi-organ failure. Patient expired after 5 days of admission.


A 36-year-old male, who was asthmatic since childhood, presented in the ED with shortness of breath for 1 week. The patient also had a history of yellowish sputum with fever for 1 week. Clinical exam revealed bilateral wheeze with prolonged expiration throughout the chest and a roentgenogram showed hyper-inflated lungs and right lower lobe infiltrate. He was intubated in the ED in response to worsening respiratory failure. The initial diagnosis was exacerbation of asthma and community acquired pneumonia. Blood gases before (pH 7.01; PaCO2 108; PaO2, 106 HCO3 27.8) and after the intubation showed acute respiratory acidosis (pH 7.16; PaCO2 90.2; PaO2 110; HCO3 23.7). Initial treatment included inhaled bronchodilators, inhaled and intravenous steroids, antibiotics (ceftriaxone and azithromycin), and a bolus dose of magnesium sulfate. Patient was placed on mechanical ventilation (Draeger infinity 500) with settings of assist control, rate 12 per min; tidal volume 6-7 mL/kg; PEEP 05 cm H2O; inspiratory flow rate 70 L/min and FiO2 1.0. Lung mechanics revealed high peak and plateau pressures of 70 and 28 cm H2O respectively, whereas intrinsic PEEP (PEEPi) was measured 12 cm H2O. Inspiratory flow rate was increased to 80 L/min to reduce the PEEPi.
Intravenous infusion of salbutamol and intermittent subcutaneous adrenaline 0.5 mL (1:1000) was started due to progressive worsening of clinical condition. PEEPi and peak airway pressure improved from 12 to 4 cm H2O and 70 to 56 cm H2O respectively. Arterial blood gases showed little improvement (pH 7.26; PaCO2 74.9; and PaO2 146). On 3rd day of hospital admission bronchoscopy was planned for bronchial toilet. It revealed inflamed airways and obstruction of middle-sized airways with mucus plugs []. Effective suction and lavage were done.
The patient's clinical condition and ventilator requirement were reduced and ABG was improved [] after therapeutic bronchoscopy. The patient was successfully weaned on the following day. Patient was discharged from intensive care 48 h after extubation.


A 34-year-old male, a clerk by profession underwent a living donor renal transplantation in 2006 and was maintained on cyclosporine (150 mg daily), prednisolone (10 mg daily), and mycophenolate mofetil (1500 mg daily). He did not receive lytic induction. He was anti-HCV positive and received a 6-months course of interferon alpha 2b before transplantation. During early post-transplant period, he had acute cellular rejection Banff type II A, requiring three doses of methyl prednisolone. There were no opportunistic infections or reactivation of HCV during the 1st year of follow-up.
A year after transplantation, he developed multiple warty lesions on the dorsum of the fingers of both hands suggestive of verruca vulgaris. These lesions were treated with cryotherapy, cauterization, and radiosurgery with marginal improvement. However, 4 months later, the distal end of the right middle finger revealed ischemic changes and necrosis, needing amputation of distal two phalanges []. Histology of the amputated finger showed nests of malignant squamous cells with keratin pearls infiltrating the dermis []. He returned to our center where excisional biopsies of few existing warts were done. Histology showed hyperkeratosis, parakeratosis, acanthosis and prominent giant eosinophilic keratohyalin granules and eosinophilic intranuclear inclusions with viral cytopathic effect, and mild dysplasia consistent with verruca vulgaris []. Human papillomavirus (HPV) genotype Ia was identified from the specimen. Having lost part of the finger on the right hand, the patient had crippling anxiety and fear that the remaining warts would claim his other fingers and his livelihood. Cyclosporine was replaced with everolimus. Ketoconazole augmentation was given for cost reduction. Cryotherapy and cauterization failed over the next 6 months. At this time, the patient was treated with Thuja occidentalis (T. occidentalis) extract, orally and topically for a period of 7 days at his native place. For external applications, he received mother tincture and as oral preparation he was given potentized medium (power 1m= 1000 times) T. occidentalis as 2 globules thrice a day. By the end of 3rd week of therapy, the warts dropped off leaving only small superficial scars []. The allograft function remained unaffected at creatinine of 1.5 mg/dl. He has been followed up for one year and has not had any recurrence.


A 37 year old male presented with a history of hypertension for the last 3 years. He was not a smoker and had no family history of hypertension. The blood pressure was 220/120 mm of Hg despite being on nifedipine 20 mg thrice daily, prazosin 5 mg twice daily and clonidine 0.1 mg 3 times daily. He was found to have severe renal insufficiency (serum creatinine: 8.9 mg/dl), hypokalemia (serum potassium 2.9 meq/l), bland urine sediment, contracted left kidney (6.3 cm × 3.4 cm) and normal sized right kidney (9.4 cm × 4.0 cm) with increased echotexture. The cardiac evaluation showed concentric left ventricular hypertrophy with good LV function (EF: 71%) and mild diastolic dysfunction. Color Doppler showed high resistive indices (RI > 1.0) and peak systolic velocity (>180 cm/sec) in both main renal arteries suggesting ostial stenosis. Renal arteriogram showed hemodynamically significant ostial stenosis on both sides. Renal angioplasty and stenting was carried out on the right side with balloon expandable chromium cobalt stent. He received 5000 units of unfractionated heparin in the post procedure period and was started on anti-platelet agents. His serum creatinine decerased to 1.5 mg/dl over the next 4 weeks. The blood pressures were within the normal range on 40 mg of nifedipine daily. He continued to use anti-platelet agents (aspirin 150 mg and clopidogrel 75 mg daily).
He presented with flash pulmonary edema after 1½ years of initial stent placement. When his follow-up visits with the local physician were reviewed it revealed a slowly rising blood pressure levels for which an angiotensin converting enzyme inhibitor (ramipril 5 mg) was added in the last 2 weeks. Re-evaluation showed severe renal insufficiency (serum creatinine 10.2 mg/dl). Color Doppler showed no flow across the stent. Renal arteriogram showed near total stent occlusion with no collateral flow into the kidney [].
Ramipril was discontinued and he was given two sessions of hemodialysis. A percutaneous balloon dilatation and stent-in-stent (Medtronic racer: 5.0 mm × 18 mm, cobalt chromium) was placed [Figures and ]. On the 2nd day of stent placement his urine out put improved and serum creatinine started to decline and reached a nadir of 1.5 mg/dl on the 7th day.


A 56-year old man was referred by an emergency physician to our hospital with an impression of ST-segment elevation myocardial infarction (STEMI). The patient was stung on the arm, neck and head several times by wasps while working on his field about 7 hours prior to admission. He had a mild allergic reaction involving local pain and urticarial swelling immediately after the incident without signs of anaphylaxis or shock. Just a few minutes after being stung, he started complaining of chest pain and called the emergency service. His blood pressure was 120/80 mm Hg, pulse rate was 90 beats per minute and electrocardiogram revealed ST-segment elevation with Q wave formation in the anterior leads and reciprocal ST-segment depression in the inferior leads (). His troponin T level was elevated to 1.86 ng/mL. After being given intravenous dexamethasone and antihistamine, he was promptly transferred to our catheterization laboratory. He had undergone an everolimus-eluting 3.5×15 mm stent placement (Promus®, Boston Scientific, MN, USA) in the mid-left anterior descending (LAD) artery for stable angina 3 years prior in our hospital. Clopidogrel (75 mg/d) was withdrawn 24 months after stent implantation, while aspirin (100 mg/d) had been continued until that day. Coronary angiography demonstrated a thrombosis in the previous stent in the LAD artery, completely occluding the vessel (). The remaining vessels showed insignificant stenosis. The lesion was crossed with a Runthrough® NS guidewire (Terumo) and sequential inflations using Nimbus PICO® (BARD) 1.25×12 mm, followed by 2.0×12 mm balloons to disperse the thrombus. Next, thrombus aspiration with a thrombus aspiration catheter (Thrombuster II®, Kaneka Corp., Japan) was performed. Abciximab infusion was started, of which half of the initial bolus was given directly into the left coronary system. However, Thrombolysis in Myocardial Infarction flow 3 was not established despite these measures. In the end, an everolimus-eluting 3.5×15 mm stent (Promus Element™, Boston Scientific, MN, USA) was deployed with an excellent angiographic result (). We did not measure serum tryptase and histamine levels with a half life of 90 minutes and of less than 30 minutes respectively because 7 hours had passed after the onset of symptoms. He was discharged from the hospital 6 days after the index procedure with dual anti-platelet therapy (DAPT). The patient is currently doing well and is being followed up in the outpatient department.


A 53-year-old Korean-Chinese woman was brought into the emergency department of our hospital by an ambulance, with complaints of progressive chest pain and dyspnea. She had a high fever, cough, and general fatigue over the three days. Upon arrival, she was fully conscious and had signs of cold sweating, cyanosis and general pallor. The initial creatine kinase (CK), CK-MB and Troponin-I levels were 626 U/L, 47.27 ng/mL, >50 ng/mL, respecitvely. Emergent coronary angiogram was performed because of low blood pressure (88/56 mm Hg), ST-segment depression in the precordial leads of ECG (), and systolic dysfunction with left ventricular wall motion abnormality on echocardiography. Coronary angiographic findings were normal, and an intra-aortic balloon pump (IABP) was immediately inserted for hemodynamic support (). On the basis of prodromal symptoms, elevated cardiac enzymes and normal coronary angiographic findings with ventricular wall motion abnormality, we contemplated acute decompensated heart failure due to clinical suspicion acute myocarditis. She was admitted to the coronary care unit, and mechanical ventilation and inotropic agents were started. Although aggressive supportive therapies were provided, her blood pressure continued to decline. We decided to support the patient with ECMO, which was inserted in a veno-arterial configuration by cannulation on both femoral vessels. We were able to reduce the amount of inotropic agents using mechanical circulatory support. However, ECG showed wide QRS tachycardia with left bundle branch block (), and echocardiography showed severe global hypokinesia (). The serum creatinine level was elevated, and the amount of urination was decreased. Soon after, pulmonary edema developed. Because of low blood pressure and the lack of diuretic effect, continuous renal replacement therapy was started using the ECMO circuit on day 1. Ventricular wall movement was gradually decreased, and ECG showed little or no electrical activity ( and ). On day 2, IABP had to be removed because of its malfunction. We continued intensive supportive care. However, the laboratory data and general medical conditions gradually deteriorated. ECG showed little or no electrical activity. On day 5, ECG revealed weak electrical activities (), and echocardiography showed a slight improvement of systolic function (). She gradually recovered, and her ECG showed sinus rhythm ( and ). Since then, her condition started to gradually recover. Mechanical ventilator was weaned off on day 18, and ECMO was weaned off on day 20. She underwent cardiac magnetic resonance imaging after making sure that she was medically stable, which showed diffuse wall thinning, decreased wall motion and delayed enhancement of diffuse ventricular wall sparing of the infero-septal wall (). During hospitalization, she was complicated with ischemic insult in the lower extremities, hepatitis with jaundice, and acute tubular necrosis. On day 76, she was discharged from the hospital. The ejection fraction on the echocardiogram before discharge was approximately 30%. She receives wound dressing once a day and maintains hemodialysis every other day.


This 11-year-old boy presented with 3 days history of progressively increasing radicular pain over the sacrogluteal region bilaterally; left side more than the right side, along with lower limb weakness and sensory impairment in both lower limbs. He also developed urinary retention and was catheterized elsewhere 1 day prior to his presentation. On examination, his cranial nerves and upper limbs were normal. He had asymmetrical lower limb weakness with the left side worse than the right. His sensory examination also revealed an asymmetrical sensory impairment in the lower limbs with the upper limit being D12 dermatome. Both knee jerk and ankle jerk were absent with plantars not being elicitable. His muscle tone and bulk were normal. He did not have any neurocutaneous markers, palpable lymph nodes or spinal deformity. With this presentation and neurological examination, a diagnosis of spinal cord pathology with clinical localization to cauda equina was made. An emergency magnetic resonance imaging (MRI) of the lumbosacral spine with screening was performed, which showed a well-defined sausage shaped intradural lesion at L2, L3 level, without evidence of any other central nervous system (CNS) lymphomas. The lesion was iso-intense in T1- and T2-weighted images []. He underwent emergency L2, L3 laminectomy and excision of intradural extramedullary lesion. The lesion was removed piecemeal. Intra-operatively the lesion had some attachment to the anterior dura. Total removal was carried out, with coagulation of the anterior dura.
Post-operatively he had total relief of pain and his motor power improved by one Medical Research Council grade and sensations were slowly improving. Histoplathological examination of the tumor revealed a dense infiltration of round cells admixed with cells with a large eosinophilic cytoplasm and vesicular nucleus with prominent nucleolus, which was consistent with non-Hodgkin's lymphoma []. The diagnosis was confirmed by immunohistochemistry showing CD20 positivity. Detailed investigation was carried out to stage the disease, which included complete hematological examination, including bone marrow aspiration and computerized tomography of the chest and abdomen. All the above investigations were normal.
On follow-up after 1 month he had received radiotherapy to the local area of 32 Gy in 20 fractions and was on chemotherapy; cyclophosphamide, hydroxydaunomycin, oncovin-vincristine, and prednisone regimen. Post-operative MRI showed total excision of the lesion []. At 1 year follow-up, he was having near normal power, normal sensations, and normal bladder control.


A 40-year-old male patient presented with complaints of intermittent claudication in the right lower limb for past 6 months. There was no history of fever, trauma, diabetes mellitus, or hypertension. He was an occasional smoker. There were no other significant associated complaints. Physical examination revealed diminished pulses in right lower limb arteries, for which Doppler USG (ultrasound) examination was requested. Doppler study revealed multiloculated cystic lesion in relation to the popliteal artery, causing significant luminal narrowing with dampened low resistance flow in distal arteries []. It was also causing focal narrowing of popliteal vein. Subsequently, the patient underwent computed tomography angiography (CTA) on 128-slice multidetector computed tomography (MDCT) scanner (Ingenuity CT, Philips Healthcare, Cleveland, OH, USA). CTA revealed multiloculated cystic lesion in relation to right popliteal artery, with mild peripheral enhancement. There was significant focal eccentric narrowing of popliteal artery. Distal vessels were normally opacified. It was also causing narrowing of popliteal vein []. Based on the characteristic imaging findings, diagnosis of cystic adventitial disease of popliteal artery was made. Patient underwent surgery with partial resection of the cysts and the diagnosis was confirmed on histopathology. Patient improved symptomatically. Postoperative CTA revealed significant reduction of cystic disease and reduction of popliteal artery stenosis [].


A 10-year-old girl presented with multiple asymptomatic papules over right lower abdomen present since the age of 2 months. The lesions were gradually progressive with a rapid enlargement in the last 1 year. There was no history of any neurological, ocular or skeletal abnormality. On examination there were multiple erythematous papules and coalescent plaques (0.5 cm to 5 cm) in a linear pattern over the right lower abdomen []. Most papules were discrete, pink, dome shaped with a few papules showing central umblication and crusting. The papules coalesced to form numerous papillomatous plaques of varying sizes (1 to 5 cm). Yellowish slough and crusting was seen on some of the lesions. The discharge from the lesions foul smelt. No regional lymphadenopathy was present. The routine hematological and biochemical tests, chest radiograph and abdominal ultrasonography were normal.
The skin biopsy revealed cystic invagination of epidermis with papillary projection lined by two rows of cells. There were columnar cells towards the lumen and cuboidal cells in the outer layer. Decapitation was seen in the luminal columnar cell layer. The fibrovascular core of papillae showed mixed inflammatory infiltrate comprising of plasma cells, lymphocytes and neutrophils. The underlying deep dermis showed apocrine sweat glands []. The histopathologic features were consistent with the diagnosis of syringocystadenoma papilliferum. Immunohistochemistry (IHC) staining using epithelial membrane antigen (EMA), CD56, CK 19, CK 5, P 63 and smooth muscle antigen (SMA) revealed EMA positivity in columnar cells. Focal positivity of CD 56 was seen in columnar cells. CK 19 was positive in both columnar and basal cells. CK 5 and p63 were positive in basal cells. SMA was focally positive in basal cells []. These findings were consistent with the diagnosis of SCAP of apocrine origin. There was no evidence of malignant transformation. The patient was referred to Plastic surgery for surgical excision with skin grafting. However, the patient was lost to follow up.


A 52-year-old male presented to our department with a painless swelling in front of neck progressing slowly over the past 6 years. He complained of a rapid increase in size over the past 6 months. No history of irradiation. Clinical examination and CT evaluation suggested the presence of an irregularly-shaped complex TGDC measuring 6 × 5 cm with solid and cystic components. There was also evidence of fine calcification within the solid areas []. There was also a mildly enhancing nodule found in right lobe and isthmus of thyroid with fine calcification within the nodules. There was no cervical lymphadenopathy. Ultrasound-guided FNAC from the solid area of the TGDC suggested papillary carcinoma. Sistrunk operation for thyroglossal cyst done using a single transverse neck incision, and per-operative thyroid exploration revealed a hard nodule in the right lobe of thyroid with few enlarged paratracheal nodes. Since there was a strong suspicion of malignant thyroid nodule as well, total thyroidectomy and central compartment dissection was completed in the same sitting. Gross examination revealed TGDC, which was multiloculated and had solid and cystic areas (about 2 cm) []. There was a 0.5 cm nodule in the isthmus and a 1 cm nodule in the right lobe of thyroid gland. Microscopic diagnosis [Figures -] was multifocal papillary carcinoma of thyroid and thyroglossal cyst with no metastasis in level VI nodes. Post op I131 scan showed 0.3% uptake in the thyroid bed and no evidence of functioning distant metastasis. Patient is on suppressive thyroxin therapy.


Patient 1 is a 31-year-old female with a history of unprovoked pulmonary embolism at age 20. Thrombophilia testing was completed due to her young age and a family history of pulmonary embolism in her brother. The patient was found to be AT deficient with an AT activity of 37%. She was maintained on long term anticoagulation with warfarin. Her other past medical history was significant for supraventricular tachycardia, rheumatoid arthritis, endometriosis, pyelonephritis, Crohn’s disease, and gastroesophageal reflux disease. The patient became pregnant in 2010 and was switched to enoxaparin at 4 weeks gestation. Her pregnancy was complicated by gestational diabetes, which was controlled by diet and exercise. Additionally, she had one admission due to supraventricular tachycardia and was found to have irregular uterine contractions. Due to the AT deficiency, anticoagulation was monitored using anti-Xa levels with goal peak level >0.6 IU/mL. At the highest dose, she required enoxaparin 120 units (~1.4 units/kg) subcutaneously every 8 hours ().
Patient 1 was admitted at 35 weeks and 4 days due to concerns for preterm labor. She was continued on enoxaparin until the evening of hospital day (HD) 2. She started rhAT on HD3 with a loading dose of 48.5 IU/kg (calculated from [100-baseline activity]/1.3) and maintenance dose of 11 IU/kg/hour (calculated from [100-baseline activity]/5.4). She underwent induction of labor via cervical ripening catheter and oxytocin when the AT level was in the normal range. Amniotomy was performed on HD5, and the patient vaginally delivered a healthy infant weighing 2,268 grams on HD6. Apgar scores were 7 and 9 at 1 and 5 minutes, respectively. The estimated blood loss was 250 mL. The rhAT infusion did not require dose modifications and the patient’s AT levels remained between 90%–108% (). Intravenous unfractionated heparin was started immediately postpartum and was adjusted by anti-Xa levels. Additionally, the patient was started on warfarin on the evening of delivery. Admission hemoglobin of the patient was 14.4 g/dL and postpartum hemoglobin was 11.5 g/dL. She was continued on an unfractionated heparin and AT3 infusion until the international normalized ratio (INR) was greater than 2.0 and she was subsequently discharged.


Patient 2 is a 40-year-old female with a past medical history significant for viral encephalitis and a left leg superficial thrombosis at age 32 while taking oral contraceptive pills. Her oral contraceptive pills were discontinued and she was treated with anti-inflammatory medication. At age 40, patient 2 was 8 weeks pregnant with her third child and sought evaluation for right calf and popliteal pain. She was diagnosed with a non-occlusive deep vein thrombosis of the distal femoral, popliteal, and posterior tibial vein. A hypercoagulable evaluation showed an antithrombin activity of 38%–41%. Her sister, father, and daughter were subsequently diagnosed with antithrombin deficiency but have not experienced thrombosis. Patient 2 was initially treated with enoxaparin at 1.5 mg/kg daily, and was switched to twice daily dosing after the antithrombin deficiency was diagnosed (). At the highest dosage, she required enoxaparin at 1.8 mg/kg twice daily to maintain therapeutic anti-Xa levels. Her pregnancy was otherwise uncomplicated and she was admitted at 37 weeks 4 days gestation for induction of labor. She received a bolus of 41.4 IU/kg and maintenance infusion of 10 IU/kg (calculated as above). Labor induction began once antithrombin levels had normalized. The patient vaginally delivered a healthy male with Apgar scores of 8 and 9 at 1 and 5 minutes, respectively. Estimated blood loss was 300 mL. Her antithrombin levels remained between 96%–127% without adjustment of her infusion (). An unfractionated heparin infusion was started 4 hours after delivery. She was discharged on HD9 on warfarin and twice daily enoxaparin until her INR was >2.0 two days later. She has been maintained on therapeutic anticoagulation due to her history of thrombosis in the setting of antithrombin deficiency.


Patient 3 is a 27-year-old female with a history of pulmonary embolism 4 days after cesarean delivery of her first child. She was treated with weight-based enoxaparin without monitoring of anti-Xa levels. The patient sought hematology evaluation when she was 8 weeks pregnant with her second child. A hypercoagulable work-up was notable for an antithrombin level of 63%. Repeat testing showed antithrombin activity levels of 64%–73% with normal antigen levels. The patient had no family history of thrombosis. Due to the discrepancy between the amount of clinical heparin resistance and her antithrombin activity, sequencing of the SERPINC1 gene was completed. She was found to have a heterozygous mutation in the heparin binding site (c.218C > T, p.Pro73Leu) which is associated with type II antithrombin deficiency. To achieve therapeutic anticoagulation, the patient was treated with 1.8 mg/kg of enoxaparin. She did not require further increase in her enoxaparin dose after therapeutic levels were obtained (). She underwent elective induction at 37 weeks 3 days after rhAT infusion was initiated. Her last dose of enoxaparin was 24 hours prior to induction. Patient 3 required a cesarean delivery on HD2 due to intrapartum spontaneous conversion to breech presentation. A healthy male infant was delivered with an estimated blood loss of 1,200 mL due to uterine atony. Eight hours postpartum the patient was started on heparin infusion and warfarin. She achieved therapeutic anticoagulation within 4 hours. Her AT activity remained in the normal range without adjustments of her rhAT infusion (). On HD3, the patient developed right arm pain and was noted to have an occlusive superficial thrombus of the right basilic vein and a nonocclusive deep thrombosis of the distal right axillary vein associated with the peripherally inserted central catheter (PICC). The PICC was removed as it was considered the etiology of the thrombosis, and the patient continued the rhAT via a peripheral intravenous infusion. The patient’s right arm pain resolved and she was discharged on HD8 after therapeutic anticoagulation with warfarin was achieved.


A 62-year-old woman with relapsed diffuse large B cell lymphoma (DLBCL) after autologous HSCT received an allogeneic peripheral blood stem cell transplantation from a sex-mismatched and ABO- and human leukocyte antigen-matched related donor after conditioning with fludarabine (30 mg/m2/day for 6 days) and intravenous busulfan (0.8 mg/kg every 6 hr for 2 days). She had been diagnosed with DLBCL 2 years previously, and treated with autologous HSCT as salvage therapy after the first relapse of the disease. Graft versus host disease (GVHD) prophylaxis consisted of 3 mg/kg/day of intravenous cyclosporine A (CsA) and intravenous methotrexate (15 mg/m2 on day 1 and 10 mg/m2 on days 3, 6, and 11). This therapy prevented development of acute GVHD. The serum level of CsA was adjusted to maintain a target trough serum level between 200 and 300 ng/mL. No hemorrhagic cystitis occurred during the course of immunosuppression.
On post-transplant day 25, while the patient was still receiving CsA, memory loss, disorientation to time and place, and slurred speech were observed. Diffusion magnetic resonance imaging (MRI) showed no evidence of diffusion restriction, and only non-specific findings suggesting a subacute or chronic lacunar infarction at the right basal ganglia were found. The patient's disorientation recovered transiently over the next 24 hrs, although her neurological symptoms became progressively worse during the next 48 hrs. A repeat contrast-enhanced MRI performed 5 days after the onset of these symptoms showed no abnormal findings, with the exception of mild leukoaraiosis in the bilateral cerebral white matter, basal ganglia, and pons. A sleep and waking electroencephalogram (EEG) showed a slow, continuous generalized theta rhythm suggesting the presence of diffuse cerebral dysfunction. Based on this finding, CsA was switched to mycophenolate mofetil to exclude the possiblity of reversible posterior leukoencephalopathy syndrome, neurotoxicity caused by the immunosuppressive agent. Analysis of cerebrospinal fluid (CSF) showed normal glucose (71 mg/dL) and protein (19.5 mg/dL) levels and no evidence of pleocytosis. Microbiological examination of the CSF showed negative results for bacteria, mycobacteria, toxoplasma, herpes simplex virus type (HSV) I and II, cytomegalovirus (CMV), enterovirus, varicella-zoster virus, Epstein-Barr virus, and cryptococcus. Examination for BKV or John Cunningham (JC) viruses was not performed because there was no evidence of BKV encephalitis or progressive multifocal leukoencephalopathy on the MRI findings. The mental state of the patient deteriorated progressively with stupor without fever developing on post-transplant day 40. A follow-up sleep and waking EEG showed moderate to severe diffuse cerebral dysfunction, with evidence of progressive worsening of cerebral dysfunction. This finding led us to carry out a repeat MRI that showed the findings had changed since the initial scan. A diffusion-weighted image () identified diffusion restriction areas in the post-frontal and parietal periventricular white matter, and along the precentral and postcentral subcortical white matter, suggesting new development of encephalitis.
Because diffusion restriction is a common MRI finding in encephalitis cases, a follow-up CSF analysis including real-time PCR and PCR for BK virus was carried out on post-transplant day 48. Real-time PCR test and PCR were performed using a BKV quantitative real-time PCR kit (Bio-Core. Inc., Seoul, Korea) and a BKV PCR Kit (Bio-Core. Inc., Seoul, Korea), respectively, and showed positivity for the BK virus (). The viral load for BKV was 3,356 copies/mL, confirming the diagnosis of BKV encephalitis. PCR for BKV with a peripheral blood sample was also shown to be positive ().
PCR analysis of a urine specimen yielded negative results. PCR for other viruses such as HSV I, HSV II, enterovirus, varicella-zoster virus, Epstein-Barr virus, CMV, and JC were all negative. We did not discontinue immunosuppressive therapy when the diagnosis was established because we considered it too early to stop prophylaxis for GVHD. The patient died on post-transplant day 79 owing to probable aspiration pneumonia without recovery of mental stupor.


A 22-year-old lady presented to the Joint Ophthalmology & ENT watery eye clinic with a 12-month history of a painless lump in the medial corner of her left eye, which was not increasing in size. Six months after noticing this painless lump, she developed left-sided intermittent epiphora. At the age of 10, she first had a watery left eye, and following a DCR when she was 15 years old, her symptoms seemed to resolve until this episode. She denied any nasal symptoms.
She had a history of depression, for which she was on fluoxetine but was otherwise well. She smoked three cigarettes per day and drank alcohol occasionally.
Clinical examination revealed a small cystic swelling in her left medial canthus (Fig. ). There was no discharge on pressure, mild tenderness was elicited and the swelling was not compressible. The rest of the eye examination was normal with a visual acuity of 6/6 in both eyes.
Anterior rhinoscopy showed a reasonable nasal airway with healthy mucosal lining. Flexible nasendoscopy revealed no nasal lesions with the septum slightly deviated to the right.
An MRI scan of the orbits showed a well-defined, thin-walled 22 × 16 mm cyst medial to the left orbit containing fatty/proteinaceous material, which was lying within and mildly expanding the left ethmoid air cells (Figs –).
A CT scan of the paranasal sinuses and orbits revealed the cystic expansile 1.6 cm mass at the left medial canthus to be of soft tissue density. The lateral wall of the mass expanded outwards into the orbit (suggesting an anterior ethmoidal mucocele) rather than being pushed medially (which could have been indicative of a dacryocystocele) (Fig. ).
All pre-operative blood tests were normal. A joint operating session by the ENT and Ophthalmic surgeons was planned with a view to performing an endoscopic left anterior ethmoidectomy with marsupialisation of the mucocele in combination with an endoscopic DCR.
The puncti were probed (Fig. ) and fluorescein dye instilled with no dye outflow to the left inferior meatus. It was not possible to pass the probe through the upper punctum so a mini-monoka DCR stent was inserted and secured (Figs. and ). Chloramphenicol eye drops were instilled.
The nasal cavity was prepared with modified Moffet's solution and a Storz 30° endoscope used with visualisation of the nasal cavity on a monitor. An inferiorly based mucosal flap was elevated on the lateral nasal wall (Fig. ) with the incision performed using a small myotome. Removal of part of the lateral nasal wall anterior to uncinate process was performed for access to the lacrimal system (unciformian endonasal DCR)
30° punch forceps were used to nibble bone sequentially for adequate exposure. Further drilling of the lateral bony wall was undertaken with a small cutting burr. An endoscopic left anterior ethmoidectomy was performed (Fig. ) with marsupialisation of the mucocele (Fig. ) and trimming of the DCR stent (Fig. )
Post-operatively, she was discharged the next day and advised to administer chloramphenicol eyedrops as well as betnesol nasal drops for a week. The DCR stent remained in situ for 3 months and was removed in the clinic. There was clinical resolution of the medial canthal swelling and epiphora.


A 67-year-old female patient presented to the emergency department of the American University of Beirut Medical Center because of the progressive appearance of painless jaundice of two weeks duration.
The patient's past medical history was noted for left breast cancer (in remission). She denied alcohol intake or illicit drug abuse.
Six weeks prior to the onset of jaundice, she had presented with high-rate atrial fibrillation and was commenced on propafenone at 300 mg/day.
Upon presentation, she was icteric. The physical examination revealed minimal nontender hepatomegaly.
A computed tomography scan performed at another facility showed prominent common bile and pancreatic ducts suggesting a double duct sign. Her initial serum bilirubin was 9.4/7.7 mg/dL, alkaline phosphatase of 384 IU/L. Her alanine transferase was 213 IU/L and aspartate transferase 228 IU/L. Her CA19-9 was 70 IU/mL []. Endoscopic ultrasound done at our center showed normal common bile and pancreatic ducts and no ampullary or pancreatic masses. Subsequently, viral serologic markers (IgM hepatitis A virus, IgM Hepatitis B core, Hepatitis C virus antibodies, Epstein-Barr virus, Cytomegalovirus) were negative. The anti-nuclear, anti-smooth muscle, anti-mitochondrial, and anti-liver and anti-kidney microsome antibodies’ levels were within normal limits. A Magnetic resonance cholangiopancreatography suggested a left hepatic stricture, but Endoscopic retrograde cholangiopancreatography was normal.
A liver biopsy via a trucut needle showed active portal and periportal inflammation with moderate macrovesicular steatosis, and bile ductular proliferation [Figure and ].
Withdrawal of propafenone was associated with gradual decrease in serum alkaline phosphatase and gamma-glutamyl transferase along with normalization of the aminotransferase levels and CA19-9.


A 28-year-old male patient reported to Dental Department of a Private Hospital with the chief complaint of rapidly increasing swelling at left body of mandible []. Patient had visited an oral and maxillofacial clinic for tenderness at same site, and extraction of 38 was performed. After extraction, patient noticed fast progression of swelling with no relief in pain. Swelling was bony hard. Submandibular lymph nodes of involved side were palpable and non-tender. Intraoral examination revealed obliteration of buccal vestibule in relation to 35, 36 and 37. Intraoral radiograph, in early stage of disease, revealed widening of periodontal ligament (PdL) space in relation to 35, 36 and 37 without any evidence of odontogenic or periodontal disease.
Radiographic imaging using CT, 3-D CT and CT angiography techniques were performed. CT scan revealed a large tumor mass originating from surface of outer cortex of body and angle of mandible []. Lesion extended from first molar to posterior border of ramus anterio-posteriorly. Tumor involved coronoid process above and extended 1.5 cm below lower border of mandible. Lower border of mandible was seen destroyed and replaced by connective tissue stroma of tumor. A mixed radiopaque and radiolucent mass with typical “sunburst” appearance at outer cortex with “codman's triangle” at the margins of tumor led to the diagnosis of OS []. 3D CT images revealed extensive spread of tumor mass. Tumor osteoid was seen forming a complex network radiating from body and angle of mandible and reaching coronoid notch []. Study of bone destruction pattern on CT scans revealed a predominant bone-destruction negative pattern. At most areas of tumor involvement the continuity of outer cortical plate is intact, with tumor osteoid radiating outwards. However, at lower border of mandible tumor mass is seen destroying entire thickness of bone and replacing with radioluscent soft-tissue mass. CT angiography was performed to assess the vascularity of tumor. The tumor was found to be extensively vascularized and the feeder vessel was identified to be external carotid artery []. Incisional biopsy showed osteoid areas lined by plump osteoblasts with hyperchromatic nuclei, mitotic figures, and sheets of cells showing nuclear and cellular pleomorphism, inflammatory cells, numerous blood vessels and hemorrhage []. Case was operated upon under general anesthesia, tumor mass resection with reconstruction using iliac crest was done []. Final diagnosis was consistent with that of representative specimen.


A 25-year-old female patient was referred to our department with a chronic headache. Patient's first diagnosis hypothesis was sinusitis and she had previously been referred to an otolaryngologist. Waters’ radiograph was performed, which demonstrated a limited radiopacity area into the right maxillary sinus. The patient's medical history was unremarkable. On physical examination, the patient was healthy, without swelling. The mucosa overlying the area of the lesion was the same color and texture as the surrounding mucosa. The sensory examination of the maxillary branch of the trigeminal nerve was normal bilaterally. Furthermore, she had aesthetic concerns about her high smile. Facial and cephalometrical examination revealed an excessively facial height and an excessive incisal and gingival display upon smiling. She was diagnosed with vertical maxillary excess and Class I malocclusion []. Initially, the patient was treated for third molar extraction 7 years ago; in this panoramic radiograph, was observed a discrete radiopacity area in the left maxillary sinus. It was probably an early stage of the lesion.
A biopsy was taken with a Caldwell-Luc approach; histological result show abundant myxoid stroma with collagen fibrils presenting a diagnosis of OM.
The treatment planned was Le Fort I osteotomy with down-fracture to remove the tumor with segmental maxillectomy and 5 mm superior maxillary repositioning for better occlusion and facial esthetic.
Surgery was performed under general anesthesia and nasal endotracheal intubation. Pre-orthognathic surgical models, radiographs, computed tomography face, photographs and biomodels were obtained before the surgery []. When the maxilla was down fractured, the tumor mass was visualized in the right maxillary sinus with four teeth involved in the lesion, which were removed. After the segmental maxillectomy, maxillary segment was stabilized with plate and screw in the anterior area on the right side and fixation on the anterior and posterior maxillary buttress on the left side. No intermaxillary fixation was used and it was not necessary turbinectomy.
The 3 years follow-up show satisfaction for the occlusal and esthetic result and the patient is disease-free []. A removable dental prosthesis without functional or aesthetic compromise is used [].


A 24-year-old woman who lived in Saitama, Japan had three pregnancies, two childbirths, body mass index (BMI) of 22.3, and unremarkable past medical and family histories. Furthermore, her pre pregnancy weight was 55 kg and her height 163 cm.
She also had an uneventful first trimester, but developed a fever of >39°C at 22nd week, 1st day of pregnancy. Because of prolonged headache and nausea, she was referred to our hospital in Saitama for complete physical examination on October 2008. On admission, she had blood pressure of 103/51 mmHg, heart rate of 100 beats per min (bpm), body temperature of 39.0°C, mild stiffness in the neck, and cold extremities. No neurological abnormalities, such as consciousness disturbance or paralysis, were observed. However, brain computed tomography (CT) for the prolonged headache revealed a 1.5 cm mass in the right frontal lobe, while hematological analysis showed an elevated white blood cell count of 12,400 cells/µl (neutrophils, 87.7%). Cerebrospinal fluid findings were positive for gram-positive bacteria, an increased cell count (especially for neutrophils) of 2,332 cells/µl, and a low glucose concentration of 30 mg/dl. Brain MRI revealed a 1.5 cm mass with a high intensity signal inside and a low intensity T2 signal on the margin in the deep white matter of the right frontal lobe. Based on the above findings and a high intensity zone surrounding the mass on diffusion-weighted images, she was immediately placed on intensive therapy with concurrent administration of antibiotics cefotaxime (2 g/day) and meropenem (3 g/day), as well as glycerin 20 g/day to reduce intracranial pressure. shows a list of examinations performed in search of causal factors, while the results show the isolation of methicillin-sensitive Staphylococcus aureus (MSSA) from the throat. On the other hand, she had no dental problems. Because of unremarkable upper gastrointestinal endoscopy findings and a negative fecal occult blood test result, the possibility of brain metastasis of a malignant tumor was ruled out. After six weeks of intensive therapy with concurrent administration of two antibiotics and glycerin, the headache and nausea disappeared along with a reduction in the number of white blood cells. Subsequent brain MRI at 28th week, 4th day of pregnancy showed no enlargement of the abscess and disappearance of the surrounding edema, with no indication of puncture drainage. At this point, she was switched to oral administration of amoxicillin 750 mg/day for four weeks and was discharged at 29th week, 3rd day of pregnancy. shows the post admission course.
She vaginally delivered a 2,890 g girl baby at 38th week, 5th day of pregnancy, with no abnormalities. No neurological abnormalities were evident during a five-year follow-up observation conducted over the phone.
MRI findings at the 22nd and 28th week of pregnancy are shown in .


A 69-year-old female weighing 78 kg, a medically managed (atenolol 25 mg and amlodipine 10 mg once daily) case of HOCM was scheduled for bilateral knee arthroplasty. She had intermittent episodes of dyspnoea and fatigue. There was no history of angina, syncopal attacks, or any sudden death in her family. Systemic examination revealed a regular pulse rate of 68 beats/min , and a grade 3/6 crescendo-decrescendo systolic murmur was heard between the left sternal border and apical area, not radiating to the carotids. Electrocardiography (ECG) showed normal sinus rhythm with nonspecific T wave changes in leads II, III, and aVF with left ventricular hypertrophy and left axis deviation. Chest X-ray showed cardiomegaly with clear lung fields. Echocardiography showed asymmetrical septal hypertrophy, left ventricular outflow tract obstruction (LVOT) with peak systolic gradient (PSG) of 56 mmHg, moderate mitral regurgitation and moderate diastolic dysfunction with ejection fraction of 56%. Computerised tomographic (CT) angiogram showed normal coronaries.
Both cardiac drugs were continued till the morning of surgery along with a premedication of oral ranitidine 150 mg and alprazolam 0.25 mg. In the operating room, baseline blood pressure (BP), heart rate (HR) and respiratory rate (RR) were 160/90 mmHg, 68/minute and 14/minute, respectively. The patient was given injection metoprolol 2 mg, 80 mcg fentanyl and midazolam 2 mg intravenously, before establishing invasive monitoring (left radial blood pressure and right jugular venous pressure), opening central venous pressure (CVP) was 8 mmHg. Bilateral perineural femoral nerve catheters were placed with the help of a nerve stimulator. A bolus of 8 mL of 2% lignocaine with 8 mL of 0.2% ropivacaine was injected in each femoral catheter before the incision of each side, followed by a continuous infusion of ropivacaine 0.2% 8 mL/hour intra and postoperatively. Half an hour later, induction and intubation were accomplished using propofol 100 mg, morphine 8 mg, midazolam 1 mg and vecuronium 8 mg. Mild hypotension occurred with BP falling to 100/50 mmHg, which was managed with a bolus of 200 mL crystalloid and injection phenylephrine 50 μg. To prevent intubation stress, esmolol 30 mg was given intravenously 90 seconds before intubation. Anaesthesia was maintained with 66% nitrous oxide in oxygen and isoflurane 0.2-0.4% (because of its myocardial depressive properties, halothane is an ideal agent in such patients but due to its nonavailability in our institute, isoflurane was used without any adverse haemodynamic changes); the average duration of both tourniquets was 35 to 40 minutes. At the time of both tourniquet deflations, systolic pressures dropped by more than 20% each time which responded to a judicious administration of crystalloid and phenylephrine 100 mcg. CVP remained between 8 and 10 mmHg and urine output was 500 mL with an input of 2.5 L of crystalloids. The surgery lasted for four hours; neuromuscular blockade reversed with neostigmine 3.5 mg and glycopyrrolate 0.6 mg and esmolol 30 mg was given again to prevent exaggerated haemodynamic response at extubation. Post extubation, the patient was haemodynamically stable (BP: 124/62 mmHg, HR: 74/minute) with saturation of 100% on oxygen of 2 L/minute. Postoperatively, the patient was transferred to a special intensive care unit (ICU) for further management.
Two hours postoperatively, the surgical drains were opened. Four hours later, we noted increase in heart rate upto 94-96 beats/ min; BP was 110/75 mmHg, CVP and RR were10 mmHg and 33/ min respectively and desaturation up to 90% on room air, with bilateral drain loss of about 100 mL each. Her pain assessment on a verbal analogue score was 6 (on a scale of 0-10). Immediately, the oxygen was increased from 2 to 5 L/minute. For pain and tachycardia, a bolus of ropivacaine 0.2%, 8 mL was given through each femoral catheter along with metoprolol 2 mg intravenously, and liberal fluids continued. Also, other parenteral analgesics like diclofenac, paracetamol and tramadol were started on a regular basis, as per our ICU protocol. Six hours postoperatively, dyspnoea persisted with the occurrence of bilateral fine crepts in chest now and CVP increased to 12 mmHg with heart rate and BP being 88-90 beats/min and 108/70 mmHg, respectively. Echocardiography showed a decreased PSG of 45 mmHg. So, furosemide 20 mg and another dose of metoprolol 2 mg were given intravenously. The patient passed about 1200 mL urine over the next three hours; her tachycardia and tachypnoea both settled with an HR of 78/minute and RR of 20/minute and blood pressure increased to 136/67 mmHg. Her daily dose of atenolol was increased from 25 mg once a day to 50 mg orally twice a day. Forty-eight hours later, the patient was shifted from the ICU after removing femoral catheters. The rest of the hospital stay was uneventful.


24 year old male patient came to the Department of Conservative Dentistry and Endodontics Darshan dental college and hospital, Udaipur, Rajasthan, with the complaint of fractured tooth of upper front region of jaw since five year.
On investigation, periapical radiolucency involving 21, 22 was seen on IOPA and Color Doppler Echographic imaging revealed a granuloma of diameter 13 × 5 mm in size [].


32 year old male patient came to the Department of Conservative Dentistry and Endodontics with the complaint of draining sinus from upper front region of jaw. Patient had undergone Root canal treatment elsewhere two years ago in the same tooth.
On investigation, periapical radiolucency involving 12 was seen on IOPA and Color Doppler Echographic imaging showed granuloma of diameter 10 × 8 mm in size [].


35 year old male patient came, with a complaint of discoloured tooth of upper front region of jaw since 8 years. Patient had history of trauma 17 years ago.
On investigation, periapical radiolucency involving 21, 22 was seen on IOPA and Color Doppler Echographic imaging showing periapical cyst of diameter 17 × 15 mm in size [].


A 38-year-old Indian woman reported to the Department of Periodontics, Government Dental College and Hospital, Hyderabad, India in July 2011 with a chief complaint of burning sensation and itching in relation to mandibular anterior lingual gingiva for past 1 month. Patient had provided informed consent to be profiled. Past dental history revealed that the patient had visited a couple of private general dental practitioners where the lesion was misdiagnosed as an aphthous ulcer and palliative care was provided for the same. As there was no improvement in her complaint, she decided to come to the dental school for an additional opinion. She was referred for diagnosis and treatment in post-graduate periodontics clinic. There was no contributing medical or family history except that the patient had undergone hysterectomy and appendectomy 10 years back. Patient was in good health and denied any deleterious habits like smoking, alcohol consumption or recreational drug use. No lymph nodes were palpable or tender in a head and neck examination.
Intraoral examination revealed a clean mouth with good gingival health and minimal deposits with the full complement of teeth. Clinical examination of the lingual gingiva revealed a 1 cm × 1 cm ulcer extending mesiodistally from mid lingual surface of 41 to mesiolingual surface of 43 and corono-apically from the gingival margin to the floor of the mouth, not extending beyond the anterior part of lingual frenum. The surface of the lesion appeared to be ulcerated and pebbly with isolated areas of erythema and had well-defined borders that were found to be in level with the adjacent tissue. The ulcerated part of the lesion had rhomboid appearance. The surface of lesion toward the lingual frenum appeared to have a shaggy base covered with slough and there was no exudation []. Intraoral periapical X-ray showed bone loss extending up to the apical 3rd in relation to 41, 42 []. Since the clinical findings of the existing lesion didn’t correlate with any of the features of periodontal lesions and the fact that it has been present for the past 1 month was enough to suspect a malignant ulcer. At this stage, a provisional diagnosis of GSCC was made and after obtaining the patient's consent, an incisional biopsy was taken immediately. The specimen was then sent for histopathological examination.
The histological examination of the soft-tissue specimen revealed severe dysplastic changes of the epithelium. There were many sheets and clusters of cells, which were polygonal in shape and contained moderate to abundant pale acidophilic cytoplasm and sharp cellular margins. The nucleus was round to oval in shape and showed moderate pleomorphism, disorganization, coarse chromatin clumping and prominent nucleoli. Mitotic activity was high. There were patchy dense infiltrates of lymphocytes, plasma cells and neutrophils []. A clear and prominent feature was the presence of multiple, keratin pearls in connective tissue []. The above clinical and histological features are conclusive of invasive keratinizing GSCC.
The patient was immediately referred to a specialty hospital for cancer (Indo-American Cancer Institute, Hyderabad, India) where a computed tomography scan was taken to evaluate any alveolar bone invasion. Subsequently, the lesion was staged as T1N0M0. The involved teeth 41, 42 were extracted and the lesion was treated with radiation therapy alone (intensity modulated radiation therapy, 6600 U/33 fractions using ×6 photons). Six months follow-up revealed uneventful healing and no recurrence.


A 54-year-old male patient was diagnosed with pancreatic cancer and suffered from intractable, severe epigastric pain with a score of 5 to 8 out of 10 on the Numeric Rating Scale (NRS). Furthermore, the abdominal pain was not responsive to opioids and other medications.
Therefore, we planned to perform celiac plexus neurolysis and reviewed the patient's anatomy on the abdominal CT image with contrast to determine the target point, ideal depth, and insertion angle through CT simulation. The celiac trunk was located at the T12 vertebral body level. At this level, the classic conventional transcrural approach via "walking off" the vertebral body was simulated, but the needle pathway was impeded by the kidney on the right side and by the aorta on the left side (). Then, we simulated the transdiscal pathway through the T11-12 intervertebral disc. The pathway was drawn from the target point to the lateral side of the right superior articular process of the T12 vertebra and extended to the skin.
The point at which the pathway crossed the posterior skin surface was designated as the needle insertion point (I). The distance from the midline spinous process of the T12 (S) to the needle insertion point was measured against the scale printed on the axial CT image (IS: 3.6 cm). The angle between the proposed needle pathway and the midline was designated as the needle insertion angle (*) (). The distance between the target point and the anterior margin of the vertebral body was measured, and the anteroposterior (AP) diameter of the vertebral body was also measured. The proportion of these two values was used to estimate the proper depth of the needle in the fluoroscopic image.
In the operating room, the patient was placed in a prone position, and we identified the T11-12 intervertebral disc space. In this case, the predetermined insertion angle was 18 degrees on the right side. Therefore, we rotated the fluoroscopy tube 18 degrees to the right side. The insertion point was the lateral margin of the superior articular process of the T12, and it was marked 3.6 cm to the right of the midline. After anesthetic infiltration was deepened in a fan fashion, the skin was punctured with a 16 g needle, and a 20 g Chiba needle was introduced through the 16 g needle. After contacting the disc, the fluoroscope was rotated to the lateral position. We inserted the needle through the disc while checking the tip position with the AP and lateral fluoroscopic images. After penetrating the disc, the 20 g Chiba needle was advanced up to the predetermined depth, which was 2/3 of the AP diameter of the vertebral body from the anterior margin of the vertebral body. Frequent fluoroscopic images for both the AP and lateral views were used to guide the needle when advancing it in the correct plane. While advancing the needle, we checked the loss of resistance using saline to penetrate the crura of the diaphragm. Contrast was injected to confirm the proper spread; the contrast flow showed a smooth curvilinear contour corresponding to the anterolateralaortic space, and it silhouetted the runoff of the celiac artery. On the AP view, the contrast spread across the midline. On the lateral view, the needle penetrated the disc, and its tip was located at 2/3 of the AP diameter anterior to the vertebral body. Then, 15 ml of 2% lidocaine followed by 15 ml of 99% ethyl alcohol was injected for neurolysis ().
There were no adverse events during the procedure. The patient tolerated the entire procedure well and did not complain of pain related to the procedure. The next day, during follow-up, the patient reported an abdominal pain score of 2 to 3 out of 10 on the NRS. After 1 week, the patient expressed great satisfaction with the results and was discharged.


A 41-year-old Hispanic female diagnosed with type 1 myotonic dystrophy (Steinert disease) was referred for ophthalmologic examination with the chief complaint of progressive vision loss. Her best-corrected visual acuity was 20/32 in her right eye and 20/40 in her left eye. Ocular motility was normal. She had bilateral ptosis with abnormal elevator function. Slit lamp examination revealed the presence a bilateral polychromatic cataract with posterior subcapsular component.
Dilated fundus examination was remarkable for macular pigmentary changes with multifocal yellowish depigmented patches within the macular area in both eyes (fig. ). Fundus autofluorescence highlighted a branching linear pattern of mixed hyper- and hypoautofluorescence limited to the macular area in both eyes (fig. ).
Optical coherence tomography images showed diffuse subretinal hyperreflective material between the photoreceptor layer and the RPE in both eyes. Larger focal vitelliform lesions were also evidenced. No subretinal or intraretinal fluid was found in association with the deposits (fig. ).


A 37-year-old male patient presented with complaints of transient loss of consciousness and persistent headache after minor head injury. He had no past history of head injury or brain surgery. Neurological examination was normal and there was no stigma of neurofibromatosis. Plain CT head did not show any brain parenchymal or bony injury. Contrast-enhanced 3-mm axial and coronal CT images of paranasal sinuses [Figure and ] revealed a large (approximately 12 mm in size) defect in the right lateral wall of the sphenoid sinus with herniation of a part of the right mesial temporal lobe through the defect, to occupy the ipsilateral lateral recess of the sphenoid sinus. The remaining part of the right sphenoid sinus showed mucosal thickening. The bones around the defect and encephalocele showed remodeling and appeared thinned out [Figure and ]. There was no evidence of meningitis or any other intracranial abnormality. CT cisternography was not performed as there was no history of nasal discharge. Further evaluation of the lesion with MRI was not possible because the patient was claustrophobic and refused to undergo sedation.
The surgical exploration confirmed the CT finding of a large bony defect in the right lateral wall of the sphenoid sinus, lateral intrasphenoidal encephalocele occupying the lateral recess with otherwise intact dura. Mild ipsilateral sphenoid sinus mucosal thickening was also documented. Endoscopic transpterygoid approach was used and the herniated brain tissue with intact dura was gently pulled up and the bony defect was closed to prevent future risk of CSF leak, ascending meningitis or brain abscess. The abnormal mucosal thickening was stripped off and space within the right sphenoid sinus was filled with free fat graft. The patient had a good postoperative recovery and was advised cross-sectional follow-up study after six months to confirm the integrity of the repair.


A 76-year-old man with a history of hypertension, diabetes mellitus, benign prostate hypertrophy and tobacco use was presented with right flank pain. A retrograde pyelography revealed an extrinsic indentation of the right pelvic ureter. Computed tomography (CT) angiography demonstrated an AAA with bilateral CIA involvement (). The maximal diameter of the distal abdominal aorta was 34 mm and the diameter of the aorta at renal artery level measured 19.2 mm. The right CIA was 55 mm and the left CIA was 24 mm in their maximal diameters. The diameter of the right CIA at its ostium was 27 mm, whereas that of the left CIA was 11 mm.
In this patient, we decided to perform EVAR using a bifurcated stent graft. In order to preserve at least one IIA for pelvic perfusion, we planned to apply the sandwich technique. The right IIA was embolized using a 14 mm Vascular Plug (Amplatzer, St. Jude Medical, St. Paul, MN, USA) after the engagement of a 7 Fr sheath into the right IIA from the left common femoral artery. The main body of the bifurcated stent graft (Excluder 23-14-160 mm, Gore, Newark, DE, USA) was introduced through the left common femoral artery and deployed below the left renal artery origin.
Thereafter, a tubular-type stent graft (Viabahn 8×150 mm, Gore, Newark, DE, USA) was inserted into the left IIA through a 8 Fr Shuttle sheath from the left brachial artery. An iliac extender stent graft (Excluder 12×140 mm, Gore, Newark, DE, USA) was inserted through the left common femoral artery. The two distal stent grafts were deployed in parallel with the overlapping of the proximal main body stent graft and dilated synchronously by a kissing balloon method (). A contralateral limb (Excluder 12-140 mm, Gore, Newark, DE, USA) and an iliac extender (Excluder 12-100 mm, Gore, Newark, DE, USA) were inserted through the right CFA in order to cover the right CIA and the proximal segment of the right EIA sheath.
After the procedure, angiography showed proper positions of the deployed stent grafts with good blood flow to the left IIA and minimal endoleaks (types Ib and III). Follow-up aorta CT scans taken at 3 days () and 8 months after the procedure showed patent stent grafts without significant endoleak. During the 8-month follow-up, the patient remained uneventful.