A 24-year-old Thai male presented with high fever and abdominal pain for 4 days. The patient first noticed his fever accompanied with fatigue and a bitemporal throbbing pain without organ-specific symptoms, 2 weeks prior to admission when attending an outpatient clinic. Viral infection was the presumptive diagnosis. His low-grade fever remained for several weeks until 4 days prior to admission, when high fever and a progressive maculopapular rash developed. He also experienced epigastric pain, which brought him to our hospital again seeking medical attention.
The patient was diagnosed with bilateral chronic uveitis 2 years ago, when topical steroids had been prescribed. Low-dose oral prednisolone (15 mg/day) was subsequently added before tapering off within 11 months. Two months later, a diagnosis of spondyloarthropathy was suspected by the rheumatologist, when Achilles tenosynovitis, plantar fasciitis, and tenderness over the sacroiliac joints developed. Sulfasalazine was then prescribed starting at 1 g/day, gradually increasing to 2 g/day for 2 weeks prior to the development of fever.
Physical examination revealed high fever (38.5℃), cervical lymphadenopathy, pharyngitis with whitish patches on soft palate and buccal mucosa. The patient had a scattered maculopapular rash over his trunk and extremities and abdominal examination revealed mild epigastrium tenderness. A complete blood count revealed marked leukocytosis with a total white blood cell count of 23,740/µL, 50% neutrophils, 16% lymphocytes, 31% monocytes, and 3% eosinophils. Atypical lymphocytes were detected in peripheral blood smears. Blood culture and anti-viral antibody profiles were investigated; sulfasalazine was promptly discontinued.
On the third day of admission, the patient developed severe abdominal pain and mild icteric sclera was noted. Liver function tests showed direct hyperbilirubinemia with total bilirubin 3.34 mg/dL and direct bilirubin 2.94 mg/dL. ASL and ALT levels were 536 and 734 U/mL, respectively, and serum alkaline phosphatase was 301 IU/mL. Upper abdominal ultrasonography revealed gallbladder wall thickening with pericholecystic fluid collection and positive sonographic Murphy's sign. Intravenous ceftriaxone was then administered. On the ninth day of admission, he developed hypotension (blood pressure of 70/40 mmHg) before being rescued with 1,500-mL intravenous fluid. Abdominal computed tomography scans showed a collapsed gallbladder with a moderate amount of pericholecystic fluid, but no gallstones could be demonstrated (); hepatosplenomegaly and minimal ascites were also noticed. Dexamethasone (5 mg) was administered every 12 h intravenously for six doses, resulting in cessation of the fever and abdominal pain, after the third dose.
The viral studies yielded negative results for IgM and IgG against Epstein-Barr virus, cytomegalovirus, and Dengue virus. Blood culture results showed no bacterial growth. Anti-HIV and anti-human herpes virus 6 (HHV-6) IgM antibodies were also negative, but anti-HHV-6 IgG was positive (17.05 units with a cut-off value of 11 units). Two days after the initiation of steroids, the numbers of IFN-γ-releasing cells in the peripheral blood were measured by ELISPOT assay (Mabtech, Stockholm, Sweden) upon stimulation with four drugs as described previously. Significant numbers of IFN-γ-secreting cells were demonstrated (1,048 spots forming cells/106 PBMCs) upon incubation with 100 µg/mL sulfasalazine, but not with other drugs administered concurrently (ceftriaxone), previously (amoxicillin), or never (ceftazidime) (). Dexamethasone was then replaced with prednisolone 1 mg/kg/day before being tapered off over 3 weeks. His liver function tests returned to normal levels in 1 month; no complications were noted after 2 years of follow-up. His symptoms are now well controlled with NSAIDs and methotrexate.


A 70-year-old female.
Fever and systemic debilitation.
The patient was transferred to our hospital due to the finding of thyrotoxicosis during an in-patient stay at another hospital where she was being treated for a 2-week fever and systemic debilitation.
The patient had hypertension and had taken antihypertensive medication for 20 years.
There was nothing specific.
The patient was quite alert, but showed signs of acute illness. Her blood pressure measured 120/80 mm Hg, pulse rate was 110 bpm, respiratory rate was 20 times per minutes and axillary temperature was 38.4℃. Based on examinations of her head and neck, a lump was detected and palpitation of the lump was accompanied by local heatness and minor tenderness. The lump was fixated and soft. There was no finding of tenderness of the paranasal sinus or pharyngolaryngeal flare, tonsillar hypertrophy, or enlargements of lymph node.
The blood assay revealed that white blood cell (WBC) count was 13,500/mm3 (neutrophils, 80.9%), hemoglobin was 9.3 g/dL, and platelet was 456,000/µL. The erythrocyte sedimentation rate (ESR) increased to 151 mm/hr, and C-reactive protein increased to 24.7 mg/dL. The endocrinology report showed that T3 was 228.0 ng/dL (normal range, 80 to 200), free T4 (FT4) was >7.77 ng/dL (normal range, 0.93 to 1.7), thyroid stimulating hormone (TSH) was 0.02 µIU/mL (normal range, 0.27 to 4.2), and thyroglobulin was >5,000 ng/mL (normal range, 1.4 to 78). Antimicrosome antibody (Ab), antithyroglobulin Ab, and thyroid stimulating Ab were in the normal ranges. Serum calcitonin was in the normal range of less than 1.0 pg/mL, and the HIV Ab test was negative.
The 99mTc thyroid scan showed that the radioactive isotope intake of the thyroid was reduced and irregular ().
The margin of the right side of the thyroid was unclear and a multilobulated lump with poor contrast was observed. Multiple lymph nodes were observed from the IV, V, and VI areas of the right side of the neck ().
Neck sonography revealed that there were no abnormal structures found in the homogeneous image of the left lobe of the thyroid, but in the right lobe, there was a mass that was about 4.5×2.5×4.6 cm in size with heterogeneous echogenicity (). Using fine needle aspiration biopsy, we obtained chocolate-colored abscess fluid that was chocolate in color (), and a cytopathogenic test revealed no atypical cells or malignant cells, but many neutrophil cells and histiocytes were observed.
Immediately, we commenced with treatment by administration of amoxicillin/clavulanate 1 g/200 mg three times a day and prescribed 40 mg propranolol four times a day for relieving the symptoms of thyrotoxicosis. No microbes were identified from the culture test of aspirated samples from blood or thyroid gland. Hyperpyrexia gradually disappeared within 3 days after administration of antibiotics, but the feeling of local fever, neck swelling and tenderness continued for up to 10 days after administration of antibiotics. We performed a thyroid lobectomy and found that the abscess was accompanied by fibrosis in the right lobe of the thyroid. The pathological findings revealed inflammation accompanied by necrotic tissue and abscess.
After the surgery, the patient showed symptomatic recovery from neck pain and swelling, and was discharged from the hospital. We performed outpatient follow-up with esophagography and neck computed tomography (CT) and we could not find any anatomical defect such as fistula. A thyroid function test in the outpatient department at 2 months after surgery revealed that FT4 was 1.02 ng/dL and TSH was 2.40 µIU/mL, indicating that thyroid function had been restored to normal.


A 42-year-old female presented with Hunt and Hess grade IV subarachnoid hemorrhage (SAH), which improved to grade III after placement of a ventriculostomy. Computed tomography (CT) and CT angiography revealed a diffuse SAH and ruptured basilar tip aneurysm []. Digital subtraction angiography (DSA) confirmed the diagnosis of a basilar bifurcation aneurysm with a wide neck and shallow dome []. Due to its unfavorable neck/dome ratio, endovascular obliteration of this aneurysm was thought to be high risk. The basilar bifurcation was noted to be quite high in relation to the dorsum sella []. A right cranio-orbital approach was used for the clipping of the aneurysm in this patient. After wide opening of the Sylvian fissure and arachnoid cisterns, the PComA, and the P1 and P2 segments of the PCA were isolated. Due to the high riding basilar bifurcation, dissection of the basilar bifurcation was restricted by the PComA, which was tethering the PCA. Because the PComA was not a fetal type, the decision was made to divide the PComA. However, before dividing it in its perforator-free segment, we performed ICG-VA with a temporary clip on the perforator-free segment, and demonstrated that both perforators were filling from both the PCA and the internal carotid artery (ICA). The PComA was divided between the proximal and distal perforators. Another ICG-VA was performed and this showed that the perforators were still filling. The aneurysm was then clipped (see video, , which demonstrates the surgery, 3 min 18 s, and 71.8 MB). Postoperatively the patient's clinical status improved and she was extubated on the 7th postoperative day with intact speech and was able to follow verbal commands. A postoperative angiogram showed the total obliteration of the aneurysm []. Two days after the removal of the external ventricular drainage, the patient suffered a rapid decline because of right intraventricular hemorrhage. Emergency evacuation of the hematoma was performed. She eventually made a good recovery and was discharged to a rehabilitation center. On postoperative 3rd month follow-up she was neurologically intact.


A 47-year-old female presented with headache. CT angiography and a four-vessel angiogram revealed a PComA–PCA junction aneurysm on the right hemisphere and P1 segment aneurysm on the left side [Figure and ]. The patient elected to undergo coil embolization of both aneurysms. Although the right-sided P1–PComA junction aneurysm was successfully coiled the left-sided P1 aneurysm was not amenable to safe coiling due to its broad neck involving the P1 posterior thalamoperforating artery. Therefore, the patient underwent a cranio-orbital approach for the clipping of the left P1 aneurysm. After wide splitting of the arachnoid cisterns, the ICA, PComA, PCA and basilar bifurcation were all exposed. The aneurysm was originating from the P1 segment of the PCA in relation to the P1 perforating artery. The tethered PComA was obstructing the view of the aneurysm neck and origin of the P1 perforator. Preclipping ICG-VA was performed to lay out the vasculature. Although few clip options were exercised, it was felt that without dividing the PComA, safe clipping would not be possible. As such, a temporary clip was placed along the distal P1 vessel and then ICG-VA performed to ensure that there was flow through the PComA perforators. After this was confirmed, the distal portion of the PComA was divided. The aneurysm was then dissected free and good clip purchase was provided. Postclipping ICG-VA revealed no flow through the aneurysm dome and persistent flow in the P1 perforator and rest of the P1 (see video, , which demonstrates the surgery, 3 min 18 s, and 97.5 MB). The patient refused to undergo postoperative arterial DSA, so intravenous-DSA was performed and revealed the total obliteration of the aneurysm [Figure and ]. The postoperative course was uneventful and the patient was discharged home in stable and neurologically intact condition.


66-year-old gentleman, ASA 3 was scheduled for laparotomy for duodenal tumour excision. His other medical conditions were type 2 diabetes mellitus, cardiomyopathy, chronic smoker, and obstructive sleep apnoea on Continuous Positive Airway Pressure (CPAP) machine. Postoperative analgesia options were discussed with the patient. He was not keen on epidural, but happy to consider other options. He was offered patient controlled analgesia (PCA) fentanyl, QL block, and multimodal analgesia. We had explained the QL block as a novel technique. He preferred to undergo the block while sleeping. After taking informed consent, anesthesia was induced with propofol (Fresofol® fresenius, Sydney, New South Wales, Australia), fentanyl (fentanyl citrate DBL Hospira, Melbourne, Australia), and rocuronium (Esmeron, MSD, Sydney, New South Wales, Australia) for Neuro muscular (NM) paralysis. Maintenance of anesthesia was with 50:50 O2 and air with sevoflurane. The abdomen was opened via right-side large subcostal incision. The procedure lasted 2.5 h and was uneventful. At the end of the procedure, he was positioned in left lateral to obtain appropriate view of QL and TAP extensions of lateral abdominal muscles. Aseptic precautions were taken by wearing sterile gown and sterile drapes. Ultrasound Macro Maxx™ (SonositeInc, Bothell, Washington, USA) was used with linear probe (HFL38_10-5 MHz) covered with sterile plastic sheath SiteRite (Bard Access Systems Inc., Salt lake city, Utah, USA) placed in the anterior axillary line to visualize the typical triple abdominal layers. Then, the probe was placed in the midaxillary line and at this juncture the layers of abdominal layers started to taper. When the probe was placed in the posterior axillary line as per the posterior approach, sonoanatomy showed first the transversus abdominis disappearing then the internal oblique and external oblique forming aponeurosis and appearance of QL noticed []. shows typical muscles layers and the fascia. At the junction of the tapered ends of abdominal muscles and QL, a 21 g 100 mm SonoPlexStimu cannula needle (Pajunk Medizintechnologie Geisingen, Germany0) was inserted in plane [] and confirmed its position by injecting saline. Under ultrasound (US) guidance, saline separating the fascia similar to what is seen in the TAP plane was observed. Then in that space 25 mL of 0.5% ropivacaine (Naropin-AstraZeneca, Sydney, North South Wales, Australia) was injected []. Pain scores using the numerator rating scale (NRS) from 0 to 10 were recorded hourly in recovery room and then in the high dependency ward and fentanyl use was monitored for 24 h. He received a fentanyl PCA with bolus dose of 20 mcg with lock out interval of 5 min and multimodal analgesia comprising paracetamol1g every 6 h and parecoxib (Dynastat, Pfizer Pty Ltd, North South Wales Australia) 40 mg daily.
Postoperatively in recovery, he did not require any further analgesia. Pain scores were 0/10 and the ipsilateral sensory block was T8-L1. The first analgesic request was about 3 h postoperative. After 15 h, he started experiencing pain requiring more fentanyl PCA amounting to 720 mcg for the remaining day. The average pain scores on day one were 4/10 at rest and 6/10 on coughing and comfortable. The 2nd day, the pain scores were 7/10 and 9/10 requiring 1000 mcg of fentanyl.


A 33-year-old woman in the 16th week of her first pregnancy experienced two episodes of upper abdominal pain suggestive of biliary colic. Hematological and biochemical parameters were normal but ultrasonography showed previously undiagnosed multiple small gallbladder calculi. Two weeks later she experienced another episode of abdominal pain during which the liver function tests including bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase were marginally elevated. An endoscopic ultrasound (EUS) showed a patulous ampulla indicative of a recently passed bile duct stone and normal calibre bile ducts. At this point she was referred for a surgical consultation and was counselled regarding a LESS-chole. While awaiting her surgery scheduled 3 days later she developed another episode of abdominal and back pain. The serum amylase and lipase were elevated but the white cell count, liver function tests, serum calcium, and lactate dehydrogenase (LDH) were normal. This episode of mild acute pancreatitis settled within 48 h and a repeat EUS was normal. A LESS-chole was undertaken during the same admission. At the time of surgery she was in the 20th week of her pregnancy. An obstetric consultation was obtained and she was started on inj. terbutaline (Bricanyl, Astra-Zeneca, Mumbai, India) 5 mg subcutaneously on the evening before the surgery. Fetal heart monitoring was initiated on the morning of surgery and continued at an interval of 2 h in the postoperative period until discharge.


A 25-year-old lady presented to dental out-patient services with swelling and pain in the right side of the face. Local examination showed a fluctuant swelling measuring 5 mm × 3 cm over the right side of the angle of mandible []. The swelling was warm and tender on palpation with signs of impending rupture. Clinical examination of the orofacial region did not reveal any odontogenic or non-odontogenic foci of infection. Patient's vitals were in the normal limits. All the hematological parameters were normal except for borderline leukocytosis and a low hemoglobin level. Incision and drainage (I and D) of the abscess was carried out under local anesthesia. As the patient was in her 12th week of gestation, antibiotics were prescribed in consultation with the gynecologist.
On a follow-up visit after 2 weeks, a painless indurated swelling at the same site was noted [, inset]. Pus culture carried out during the incision and drainage had not revealed any bacterial growth. As the condition was not resolving, a fine needle aspiration cytology (FNAC) was advised in consultation with the pathologist, to rule out tubercular infection.
Aspirate from the swelling yielded purulent material. The smears were moderately cellular and showed abundant necrotic debris within which were seen polymorphs and histiocytes. One of the smears revealed the presence of a single microfilaria of W. bancrofti, which was rounded anteriorly and tapered posteriorly []. The caudal end of the microfilariae had a clear space free of nuclei. After the aspiration, the patient was admitted and a midnight blood sample was taken. The wet mount preparation showed motile microfilariae, which confirmed the diagnosis of filariasis.
Since, the patient was in the first trimester of pregnancy, decision was taken to start the anti-filarial drugs after delivery.


A 21-year-old male presented with sudden onset flaccid quadriparesis with no preceding history of fever, dysphagia, dysphonia, diplopia, bladder, or bowel involvement. There was no relation with heavy carbohydrate meal, exercise or diarrhea, and no past history of similar episode.
Examination revealed lower limb proximal muscle power of 3/5, diminished deep tendon reflexes (DTR) in all four limbs, bilateral flexor plantar responses, no cranial nerve palsy, and no respiratory muscle involvement. Goiter and clinical feature of thyrotoxicosis were absent. Serum potassium was 2.2 mmol/l (normal [nl.] –3.5-5), and ESR 38 mm/h (nl.–1-25). Thyroid function tests (TFT) showed TSH 0.06 μU/l (nl. –0.5–5), free T4 2.4 ng/dl (nl. 0.7–2.0), T3 210 ng/dl (normal –70–190), and TPO antibody 54 IU/ml (nl. <35). 99mTc pertechnetate thyroid scan uptake was 0.15% (nl.–0.4–1%).


A 35-year-old male presented with sudden onset quadriparesis with a history identical to that of case 1. He had upper limb proximal muscle powers MRC 3/5, distal muscles 4/5, lower limbs proximal, and distal muscles 2/5. Mild respiratory muscle involvement was evidenced by reduced single breath count of 11 seconds. DTR on all limbs were diminished with bilaterally flexor plantar responses and no cranial nerve palsy. He had a grade 1 goiter and no signs of toxicity. His serum potassium was 1.5 mmol/l, ESR 42 mm/h, TSH 0.005 μU/l, free T4 2.5 ng/dl, TPO antibody 68 IU/ml, and decreased uptake (0.1%) on 99mTc scan.


A 32-year-old male presented with acute onset flaccid paraparesis, tremors of both hands and palpitations. He had a history of transient proximal weakness 6 weeks back which recovered spontaneously. He had no dysphagia dysphonia, bladder, or bowel involvement.
He had power 2/5 in proximal muscles, depressed jerks on all four limbs, bilateral flexor plantar responses, and no signs of cranial nerve palsy. He had tachycardia, fine tremors of both hands, and grade1 diffuse goiter. His serum potassium was 1.8 mmol/l, ESR 30 mm/h, TSH 0.03 μU/l, free T4:3.2 ng/dl, TPO antibody 117 IU/ml (nl < 35), and there was decreased uptake (0.21%) on 99mTc scan.
All three cases had normal TSH receptor antibodies, serum creatine kinase (CK) and collagen vascular profile. Blood gas analysis in all three patients excluded acidosis. NCV was normal but EMG showed a myopathic pattern with no decremental muscle action potential. In all three cases fine-needle aspiration cytology (FNAC) was consistent with lymphocytic thyroiditis. Based on clinical features and investigations our diagnosis for each patient was thyrotoxic periodic paralysis secondary to painless or silent thyroiditis.
Case 1 was managed with oral potassium chloride (KCl) at the rate of 0.2-0.4 mmol/kg and propanolol 120 mg/day. Cases 2 and 3 initially required intravenous KCl at 10 meq/h. All showed marked improvement of paralysis within a week of treatment. All patients were discharged after a week with oral propranolol (80-120 mg/day). After 4 weeks of mean follow-up none had any residual paralysis. At the end of 2 months case 1 presented with normal thyroid profile and propranolol was completely withdrawn. At 3 months the thyroid profile became completely normal in cases 2 and 3 and propanolol was stopped. There was no relapse in any of the three cases even at 6-month follow-up.


A 42-year-old woman presented with acute onset lower limb paralysis associated with severe proximal muscle pain. These symptoms were not associated with respiratory difficulty, dysphagia, dysarthria or sensory symptoms and there was no associated backache, fever, rash or constitutional symptoms. She had a 2 year history of hypertension, which was poorly controlled despite treatment with a combination of nifedipine, atenolol and losartan. She was treated by a general practitioner and at initial diagnosis of hypertension had undergone biochemical evaluation including serum electrolyes, which had been within normal limits. She experienced two similar, but short lasting episodes of weakness in the preceding year, but had not been investigated. Three days prior to admission she had been given Frusemide as add on therapy by her general practitioner due to uncontrolled hypertension. Her blood pressure on admission was 160/100 mmHg. Clinical examination favored an acute onset myopathy with symmetric flaccid paralysis of lower limbs (muscle power - 3/5) with normal muscle power (5/5) in the upper limbs.
Initial work-up revealed severe hypokalemia (potassium - 2.0 mmol/l) with an elevated creatine kinase (CK) of 11347 IU (16-190) and increased lactic dehydrogenase of 856 IU/l (240-480). Patient's urine was positive for myoglobin with a high urinary myoglobin 4,170 μg/l. Serum creatinine was 130 μmol/l. In addition, patient had high urinary potassium of 19.45 mmol/24 h with metabolic alkalosis (pH - 7.540, HCO3-38 mmol/l, base excess - 15 mmol/l and PCO2-44 mmHg).
The other biochemical values on initial evaluation were as follows; serum aspartate aminotransferase - 244 IU/l (up to 35 IU/l); alanine aminotransferase - 193 IU/l (2-40); Sodium - 145 mmol/l; blood urea - 45 mg/dl; calcium - 0.9 mmol/l (1.12-1-32); phosphorus - 2.7 mg/dl (2.7-4.5); magnesium - 1.4 mg/dl (1.58-2.55); fasting blood glucose 110 mg/dl and the total protein was 7.6 g/dl with albumin 3.2 g/dl. Thyroid function tests were normal with a free T4 level of 1.02 ng/dl and thyroid-stimulating hormone 3.2 μIU/ml.
Based on the above findings, patient was diagnosed as having hypokalemic paralysis and rhabdomyolysis. Treatment was initiated by oral and intravenous supplementation of potassium and after 10 days, muscular strength and CK levels had returned to normal. Conduction studies and electromyography, which were performed after the correction of hypokalemia, were normal.
The coexistence of hypertension, hypokalemia with high urinary potassium loss in association with metabolic alkalosis raised the possibility of primary aldosteronism (PA), which lead to further hormonal evaluation. Aldosterone levels were 22,600 ng/dl (normal, 3.6-24.0 ng/dl) and the plasma renin activity (PRA) value was below the detection limit of our method (0.2 ng/ml/h). Aldosterone/renin ratio (ARR) was 113,000 ng/ml per ng/ml/h (<10). Abdominal ultrasound did not reveal adrenal lesions, but abdominal computed tomography scan showed a 20 mm × 16 mm hypodense mass in the medial limb of the right suprarenal gland []. She underwent right sided adrenalectomy and pathological examination of the gland confirmed a 20 mm adrenal adenoma. Post-operatively the patient was normokalemic without spiranolactone and the PRA was 0.52 ng/ml/h; aldosterone was 1.3 ng/dl with a reduced ARR of 2.5 (<20) ng/ml per ng/ml/h. After 4 weeks of discharge, her BP was normal without any antihypertensives and she was normokalemic with normal muscle strength.


A 62-year-old man presented with fever, cough, dyspnoea, and unintentional weight loss of 3 kgs within 3 months. Chest X-ray revealed some scattered pulmonary shadows for which a CT scan of chest was planned. During the hospital stay patient developed documented symptomatic and asymptomatic hypoglycaemia almost daily especially in morning hours including two episodes of severe hypoglycaemia for which endocrine opinion was taken.
On reviewing the history, the patient was on metformin 500 mg and glimepride 1 mg, each twice a day after meals since 8 yrs. His blood glucose and other metabolic parameters were well controlled on this medication and he was very regular with regards to his diabetic diet and physical exercise. He did regular self blood glucose monitoring with a periodically calibrated glucometer and maintained a good record of his data. He had never been hospitalized for hypoglycaemia or ketoacidosis, so far. The patient had never recorded any severe hypoglycaemic events, so far. However, he noticed that his blood glucose values started to follow a downward trend since last 6 months with an appreciable drop of his fasting capillary blood glucose values by an average of 10-15 mg/dl, despite of regular and relatively liberal diet. Patient also confirmed some of these relatively low values with laboratory plasma glucose values. At this point of time the patient self adjusted his medications by gradually reducing the doses of Oral Hypoglycaemic Agent (OHA) or oral antidiabetic agents. Due to persistent low blood glucose values despite of liberalized diet, he stopped all OHA after 3 months. There was no history suggestive of any renal, hepatic disorder, alcohol consumption, diabetic retinopathy or any other underlying autoimmune disorder. The patient was not on angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) ACEI or ARBs, fluoroquinolones, sulphonamides. He was receiving paracetamol and cefuroxime for his current illness.
On examination, patient had a BMI of 23.5 kg/m2. He had no stigmata of chronic kidney disease. However, he had a palpable liver of two finger breadths below the costal margin which was non-tender but there were no other features suggestive of chronic liver disease.
On investigation, liver function tests were normal and his serum creatinine was 1.04 mg/dl with a clearance of 88 ml/min. CT scan of the chest performed to diagnose his chest pathology revealed right lower lobe consolidation with multiple pulmonary densities with pleural effusions in both lobes along with a large hypodense mass occupying almost entire right lobe of liver consistent with the provisional diagnosis of hepatocellular carcinoma with pulmonary metastasis, which was confirmed with biopsy [].
Biochemical tests done during hypoglycaemia (blood glucose 44 mg/dl) showed a serum cortisol level of 36.5 μg/dl, suppressed serum insulin 0.6 IU/ml (3-35 μIU/ml, RIA) and C-peptide level 0.2 ng/ml (0.85-3.3 ng/ml, RIA) with negative serum ketones [], which ruled out endogenous hyperinsulinism. IGF-1 done was normal. In the given clinical scenario, ectopic secretion of big IGF-2 from the tumor mass was suspected but big IGF-2 assay was not available. Hence, a provisional diagnosis of non-islet cell hypoglycaemia as a part of paraneoplastic syndrome due to IGF-2 secreted by hepatocellular carcinoma was made.


A 42-year-old house wife (P2 + 0, last child birth 24 years ago) was admitted with complaints of generalized body ache of 1 year duration. It was more at night and progressively increasing in severity. The patient had numbness and severe burning sensation over her feet, ascending rapidly to involve her legs and thighs. It was associated with loss of weight (approximately 8 kg), loss of appetite, nausea, frequent vomiting, and altered bowel habits without history of fever or pain abdomen. She was detected to have diabetic 1 year ago and put on oral hypoglycemic agents (OHAs). There was no history suggestive of any acute diabetic complication. Past medical history was nonsignificant. She had undergone cholecystectomy 2 months back (Histopathological examination (HPE) suggestive of chronic cholecystitis without malignant change). She was amenorrhoic for last 2 months. On admission, she was biochemically euthyroid with normal creatinine phosphokinase (CPK) level, negative antinatriuretic factor (ANF), rheumatoid factor, anti-double stranded deoxyriobonucleic acid (dsDNA), and poor glycemic status (HbA1C 16.9%).
Weight: 36.5 kg, body mass index (BMI): 15.7 kg/m2, blood pressure (BP): 100/70 mmHg, pulse: 70/min, regular, all peripheral pulses palpable, pallor: +, icterus: nil, edema: nil, goiter: Gr I, acanthosis: absent, muscle function test (MFT): 6/6 b/l, ankle brachial pressure index (ABPI): left 0.9, right 1.0. Fundus was normal. Profound symmetrical wasting was noted in all extremities with associated bilateral weakness more in proximal muscle groups of the lower extremities. Reflexes were symmetrically decreased in all extremities with absent ankle jerks. The gait was unsteady due to muscle weakness and paresthesias. Otherwise, systemic examination was normal.
Hemoglobin (Hb): 9.4; total leukocyte count (TLC): 12,400; differential leukocyte count (DLC): neutrophils (N)-78, lymphocytes (L)-18, monocytes (M)-2, eosinophils (E)-2; erythrocyte sedimentation rate (ESR): 86; adequate platelet.
Renal and hepatic profile was normal except hypoproteinemia (albumin/globulin (Alb/Glb):2.6/2.2) and hypokalemia. Human immunodeficiency virus (HIV) was nonreactive. Serum protein electrophoresis did not show any monoclonal band. Whole body bone scintigraphy and bone marrow aspiration study were normal. Nerve conduction velocity (NCV) revealed symmetrical distal axonal and demyelinating type of sensorimotor polyneuropathy involving lower limbs more than upper limbs. Computed tomography (CT) scan abdomen suggested hepatomegaly with mildly dilated common bile duct (CBD) (post cholecystectomy) along with suspected stricture ileum along with proximal narrowing. Chest X-ray, CT scan brain, ultrasonography (USG) abdomen, upper gastrointestinal (GI) endoscopy, colonoscopy, Ba meal follow through, CT enteroclysis were normal.


A 23 year old male presented to us with right testicular swelling for 4 months. There was no significant past history or family history of testicular tumors. On examination, the right testis was enlarged and hard while the rest of the clinical examination was unremarkable. Tumor markers were found to be marginally raised. The levels of α-foetoprotein and β-HCG were 370 ng/ml and 650 U/L respectively. A computed tomography (CT) scan abdomen, however, revealed only subcentrimetric lymhnodes (clinically insignificant) in the retroperitoneum []. A right high inguinal orchidectomy was performed and the histopathology showed mixed NSGCT with predominnent embryonal component with vascular and lymphatic invasion. The tumor markers after 6 weeks were normalized. The patient was staged as clinical stage Ib American Joint Committee on -T2N0M0. He was given the option of RPLND or chemotherapy, and after explaining about the implications of both forms of treatment, he opted for RPLND. The patient was subsequently taken up for right modified template robot assisted laparoscopic transperitoneal RPLND.
The patient was placed in right lateral oblique position (60°) and pneumoperitoneum was created using Verres’ needle. A total of 6 ports were used []. The camera port (12 mm) was placed just lateral to umbilicus on the left. Two 8 mm robotic metallic ports were placed just lateral to umbilicus on the right at a distance of 8 cm from the camera port. A third robotic port was placed for the 4th robotic arm just medial to the anterior superior iliac spine. One 5 mm port was placed for liver retraction at the subxiphoid area. An assistant port (12 mm) for retraction, suture transfer and specimen retrieval was placed below the camera port towards the pelvis. The robot was docked with the cart being kept behind the back of the patient. On the right robotic arm, a monopolar curved scissors and needle holder were used. On the left, a bipolar Maryland forceps, needle holder and prograsp forceps were used. The prograsp forceps was very useful in holding and retracting tissues. However, the third robotic arm was not helpful because of crossing over and collision of the robotic instruments.
The dissection was started with mobilisation of hepatic flexure, ascending colon and caecum followed by kocherisation of the duodenum. The right gonadal vessels were identified and dissected from the inferior vena cava (IVC) till the right deep inguinal ring. The silk suture, which was used to ligate the vessels and cord during orchidectomy was identified and the right gonadal vessels along with a part of spermatic cord were excised. The right ureter, which was the right lateral limit of dissection, was identified, and carefully dissected from the paracaval tissue. Paracaval lymphatic tissue was dissected from the right renal hilum (proximal limit) to the right common iliac artery bifurcation [distal limit, ]. Excised tissues were retrieved through the 12 mm assistant port using home made plastic bag at the end of the procedure. The retrocaval tissue behind the IVC and the interaortocaval tissue between aorta and IVC were carefully dissected, and divided between clips (liga, weck). We didn’t use any hemostatic agent. During this dissection, the aorta and IVC were gently retracted by the assistant and the lumbar vessels were identified and preserved. With the help of 3D view and magnification, postganglionic sympathetic fibres and sympathetic ganglia were also identified and preserved. Pre-aortic dissection was done from the left renal vein (proximal limit) to the inferior mesenteric artery (distal limit). While dissecting, the wall of the aorta was injured, which was easily repaired with the 5-0 prolene suture. At the end of the dissection, we could see the skeletonised IVC, exposed aorta, right ureter and right and left renal hilum []. Hemostasis was ensured at the end of the procedure and the mobilised colon was repositioned.


An eight-year-old girl first seen at the Paediatric Out-Patient Department of Aminu Kano Teaching Hospital, Kano, with left anterior chest wall deformity since birth and recurrent loss of consciousness of two years duration. There was no history of breathlessness, paroxysmal nocturnal dyspnea or orthopnea. About a year ago, she developed a swelling on the left side of the jaw which was incised by a traditional barber and a thick whitish secretion was drained. However since then mother noticed that the site had been discharging clear fluid intermittently whenever She laughed, coughed, ate or cried. There was history of syncopal attacks lasting for few minutes noticed whenever she was carried on the back and the left side of the chest is compressed and also during play when she is being hit or pushed on the chest. She was a product of full-term gestation and pregnancy was not supervised. The pregnancy and delivery were not adversely eventful. The child was the fourth of the mother's five children in a polygamous family setting of a non-consanguineous marriage. There was no family history of congenital anomalies.
Examination findings revealed a girl with normal growth parameters and good mental status. She had an actively discharging tract at the region of the angle of the left mandible which was about 2 cm below the left earlobe []. A rudimentary accessory nipple was seen on the left side with depression of the left hemithorax. Pectoralis major muscle, the third, fourth and fifth ribs were absent on the left side []; the left scapula was hypoplastic and displaced upward [], but the left latissimus dorsi was well preserved. No limbs abnormalities were seen. She had normal cardiovascular examination findings.
She had a chest radiograph which showed absence of the left 3rd, 4th and 5th ribs []. Abdominal ultrasound, electrocardiogram and echocardiogram were normal. A diagnosis of Poland syndrome, esophago-cutaneous fistula and recurrent cardiac syncope was made. The patient and parents were counseled, and she is awaiting reconstructive surgery for the chest defect.


A 10-year-old girl, product of consanguineous marriage was referred for evaluation of palpable gonads in the inguinal region. She was born at term after an uneventful pregnancy by normal vaginal delivery with a birth weight of 2.6 kg and length of 48 cm. Bilateral inguinal gonads with short and blind ended vagina were detected at birth. She was followed-up over a period of 8 months when assignment of the female gender was decided; corrective procedure for inguinal gonads was planned, but did not occur. On physical examination, she had typical female external genitalia. Palpable gonads were found bilaterally in the inguinal region [], pubertal stage was B4P5. The uterus was absent under pelvic sonograms. Hormonal evaluation revealed follicle stimulating hormone (5.4 mIU/mL; normal: 1.5-12.4), luteinizing hormone (21.2 mIU/mL; Normal: 1.7-8.6) and total testosterone (15 ng/mL; Normal: 2.86-8.1); chromosomal analysis showed diploid 46 XY karyotype. Testosterone and DHT synthesis defects were excluded by the normal rise of T and DHT after human chorionic gonadotrophin (HCG) stimulation (basal T: 15 ng/mL; basal DHT: 9.3 ng/mL, T/DHT ratio after HCG stimulation: 7:9). Gonadectomy was performed a few months later and histological analysis revealed bilateral testes with no evidence of malignancy. She subsequently underwent vaginoplasty and received therapy with estrogens. Three maternal aunts presented with primary amenorrhea with an adequate breast and pubic hair development and palpable gonads in the age group between 15 and 20 years and were treated with bilateral gonadectomy, vaginal reconstruction and estrogen supplementation.
Peripheral blood samples were obtained from the girl and her maternal family members for molecular analysis. Genomic DNA was extracted with the use of polymerase chain reaction (PCR) amplification of AR exonic fragments 1-8 followed by direct sequencing analysis of the PCR products was performed. It revealed C 2754 to T transition in exon 6 []. The same mutation was confirmed in her mother and the 3 maternal aunts [], maternal grandmother []. Her mother and maternal grandmother were fertile carriers with 46 XX karyotype.


A 28-year-old male patient with a body mass index (BMI) of 25.1 kg/m2 and positive family history of DM reported to the out-patient clinic of the department of Endocrinology, Medwin hospital with the clinical features of polyuria and polydipsia for last 1 year. There was no history of weight loss or any significant past medical history. Physical examination revealed typical mongolian facies and other features of DS such as short stature (145 cm), brachycephaly, short neck and pot belly, small mouth with protruding tongue, wide occipital region and characteristic small eyes of DS. Thyroid was not palpable. Laboratory data revealed diabetes with fasting plasma glucose of 256 mg/dl, postprandial plasma glucose of 375 mg/dl and glycated hemoglobin (HbA1C) level of 9.9%. Urine was negative for ketone bodies. C-peptide assay showed fairly well-preserved pancreatic β cell function: Fasting values of 1.3 pmol and stimulated values of 2.4 pmol/ml (normal values in non-diabetic subjects, fasting >1.5 pmol/ml and stimulated >4.0 pmol/ml). Glutamic acid decarboxylase (GAD) antibody testing (3.2 IU/ml) was negative. These values were suggestive of type 2 DM. He also had primary hypothyroidism with a thyroid stimulating hormone level of 54 mIU/l and T4 value of 3.5 μg/dl. Other investigations (hemogram, renal and liver function parameters, serum electrolytes and lipid profile) were within the normal limits. He was initiated on basal glargine insulin at a dose of 15 units subcutaneously at night along with oral hypoglycemic agent (glimepiride 2 mg/metformin 1000 mg) once daily and L-thyroxine 100 μg daily. Later, the doses of insulin were reduced and subsequently withdrawn completely and he is maintained well on oral hypoglycemic agents alone.


A 26-year-old female patient with a BMI of 33.4 kg/m2 with strong family history of DM were admitted in the in-patient Department of Endocrinology, Medwin Hospital for proper control of hyperglycemia. She gave a history of polyuria, but denied any weight loss. Physical examination revealed features of DS (short stature, obesity, brachycephaly, gynecomastia, protruding tongue, simian crease, pot belly, short neck and acanthosis nigricans, wide occipital region with characteristic small eyes). The laboratory evaluation revealed fasting and postprandial sugar levels as 175 mg/dl and 240 mg/dl, respectively HbA1c of 8.9%. Urine was negative for ketones. His fasting and stimulated C-peptide levels were 1.4 pmol/ml and 2.5 pmol/ml with negative GAD-antibody test (4.1 IU/ml). Other investigations were within normal limits. Glycemic control was achieved with gliclazide 40 mg with metformin 500 mg twice daily.


A 76-year-old man, a known case of dilated cardiomyopathy, presented to the Emergency Department with severe breathlessness and cough productive of blood stained sputum of 2 days duration. His compliance with diet and medication was poor.
At admission, he was orthopnic, had an RR of 40 bpm, BP of 140/100 mmHg, HR of 110/min, and body temperature of 37.2°C. His neck veins were full, and there was pedal edema. Respiratory system examination revealed impaired percussion note and fine crackles in the entire left hemithorax. Cardiac auscultation revealed S3 gallop and a high-pitched, holosystolic murmur at apex radiating to the left axilla.
Laboratory investigations revealed a TLC of 14000/μL with 75% neutrophils. Chest radiograph showed left-sided airspace disease with cardiomegaly [] and electrocardiogram showed LBBB. His creatinine 1.4 mg/dL, sodium 140 mEq/L, potassium 4.0 mEq/L, B-natriuretic peptide 1200 pg/mL, creatine kinase isoenzyme MB 6.1 ng/mL, and troponin I 0.14 ng/mL.
Differential diagnosis of pneumonia versus UPE was kept. He was started on oxygen, diuretics, low molecular weight heparin, GTN infusion, anti-platelets, statins, intravenous antibiotics (cefepime and azithromycin), and non-invasive mechanical ventilation. Echocardiography done revealed a reduced global left-ventricular ejection fraction (LVEF 35%), and a large eccentric mitral regurgitation jet reaching the left pulmonary veins. His serial CRP and PCT were low. His cultures (sputum and blood) did not grow any organism, and therefore antibiotic were discontinued on day 4. With decongestive therapy, there was significant clinico-radiological improvement. Repeat chest radiography done after 48 h of admission showed significant resolution of the unilateral opacities []. The patient was discharged uneventfully on day 5 of hospitalization, and presently he is on a regular follow-up with the Cardiology Department.


A 29-year-old female, working in a pharmaceutical company, presented with sudden-onset diplopia, slurred speech, imbalance while walking, and behavioral changes which had developed over a period of 2-3 days. She reported to have headache for 2 weeks. On examination, she had cerebellar signs, bilateral extensor plantar reflexes, and bilateral VI nerve palsy. After ruling out other possibilities clinically, the clinician raised the possibility of probable toxic encephalopathy. A detailed personal and occupational history was obtained. Occupational history revealed that the pharmaceutical company used MI as a chemical intermediate. There was increase in its production in last 2 months probably leading her to sudden exposure of excessive amounts of MI before she presented. In view of the rapid onset of neuropsychiatric symptoms, acute MI toxic encephalopathy was suspected and MRI brain was advised.
MRI brain was done at our center. T2-weighted and fluid-attenuated inversion recovery (FLAIR) images revealed bilateral symmetrical hyperintense signal in peri-third ventricular thalami [], peri-aqueductal region [], dorsal pons in the region of superior colliculus [], medial leminiscus and abducens nuclei [], and dorsal medulla and inferior olivary nuclei []. Bilateral symmetrical hyperintense signal was also noted in dentate nuclei []. Dentate nuclei lesions had target appearance; they were extremely bright in the center on T2-weighted images and were surrounded by a rim of ill-defined mild hyperintensity.
All these lesions were hypointense on T1-weighted images []. No restriction of diffusion was noted on diffusion-weighted images (DWI) []. Mild cortical and cerebellar atrophy was evident. However, the basal ganglia appeared normal. No evidence of altered signal was noted in the corpus callosum. No contrast was administered and MR spectroscopy was not performed.
Based on the clinical profile, possibility of MI toxic encephalopathy was considered and other differentials with similar MRI features were excluded. Patient was advised follow-up MRI after avoiding exposure to MI.
Repeat MRI brain was done after 4 months which showed complete resolution of the above-mentioned findings [], confirming the diagnosis.


An 82-year-old man was admitted to our institution for treatment of a colonic anastomotic stricture. He had undergone a laparoscopic left hemicolectomy for cancer of the descending colon. One week after surgery, anastomosis leakage developed, and loop ileostomy was performed. Three months after ileostomy, a colonoscopic exam was performed prior to ileostomy repair, which revealed a stricture at the site of the end to end anastomosis, 17 cm from the anal verge, measuring approximately 3 mm in diameter and 8 mm in length. The patient showed no symptoms.
After bowel enema, the anastomotic stricture was dilated under endoscopic and fluoroscopic guidance, and a guide wire was inserted endoscopically through the stricture site. The controlled radial expansion balloon (5.6 cm in length; CRE Wireguided Balloon Dilator, Boston Scientific Co., Natick, MA, USA) traversed the stricture under fluoroscopic guidance, and the balloon was inflated to a diameter of 15 mm. Just after balloon dilatation, sigmoidoscopy revealed a perforation adjacent to the anastomotic site (). A simple abdominal X-ray showed free air below the diaphragm. A guide wire was inserted via the scope (TTS) method, and a fully covered, colonic, SEMS, 8 cm in length and 20 mm in diameter (Hanarostent, MI Tech Co., Seoul, Korea) was inserted across the stricture under fluoroscopic guidance to completely cover the perforation ( and ). After the procedure, the patient complained of abdominal pain with no evidence of peritonitis. The patient was managed conservatively with intravenous antibiotics. An endoscopic examination 2 days after the insertion of the stent showed satisfactory re-establishment of luminal continuity (). After 4 days of fasting after the procedure, the abdominal pain resolved and gas was gone. The patient was then put on a diet and remained symptom free. Eight days after the procedure, the patient was discharged.
The stent was successfully removed 3 weeks after placement, with no complications. Follow-up sigmoidoscopy showed that the perforation had healed completely (). Two months after the procedure, repair of the ileostomy was performed. The patient did not complain of any difficulty with defecation, and there was no evidence of recurrence of the anastomotic stricture.


A 16-year-old boy was admitted to the hospital with fever and weakness. His systemic examination was normal. His past history included history of seizure for the last 10 years. He was on oral PHT, 5 mg/kg daily once daily. After initiating therapy with PHT 10 years back, he was seizure free for 2 years. Then he started getting seizures that required adjustment in his medication. Patient was also occasionally prescribed clobazam, 5 mg, oral, as and when required. The episodes used to last for a brief period of over 6-7 days. He would then be seizure free for the next 3-4 months. Seizures used to occur at every 3-4 months interval. The boy had history of birth asphyxia and delay in developmental milestones. His previous MRI scans of brain revealed no abnormality. There was no family history of seizure. The boy was managed conservatively for viral fever. After the patient recovered, he was evaluated again due to complaint of difficulty in walking. CNS examination revealed normal mentation with cerebellar signs including gaze-evoked nystagamus, truncal, and appendicular ataxia. MRI scan of the brain was advised and it showed cerebellar atrophy as shown in . The patient had no other neurological and other systemic problems other than epilepsy. Serum phenytoin level was high (30 mcg/ml) and PHT was withdrawn immediately. Patient was started on valproic acid and followed up. The causality assessment was done using the Naranjo scale.[] The causal analysis showed a probable association of the ADR with phenytoin.


A 28-year-old male presented at the Restorative dental clinic, University of Benin Teaching Hospital, Benin City, Nigeria with a discolored maxillary left central incisor (tooth #11) of 4 years duration [], patient could not remember what happened to the tooth, examination of the tooth revealed Ellis class I fracture on the mesial incisial edge of the tooth. However, there was no carious lesion on the tooth. Pulp sensibility test with electric pulp tester was not responsive, and periapical radiolucency was evident in the periapical radiograph. Root canal treatment was commenced on tooth #11 immediately, through an access cavity on the palatal surface of the tooth. The canal was irrigated with 0.9% saline and 2.5% sodium hypochlorite solution. Intracanal medicament (calcium hydroxide) was placed in the canal, and the access cavity was temporarily sealed with zinc oxide eugenol. Patient was given a 2 day appointment for determination of working length of the tooth since the working length was not determined during the initial visit because of time constrains and continuation of the root canal treatment. Patient showed up for his appointment, examination revealed that the tooth was asymptomatic, but there was a discharging sinus in the floor of the right nostril [].
A further history revealed that the patient had been under the care of an Otorhinolargngologist for about 2 years for the treatment of the discharging sinus that he had been on several antibiotics, which he could not remember their names. The temporary seal and intracanal medicament were removed and the canal was checked using paper points, pus was revealed in the canal. Canal was the irrigated with 2.5% sodium hypochlorite and 0.9% saline alternatively. The working length was established at 29 mm using radiographic method [].
Biomechanical preparation of the canal was done using the step back under copious irrigation. Non-setting calcium hydroxide dressing was placed in the canal as inter-appointment medicament and the patient was giving a 4 week appointment. Patient returned 4 weeks later symptom free and complete healing of the sinus in the floor of the right nostril. Canal was obturated with guttapercha using the cold lateral condensation technique []. Access was sealed with glass ionomer cement and the patient was given a 1 month review appointment. Review after 1 month showed that the patient was asymptomatic, and there was no sinus in the floor of the nose, Subsequent reviews at the 3 months and 6 months revealed no symptoms.


A 44-year-old male with a diagnosis of intellectual disability presents with a many year history of enlarging cauliflower-like tumours of both feet (Fig. ).
Eight years prior to presentation, he had similar warty lesions resected from between the clefts of three toes on the left, with an amputation of one toe on the right. The histopathological report showed warty Bowen's disease with well-differentiated SCC.
The growths involved the interdigital folds of the toes of both feet. A CT scan showed tumour bony cortical disruption of the left second toe, with features suspicious for bone marrow invasion. The patient was further investigated with MRI, which showed tumour appearing to be closely related to bone and interphalangeal joints.
The extent of the lesions and possibility of bony involvement resulted in the decision to perform bilateral forefoot amputations.
The patient was followed up for 1 year and no further recurrences or metastasis were detected. He was able to ambulate with the assistance of orthotics.
Histologically, the specimen displayed both endophytic and exophytic morphology, comprising of warty papillomatous projections lined by variably atypical stratified squamous epithelium and overlying hyperkeratosis and parakeratin. The endophytic component showed deep acanthotic growths with a periphery of mitotically active basaloid cells and variable atypical squamous cells with frequent atypical mitoses. The endophytic downgrowths of tumour formed burrows filled with keratinous material, in keeping with verrucous carcinoma. No lymphovascular or perineural invasion was identified. Immunohistochemical staining for p16 showed strong nuclear and cytoplasmic reactivity, suggesting an human papillomavirus (HPV) related tumour.


A 73-year-old female presented with vague cough and dyspnea on exertion. She was previously healthy with no pulmonary or heart problems. There was no history of odynophagia, dysphagia or weight loss. Initial chest X-ray showed a mass in the mediastinum (fig. ). A CT scan of the chest with contrast revealed a hypodense, soft tissue mass/lymphadenopathy in the posterior mediastinum measuring 2.0 × 3.0 cm, contiguous with the esophagus (fig. ), suggestive of neoplastic etiology. Further imaging with PET revealed a mediastinal soft tissue mass/lymph node and a standardized uptake value (SUVmax) of 5.1.
The patient underwent a bronchoscopy and mediastinoscopy with fine-needle aspiration of the mass. Pathology showed increased cellularity with moderate nuclear atypia and pleomorphism with a mitotic count of 2–3 mitoses/10 high-power fields. Immunohistochemistry was positive for vimentin, SMA, caldesmon and desmin. EMA was focally positive and there were a few positive CD34 cells. It was negative for S100, AE1/AE3 and CD68. The Ki67 index was 3–5% and, finally, the sample was reported as spindle cell well-differentiated leiomyosarcoma (fig. ). The patient was referred to us for further management.
Given the possibility of a GIST, CD117 immunostaining was requested and yielded a positive result (fig. ). Then, the patient underwent bronchoscopy with right thoracotomy and esophagoscopy. Esophagoscopy and double lumen bronchoscopy were unremarkable. Thoracotomy findings showed the mass in the posterior mediastinum, which was dissected free from the trachea and inferior aspect of the aorta. The tumor involved muscle layers of the esophagus but not the mucosa. Six weeks after surgery, a repeated PET-CT scan showed no recurrence. On further follow-up, she was free of dyspnea and is currently under surveillance.


A 15-year-old white girl was admitted with abdominal pain and vomiting for 2 days. Two days prior, she was seen by her primary physician for vomiting. She was prescribed intravenous metoclopramide without improvement. She was referred to the pediatric emergency unit for appendicitis suspicion. The girl was febrile with a body temperature of 38 °C. On physical examination, signs of puberty were appropriate for her age (she had menarche at age 14). A mass that was painful on palpation was located in the right lower quadrant. Headache was reported without alterations in level of consciousness, or other neurologic symptoms. Her vital signs were significant with respiratory rate of 24 breaths per minute, oxygen saturation of 96%, heart rate of 120 beats per min indicating tachycardia, and blood pressure of 136/85 mm Hg. Laboratory examination showed normal urea and creatinine, but corrected serum calcium was 14.9 mg/dl (3.70 mmol/l), phosphorus 0.50 mmol/l, LDH 348 U/l, and C-reactive protein level 259 mg/l. Serum parathyroid hormone-intact (PTH-i) level was 10 pg/ml (normal 10–65). Alpha fetoprotein and beta human chorionic gonadotropin were both normal at < 10 IU/ml. Serum CA-125 was 204 (normal, 0–35) U/ml, while serum CA-15-3 was normal. Serum inhibin was not ever checked. Electrocardiograph was normal. Abdominal ultrasonography demonstrated semisolid pelvic mass measuring 125 mm × 105 mm × 65 mm. An abdominal contrast-enhanced computed tomography scan revealed a right ovarian mass with pelvic ascites, without involvement of pelvic structures (). She was referred to intensive care unit for an antihypercalcemic treatment. Isotonic saline hydration was started together with intravenous infusion of pamidronate (1 mg/kg) and furosemide. An isotopic (99 mTc-HMDP-“Osteocis”) bone scanning did not detect bone metastasis.
On the six day after starting the management of hypercalcemia, she underwent a median infraumbilical laparotomy with right salpingo-oophorectomy, omentectomy and drainage of ascites. Her serum calcium remained normal.
The tumor measured 120 mm × 90 mm × 65 mm with soft consistency. Its external surface was smooth and intact. The cut surface was heterogeneous, showing bright yellow nodular areas alternating with hemorrhagic areas and small cystic structures (Fig. 2). The right fallopian tube and the omentum were normal.
Microscopic examination revealed a solid nodular proliferation of medium-sized cells with hypocellular edematous areas, tumor cell necrosis and some pseudofollicular structures. The tumor cells had moderate to large amounts of pale or eosinophilic cytoplasm with focal features of luteinization. The nuclei were round to oval without groove. The cells were mitotically active, averaging 7 mitoses per 10 high power fields (Fig. 3A). Immunohistochemical profile was the following: the tumor cells demonstrated positive reactivity for alpha-inhibin (B) which confirms the histological suspicion of a sex-cord stromal process. The tumor also expressed reactivity to calretinin, estrogen and progesterone receptors, CD56 and smooth muscle actin. The cells were focally positive for cytokeratin KL1. The tumor was negative for TTF1, synaptophysin and chromogranin, pS100, EMA, and CD99.
These morphological and immunohistochemical features were the ones of a juvenile granulosa cell tumor, excluding the hypotheses of a neuroendocrine carcinoma or a clear cell carcinoma of the ovary which are however the most common ovarian tumors associated with hypercalcemia.


A 20-year-old woman underwent bilateral LASIK in July 2007. By 21 months postop, the patient began to experience blurred vision OD, with UCVA of 20/30 in the right eye (OD) and 20/20 in the left eye (OS); the best corrected visual acuity (BCVA) was 20/20 OD and 20/15 OS, and corneal topography showed inferonasal steepening OD (), with a normal post-LASIK appearance OS. At the most recent follow up, the UCVA was 20/50 OD and BCVA was 20/25. Topography demonstrated inferonasal corneal ectasia OD, with simulated keratometry (SimK) measurements of 42.12/48.75 and Orbscan pachymetry thickness of 392 mm OD at the tip of the cone. The postoperative course of her left eye remained uncomplicated. The patient currently wears a rigid gas permeable lens in her right eye.
The postoperative retrospective chart review revealed FFKC bilaterally, with an acceptable central corneal power (<47.2 D) and an inferosuperior asymmetry value of 3.0 D in the affected eye (). There was no noted family history of keratoconus.


A 39-year-old woman underwent bilateral LASIK in January 2008. At 44 months after surgery, the patient complained of decreased vision in her right eye. At that time, the patient had UCVA of 20/30 in each eye and BCVA of 20/30 OD and 20/20 OS. The result of the Orbscan study showed signs of inferior steepening OD () and a normal post-LASIK central flattening OS. The most recent postoperative evaluation showed UCVA of 20/30 OD and 20/25 OS. The keratometry measured 40.90/43.80 OD and 41.80/43.10 OS, with Orbscan pachymetries of 421 μm OD and 407 μm OS. She currently wears spectacles to achieve BCVA.
The postoperative retrospective chart review revealed inferior steepening in the right eye () as well as a preoperative pachymetry measurement of 458 μm and a RSB of 254 μm in this eye, which suggests a previously unrecognized FFKC. There was no noted family history of keratoconus.


A 34-year-old female underwent bilateral LASIK in December 2008. At 12 months postop, the patient complained of progressive blurring in both eyes. The UCVA was 20/50 OD and 20/80 OS, and the BCVA was 20/20 OD and 20/25 OS. The Orbscan revealed inferior steepening bilaterally (). The UCVA at the most recent follow up, at 32 months postop, was 20/60 in both eyes (OU). Keratometry at this visit measured 40.60/42.00 OD and 41.20/42.80 OS (), with Orbscan pachymetry of 479 μm OD and 462 μm OS. The patient currently has a spectacle-corrected BCVA of 20/25 OD and 20/15 OS.
As in cases 1 and 2, a retrospective review of the preoperative corneal topography demonstrated inferior steepening bilaterally ( and ). There was no noted family history of keratoconus.


A 30-year-old male underwent bilateral LASIK in June 2007. At 20 months postprocedure, the patient experienced progressive blurring in his left eye. The UCVA was 20/25 OD and 20/150 OS, with a BCVA of 20/20 OU, corresponding to a manifest refraction of −0.50 +0.75×153 OD and −4.50 +3.25 ×030 OS.
By 22 months he complained of progressive blurring of his left eye. The UCVA was 20/200 OS and BCVA was 20/25, with an increase in average keratometry from 40.30 D to 42.37 D. Corneal topography showed significant inferior ectasia (), and Orbscan pachymetry measured 523 μm. The patient currently wears rigid gas permeable contact lenses to achieve a BCVA of 20/20 OS.
The retrospective review of the preoperative data showed relatively normal topography with no clear indication of keratoconus and no other risk factors for the development of postoperative ectasia (). There was no noted family history of keratoconus.


A 22-year-old woman, gravid 2, para 1-0-0-1, was referred to our institution for fetal echocardiography at 23 weeks of gestation because of abnormally looking great arterial arches. The pregnancy had not been complicated. The mother had not had any diseases or taken any drugs or herbal medications. There was no family history of congenital heart disease. Obstetric evaluation showed normal fetal growth, normal amount of amniotic fluid and normal placenta. The fetal echocardiography revealed the normal four chamber view, where two atria and two ventricles were normal in size and thickness (). The two atrioventricular valves moved normally. Two great arteries arose normally from the appropriate ventricles. The pulmonary and aortic valves looked normal and the size of the main pulmonary artery and aortic root was within normal limits. The aortic arch was normal in size and in location, but the ductal arch was not visualized in any views. The main pulmonary artery bifurcated into two branch pulmonary arteries but was not continuous with the DA (). However color Doppler examination showed a tortuous 'S' shaped ductus cuddled inside the aortic arch (). The DA joined the descending aorta with an obtuse angle and showed a flow signal from the main pulmonary artery to the descending aorta (). Color aliasing occurred along the course of the ductus but pulsed Doppler measurement of velocity was not attempted because of the poor angle of insonation. Flow velocity and waveforms of the two great arteries were within normal limits and no TR was found. A diagnosis of S-shaped DA with mild narrowing was made and follow up examination was arranged.
A repeat examination was performed at 27 weeks of gestation and showed nearly the same findings as before. The RV was normal in size and thickness and no TR was noted. Because the DA was S-shaped, it was very difficult to assess size along the whole range of the DA. However, the color Doppler examination showed tortuous turbulent flow in the ductus and suggested mild obstruction. The sagittal section of the aortic arch showed a ductal junction through which low velocity forward flow from the DA to the descending aorta was noted. Obstetric evaluation showed that fetal growth was appropriate and the amniotic fluid index was adequate. No signs of hydrops were noted.
The third examination was performed at 33 weeks of gestation. The right atrium was big and the RV was hypertrophied and globular in shape. The intracavitary volume of the RV looked slightly smaller than normal because of the thick ventricular wall and hypertrophy of the trabeculations. The right ventricular endocardial lining and the chordae of the tricuspid valve were very bright (). Color Doppler examination showed moderate TR and its velocity was 4.5 m/sec (). Every attempt failed to demonstrate any flow through the ductus. In spite of the right ventricular overload, fetal growth was within normal range and there was no evidence of fetal hydrops.
After a discussion, we decided to deliver the baby. A female infant weighing 2625 g was born at 34 weeks gestation by induced delivery. Apgar scores were 7 at 1 minute and 8 at 5 minutes. Symptoms and signs immediately after birth were tachypnea, chest retraction, grunting sound and low oxygen saturation. An echocardiography performed at 20 minutes after birth showed a small hypertrophied RV and increased echogenicity of the moderator band and chordae of tricuspid valve (). There was a moderate TR with a velocity of 3.7 m/sec (). The short axis view showed a hypertrophied RV (). The ductus was searched for but no ductus was found in 2-D and color images (). Shunt flow through the foramen ovale was mainly right to left (). She required respiratory support with a mechanical ventilator for the first 3 days. She was successfully weaned from the ventilator on her fourth day and discharged at 12 days old. Follow-up examination at the outpatient clinic showed that she did not have any cardiac symptoms or signs. Echocardiography taken at 2 months of age showed much improvement. The RV was nearly normal in size and thickness. Increased echogenicity of the RV was also nearly normalized. There remained TR with a velocity of 3.0 m/sec. At 7 months of age, all echocardiographic findings returned to normal with resolution of TR.


A 46-year-old male patient was admitted to Dongguk University Gyeongju Hospital because of a perineal mass. The patient was born with the mass but he didn't undergo any treatment. There was no history of rapid growth or other complications. Recently, he has felt discomfort from the mass, especially during defecation. He was a hepatitis B virus carrier and he had a 20-year history of rheumatoid arthritis. Physical examination revealed a round, pedunculated mass arising from the left lateral aspect of the anus. The mass was soft, nontender and movable, measuring 5 cm × 4 cm. There was a 3.5 cm × 1.5 cm sized elongated skin-tag-like protuberance on the left lateral portion of the main mass. The rugated skin of the protuberance was contiguous with the covering skin of the main mass. Anal sphincter was normal. There were no abnormalities in the anorectal and genitourinary system. Under the impression of a lipoma, we completely excised the mass. On section, the main mass was a lump of ill-defined yellow adipose tissue partly divided by whitish fibrous septa. The elongated small protuberance was composed of whitish soft tissue and had a rubbery texture (). At the junction of the two lesions, adipose tissue was intermingled with whitish soft tissue of the small nodule. Microscopically, the main mass consisted of predominant mature adipose tissue that was neither encapsulated nor well circumscribed from surrounding tissue (). Small bundles of bland smooth muscle fibers, mature neural tissue and blood vessels were scattered within the adipose tissue mass (). Atypical cells or malignant cells were absent. The main mass was diagnosed as a hamartoma with predominant adipose tissue (lipomatous hamartoma). The skin-tag-like protuberance was composed of numerous, irregularly oriented smooth muscle bundles, resembling the tunica dartos (). It was confirmed as an accessory scrotum. The perineal mass was diagnosed as perineal accessory scrotum with a lipomatous hamartoma. There was neither postoperative complications nor functional sequelae.


A 22-year-old male was admitted because of discomfort due to repeated upper respiratory tract infection symptoms, chronic cough, and sputum for several years. There were no abnormal findings reported in the initial laboratory results and electrocardiogram. Chest X-ray and enhanced chest computed tomography (CT) scans were taken; these revealed bilateral cystic lesions on both the lower lobes. Like the chest X-ray, the chest CT also revealed bilateral cystic lesions. In particular, pneumonic consolidations were found on the lesions of the right lower lobe (RLL) (), and both the lesions were fed directly from the thoracic aorta and drained into the pulmonary vein (). On the basis of the CT image analysis of the chest, the patient was diagnosed as having bilateral intralobar pulmonary sequestration on the RLL and left lower lobe (LLL).
The patient wanted surgery for repeated chronic cough and sputum. We planned staged bilateral lobectomy for both lungs and prophylactic embolization of the feeding vessels for preventing unexpected hemorrhage during the operation. On hospital day (HD) 1, angiography was done for embolization of feeding vessels of the pulmonary sequestration. Each of them was occluded with embolic coils (). On HD 3, right lower lobectomy of lung with video-assisted thoracic surgery was done because of the pneumonic consolidations.
The patient was discharged on postoperative day 10 without surgery of the LLL because of personal schedules and recovery. In the serial outpatient department follow-up, the patient did not feel any respiratory discomfort and was satisfied with the result of angiographic embolization; he refused additional surgery of the LLL.


A 58-year-old male patient presented with a rapidly growing mass at the right posterior chest wall for one month. Initially, the patient had found an egg-sized lump at his right posterior chest wall. The patient received acupuncture at an oriental medicine clinic 10 days before admission. The soft mass showed relative hardening and rapid growth after the acupuncture.
In the physical examination, an approximately 5-cm mass was palpable at the right posterior lateral chest wall around the inferior angle of the scapula. The mass was mild and tender, without heat or redness. The patient had no history of trauma and had played golf excessively for the last six months.
Chest radiograph showed no bony abnormality or lung infiltration. Chest computed tomography showed a heterogeneous cystic mass on the right chest wall. A magnetic resonance axial T1-weighted image showed a well-demarcated lenticular mass lesion located in the right subscapular region between the serratus anterior muscle and the thoracic rib cage ().
We first recommended sonographically guided aspiration; however, the patient refused to undergo this procedure because of the possibility of recurrence after aspiration and rapid growth of mass. Excision of the mass was performed under general anesthesia. The patient was placed in a left lateral decubitus position. The latissimus dorsi and serratus anterior muscle were dissected after an incision was made over the right subscapular area. A soft, movable scapulothoracic mass, which was loosely attached between the serratus anterior and the intercostal muscle, was observed.
A well-encapsulated cystic mass measuring 8×5×5 cm in size was excised. A hemorrhage occurred, which was suspected to be a result of acupuncture in an oriental medicine clinic (). A histopathologic examination showed a pseudocyst with a thickened fibrotic wall, which was filled with blood clots. Many lymphocyte proliferations were observed in the cystic wall without neoplastic cells ().
This patient's history included playing golf, pathological features, and radiological images; therefore, this patient was diagnosed with scapulothoracic bursitis. The patient recovered well after surgery. No chest wall pain was observed, and no recurrent mass was found at the 10-month follow-up. The patient still enjoys playing golf.


An 81-year-old female patient was admitted to a local hospital for weight loss, goiter, and hoarseness. The goiter and hoarseness had been present for about 10 years; the weight loss was 10 kg over the prior 6 months. However, there were no symptoms of fever or night sweats. She had a history of hypertension, but had no family history of cancer, and had no history of thyroid disease or radiation exposure. On physical examination, the thyroid was firm, fixed, and diffusely enlarged; however, there was no pain or tenderness. The thyroid gland measured approximately 10 cm in width and 12 cm in length. Other than the goiter, physical examination was unremarkable. Laboratory tests were as follows: white blood cell count, 6,760/µL; hemoglobin, 13.4 g/dL; platelet count, 207,000/µL; total protein, 9.5 g/dL; albumin, 3.7 g/dL; aspartate aminotransferase, 25 IU/L; alanine aminotransferase, 16 IU/L; lactate dehydrogenase, 257 IU/L (normal range, 135 to 214). Thyroid function tests: free T4, 0.79 ng/dL (normal range, 0.75 to 2.00); T3, 99.5 ng/dL (normal range, 79.8 to 200); thyroid stimulating hormone (TSH), 2.55 µU/mL (normal range, 0.3 to 5.0); and antithyroglobulin antibody level, 14.75 U/mL (normal range, 0 to 60) were within normal limits, but antithyroid peroxidase antibodies were elevated (165.22 U/mL; normal range, 1 to 60).
Initial ultrasonography revealed diffuse enlargement of the thyroid gland, with heterogeneous background parenchyma. Transverse imaging revealed an ill-defined hypoechoic nodule measuring 3.7×3 cm in the right thyroid gland. The left thyroid gland and isthmus showed a diffuse goiter with ill-defined multiple patchy hypoechogenicities and heterogenecity (). Fine needle aspiration revealed the nodule to be suspicious for PTC. Thereafter, the patient was admitted to our hospital for surgery. Preoperative computed tomography (CT) of the neck revealed a diffusely enlarged thyroid gland with nodules in both lobes ().
A total thyroidectomy and right and left central neck node dissection was performed. Gross and microscopic examination disclosed a 3.7×3.0 cm papillary carcinoma in the right thyroid gland (). There was minimal extrathyroidal extension, all surgical resection margins were negative and no metastatic lymph nodes were found (pathologic TNM staging, T3N0Mx, stage III). Background thyroid tissue showed diffuse lymphocyte infiltration, the presence of Hürthle cells, small follicles with scanty colloid, and germinal center formation, which are all characteristics of HT. The left thyroid gland weighed 116 g and was measured 9.6×6.9×2.9 cm; microscopic histopathology revealed a nodular proliferation of small B cells, with a lymphoepithelial lesion suggestive of MALT lymphoma in the left thyroid gland. Much of the normal thyroid architecture was replaced by dense, diffuse infiltrates of atypical small B lymphocytes, showing strong CD20- and lambda light chain-immunopositivity, and an absence of κ light chain (). IgH gene rearrangement assay confirmed the diagnosis of MALT lymphoma.
Bone marrow examination is necessary in order to set the stage of lymphoma. However, the patient refused invasive evaluation due to her age. Postoperative neck CT and 18F-fluorodeoxyglucose positron emission tomography of the neck performed within 1 month of surgery demonstrated no persistence or recurrence of either neoplasm. There was no evidence of lymph node enlargement in the neck, mediastinum, or abdomen. Although a bone marrow biopsy was not performed, MALT lymphoma was considered to be confined to the thyroid gland, corresponding to stage IE according to Ann Arbor classification.
The patient is currently taking levothyroxine as a sole postsurgical therapy. Based on age and health status, radioiodine treatment was not administered. Symptoms of hoarseness and weight loss improved after surgery. One year after surgery, a thyroid function test was performed and antithyroglobulin antibody levels and thyroglobulin levels were measured (free T4, 1.61 ng/dL; T3, 122.1 ng/dL; TSH, 0.00 µU/mL; antithyroglobulin antibody, 11.02 U/mL; thyroiglobulin, 0.227 ng/mL). Neither tumor has recurred during the 1-year follow-up period.


A 76-year-old man was referred for evaluation of various cutaneous lesions. He had a
prior history of total prostatectomy due to prostate adenocarcinoma 6 years before the
current observation and myelodys plastic syndrome (MDS) presenting with neutropenia
followed-up in hematology for 4 years. His neutropenia had been extensively studied
through imaging studies and bone marrow aspirate and biopsy. MDS of the refractory
cytopenia with multilineage dysplasia subtype was diagnosed and an expectant approach
with careful observation was undertaken.
Two months before referral, he progressively developed multiple violaceous plaques and
nodules on the face and scalp. He denied any constitutional symptoms and mentioned just
a prior episode of minor head trauma. The physical examination revealed multiple
well-demarcated, indurated plaques and nodules scattered throughout the right
frontotemporal and biparietal areas as well as a 7 cm wide tumor in the anterior
interparietal area ( and ). Several mandibular, cervical and supraclavicular
lymphadenopathies were noted. He was otherwise well, which contrasted with the severity
of the cutaneous findings. Laboratory results revealed hemoglobin 127 g/L, white blood
cell count 6.0 x 109 /L with 55% lymphocytes; an additional decrease in
neutrophils (0.7 x 109 /L) and platelet count of 241 x 109 /L were
noted. Lactate dehydrogenase was elevated at 1139 U/L. Chest radiography was
unremarkable. Thoracoabdomino-pelvic computerized tomography revealed enlargement of
several mediastinal, axillary, celiac, retroperitoneal, obturator and inguinofemoral
lymph nodes (some larger than 25 mm).
Histology of skin and 2 cervical lymph nodes revealed a monomorphous, non-epidermotropic
diffuse infiltration of small-to-medium sized cells with pleomorphic nuclei () in the skin. This dense infiltrate effaced
the nodal architecture and was located in the dermis and hypodermis, separated from the
epidermis by a grenz zone.
By immunohistochemistry, the cells coexpressed CD4, CD43, CD45 CD56, showed partial
positivity for CD68 ( and ) and were negative for CD3, CD5, CD8, CD20, CD30,
CD34, CD38, CD117, TDT, myeloperoxidase, light IgG chains and PAX5 (). The proliferative index (Ki-67) was high, approximately
60%.
Bone marrow biopsy showed a markedly hypercellular marrow, with CD4+, CD43+,CD45+,
CD56+, CD123+ and HLA-DR+ small blast cells accounting for 80% of cellularity. No
expressions of other T or B cell lineage were observed.
Based on clinical and laboratory findings, the patient was diagnosed with BPDCN with
extensive cutaneous, nodal and bone marrow involvement.
Six cycles of CHOP (cyclophosphamide, adryamicine, vincristine, and prednisolone) were
prescribed, with remission. Only post-therapy inflammatory reactive lesions remained on
the face and scalp.
Two months later, the disease relapsed. Left-sided brachial monoparesis developed and a
paravertebral cervical (C2-C3) mass with medullary compromise through the intervertebral
foramen was detected on magnetic resonance imaging. The patient was hospitalized in a
status of rapid progression of the disease, with enlargement of the cervical mass,
hyperleukocytosis (> 100.000/ml), mental status deterioration and died 7 months after
the diagnosis (9 months after onset of the first clinical symptoms).


This is a five year-old, brown-skinned female patient, with a history of developing
erythematoushyperchromic plaques with slightly elevated edges and atrophic center
located on the face (malar areas bilaterally, inferior eyelids, nose and chin) since the
age of one and a half years ( and ). Similar lesions were presented, although with
more elevated borders, on the dorsal area of the left-hand and the lateral region of the
second right-hand digit (). Dermatologic
examination showed that the inferior palpebral lesions extended to the mucosa of the
eye, starting an ectropion growth and in the left nasal lesion there was a meliceric
crust, by a recent impetigo process (already in treatment). There were not any relevant
personal antecedents. Family members were also examined and no important cutaneous
alterations were found.
Histopathological examination of the material collected from the dorsal area of left
hand revealed cornoid lamella and hypogranulosis, confirming the diagnosis of
porokeratosis ().


A 48-year-old male, a known case of carcinoma buccal mucosa stage III and had already undergone commando procedure followed by chemotherapy and concurrent radiotherapy 3 months back, presented to triage with complaints of breathlessness, cough, difficulty in speaking of 1 day duration. On evaluation, there was an inspiratory stridor and labored respiration along with hypoxemia on room air (oxygen saturation (SpO2) 77% and PaO254 mm Hg). After an initial stabilization, he was immediately shifted to the hemato-oncology intensive care unit (ICU).
He was managed conservatively on the lines of laryngeal edema with adrenaline nebulization, steroids, antibiotics, and urgent surgical consultation. However, in next few minutes, patient’s condition worsened with increasing stridor, respiratory distress, and hypoxemia. He went into cardio-respiratory arrest, and resuscitation was started as per Advanced Cardiac Life Support (ACLS) protocol.
The call for definitive airway protection was taken as there was no improvement with the primary resuscitation. Orotracheal intubation was tried thrice by senior intensivist, however, it was unsuccessful. A rapid decision for PCT was taken by the critical care team along with on-call surgeon and was performed by Ciaglia technique using Blue Rhino PCT kit (Cook Critical Care Inc, Bloomington, IN) with size 7.0 tracheostomy tube. The time taken to secure an airway was less than 2 minutes, and position was confirmed with capnography. After tracheostomy, there was improvement in ventilation and SpO2. He was successfully resuscitated with the return of spontaneous circulation in approximately 11-12 minutes. Hypothermia protocol was initiated as per our hospital protocol.
Patient showed gradual recovery, vasopressors and ventilatory support were subsequently tapered off, and the patient was transferred out, neurologically alert and oriented, with T-piece on day 5 [Figures and ].


A 62-year-old male who was a known case of carcinoma right bronchus stage IV with bone and brain metastasis was admitted with left-sided chest pain, progressively increasing breathlessness since 4 hours. On examination, he was drowsy, hypoxemic on room air (SpO2 88%, PaO2- 64 mm Hg on FiO2- 0.6), with decreased air entry and tympanic node on percussion on left side of the thorax. Chest X-ray revealed left-sided pneumothorax, and 28 Fr intercostal drain was immediately placed. There was transient improvement in SpO2 and respiratory acidosis. After 1 hour, he had generalized tonic clonic seizure, for which lorazepam was given, and he was started on bag and mask ventilation.
The decision to secure definitive airway was taken in view of an altered mental status with persistent respiratory failure. Orotracheal intubation was tried; however, it failed due to restricted mouth opening and restricted lower jaw movement, with Cormack and Lehane grade III on direct laryngoscopy. The decision for emergency PCT was then taken and performed by Ciaglia technique using Blue Rhino PCT kit with 7.5 tracheostomy tube. Procedure was completed in less than 3 minutes. The tube position was confirmed with capnography []. In spite of obtaining definitive airway and using all aggressive medical measures, patient failed to show any clinical improvement and died of refractory shock after 4 days of ICU stay.


A 67-year-old man was admitted to Chonnam National University Hospital with sudden onset of epigastric pain. The pain did not radiate along his back but was relieved to some extent by his leaning forward. He had a history of diabetes mellitus, essential hypertension, and an old cerebrovascular accident. He had no previous history of peptic ulcer diseases, cholecystitis with gallstones, any alcohol ingestion, or abdominal surgery. On admission, he was afebrile, his blood pressure and pulse were normal, and he appeared well-nourished. Scleral icterus was not present. His abdomen was mildly distended, with tenderness in the epigastrium. No abdominal masses were seen; the liver, gallbladder, and spleen were not palpable; and bowel sounds were slightly hyperactive. Laboratory indexes were as follows: white blood cell count, 9,000/mm3; hemoglobin, 15.7 g/dl; platelet count, 135,000/mm3; serum albumin, 4.4 g/dl; aspartate aminotransferase, 29 U/L; alanine aminotransferase, 29 U/L; alkaline phosphatase, 84 U/L; and γ-glutamyl transpeptidase, 148 U/L. Serum amylase and lipase were 293 U/L and 660 U/L, respectively. C-reactive protein was 2.6 mg/dl. The results of the renal function study were within normal limits. Serum triglyceride was 93 mg/dl and serum total calcium, ionized calcium, and inorganic phosphate were 10.3 mg/dl, 2.8 mEq/L, and 1.9 mg/dl, respectively. Abdominal computed tomography (CT) revealed mild swelling of the pancreatic head with peri-pancreatic fat infiltration () and fluid collection around the pancreatic tail (). The follow-up serum ionized calcium level was still elevated at 3.0 mEq/L. The serum level of parathyroid hormone (PTH) was 113 pg/ml. The results indicated hypercalcemia caused by hyperparathyroidism.
Ultrasonography and CT of the neck showed an approximately 5-cm cystic lesion at the inferior portion of the left thyroid gland, which suggested a parathyroid cyst (). The fine needle aspiration biopsy specimen suggested a cystic lesion. 99mTc sestamibi scintigraphy showed no evidence of parathyroid adenoma. The patient had prolonged hypercalcemia despite hydration and diuretics. He underwent surgical resection, and the histological examination with PTH stain was interpreted as a parathyroid cyst with focal parathyroid hyperplasia ().
At 3 weeks after the operation, his serum levels of PTH, total calcium, ionized calcium, inorganic phosphate, amylase, and lipase were normalized. Since the operation, he has had no recurrent episodes of acute pancreatitis.


Male patient, white, 54 years old, was admitted in the Oral and Maxillofacial Trauma and
Surgery Team at Hospital de Base de Bauru (Bauru Base Hospital), in March 2009. The
patient's main complaint was pain in the left mandibular region above the median line
and paresthesia of the anatomical areas sensitized by the Left Alveolar Inferior Nerve,
branch of the Mandibular Nerve and Trigeminal Nerve. The first signal related by the
patient was a pathology originated from a root treatment about one year before, which
developed a mandibular abscess clinically treated. Once healed from this abscess,
chronic pain persisted in half mandible associated with localized paresthesia. Because
of the posterior absence of dental symptoms even as mandibular pain and face
paresthesia, the clinical dentist referred the patient to the one who suggested the
diagnosis of Trigeminal Neuralgia, establishing treatment with Carbamazepin 200 mg and
Gabapentin 300 mg, both once a day, that lasted about 1 year or more.
The patient's medical history revealed pharmacologically controlled diabetes and
prostate acinar adenocarcinoma Gleason score 7 (3+4), with initial PSA score on 4.78.
This latter treated in 2005 by means of radical prostatectomy performed in January 2006
(pT3N0M0), having follow-up procedures with urology, but in a random and intermittent
manner, a history not explored or valued by neurology.
Physical examination revealed left mandibular bulging in the buccolingual aspect and
tooth mobility involving bulging region extending to the opposite canine tooth
associated with a slight gums erythema, but without symptoms compatible with periodontal
disease. In addition, we observed the absence of pathognomonic signs and symptoms of
classic Trigeminal Neuralgia, showing no intermittent pain, neither specific localized
pain spots (trigger-points). Based on this clinical symptomatology, we established a
hypothesis of diagnosis as osteomyelitis and/or cancer, not yet discarding the
possibility of Atypical Neuralgia of the Trigeminal Nerve ().
Through a radiography exam, it was possible to define a mild, diffuse radiolucency in
the left mandibular body. The Computed Tomography Scan showed an anatomical structure
alteration with osteolysis areas in the premolars, molars and in the left region of the
chin ( and ).
Because of that, we carried out an incisional biopsy and culture/antibiogram of
sensitivity of the affected area. The results showed adenocarcinoma (clear cell type)
with necrosis areas and infiltrating bone and soft tissue. The isolated microorganism
was Staphylococcus aureus. These findings suggest a metastatic tumor
infected by via hematogenous route. The tumor had no communication between the internal
and external environment, without skin or mucosa fistula, confirmed by whole-body bone
scintigraphy with special interest in the mandibular region, where increased uptake of
the radiocontrast agent was observed, as well as in many areas, such as the right
clavicle and scapula, humerus, ribs, spine, sternum, hip bone and femur (right/left)
().
After confirming a definitive diagnosis, the patient was taken to the Oncology Clinic,
where in May 2009 was admitted to the Clinical Oncology Department with a metastatic
bone disease diagnosis (prostate acinar adenocarcinoma) confirmed by three different
methods: bone scintigraphy, incisional biopsy and immunohistochemical analysis of
mandibular lesions. The treatment consisted of the use of goserelin acetate (3.6
mg/month) and bisphosphonate (clodronate, 4 ampoules/month). The patient was evaluated
as having good disease control and good tolerance to treatment for some months, when
disseminated neoplasm and pulmonary involvement led to a lethal outcome, with the
patient's death in less than a year.


A 35-year-old non-smoking male patient presented for consultation at the Endodontic Department with a chief complaint of swelling and pus discharge in the upper left canine [Figures and ]. Patient's medical history was non-contributory. Patient reported trauma to his upper teeth when he was about 20 years old. After performing sensitivity tests, tooth #11 was diagnosed as having pulpal necrosis. Clinical examination revealed localized gingival recession and gingival enlargement in relation to tooth #11. Probing pocket depth on the mesial surface of the tooth #11 was 10 mm with a high bleeding score. Radiographic examination showed two bowl shaped radiolucency at mesial aspect of the root. Based on the clinical and radiological finding, we came to the diagnosis of localized chronic periodontitis and pulpal necrosis with external inflammatory root resorption. The treatment plan was informed to the patient, which included patient motivation, oral hygiene reinforcement, scaling and root planning, endodontic procedure and lastly surgical intervention. Patient and his parents were informed of possible discomforts and potential risks concerning the planned treatment procedure and prognosis.
In phase one therapy oral prophylaxis was performed. Endodontic access cavity was prepared after placing a rubber dam and disinfecting the area with 2% of chlorhexidine digluconate (Calypso, Septodont, India). Working length was determined by using the electronic apex locator Root ZX (J. Morita MFG. Corporation, Kyoto, Japan) and file in-radiograph with 15 number K-files. The root canal was cleaned and shaped by Rotary Ni-Ti Protaper System along with GLYDE (Dentsply Maillefer Company, USA) using the crown down technique. The root canal was copiously irrigated with 2.5% sodium hypochlorite (Novo Dental Product, India). Access cavity was temporized with calcium hydroxide and temporary endodontic restorative material (TERM). Patient was recalled after 1 week; the tooth was asymptomatic. Root canal was irrigated again with normal saline and dried using paper points. Before obturation, master points were seated to test their suitability to canals and radiograph was taken. The canals were obturated with selected master gutta-percha cone (variable taper) and AH-Plus sealer (Dentsply Maillefer Company, USA). The coronal gutta-percha cones were sheared off using heated instrument and vertical compaction was done using the heated pluggers at the canal orifices. The access cavity was restored with a composite (Clearfil Majesty; Kuraray, Osaka, Japan).
The surgical procedure was performed under local infiltration anesthesia (2% of lidocaine with 1:100,000 adrenaline) on vestibular mucosa. An intrasulcular incision was made from the distal surface of the maxillary left central incisor to the distal surface of the maxillary left canine and full-thickness mucoperiosteal flap was elevated. Surgical exploration revealed that two lesions were present on the mesial surface of upper left canine and there was no palatal intercommunication []. Granulomatous tissue within the defect area was removed and 90% of trichloroacetic acid was applied to the resorptive defect for coagulation necrosis. The resorptive defects were restored with microfilled composite (Durafill VS; Heraeus Kulzer GmbH, Dormagen, Germany) to a thickness of about 1 mm and light cured for 20 s. The rest of the defects were restored with Resin modified glass ionomer cement (RMGIC) (Fuji II LC; GC Corporation, Tokyo, Japan) to a smooth finish with a cervical matrix and light cured for 20 s [].
A test dose of 12 ml sample of whole blood was drawn intravenously from the patient's right antecubital vein and centrifuged (REMI Model R-8c with 12 ml × 15 ml swing out head) under 3000 rpm for 10 min to obtain the PRF, which was jelly like in consistency. PRF clot started to release its serum (PRF-clot exudates) and was ready for compression into the membrane. The bony defect was filled with freeze-dried bone allograft (LifeNet, Virginia Beach, VA) and PRF []. Without delay autologous PRF membrane was placed [] and the flaps were secured with 4-0 polyglactin 910 sutures (Vicryl, Ethicon, Inc., Piscataway, NJ). After the surgery, the patient was prescribed amoxicillin 1 g twice a day for 1 week and 0.2% of chlorhexidine mouthwash 15 ml twice a day for 2 weeks. The desired gingival contour was achieved; the patient was asymptomatic 1 week after the surgery and the sutures were removed. Patient was followed-up for 6 months, [] 1 year [] and 2 year. At 2-year follow-up period, periodontal status of related tooth demonstrated mild mobility with normal probing depth, no gingival recession and no loss of clinical attachment [Figures and ].