A 60-year-old woman was admitted to our ward with recurrent falls of 1 month duration. She was a long standing diabetic of 10 years duration on insulin and oral hypoglycemic agents. Her husband had noticed that she had developed a voracious appetite, eating every 2 h; although, there was no evident weight gain. For the past 3 days, the falls had increased in frequency and now she was falling 2-3 times a day. She complained of an abnormal sensation in the epigastrium followed by sudden buckling at the knee. She usually fell backward; although, she could fall to either side. On the day of admission, she had fallen 4 times and bruised her left side of the chest and sustained lacerations over the forehead and the occipital region []. She denied any palpitations or loss of consciousness during the episodes and was able to pick herself up immediately after the falls. There was no history of tongue bite or urinary or bowel incontinence associated with these episodes. She was admitted for further evaluation of drop attacks. Prolonged EEG monitoring was normal. Recurrent clinical episodes were recorded without any EEG correlate or recordable movement. MRI brain with contrast was normal. Holter monitoring was normal. Audiometry revealed mild sensorineural hearing loss bilaterally 1 week after admission; she continued to have recurrent falls with injury. Owing to hyponatremia (serum Na of 115 meq/l) and drowsiness, she was shifted to the intensive care unit for observation. At this time, she was noticed to have frequent brief alternating facial grimacing and upper limb dystonic posturing lasting a few seconds. Each of these episodes was preceded by the typical discomfort or aura that she experienced prior to fall and a feeling of weightlessness. These episodes were now noticed to occur every time she became drowsy or woke up from sleep (approximately 30 times a day) []. She was noticed to be very confused and disoriented. Her Addenbrooke's cognitive examination (ACE) score was 68/100 with prominent deficits in attention, concentration and recall. Patient was treated with 1 g of intravenous (IV) methylprednisolone for 5 days followed by oral prednisolone 40 mg/day. She was shifted back to the ward where her husband continued to notice milder attacks with occasional posturing of the leg on the side of the attacks []. The attacks gradually declined in frequency and by day 7 after initiation of therapy, she was asymptomatic and ambulant. Routine blood evaluation, liver function test, renal function test, thyroid function test and vasculitic work-up were normal. The cerebrospinal fluid study showed 0 cells and normal sugar and protein levels. Her ACE score had improved to 82/100. Serum was sent for anti LGi1 and contact in associated protein 2 (CASPR2) antibodies to Oxford University, UK. She tested positive for LGi1 antibody and negative for CASPR2. A second simultaneous sample sent to Statens Serum Institute Copenhagen was positive for LGi1 immunoglobulin G (IgG) antibodies at a titer of 1:320 and negative for LGi1 IgA & IgM, CASPR2, ANNA-1 (Hu), ANNA-2 (Ri), PCA-1 (Yo), Tr, Myelin-associated glycoprotein (MAG) antibody, myelin, PNMA1 (Ma/Tr), glutamic acid decarboxylase antibody (GAD), Amphiphysin, Aquaporin-4 (Aqp4), glycine receptor (GlyR), Abs, GABAbR, GluR (AMPA type) glutamate receptor and (GluR) (NMDA type) antibodies.
Owing to financial constraints, the family declined further testing. She was discharged on oral prednisolone 40 mg/day. At follow-up 45 days later, there were no further falls or dystonic episodes; however, she complained of disabling persistent amnesia and her ACE score was 80/100 with predominant recent memory impairment.
After review of the second case, serum of the 1st patient was sent to Oxford University for LGi1 and CASPR2 antibodies. Serum was positive for LGi1 antibodies and negative for CASPR2 antibodies.


A 63-year-old female patient was admitted to the psychiatry emergency clinic for hallucinations, nervousness and agitation, which had started abruptly before 2 days. She was described to be a little bit aggressive and conversable person before but neither the patient nor her family had a previous history of psychiatric disease. She was consulted to neurology as a late-onset psychiatric disorder to rule out an organic etiology. She had hypertension and had an ischemic cerebrovascular accident before and stopped taking acetylsalicylic acid treatment for 3 days.
Before 2 days, she had suddenly seen her sister was plastering the house she lived before and it had lasted nearly 5-6 min. After a few hours later, she had seen her dead mother calling her “come here” and this also had lasted nearly 5-6 min. After several hours, she had heard some voices calling “get out and walk” and she had walked aimlessly in the house. Then, she had become agitated and had thrown her grandson's toys around and had broken a window. After that she had attempted to jump down from the balcony and had slapped her daughter's face while she was trying to hold her. After she had calmed down, she had recognized these all as hallucinations and her children had brought her to the psychiatry emergency clinic.
At the neurological examination, she was cooperative, orientation for the person and the location was normal, but she was disoriented to time and couldn’t distinguish night and day. Cranial nerves were intact; there was no paresia other than a left upper monoparesia, which was the sequel of a previous ischemic cerebrovascular accident. She was aware of the hallucinations that she had.
There was no metabolic abnormality in blood examination; electrocardiogram and electroencephalogram (EEG) was normal, no acute pathology was found in cranial computed tomography. Acute infarction was found at the left side of pons with diffusion weighted magnetic resonance imaging (MRI) investigation [Figures and ].
She was diagnosed as a cerebrovasculer accident presenting with pedincular hallucinosis and was treated with heparin and 100 mg/day acetyl salicylic acid and ketiapin 50 mg/day was given for hallucinations. One week later, her hallucinations were resolved almost completely.


A 31-year-old male presented in February 2009 with subacute onset occipital and sub-occipital moderate “pressure-like” headaches and neck pain for 2 years. The headache was precipitated by standing or walking and relieved on assuming recumbent position. There was no history of nausea, vomiting, photo-phonophobia, auras, seizures, loss of consciousness, neurological deficit, trauma, cranial/spinal surgery or fever. He had been evaluated at another hospital 1 year back where his MRI brain was normal, but CSF pressure was reported to be “low.” He had been treated with EBP, following, which he had shown good recovery. Clinical examination was normal. CSF opening pressure was 80 mm water. CSF analysis was normal. MRI brain revealed thin subdural hygroma, absence of meningeal enhancement, and mild tonsillar descent [Figure –]. Contrast MRI spine and myelography, and radioisotope cisternography did not reveal an area of CSF leak. Routine laboratory parameters were normal. He was given autologous EBP with reduction in headache by 40% after 5 days followed by complete relief over days without recurrence of headache since then. Follow-up MRI showed normalization of CSF space in the posterior fossa [].


A 41-year-old male presented in Oct 2009 with subacute onset, severe bifrontal throbbing headaches for 1 month. It was precipitated within 10 min of standing and relieved after few minutes in the recumbent position. He was so incapacitated with his headache that he was very fearful of getting off his bed for activities of daily living. Rest of the history, clinical examination and routine laboratory parameters were unremarkable. On clinical suspicion of SIH, MRI brain was carried out, which revealed bilateral subdural hygromas [Figure –], diffuse meningeal enhancement [Figure ,], venous distension sign [], sagging of the brain and tonsillar herniation []. Contrast MRI spine did not reveal CSF leak. CSF opening pressure was 80 mm water. CSF analysis was normal. Patient did not respond to bed rest, analgesics and fluids. He responded remarkably to EBP with reduction of headache by 75% in 72 h, and was headache free after 4 weeks with no recurrence on follow-up. MRI after 3 months revealed resolution of findings [Figure –].


A 43-year-old male was diagnosed in November 2008 as HIV-positive and was on regular ART. He was admitted to hospital with complaint of passing loose stools 8-10 times per day since 1 month without associated pain abdomen, passage of blood or mucus in stool. He had an episode of diarrhea about 6 months back. It was diagnosed as cryptosporidial diarrhea on stool examination and he was treated with nitrazoxamide successfully.
The patient had several associated comorbidities. He was a documented case of disseminated tuberculosis since August 2010 and was on ATT. Presently, he is also a patient of Herpes Zoster (T6-T10 dermatome) and is on acyclovir therapy. On general physical examination, he was found to be a thinly built, well oriented, afebrile with a supine blood pressure of 90/66 mmHg and a regular pulse rate of 88/min. He had a significant left cervical and axillary lymphadenopathy with matted nodes. No organomegaly on abdominal examination was seen. Upper GI endoscopy revealed essentially normal esophagus and stomach and first part of duodenum. The second part of duodenum showed nodular folds. Ultrasonography of abdomen and pelvis showed calcified areas in segment VII of liver and multiple hypoechoic focal lesions (? granulomas).
The laboratory investigations revealed hemoglobin-10.9 g/dl, total leucocytic count -4,200/μl, differential leucocytic count was lymphocytic predominant (54%), and a platelet count of 1.5 lakh/μl. His absolute CD4+ T lymphocyte count was 219 cells/μl and viral load was less than 400 copies/ml. His liver and renal function tests and urine examination were essentially normal. Upon stool examination no ova, cyst, acid-fast bacilli, or any other organism was discerned. Culture of stool showed no growth. Stool was also negative for fat globules.
Histopathological examination of biopsy from second part of duodenum revealed mild atrophy in the form of blunting, shortening, and fusion of villi with crypt elongation at places. A focal disorganization of the epithelium, loss of nuclear polarity, cell crowding, and cell vacuolation was seen []. Lamina propria showed an intense lymphoplasmacytic infiltrate along with few eosinophils and occasional macrophages. Numerous enterocytes showed intracytoplasmic loose parasitophorous vacuoles containing isosporidia schizonts and merozoites. These organisms were seen in the basal part of cytoplasm below and around the nucleus. The single organisms were the schizonts. Focally on luminal surface of occasional enterocytes, small bluish intracellular but extracytoplasmic round to oval amphophilic structures resembling cryptosporidia were seen. Also noted were foci of occasional enterocytes containing intracytoplasmic vacuoles with small, round to oval, bluish supranuclear refractile spores resembling microsporidia []. No crypt destruction, dysplasia, or granulomas were seen. Lamina propria showed dilated vascular channels at places. Special histochemical stains to identify the parasites done were – Brown – Bren modification of Gram stain, PAS, Masson's trichrome, toluidine blue [], Giemsa, modified acid fast, and Gomori's methanamine silver (GMS) stains. A histopathology opinion of enteritis due to triple infection by isosporidia, cryptosporidia, and microsporidia was offered.
Based on histopathology report, patient was put on tablets niazoxanide, Septran, Cifran, and Fluconazole. He has since improved and is under regular follow-up in the outpatient department and ART center of the hospital.


A 33-year-old male bank employee presented to our outpatient department with a 4 month history of dry cough, and breathlessness on exertion associated with wheeze. He was a nonsmoker and teetotaller. There was no history of high risk behavior, but he had a history of exposure to pigeons in his house for the past 1 year. He had a history of being treated with empirical antituberculous therapy for an exudative pleural effusion 2 years ago. For his current symptoms, he had been initially treated by his local physician with antibiotics and inhaled bronchodilators, but his symptoms persisted. At presentation, he had no neurological symptoms.
Physical examination revealed decreased breath sounds on the whole left hemithorax. Vital signs were stable. Initial investigations such as total leukocyte count, differential count, and renal and liver function tests were within normal limits. A chest X-ray [] revealed a left upper zone, mid zone, lower zone air space consolidation; and an elevated hemidiaphragm possibly due to collapse of the left lower lobe. A computerized tomography (CT) scan of the chest [] showed a mass lesion in the left main bronchus (LMB), causing complete collapse of left upper lobe and partial collapse of left lower lobe with consolidation with no mediastinal lymph adenopathy and no peripheral lung nodules.
Fiberoptic bronchoscopy [] performed under local anesthesia revealed a white polypoid endobronchial mass lesion in LMB causing complete occlusion. Bronchial washings showed no evidence of TB or fungal infection. However, bronchial biopsy of the lesion showed yeasts consistent with Cryptococcus [] and subsequent cultures grew Cryptococcus. The cryptococcal antigen was not tested in our patient as the clinical suspicion was very low. Moreover the value of serological tests in the diagnosis of this condition is doubtful. The patient was then evaluated for his immune status. Test for human immunodeficiency virus (HIV) by ELISA technique was negative. His total lymphocyte count, CD4 and CD8 counts, and immunoglobulin levels were normal. The patient was initiated on intravenous amphotericin B (0.7 mg/kg daily) and fluconazole (1,200 mg per day). A repeat chest X-ray [] after 10 days of therapy showed significant resolution of the lesion and his symptoms had improved. Intravenous amphotericin was stopped and he was discharged home on oral fluconozole 1,200 mg per day. After a month of oral fluconozole (1,200 mg per day), he was switched over to maintenance dose of oral fluconozole 400 mg per day. He remained well with good improvement in symptoms and chest X-ray findings. CT scan chest and bronchoscopy have not been repeated in our patient as he was not keen on having either of them. Further, his remarkable clinical improvement made us agree with him on this management decision.


A 16-year-old male presented with right-sided numbness, dysphagia, and right peripheral vision loss after working out during football practice. In the emergency room (ER) his right-sided visual field defect persisted, with anomia and alexia. He stated that he had experienced intermittent episodes and discreet events over the past year including weakness, numbness, and vision loss.
He had a computerized tomography scan of the head, which revealed areas of hypodensity in the left temporoparietal region suggestive of stroke. This finding was confirmed by magnetic resonance imaging, which revealed multiple strokes of different ages. Specifically, he had an acute stroke in the left temporoparietal region, along with subacute strokes in the right thalamus, spanning the corpus callosum and left cerebellum. The patient was then admitted to the pediatric intensive care unit (PICU) for observation and further workup. A cerebral angiogram revealed a focal dissection of the distal right VA with a small nonocclusive thrombus proximal to the dissection. The only suspicious event from the patient's history was a wrestling incident in the locker rooms a few days before the onset of stroke. He was followed by neurology and hematology/oncology, and had workups to rule out vasculitis, metabolic, hypercoagulable, and cardiac embolic sources, all of which were negative. Anticoagulation with enoxaparin was then initiated, and the patient was discharged home with instructions to avoid weight lifting and contact sports.
Approximately 3 months after his initial presentation and completing his 3-month course of anticoagulation with therapeutic enoxaparin, the patient experienced new transient neurological symptoms of headache, blurred vision, and confusion. Incidentally, he began weightlifting a week prior to the onset of his new symptoms. Magnetic resonance imaging of the brain revealed a subacute stroke in the left medial cerebellum, and a new area of encephalomalacia, suspicious for a stroke, in the parietal region near the vertex that occurred after his initial hospitalization. The patient was then admitted for further evaluation.
A dynamic cerebral angiogram was performed and revealed that the patient had a Bow Hunter's type phenomenon, with dynamic occlusion of the right VA in the chin up position looking to the left [].
A dynamic computerized tomography angiogram performed with the patient's head in rotated position showed a near complete occlusion of the V3 segment of the right VA resulting from an anomalous spur emanating from his right occipital condyle that pinched off his VA between the C1 ring and this condylar spur []. This was determined to be the etiology of the dissection. Therefore, the patient was managed by neck immobilization via a cervical collar, and we initiated aspirin 81 mg and coumadin with an INR goal of 2-3. At this time, the plan was to allow the dissection flap to heal and then bring the patient back for elective surgical decompression of the condylar spur.
However, 2 weeks after the treatment modality of immobilization and pharmacotherapy, the patient presented with a transient ischemic attack. He reported right hemibody numbness and tingling. His INR at that point was subtherapeutic, first at 1.8 then at 1.6. A magnetic resonance imaging and magnetic resonance angiography of the head and neck revealed persistent narrowing of the V3 segment of the VA to 50%, with new strokes noted in the occipital lobe, right cerebellum, and a thrombus in the left P2-3 segment of the left posterior cerebral artery.
Since the patient had further thrombotic episodes due to the dissection, he was admitted and placed on 325 mg aspirin, clopidrogrel (300 mg load followed by 75 mg daily), and a heparin infusion. After a thorough discussion of all treatment options, including stenting of the artery, surgery to drill off the spur, or continued medical therapy, the decision was made to proceed with coil embolization/sacrifice of the right VA so as to prevent further thromboembolic events as well as to avoid the future need for surgical decompression of the anomalous occipital condyle process. The right VA was sacrificed with coil embolization and trapping of a 4 mm thrombus over the dissected segment []. The patient tolerated the procedure without complication and was subsequently discharged home.
During his initial postoperative clinic visit, one week status-post right VA sacrifice, his cervical collar was discontinued. During his 5 week postoperative clinic visit, he reported no further episodes of seizures, paresthesias, headache, or neck pain. He was doing well on aspirin 81 mg with a plan to continue antiplatelet therapy indefinitely
Three months status-post right VA sacrifice, the patient had a baseline right homonymous hemianopsia and a mild nystagmus, especially with right lateral gaze, but was otherwise doing well and denied any symptoms. He had increased his level of activity and started weightlifting but was not cleared for contact sports.


A 25-year-old primigravida presented to our hospital at 22nd week of gestation for target scan Targetted imaging for fetal anomalies (TIFFA). Fetal biometric parameters were normal. Liquor was adequate. Anatomical survey revealed a longitudinally oval, avascular anechoic cyst measuring 14 × 9 mm in the right upper abdomen, separate from duodenum, showing continuity with hepatic hilum superiorly without identifiable gall bladder (GB). No other abnormalities were detected. Presumptive diagnosis of CDC was made.
Fetal MRI was performed 2 weeks later on 1.5T Essenza (Siemens, Erlangen, Germany) to investigate the correct anatomical location of the cyst and its relationship with adjacent organs to assist with prognostication and treatment planning for the perinatal period.
T2-weighted Half-Fourier acquisition single-shot turbo spin-echo (HASTE, TR/TE 900/86 ms, 4-mm slice thickness) sequences were obtained in the axial, coronal, and sagittal planes with respect to the fetus. Sequences were monitored in real time and manipulated to determine optimal imaging planes during the scan, as fetal orientation is unpredictable and often changes during acquisitions. In addition to the standard orthogonal planes, oblique planes were acquired for demonstrating the relationship to surrounding structures.
MRI showed a 14 × 9 mm ellipsoid [] homogenous cystic lesion at liver hilum hyperintense on T2W images. Axial images revealed the cyst posterior to the duodenum []. The cyst was longitudinally oval, coursing posteroinferiorly from hepatic hilum appreciated on sagittal images []. Intrahepatic ducts were not dilated; CBD was not visualized. Coronal images revealed hyperintense cord-like structure above the cyst, showing communication with it []. The normal morphology of fetal GB was not visualized in the inferior surface of liver in right upper quadrant. The spleen was normal. Inferior vena cava (IVC) showed normal course. Liver showed normal signal intensity and contour.
The imaging characteristics on USG and MRI are presented in .
Follow-up using serial USG scans in pregnancy revealed static size of the cyst with persistent ghost GB. Interval growth was normal till term.
A female infant weighing 2.9 kg was delivered by cesarean section at 39 weeks.
Postnatal USG, on day 3 after a 4-h fast, revealed liver extending beyond subcostal margin; echotexture was homogenous with normal surface contour. Intrahepatic ducts were not dilated. There was an echogenic area anterior to the portal vein at porta and measured 3.2 mm []. A well-defined, longitudinally oval anechoic cyst was present at the hilum ~14 × 9 mm. The cyst size, echogenicity, and morphology were the same as seen in prenatal imaging []. Maximum width and length of GB was 11 × 2 mm, with irregular, compressed lumen s/o ghost GB []. Hepatic artery was prominent, running parallel to the right portal vein, and measured 1.7 mm. Main portal vein (MPV) diameter was obtained at the same level, which measured 3 mm. The ratio of HA/MPV diameter was >0.5 (>0.45 increase) []. Hepatic subcapsular flow appeared subjectively increased. Spleen measured 3.8 cm. No varices were present. No free fluid was noted.
The imaging characteristics at porta are presented in .
Liver function tests (LFT) revealed increased γ-glutamyl transferase (831 U/L), elevated alkaline phosphatase (698 U/L), conjugated hyperbilirubinemia (2.8 mg/dL), and normal serum glutamate pyruvate transaminase (SGPT) 10 U/L, serum glutamate oxaloacetate transaminase (SGOT) 29 U/L, albumin, and International Normalised Ratio [(INR). Hepatobiliary scintigraphy was performed on day 24 which showed prompt and good uptake by the liver and absent tracer excretion into the intestines in 24-h delayed images. GB and extrahepatic ducts were not visualized [].
A diagnosis of extrahepatic cystic biliary atresia (CBA) was made based on imaging.
The child was explored with on day 31. Operative findings included firm brownish liver, fibrotic porta inclusive of non-visualized right/left hepatic duct, common hepatic duct, and proximal CBD []. GB was small and did not have a lumen. A cystic structure was seen at the site of terminal part of CBD. The cyst was going behind the duodenum and ending blindly. No communication was seen with the pancreatic duct. Corresponding schematic representation is shown in and was classified as type 3 BA according to Japanese classification system.
Excision of fibrotic hilar structures including cyst en masse with a Kasai's portoenterostomy was performed with ~30 cm of Roux-en-Y jejunal loop. Histopathologic examination confirmed the diagnosis of BA. Bilirubin returned to 1 mg by the 11th postoperative day. The child is aged 2 months now and doing well.


A 54-year-old African-American male with a remote history of prednisone treated polymyositis developed bilateral open angle glaucoma. His past ocular history included trabeculectomy in the right eye, bilateral cataract surgery and the maintenance of topical steroid drops to manage his rebound iritis. On the day of surgery, he reported some mild cold symptoms, but he insisted on having the surgery done. He had an uneventful trabeculectomy with mitomycin C performed on his left eye and did well during the first postoperative week with deep anterior chamber and an IOP in the 7–9 mm Hg range. He was on Vigamox 0.5% (Alcon, Fort Worth, Tex., USA) and prednisolone acetate 1% 4 times a day. He returned for a follow-up on postoperative day 11 with a complaint of persistent left eye pain for the last 3 days. On examination, his visual acuity was 20/80, pin holed (PH) to 20/30, and IOP was 10 mm Hg. His anterior chamber was flat with a complete iris-cornea touch except a 1/5 cornea thickness space between the cornea and the intraocular lens (IOL). The superior fornix-based bleb was slightly elevated without leakage and the peripheral iridectomy was patent. There were severe fibrin exudates in the anterior chamber with a 360° posterior synechiae of the pupil. The retina was flat on fundus exam without scleral depression. The initial differential diagnosis included: overfiltration, pupillary block, aqueous misdirection, choroidal effusion or choroidal hemorrhage. Inflammation was considered to play a role because of his history of steroid dependency, eye pain and copious fibrin in the anterior chamber. He was given oral prednisone 60 mg daily, topical Atropine 1% (Falcon Pharmaceuticals, Ltd., Fort Worth, Tex., USA) and phenylephrine 2.5% (Akorn, Inc., Lake Forest, Ill., USA) to dilate the pupil. Prednisolone was discontinued and Durezol (Difluprednate Ophthalmic Emulsion 0.05%; Alcon) was given one drop every hour []. In addition, he was given a 2-mg dexamethasone subconjunctival injection. Following the application of dilating drops in the clinic, the anterior chamber began reforming and posterior synechiae began to break down. He was sent home with Atropine 1% and phenylephrine 2.5% 4 times a day as well as Durezol every hour. The next morning, his visual acuity was 20/200 (PH 20/60), IOP was 7 mm Hg, and his anterior chamber was flat with cornea-IOL touch. His fundus exam revealed no choroidal detachment or hemorrhage. Healon (Abbott Medical Optics Inc., Santa Ana, Calif., USA) was injected to reform the anterior chamber []. His oral prednisone and topical drops were continued.
Despite this treatment, the patient returned to the clinic 2 days later. He had a totally flat anterior chamber with a normal fundus and an IOP of 10 mm Hg. Aqueous misdirection was suspected, but peripheral choroidal effusion could not be ruled out. Transverse B-scan using a temporal approach identified a shallow annular anterior choroidal effusion (fig. ). He was taken to the operating room the same day and the suprachoroidal effusion was drained from infero-nasal and infero-temporal sclerotomies []. A moderate amount of light yellow clear fluid was retrieved. The anterior chamber was reformed with Healon (Abbott Medical Optics Inc.) at the end of the surgery aiming at a high IOP to prevent choroidal effusion from recurring. He was continued on oral prednisone 60 mg daily and Durezol every 2 h and dilating drops 4 times a day.
His anterior chamber remained deep for 2 days with IOP in the mid-teens. However, on the third day after drainage of the choroidal effusion, the anterior chamber was flat with an IOP of 10 mm Hg. Aqueous misdirection was suspected, but repeat transverse B-scans showed recurrent peripheral choroidal effusion. The patient was taken to the operating room. One sclerotomy wound was reopened and a smaller amount of suprachoroidal fluid aspirated. The conjunctival incision for trabeculectomy was opened and additional 10–0 nylon sutures were placed on the sclera flap. Also, a half-thickness 3 × 3 mm donor scleral patch was placed to reinforce a thin area on the scleral flap. Postoperatively, his anterior chamber was deep with an IOP in the 40's. The IOP was lowered to the 30's over the next 2 days with paracentesis and ocular massage. Suture lysis was performed on the third postoperative day and his IOP decreased to the mid 20's. The patient developed a large corneal epithelial defect postoperatively. The oral prednisone was decreased by 20 mg every 2 days from the initial 60 mg/day, and topical Durezol was decreased from one drop every 2 h to 4 times a day to promote corneal healing.
The patient presented 7 days later with counting fingers vision due to diffuse corneal stromal edema and Descemet's membrane folds. The epithelial defect was completely healed and the IOP was 18 mm Hg with a deep anterior chamber. The corneal edema was thought to be due to the rapid steroid tapering. Oral prednisone 60 mg/day was resumed. The first dose of prednisone was given in the clinic and topical Durezol was increased to one drop every 2 h. The patient's corneal edema and Descemet's membrane folds cleared with vision improving to 20/50 the next morning. Oral prednisone was slowly tapered by 10 mg/week, while topical Durezol was continued at one drop every 2 h for 5 weeks, followed by a very slow taper. At this point, his anterior chamber depth stabilized and cornea remained clear. Suture lysis was performed cautiously and as needed. Visual acuity in the eye returned to 20/20 and IOP was 15 mm Hg, 8 months after the initial surgery, without glaucoma drops.


A 39-year-old male presented with decreased vision in his left eye for two days. Visual acuity was 20 / 20 in the right eye and hand movement in the left eye. On slit lamp examination of the left eye, severe inflammation was seen in the anterior chamber (cells +4) and the vitreous (cells +4). Fundus examination of the left eye demonstrated thick, white, confluent sheathing surrounding the retinal veins and arteries from the posterior pole to the periphery with extensive retinal hemorrhages, optic disc swelling, and macular edema (). The right eye was normal. B-scan ultrasonography and spectral-domain optical coherence tomography of the left eye showed a severely edematous and detached retina in posterior pole (). Fluorescein angiography demonstrated a prolonged arteriovenous transit time, blockage of fluorescein corresponding to extensive retinal hemorrhage, widespread area of capillary non-perfusion, and extensive staining of sheathing veessels (). A diagnosis of occlusive retinal vasculitis resembling acute FBA was made and systemic evaluation for retinal vasculitis was performed. The patient had a history of recurrent genital and oral ulcers over two years, but no other systemic manifestations of Behçet's disease on presentation. The results of laboratory examinations, including serology for herpes virus, varicella zoster virus, and human immunodeficiency virus were normal or negative. Other examinations, including brain magnetic resonance imaging and polymerase chain reaction assay for varicella zoster virus and cytomegalovirus in the aqueous humor, were negative or normal. Human leukocyte antigen typing resulted in a positive HLA-B51.
The patient was started on intravenous methylprednisolone. Vitreous opacity progressed and angle hypopyon appeared until 24-hour after treatment initiation (). However, during two weeks after treatment, the vascular sheathing and vitreous opacity gradually disappeared. Systemic steroids were slowly tapered during the next two months and cyclosporine 150 mg/day was added. Two months later, follow-up angiographic findings revealed a widespread area of non-perfusion in three retinal quadrants with neovascularization of the disc (). Although panretinal photocoagulation for non-perfusion areas was performed, neovascularization progressed by four months (). However, iris rubeosis and neovascular glaucoma had not developed by 10 months. Six months after his presentation, he developed two ulcers on oral mucosa and pseudofolliculitis on his face, along the hairline. A diagnosis of Behçet's disease was made using the international criteria following a rheumatology consultation. Eight months later, follow-up optical coherence tomography imaging revealed atrophy and disruption of the photoreceptor layer in the macular area (). The final visual acuity was hand movement in the left eye. He is currently on maintenance cyclosporine therapy.


A 60-year-old gentleman, a laborer by profession, presented with the complaints of severe low back ache of 3 days duration and low grade fever for the past 2 weeks. There was no history suggestive of tuberculosis in the past. One year back, he had low backache of moderate intensity, precipitated by lifting and carrying heavy loads on his back, which resolved spontaneously. On clinical examination, there was focal tenderness over L4-5 vertebral levels with gross restriction of spinal movements and marked paraspinal spasm. No focal neurological deficits were detected. Routine hematological and biochemical parameters were normal except for high ESR of 94 mm/1 h (Westergren). Chest X-ray did not reveal any radiological abnormality. Magnetic resonance imaging (MRI) of lumbosacral spine [] revealed collapse of L4 body with relatively preserved disc spaces. The collapsed L4 vertebral body was hypointense on T1W image and hyperintense on T2W image []. There was no area of abnormal enhancement or any prevertebral or para spinal collection. Computed tomography (CT) of spine [Figures and ] revealed L4 vertebral body collapse. He underwent L4 laminectomy, L3-5 transpedicular fixation, and the biopsy of the L4 body. Histopathology revealed thin irregular osteoporotic bony lamellae and fragments of pale ischemic bony bits []. The enclosed marrow spaces revealed fresh hemorrhage bordered by clusters of foamy histiocytes as response to fresh hemorrhage reflecting trauma []. There was abundant fibrin and early necrosis of the marrow without any osteoblastic or osteoclastic activity. There was no evidence of tuberculosis (absence of granulomatous pathology or acid fast bacilli). The possibility of post-traumatic avascular necrosis (KD) was suggested. As tuberculosis could not be conclusively excluded, he received antitubercular therapy (ATT).
On subsequent reviewing of MRI, radiological features were not favoring tuberculosis, as the disc space was well preserved. There was no pre or paravertebral collection of inflammatory granulation tissue and the collapsed vertebral body did not have abnormal enhancement or signal changes. Review of the CT scan revealed L4 vertebral body collapse with cortical breach, linear fracture of lamina on the left side, and presence of intravertebral “vacuum cleft” on radiograph [Kümmell's sign – a retrospective observation ()]. Clinical history was suggestive of mild trauma and delayed acute presentation, and hence, diagnosis of KD was made and ATT was stopped. Postoperatively, his pain improved significantly. At discharge, he was ambulatory without any neurological deficits. Serum ADA performed at 3 months of follow up, which was normal. At 12 months follow up, he was ambulatory and was doing well. There were no clinical signs or symptoms attributable to tuberculosis.


A 69-year-old man presented to the emergency room with sudden-onset abdominal pain and nausea. He had previously undergone a hybrid laparoscopic left hemihepatectomy and splenectomy for hepatolithiasis and spherocytosis approximately 20 months earlier. Since his surgery, he had occasionally taken non-steroidal anti-inflammatory drugs (NSAIDs), loxoprofen as per his prescription. During the 3 months before his current presentation, he had discontinued taking proton pump inhibitors, at his request.
Abdominal computed tomography images revealed a deformity of the duodenal bulb and a markedly dilated stomach, containing food residue (); free air in the abdominal cavity was not detected. A fibroscopic upper gastrointestinal examination revealed a giant ulcer with a prominent crater in the inferior wall of the bulb. In addition, a foreign body was detected at the ulcer floor and was strongly suspected of being a ligature associated with the previous left hemihepatectomy (). The foreign body was eliminated, and an endoscopic biopsy was performed. Histopathological examination of the biopsy showed a simple, active ulcer. The patient received conservative therapy with a proton pump inhibitor and recovered immediately.


A 33-year-old woman (married, homemaker) presented with frequent high-grade fever and left-sided abdominal pain that had lasted for 1 month. There was no history of cough, sputum, or any other respiratory symptoms. She had no history of diabetes, hypertension, TB, or other significant illness. Physical examination showed that her body temperature was 38℃, pulse rate 105 beats/min, and blood pressure 100/60 mm Hg. Abdominal examination revealed an enlarged and tender spleen. Routine examinations of other systems showed unremarkable findings. The patient's laboratory data showed a white blood cell count of 11,590/mm3, hemoglobin concentration 9.4 g/dL, erythrocyte sedimentation rate 30 mm/hr, and C-reactive protein concentration 9.02 mg/dL. Other biochemical parameters, including liver functions and levels of blood sugar, blood urea, and serum creatinine, were within normal limits. T-SPOT.TB assay (Oxford Immunotec, Oxford, UK) showed positive result and enzyme-linked immunosorbent assay showed that the patient was seronegative for anti-HIV antibodies. Chest radiography revealed no remarkable abnormalities. Computed tomography (CT) of the abdomen revealed multiple low-density lesions of variable size, with some septations, in the spleen (). We also observed several enlarged mesenteric lymph nodes, which showed central low attenuation with a peripheral rim enhancement, suggestive of TB lymphadenitis (). An ultrasound-guided splenic biopsy revealed inflammatory cells with focal necrosis, and results of acid-fast bacilli (AFB) staining and TB-polymerase chain reaction were negative. Laparoscopic biopsy of the small bowel mesentery was performed for differential diagnosis and to exclude malignancy. However, biopsy of abdominal lymph nodes could not be performed, because profuse bleeding was expected as a result of severe adhesion of small bowel mesentry. Histopathological examination of the biopsy specimen revealed evidence of both acute and chronic inflammation without granuloma. Our initial impression, based on the clinical and radiological findings, was splenic TB accompanied with abdominal TB lymphadenitis. We initiated antituberculous chemotherapy with isoniazid, rifampicin, ethambutol, and pyrazinamide. After 1 week of chemotherapy, the patient became afebrile and did not complain of abdominal pain. She was subsequently discharged.
After 10 weeks of chemotherapy, the patient returned to the emergency department of our hospital with sudden-onset dull and aching pain in the abdominal upper left quadrant. Abdominal CT scan showed more increase in the size and number of splenic abscesses with intraperitoneal rupture (), whereas more decrease in the size and number of abdominal lymph nodes than were previously observed (). The patient did not report occurrence of recent trauma. The patient was admitted for emergency splenectomy. Gross findings included multiple yellow necrotic nodules and hemorrhagic foci with a lacerated splenic capsule (). Histopathological examination showed epithelioid granulomas composed of epithelioid cells, lymphocytes, and Langerhans giant cells with variable degree of central caseous necrosis, consistent with TB (). AFB staining and culture for TB from the splenectomy specimen were negative. Considering the clinical improvement of the patient and radiological improvement of concomitant abdominal lymph nodes, we assumed that the splenic rupture was precipitated by paradoxical reaction. Antituberculous chemotherapy was continued postoperatively without regimen change, for a total treatment time of 9 months. The patient is currently clinically disease-free for 3 months after completion of chemotherapy.


A 48-year-old man with a prior history of renal transplantation was admitted to our medical center with 2 weeks of fever, chills and left upper quadrant abdominal pain. His history was significant for end-stage renal disease due to congenital solitary kidney and reflux nephropathy which required cadaveric renal transplantation in 2008. His immunosuppressive regimen included mycophenolate mofetil and tacrolimus. Three months prior to his current presentation he was admitted with Salmonella enteritidis bacteremia. During that hospitalization he was found to have a splenic artery pseudoaneurysm measuring 4.9 × 5.1 × 7.8 cm on abdominal computed tomography. This was suspected to be a mycotic pseudoaneurysm related to the Salmonella infection. After undergoing antibiotic treatment he subsequently underwent interventional radiology-guided coil embolization of the splenic artery pseudoaneurysm without complication.
At the time of his current admission, the patient reported 2 weeks of subjective fevers, intermittent chills and abdominal pain. The pain was located in the left upper quadrant, dull in quality, and was not associated with eating. On presentation he was afebrile and had normal vital signs. There were surgical scars from his prior renal transplant surgery. His abdominal exam was notable for mild tenderness in the left upper quadrant with normal bowel sounds. There was no guarding or rebound tenderness. Laboratory tests were notable for a mild leukocytosis and stable renal function (table ). Blood and urine cultures were negative.
The patient had an abdominal X-ray revealing a fragment of embolization coil in the right lower quadrant (fig. ). Abdominal/pelvic computed tomography with oral contrast revealed a migrated coil within the right colon (fig. ). The remaining coils appeared to be within the splenic artery. There was no evidence of contrast extravasation or free intraperitoneal air. The patient subsequently underwent diagnostic upper endoscopy. This identified a large mucosal defect in the proximal stomach, with numerous coils extruding into the gastric lumen (fig. ), consistent with a gastrosplenic artery fistula. The patient subsequently underwent exploratory laparotomy with splenectomy, distal pancreatectomy, partial gastrectomy, resection of the splenic artery aneurysm and removal of the splenic aneurysm coils. He had an uneventful recovery and was discharged from hospital 9 days after surgery.


A 50-year-old Caucasian female presented to the urgent care clinic with extreme headaches, fever with intermittent shivering cold spells, 10/10 generalized joint pain, excessive thirst and fluid intake, and a progressing rash on her back. The patient described the headaches as tremendous pressure pushing inwards “as though she was wearing a heavy helmet,” such pressure that sneezing and coughing gave her the perception that her “head would explode.”
Three days before her visit to the urgent care clinic (day one), the patient noticed an initial small, slightly raised lesion resembling an insect or spider bite. The patient did not examine her back, but described what she thought to be a scab covering the bite while she scratched. On day two, the patient’s fever reached 39.3°C (102.8°F), and she had an increasing burning sensation at the site of the bite. A family member examined the bite, and recognized that the bump had developed into a circular rash. The patient took over the counter ibuprofen and Benadryl, and was able to sleep through the night. On day three, the patient felt poorly, but completed a normal working day. By day four, the patient awoke feeling worse, with 10/10 joint pain, high fever, and excessive thirst and fluid intake; this led her to seek medical attention.
On exam, her temperature was 40.2°C (104.4°F). She had a large circular red rash on her back with bull’s-eye appearance, 16 × 18 cm in diameter ( and ). The rest of her physical examination was unremarkable. Her prior medical and surgical history is not significant to this case. The patient recalled a walk in the woods 3 weeks prior to her exam, but denied finding a tick on her body.
Initial laboratory investigation results are shown in and . The patient’s white blood cell count and platelet count, hemoglobin, and hematocrit were within normal ranges. Her serum chemistry was unremarkable, except for elevated glucose, borderline low alkaline phosphatase, and slightly depressed osmolality.
A serologic test for LD (antibody response to B. burgdorferi by enzyme-linked immunosorbent assay [ELISA]) was ordered and showed negative results (). A 10-day treatment of doxycycline (500 mg twice a day) was prescribed. The patient gradually began feeling better, and was able to return to work after 4 days of antibiotic medication. On day nine, her body temperature was within normal limits, the polydipsia and headaches had dissipated, and the rash had decreased to 11 × 14 cm. The patient expressed concern that a 10-day treatment was inadequate in proportion to her symptoms and to the size of her rash. Her doxycycline prescription was extended to 30 days by her primary care physician, continuing at 500 mg twice daily.
A second set of serologic tests were ordered on day 28, which demonstrated the presence of immunoglobulin (Ig)-M without IgG antibodies to B. burgdorferi. The patient also sought a dermatology consultation, and the lesion was biopsied. The pathology report described microscopic changes consistent with lichenoid and spongiotic dermatitis. A Steiner stain failed to reveal spirochetes.
On day 48, 2 weeks after completing the antibiotics, the patient began experiencing lower-extremity neuralgia as well as tingling in her hands. She described her pain as “electrical currents running down her legs.” The patient visited her primary care provider, who started a second 30-day treatment of doxycycline (500 mg twice daily) and gabapentin (900 mg daily before bed).
The patient has been referred to a local physician who has extensive experience with LD for continued management of her medical therapy. At the time of this report, a year later, this patient reports that her symptoms include chronic fatigue and intermittent arthralgia that has required a cane to mobilize at times. Her only medication is methylphenidate (36 mg daily) for fatigue.


A 43-year-old woman awoke with left cervical discomfort 10 days before presentation. The discomfort radiated to the trapezius and scapular region, and was aggravated by neck movement. 4 days after awakening with cervical discomfort, she noted the inability to abduct her left arm. In retrospect, she recalled mild left upper cervical discomfort on neck rotation to the left while reversing her car about 4 days before the symptoms began. On examination, she had weakness involving the left deltoid, supraspinatus, infraspinatus and biceps muscles (4/5), with milder weakness of left forearm pronation and supination (4+/5). The left biceps reflex was absent and the left brachioradialis reflex reduced. The remainder of the neurological examination including left upper limb sensory examination and cranial nerve examination was normal.
Cervical MRI revealed an intramural haematoma in the left vertebral artery from mid-C7 to C2 (, ). MR-angiogram (MRA) demonstrated spiral arrangement of intramural methaemoglobin and irregularity of the vessel lumen from C2-C6 (). No intimal flap was evident. The vessel wall haematoma was seen to compress the left C5 and C6 nerve roots. Cranial MRI was normal. An electromyogram performed 11 days after her weakness began revealed acute denervation consistent with an acute left C5/6 radiculopathy. The lateral antebrachial sensory response and other sensory studies were normal. Nerve conduction studies including median and ulnar F-wave responses were normal. She was treated with aspirin as an antiplatelet agent. Left upper limb power returned to normal after 2 months; repeat MRI/A showed recanalization of the vertebral artery with no residual abnormality or nerve root compression.


A 43-year-old woman suffered lumbago and bilateral leg pain for one month. Neurological examination revealed paresthesia of the dorsal aspects of both legs. Magnetic resonance imaging (MRI) showed a ventrally located intradural extramedullary mass at the level of T12 (). Three-dimensional computed tomography angiography (3D-CTA) revealed that the Adamkiewicz artery (AKA) ran from the L2 foramen to the spinal cord (). The patient was placed in the prone position and treated via the posterior approach. We performed T11 to L3 hemilaminectomy on the left side to expose the dorsal aspect of the spinal cord. After opening the dura mater it was seen that part of the tumor was located at the left ventral side of the spinal cord. We detached the dentate ligament on the left side from the dura mater and gently reflected it to make space ventral to the spinal cord. The tumor capsule, partially exposed by this maneuver, was cauterized and we proceeded to perform internal decompression of the tumor from this corridor using an ultrasonic aspirator. Intraoperatively, motor evoked potentials elicited by the stimulation of nerve roots attached to the tumor capsule identified the upper lumbar nerves as the tumor origin. Sharp dissection of the tumor capsule away from the pia mater of the spinal cord was carried out with ease and total removal of the tumor was achieved with resection of the associated rootlets. Postoperatively, her symptoms improved and she was discharged 10 days after the operation. The pathological diagnosis was schwannoma. Postoperative MRI showed no evidence of a residual tumor ().


A 77-year-old man suffered progressively worsening low back pain for 5 months and mild weakness in both legs for 4 months. Neurological examination revealed paraparesis in both lower extremities (manual muscle testing [MMT] 2 in left- and 3 in the right leg). MRI demonstrated an intradural-extramedullary tumor extending from T10 to T12 on the ventral side to the spinal cord (). The tumor was isointense with the spinal cord on T1- and hyperintense on T2-weighted images (). It was also well enhanced (). On axial enhanced images at the level of T11-T12 the tumor extended laterally into the intervertebral foramina on the right side (). With the patient in the prone position and under general anesthesia we attempted total tumor removal. After the midline skin incision we performed T9 to T12 laminectomy and opened the dura mater. The tumor was not seen from the dorsal side because of its ventral location. After cutting the dentate ligament of the right side and carefully mobilizing the spinal cord by reflecting the ligament we could see a tumor with a yellowish gray hue. After internal decompression using an ultrasonic aspirator we proceeded to dissect the tumor from the spinal cord. During the dissecition of the tumor, we were able to identify one large nerve root that entered and descended into the tumor. As it was difficult to shave it into constituent rootlet bundles we cut the nerve root at the level of T12 and completely removed the tumor capsule. Based on operative findings we concluded that the exact tumor origin was T12 or L1. His somatosensory- and motor evoked potentials remained stable throughout the operation.
Postoperatively this patient suffered transient worsening of paraparesis predominantly on the right side. Over the course of his hospitalization, his motor weakness of the left lower extremity improved to MMT3, however, his right leg remained at muscle power grade 2. The histological diagnosis was typical schwannoma (). He was transferred to a rehabilitation facility 2 weeks after the operation and subsequently returned to his home. At the 6-month follow-up examination, he could walk without assistance. Postoperative MRI confirmed total tumor removal ().


A 63-year-old male, 159 cm in height and 70 kg in weight, was scheduled to undergo resection of cervical epidural mass. The patient had a medical history of well-controlled hypertension and old healed pulmonary tuberculosis. The patient had facial and neck purpuras and ecchymoses, whose cause could not be identified at a private dermatologic clinic. Blood test results concerning platelet count, prothrombin time and activated partial thrombosplastin time were normal.
General anesthesia was induced with propofol 100 mg and remifentanil 0.5 µg/kg/min. Rocuronium 50 mg was administrated to facilitate tracheal intubation. Anesthesia was maintained with 6 vol% desflurane with 50% O2 in air, remifentanil, and rocuromium. After a change from a supine to a prone position, bleeding from the lacerated facial purpuras was recognized while identifying head position on a Mayfield headrest. Swollen purpuras and eyeballs hyperemia were evident. The operation was canceled in order to evaluate the facial lesions and the patient was transported to the postanesthetic care unit when fully conscious.
Skin biopsy from the facial lesions () and serum free light chain assay were performed during the stay at the general ward, and resulted in the diagnosis of systemic amyloidosis of monoclonal gammopathy with lambda type. Multiple myeloma, which usually accompanies systemic amyloidosis, was excluded after bone marrow biopsy and immunoprotein measurement of serum and urine.
The patient had complained of dyspnea since post-anesthesia day 16. Bilateral pleural effusion and interstitial pulmonary edema were identified by high resolution chest computed tomography. Pulmonary function test revealed moderate degree of chronic obstructive pulmonary disease. Cervical magnetic resonance imaging taken 48 days after the anesthesia showed spontaneous resolution of the epidural mass. Post-anesthetic echocardiograph showed thickened myocardium, which was not confirmatory of cardiac amyloidosis. According to abdominal ultrasound, there was no hepatomegaly or splenomegaly. Symptoms and signs suggesting the involvement of other organs, such as renal, neurologic, and hematologic abnormalities, were not observed. Treatment with chemotherapy and auto-peripheral blood stem cell transplantation was planned.


A 24-year-old male, unmarried, agricultural worker by occupation and without any drug habits had come with complaint of erectile dysfunction and depressive symptoms secondary to that. These complaints started around 4 months back, when his father was looking for a bride. Prior to this, he reported never having had sexual ideas and his friends tried to give him advice on how to show sexual prowess to a woman on her first night. That night when he went to sleep he felt some shadow crawling over his body and he had spontaneous ejaculation. This was first time such thing had happened to him. His father reassured him that night. Next two nights also he had spontaneous ejaculation at night and this terrified the patient that all his semen may have drained out and consequently, his ability to impregnate a woman and his energy to carry out physical work had been depleted significantly. His friends had advised him to masturbate and told him to continue the technique to get semen out at least once a month. To his dismay, he found that he was unable to do as there was ‘no rigidity’ in the penis. When questioned about the nature and importance of semen, he said that semen is important for producing children and having a family but added that he had no idea where it came from. He consulted a Siddha practitioner for his problems and was told that if semen was not coming out through its proper channel, it would fill other body fluids and also come out in the saliva. That doctor took sample of saliva in small bottles and told the patient that after testing he had come to the conclusion that they are containing sperms. Along with this presumed ‘imbalance in bodily fluids’, he had developed depressive symptoms secondary to semen loss when he presented to us and had attempted suicide once during this period.
After evaluation, he was admitted as a case of severe depressive disorder. During ward stay and with various treatments there was improvement in biological functions and consultations also revealed acute gastritis for which he was treated adequately. He continued to believe that semen is coming out through saliva. By its taste and smell he was able to confirm what the previous Siddha doctor had told him. Few weeks later, he observed that the size of his penis had shrunken and corroborated this observation by taking his measurements. He began to worry about how he was going to live without his own family and how he would become a laughing stock among people for losing his ‘maleness’ or ability to impregnate a woman. He also worried about earning his livelihood by farming due to accompanying weakness.
During assessment we found that he has hypolibidinal state prior to onset of these problems. There were no local pathology and sex hormone study and thyroid function tests did not show any abnormalities.


A 67-year-old male with a known dolichoectasia of his vertebrobasilar artery, presented with a history of increasing falls over the past 3 months. A computed tomography (CT) scan of the head [] and magnetic resonance imaging (MRI) of the brain [] demonstrated a VBD with formation of a focal fusiform aneurysm in the proximal basilar artery. This caused mass effect on the left anterior aspect of the adjacent pons.
A magnetic resonance (MR) angiogram [] revealed fusiform dilatation of the intradural distal right vertebral artery giving rise to the dysplastic dilated basilar artery, which had increased in size. The lumen was within a larger partially thrombosed vessel. This gave rise to a short segment of normal caliber basilar artery, which then again dilated just proximal to the basilar tip. There was also a new fusiform dilatation of the posterior cavernous left internal carotid artery consistent with a fusiform aneurysm. There was presence of ventriculomegaly of the lateral and 3rd ventricle, with the 4th ventricle being collapsed.
His past medical history included: Hypertension, dyslipidemia, long time smoker, chronic obstructive pulmonary disease, previous transient ischemic attack, depression, and prostate cancer treated with radiotherapy and NSTEMI treated with PCI (two bare metal stents).
The presence of new ventriculomegaly on imaging raised the possibility of symptomatic hydrocephalus. A radionuclide cerebrospinal fluid (CSF) flow study was undertaken. It revealed normal migration of the radio tracer from the subarachnoid lumbar space to the basal cisterns and sylvian fissures, with no activity within the lateral ventricles in the 24 and 48 hour images. However, the patient also underwent a trial of lumbar drainage, during which his gait was assessed by the medical allied health team documenting an objective improvement in his gait. Consequently, the patient had a ventriculoperitoneal (VP) shunt inserted with no complications.


A 38-year-old female, gravida 2 and para 2, presented to gynecology outpatient department with a left sided mass in the vulvar region. It was noticed one year back, which was small initially and gradually increased to the present size. Local examination showed 3 × 3 cm, nontender, well defined, soft to firm swelling in the labium majus. Overlying skin was unremarkable. Systemic examination findings were noncontributory. Fine needle aspiration cytology (FNAC) was advised.
FNAC revealed moderately cellular smears composed of tissue fragments of cells with indistinct cell margins, moderate amount of eosinophilic cytoplasm and spindly nuclei of varying size. Few adipocytes were seen entrapped within the spindle cell fragments []. Background was hemorrhagic. Cytological report of benign spindle cell lesion with differential diagnosis of spindle cell lipoma and leiomyoma was offered. The complete excision of the lesion was advised for histopathological confirmation.
On gross examination, the tumor was ill circumscribed, partly encapsulated, soft to firm measuring 6 × 2.5 × 2 cm. On cut section, the tumor appeared whitish with yellowish and few tiny hemorrhagic areas [].
On microscopic examination, an ill circumscribed tumor mass composed of spindle cells arranged in interlacing fascicles and whorls, regularly interspersed with single and at places collections of mature adipocytes was observed. The spindle cells showed bland oval nuclei and moderate amount of eosinophilic cytoplasm []. No areas of necrosis and abnormal mitosis were noted. Based on histomorphologic appearance, differential diagnosis of lipoleiomyoma and neurofibroma with lipomatous differentiation was considered and representative sections were subjected for immunohistochemical studies.


A 41-year-old man with end-stage liver failure due to hepatitis B virus-associated liver cirrhosis underwent orthotopic liver transplantation (OLT). He had underlying diabetes mellitus and did not have a history of exertional angina, dyspnea on exertion, and paroxysmal palpitations. Preoperative 12-lead electrocardiography showed normal sinus rhythms. Preoperative echocardiographic evaluation showed normal biventricular size and function. Paroxysmal AF with rapid ventricular responses developed on the first postoperative day (; in the online-only Data Supplement). Given the stable vital status with no signs of heart failures or myocardial ischemia, the sinus conversion was not attempted. The patient required a prolonged in-hospital recovery period, during which, continuous renal replacement therapy, mechanical ventilation, and tracheostomy were performed. Flecainide and diltiazem were administered to control recurrent AF after normalization of liver and renal function, 5 weeks after OLT. But, such drugs had to be discontinued after development of congestive heart failures with severe ventricular dysfunction (ejection fraction, 30%) () 9 weeks after OLT. During the hospital stay, the left ventricular ejection fraction increased to 38% after administration of ramipril, carvedilol, and diuretics. The patient was discharged with these medications on top of immunosuppressive drugs including FK 506 and mycofenolate mofetil 11 weeks after OLT. Acute renal failure occurred 3 months after surgery, but resolved after discontinuation of heart failure medications. Repeated echocardiography showed improved left ventricular ejection fraction of 42%.
Six months after OLT, the patient collapsed while he was walking. The patient was transported to the emergency room under cardiopulmonary resuscitation and ventricular fibrillation was noted on electrocardiogram ( in the online-only Data Supplement). After an immediate defibrillation, AF with rapid ventricular response was noted ( in the online-only Data Supplement). He recovered without neurologic impairments. Coronary angiography showed no significant stenosis. Echocardiography showed severe left ventricular dysfunction with a left ventricular ejection fraction of 21% (). A single-chamber implantable cardioverter-defibrillator (ICD) was implanted. Heart failure treatments, including a β-blocker and an oral anticoagulant, were continued. Ventricular tachycardia with palpitation (cycle length of 290 ms, 18 beats for 5.2 seconds) was detected and terminated by antitachycardia pacing 2 months after the ICD implantation ( in the online-only Data Supplement).
Complete conversion to sinus rhythm was recorded on ICD after 5-months of alternation between AF and sinus rhythm. Echocardiography showed normalized left ventricular systolic function 8 months after the ICD implantation (). Thereafter, only a β-blocker was administered to prevent tachycardia for 18 months with no recurrences of ventricular arrhythmias.


A 49-year-old man presented with oral erosions, erythema and blistering rashes over his
trunk and limbs for 3 months. The patient first developed painful oral mucosal blisters
and ulcers, which became progressively severe and gradually spread to the eyes, perineum
and anus. The patient was admitted to our department for further diagnosis and
treatment. On physical examination, we found several small lymph nodes on his neck with
diameters of under 1 cm. Dermatologic examination revealed hyperemia on the bilateral
conjunctiva, extensive ulcers and erosions on the oral mucosa, erythema and blisters
scattered on the chest, back, perineum and anus, but with no obvious ulcers ( and ).
One week prior to admission, the patient had attended another hospital where
histological examination, serum direct immunofluorescence (DIF) and indirect
immunofluorescence (IIF) were performed. Histological examination of a skin biopsy taken
from a lesion on his left arm showed epidermal acantholysis, suprabasal cleft formation,
erythrocyte extravasation and vacuolar changes at the dermal epidermal junction and
lymphohistiocytic infiltrate in the upper dermis (). DIF revealed IgG, IgM, and C3 deposit in the basement membrane zone (BMZ).
IIF revealed IgG reticular staining with an antibody titer of 1:20. CT revealed a
prominent solid lesion in the right anterior superior mediastinum ().
The results of laboratory tests, including full blood count, urea, creatinine,
electrolytes, liver function, tumor markers and tests for infectious diseases were
normal. Percutaneous mediastinum biopsy guided by CT revealed lymph hematopoietic
hyperplasia. Immunohistological examination revealed CD20++, Pax-5++, CD43++, CD3+,
CD163+, CD68 scattered+, Mum-1-, CD30-, CD10-, EMA-, CKpan-, TdT-, Ki673%+, CD5
scattered +.
PCR analysis of Ig heavy chain genes, gene clonal rearrangement (IGH, IGK, IGL,
TCRβ, TCRγ, TCRδ) was detected by using
BIOMED-2 protocols. DNA extraction from formalin-fixed tissues was performed using
standard methods. All the results were negative ( and ).
Diagnosis: 1. Paraneoplastic Pemphigus 2. Castleman's Disease.
Upon hospitalization, the patient was given an intravenous methylprednisolone injection
60mg per day and other supportive therapy. A few days later, the lesions started to dry
up and form crusts, except for the oral mucosa. According to the advice from the
Cardiothoracic Surgery Department, the lesion in the right anterior superior mediastinum
was too large to be completely resected, since abundant blood vessels were present and
it was too close to the pulmonary artery. In any case, since the patient rejected
surgery, conservative treatment was recommended. Considering that the erythema and
crusting on the patient's chest and back could perhaps further aggravate after
radiotherapy, the Radiotherapy Department attempted to use stereotactic radiosurgery,
with an irradiated DT:32Gy/2fx and isodose line 80%. After the end of treatment, the
patient's lesions aggravated and new erythema and blisters appeared. However, these
recovered during the following week, and no new lesions manifested during the short
follow-up period.


A 42-year-old Caucasian woman with a 22-year history of severe scalp psoriasis presented
to our outpatient clinic complaining of itchy scalp and diffuse hair loss for the last
five years. Increased hair shedding was associated with episodes of greater inflammation
and pruritus. Nail and articular psoriasis were absent. Psoriatic lesions had always
been confined to her scalp. Topical clobetasol, oral cyclosporine, methotrexate, UVB-NB
phototherapy and antibiotics had been used as treatment with only temporary relief.
On physical examination, diffuse erythema, infiltration, scales and crusts were present
all over the scalp. Decreased hair density in the fronto-parietal area was observed. The
right parietal side was the most severely affected, so both dermoscopy and skin biopsies
were performed in this area ( and ). Fungal assessment, from both scalp scales and
hair shafts, were negative.
Dermoscopy showed interfollicular twisted red loops characteristic of scalp psoriasis
and lack of follicular openings (). No
pustules or tufted hairs were observed.
Horizontal sectioning of the biopsy specimen showed follicular drop-out with only one
follicle at the subcutaneous level and 3 vellus follicles at the dermis level ( and ). Sebaceous glands were not visualized at all, but isolated pili erector
muscles were present and fibrosis could also be observed (). No signs of androgenic alopecia were detected.
Vertical analysis showed epidermal changes compatible with psoriasis and a moderate
chronic inflammatory infiltrate around vessels and eccrine glands, associated with
fibrous tracts (). No interface changes
were observed at the dermal-epidermal level or affecting the follicular epithelium.
Direct immunofluorescence was negative for IgG, IgM, IgA and complement.
Findings were consistent with scarring alopecia associated with psoriasiform epidermal
changes.


A 45-year-old female was referred to the radiology department for investigation of gradually progressive abdominal lump in right lumbar region which she first noticed about 6 months back. She had complains of right flank pain, fullness and pus in urine for the same duration, but intensity of pain has increased since last 15 days and had an episode of hematuria few days back. She also gave history of off and on fever, for which she took medications from local practitioners. However, she had no previous history of diabetes, hypertension, renal disease or urinary tract infection.
On local examination, temperature was slightly raised with an ill-defined firm to hard mass palpable in right lumbar region and was tender on palpation. Laboratory investigation showed leukocytosis with increase in neutrophil count. On admission, investigations done at our hospital showed raised blood serum creatinine (1.8 mg%) and urea (60 IU) level. However, blood sugar level was normal.
An X-ray kidney urinary bladder (KUB) showed a large soft tissue density mass in right lumbar region displacing bowel loops to the left side. Loss of right psoas shadow, blurring of pre-peritoneal fat planes and mild scoliosis of spine with concavity to right side was also noted []. CT abdomen was advised immediately which showed ill defined, poorly excreting right kidney with loss of corticomedullary differentiation. There was extensive heterogeneously enhancing collection with involvement of adjacent soft tissue in perinephric and pararenal space, pelvis and under surface of liver with involvement of ipsilateral psoas, quadratus lumborum and lateral abdominal wall muscles. No evidence of calculus was seen on CT. Inferior vena cava IVC was displaced anteriorly due to retroperitoneal lymphadenopathy; however, no evidence of extension of the lesion into IVC was seen []. A radiological diagnosis of Xanthogranulomatous pyelonephritis was suggested even in the presence of negative history of diabetes, prior episode of urinary infections, absence of calculus and presence of hematuria.
Drainage of extrarenal abscess under coverage of piperacillin-tazobactum and metronidazole was performed and aspirate sent for cytology which showed lipid laden macrophages with few haemosiderin laden macrophages consistent with the diagnosis of Xanthogranulomatous type of Pyelonephritis []. This was followed by radical nephrectomy. The patient recovered well with uneventful post-operative period and patient was discharged on 7th post-operative day. The patient was last seen at 3 months follow up and has progressed well.


A 12-year-old Brazilian male reported to the Department of Pediatric Dentistry, School of Dentistry, University of Cuiabα, Cuiabα, Brazil. The child presented with bothered by a swelling on the lower of his lip. The nodule measured 0.6 × 0.3 cm and was reported to have appeared 2 years ago. On clinical examination, the asymptomatic lesion was identified at the middle border of his lower lip, presenting sessile soft tissue growth and smooth surface with a color similar to normal mucosa [].
There was neither any history of injury to the lower lip nor any source of stimulus that could be related to the lesion. Medical and familial history did not contribute to the diagnosis. Based on the clinical appearance of the lesion, differential diagnosis was either traumatic fibroma or mucocele. An excisional biopsy was planned to establish a definitive diagnosis.
The surgical procedure was performed with under local anesthesia and the lesion was completely removed by a no. 15 Bard-Parker blade. Three interrupted silk 4.0 sutures were placed to achieve hemostasis. The excised tissue was sent for histopathological investigation. On the postoperative visit after 2 weeks, sutures were removed and healing was satisfactory. After 3 weeks, the lower lip was completely healed.
Histopathological investigation revealed that the tumor was composed of interlacing bundles of elongated cells with wavy nuclei and small nerve fibers. These cells are bland and disorderly with intracellular collagen strands [Figures and ]. Immunohistopathologic assessment showed cells positive for S-100 [Figures and ]. Pathological diagnosis was a NF with no signs of malignancy. There were no signs of recurrence at the 1-year follow-up visit [].


This paper reports a case of a 23-year-old man who reported with a chief complaint of spacing in the anterior maxillary region []. An intraoral examination showed two supernumerary teeth on the palatal aspect of the maxillary premolar region bilaterally and one supernumerary tooth on the buccal aspect of the right maxillary molar region, thus constituting three fully erupted supernumerary teeth in the maxillary arch [] and a supernumerary tooth at the lingual aspect of premolars in the mandibular arch on the right side []. There was no relevant medical history and the patient was otherwise healthy. Physical and extra-oral examinations revealed no additional abnormalities wherefore, conditions such as cleidocranial dysostosis, Gardner's syndrome, ectodermal dysplasia and Apert's syndrome were excluded. There was no familial history of supernumeraries elicited by the patient. A panoramic radiograph revealed three impacted supernumerary teeth in the mandibular posterior region, of which one was on the right side and two on the left side of the mandible []. The maxilla showed one impacted supernumerary tooth in the right premolar region and one on the left side between lateral incisor and canine, thus making five impacted supernumeraries in the oral cavity. This resulted in a dental formula of 40 teeth (32 normal, 8 supernumeraries [5 impacted and 3 erupted]). The treatment of the patient began with the extraction of erupted maxillary and mandibular supernumeraries followed by fixed appliance therapy. Straight wire appliance (0.022 Roth prescription) was used. The impacted supernumeraries were left in situ as they were not asymptomatic. Space closure was performed using class III elastics and echains []. A permanent lingual retainer was placed after debonding [Figures and ]. He was advised on the need for periodic recall and observation for any cystic changes with the impacted supernumeraries.


A 54-year-old man had a large asymptomatic anterior mediastinal mass incidentally discovered by chest radiograph during a regular health check-up. He had no history of autoimmune diseases including myasthenia gravis, aplastic anemia, hypogammaglobulinemia, lichen planus, or Graves' disease. A computed tomography scan of the chest demonstrated a large mediastinal mass consisting of a mixture of fat and soft tissue contents, radiologically suggesting thymolipoma ().
The tumor was surgically removed. Grossly, it was fairly wellcircumscribed by a thin fibrous capsule, and measured 12.0×10.0×3.5 cm. The outer surface was soft, yellow fatty tumor with focal solid areas (). Histologically, the mediastinal mass was characterized by the presence of abundant mature adipose tissue admixed with areas containing remnants of thymic tissue (). The thymic tissue component varied from strands of atrophic thymic epithelium to large areas containing thymic parenchyma with medullary epithelial hyperplasia (). In areas, the tumor showed a frequent occurrence of polygonal, striated myoid cells with abundant eosinophilic cytoplasm (). These cells showed positive immunoreaction for desmin (1:200, clone D33, Dako, Glostrup, Denmark) and myoglobin (1:800, RB-9068-R7, Thermo, Fremont, CA, USA) in immunohistochemical study (), but negative reaction for alpha smooth muscle actin (1:400, Dako). The myoid cells also lacked cytological atypia and mitotic figures.


A 48-year-old female presented with a 6-week history of a tender mass inferior to the right inframammary fold following trauma.
Antibiotics were initiated for presumed infection; however, the mass persisted, prompting surgical referral. Clinical examination demonstrated a 2 × 1 cm superficial mass, with adjacent accessory nipple. An ultrasound confirmed a 15-mm hypo-echoic mass consistent with a sebaceous cyst; however, a core biopsy confirmed a Grade 2 invasive ductal carcinoma (IDC), strongly positive for oestrogen and progesterone receptors (Allred scores of ER 7, PR7). Immunohistochemistry for Her 2 status was negative (0).
Magnetic resonance imaging (MRI) confirmed a 22 × 12 mm spiculated (Fig. ) mass inferior to the right inframammary fold deep to the accessory nipple, compatible with a supernumerary breast. There was evidence of overlying skin infiltration, with a clear margin of normal tissue between the tumour and costal fascia. No masses were noted in either breast.
She proceeded to a wide local excision of the entire accessory breast, nipple-areolar complex and an additional ellipse of skin. Sentinel node biopsy was negative, with no further axillary dissection performed.
Histopathology revealed a Grade 2, 19-mm IDC. There was no lymphovascular invasion and radial margins were clear by >10 mm. The deep margin was 2 mm, but the anterior subcutaneous margin was 0 mm. In view of the positive anterior margin the patient proceeded to adjuvant radiotherapy.
The patient underwent a CT planning scan to assess the depth of tissue to be treated. A 10 × 7 cm rectangular electron field was applied to the tumour bed incorporating the excision scar. The patient was then treated with 9 megavoltage (MEV) electrons to a dose of 40 Gy in 15 fractions, over 21 days receiving 2.67 Gy per fraction. The Dmax treatment depth was 12 mm, with the 90% isodose at 18 mm. The ipsilateral breast was not included in the treatment field as the tumour was in a separate accessory breast which had been fully excised. The patient subsequently commenced Tamoxifen. Twelve weeks post-radiotherapy, she was in remission and all acute radiotherapy reaction had subsided.


A 73 year old Caucasian female with a history of severe osteoarthritis developed fever, pain, redness, and swelling of her left elbow one month following a revision left elbow total arthroplasty. The original arthroplasty 10 years earlier had been complicated by infection that was successfully treated with several weeks of intravenous antibiotics according to the patient; the details of this remote infection and treatment were unattainable. She was subsequently well for many years without antibiotics until about 2 years prior to presentation when she began to develop gradually progressive joint instability and pain. She was admitted for elective total arthroplasty of the left elbow. Following surgery, she noted continuous serosanguinous drainage. Her orthopedist aspirated the joint on post-operative day 22. The joint fluid was described as cloudy with 26,000 red blood cells, 1300 white blood cells and 31% neutrophils. No organisms were seen on Gram stain, and bacterial cultures were negative. Patient was not started on antibiotics at this time. A few days later (post-operative day 25) she developed progressive elbow pain and fever and was admitted to the hospital. On admission, her temperature was 102.2°F and her white blood cell count was 11,000 cells/mm.
On surgical exploration, a large fluid collection was found in the elbow. The joint capsule appeared intact, however both wound and joint fluid cultures grew S. intermedius, as identified by the Vitek II automated microbiology system without further subspeciation. The wound was irrigated but the elbow prosthesis was not removed. Blood cultures were negative. In accordance with CLSI standards, the elbow isolates were determined to be resistant to penicillin and tetracycline but susceptible to oxacillin, erythromycin, clindamycin, chloramphenicol, gentamicin, rifampin, levofloxacin, linezolid, and vancomycin. The patient was treated with intravenous cefazolin and rifampin for six weeks and then transitioned to oral levofloxacin and rifampin with plan for a prolonged course given retention of infected prosthesis. She has not had any recrudescence of disease after 10 months on this regimen and will be reevaluated for possible cessation of therapy at one year’s time.
The patient was an avid dog lover. Although she did not recall her dog licking or biting her elbow after surgery, she did report that her dog frequently licked her face. She admitted to frequent close contact with her dog including sharing her bed at night. She denied any recent illness or skin lesions in her dog.


A 3-year-old HIV-infected boy was referred for further management in January 2005. Mother was diagnosed as tuberculous pleural effusion with HIV infection with acid fast bacillus (AFB) seen on sputum examination and was on Ofloxacin (O), INH (H), and Rifampicin (R) for the same. (Details of mother's investigations are not available.) The child was currently asymptomatic. He had oral thrush and herpes simpler in the past. He had been immunized till date. On examination, his weight was 12 kg and height was 86.5 cm. He had cervical adenopathy (non-tender, non-matted) and other systems were normal. Investigations showed positive Mantoux test (20 × 22 mm) and chest X-ray was suggestive of primary complex. His venereal disease research laboratory (VDRL) test, HBsAg, and anti-hepatitis C were negative. He was started on anti-tuberculous therapy (ATT) consisting of 2 HRZE + 10 HR (Z = Pyrazinamide, E = Ethambutol). His serial CD4 counts are depicted in . ATT was stopped in January 2006. He was asymptomatic till June 2007, when we had mild molluscum contagiosum. In February 2009, at the age of 7 years, he was hospitalized with right lower zone pneumonia and his sputum was positive for AFB. He was restarted on ATT in category 2 regime as per WHO. His sputum culture grew Mycobacterium tuberculous (MTB) complex after 6 weeks and sensitivity after another 2 weeks showed resistance to Streptomycin (S) and H. He was then shifted to REZO in May 2009 and ART was started in the same period in view of decreasing CD4 count, consisting of Zidovudine (AZT), Lamivudine (3TC), and Nevirapine (NVP at 400 mg/m2/day). He was alright and chest X-ray normalized in August 2009. Ofloxacin was stopped in August 2009 and he was advised REZ for another 6 months.


A 23-year-old primigravida at 13 weeks of gestation presented to the antenatal clinic of the urban health center with urgency, dysuria and increased frequency of urine. On examination a mobile hard mass was felt in the right iliac fossa. On per vaginal examination a large bony mass was felt and a probable diagnosis of bladder stone complicating pregnancy was made. She was referred to the tertiary hospital where an ultrasound showed mild bilateral hydroureteronephrosis and a large vesical calculus measuring 8.3 cm causing dense acoustic shadowing obscuring the bladder base []. There was no significant post void residue. Ultrasound also confirmed the presence of a single live intra uterine fetus corresponding to the gestational age. Urine microscopy showed the presence of pus cells. Urine culture grew Enterococcus which was sensitive to Ampicillin.
She was referred to the urologist and underwent open cystolithotomy under spinal anesthesia. Intra operative cystoscopy revealed bladder trabeculation with stone sitting in the anterior wall of trabeculation. Two small diverticuli were seen. Right ureteric orifice was seen refluxing and pus flakes were present. On cystolithotomy a 8 × 7 cm stone was removed. Post operatively she had continuous bladder drainage for 2 weeks and was treated with appropriate antibiotics. She also received antibiotic prophylaxis till delivery. She delivered normally a live-term baby girl of Apgar 9 and 10 and birth weight 2.42 kg at 38 weeks of gestation and is on regular follow up and doing well.


An eight-year-old male child presented to the Pediatric Outpatient Department with complaints of facial asymmetry and polydactyly with bilateral microtia since birth. The child was born by vaginal delivery at a government hospital, with a birth weight of 2.5 kg. He was the second born. There was no family history of malformations. No mental retardation was detected during examination. The child showed undernourishment and weighed 15 kg (<fiftieth percentile) and a height of 110 cm (<fiftieth percentile). On physical examination, facial asymmetry, right side infranuclear facial palsy, bilateral microtia with bilateral ear tag [], short neck, high arched palate, and skin tags on the nape of the neck were present. Dental caries were present, with normal dental development. There was lower motor neuron weakness of the facial nerve on the right side, manifested by an inability to close the right eye and loss of a nasolabial fold on the same side. Asymmetric crying facies was noted with the right lower lip being pulled down while crying or chewing. Left eye closure and nasolabial fold were normal. Left preaxial polydactyly was present [], whereas, the other hand was normal. The length of both the hands was equal. His parents were normal on clinical examination. The first and third of the children, both boys, were normal.
On ophthalmological examination, the only positive finding was presence of a right-sided iris coloboma. Cardiac auscultation revealed that S1 and S2 were normal and a soft systolic murmur was present in the pulmonary area. No other abnormality was detected on systemic examination. The patient showed moderate-to-severe bilateral conductive hearing loss on audiometry. Abdominal sonography was normal. Renal function tests, liver function tests, and thyroid function tests were normal. Echocardiography and Color Doppler did not detect any cardiac lesion. X-ray examination of the skull and vertebral column did not show any vertebral abnormality. A computed tomography (CT) scan of the temporal bone revealed bony atresia of the external auditory canal, with absence of mastoid pneumatization of the right ear and left ear, showing auricular tags with bony atresia of the external auditory canal, with a deformed ossicular chain.


An 8-year-old boy was referred to the Department of Oral Surgery with chief complaint
of volume augmentation at the left side of mandible, pain and fever for about one
week. Panoramic radiograph revealed a unilocular radiolucent cystic lesion with
sclerotic border associated lateral incisor, canine, first and second premolar
crowns. Teeth were dislocated apically and medially. After local bone aspiration and
incisional biopsy, the histological diagnosis of dentigerous cyst was established
(). Analysis of capsule fragment
showed to be lined by non-keratinized epithelium. Hemorrhagic areas were also
present. Under local anesthesia, the patient was submitted to marsupialization after
extraction of the primary molars ().
The oral mucosa was sutured to the cyst capsule and iodoform gauze dressing was
inserted within lesion cavity. Medication gauze was changed every 5 days until the
wound edges were epithelialized and afterwards an acrylic plug was inserted in order
to keep wound opening and decompression. The parents were instructed to irrigate the
cavity twice a day with saline solution and the acrylic plug was fitted when
necessary, attending lumen reduction. Radiographic follow-up was performed
periodically. The involved permanent teeth erupted naturally, without any traction
forces (). Second premolar assumed an
impacted position over the first premolar probably because of dental arch space
deficiency. Thus, under local anesthesia the second premolar was removed. One year
after the first visit, the lesion had completely withdrawn, but the lateral incisor
still remained displaced. A space-maintainer was installed and the patient was
referred to orthodontic treatment ()
for correcting tooth position. The radiographic follow-up of 7 years showed no lesion
recurrence ().


A 10-year-old girl was referred to the Oral Surgery Clinic for treatment of a cyst in
the right side of the mandible found casually on a panoramic radiograph taken for
orthodontic treatment planning. The patient came without complaint but oral
examination revealed a slight swelling of alveolar mucosa related to a primary molar
and canine. The panoramic radiograph showed a segmented radiolucent area in the right
mandible body presenting a sclerotic border. Inclusion and dislocation of the
permanent canine, first and second premolars was also associated (). After local bone aspiration and
biopsy, a diagnosis of keratocystic odontogenic tumor was established. The cyst
capsule fragment presented a stratified epithelial lining with prominent columnar
basal cell layer and parakeratinized daughter microcysts were scattered in the
connective tissue wall (). In an
attempt to maintain the permanent teeth, the patient was submitted to decompression
procedure by extraction of the primary molars and insertion of iodoform gauze (). Changing of medication gauze and
acrylic plug were performed as described for Case 1. The permanent teeth went to
natural eruption and 2 years after the first visit lesion had healed (). Patient was submitted to orthodontic
treatment and radiographic follow-up of 7 years showed no lesion recurrence ().


A 22-year-old female presented to the emergency room with a 24-h history of periumbilical pain, associated with nausea, vomiting and a low-grade fever. On examination, she was afebrile but focally tender in the right lower quadrant over McBurney's point. A computed tomography (CT) scan showed a dilated appendix with fat stranding. She was taken to the operating room for laparoscopic appendectomy. Three trocars were used. The mesoappendix was divided with the harmonic scalpel, and the base of the appendix was divided with an EndoGIA stapler (Ethicon Endosurgery, Cincinnati, OH, USA). The postoperative course was uncomplicated and the patient was discharged the next day.
Six days later, the patient returned to the emergency room with abdominal pain for <12 h in the periumbilical region. The pain was worse than when she had appendicitis. She reported chills, nausea and vomiting. On examination, she was tender in the periumbilical region and mildly distended. She underwent CT scan, which showed a small bowel obstruction with a transition point in the right lower quadrant (Fig. ). She was taken to the operating room for an exploratory laparoscopy. A staple attached to the appendiceal stump on one end had snagged a loop of small bowel and small bowel mesentery with the other end (Fig. ). It was causing an internal hernia and contained a small bowel loop. The staple was freed and removed laparoscopically with no full thickness defect of the small bowel. The staple line was imbricated with intracorporeal Lembert sutures. The patient did well and was discharged the following evening.


A 47-year-old woman presented with worsening headache and neck pain over 4 days associated with nausea and vomiting. She denied subjective fevers or chills. She reported traveling to the Dominican Republic 1 month prior to presentation. She had no other medical history and was not on any medications. She denied any recent illnesses or dental procedures.
Her temperature was 38.0℃, heart rate was 70 beats/min, respiratory rate was 18/min, and blood pressures were 140/72 mm Hg. The patient had no evident toxicity and was alert and oriented to person and time but not to place. An oral examination showed good dentition with no notable abscess, pain, or gingival disease. A cardiovascular examination revealed no abnormalities, including murmurs. There was no evidence of skin infections or lesions. She had mild expressive aphasia with clear, unpressured speech. Reception and comprehension were intact. Her cranial nerves and the results of motor and sensory examinations were normal. However, she did have a shuffling gait with loss of balance to the right and clonus at the right ankle.
The laboratory parameters of the patient at admission were remarkable for leukocytosis with a left shift (17.8×109 WBCs per liter and 90% neutrophils). The results of electrocardiogram and chest X-ray examinations were normal. Computed tomography (CT) of the brain without contrast agent demonstrated a left thalamic mass with a hypodense center and hyperdense periphery. A mass effect was noted on the left lateral and third ventricles. Well-aerated paranasal sinuses and mastoid cells were noted. Magnetic resonance imaging of the brain with and without contrast agent revealed a 2.4×2.2×1.9-cm lesion with mild surrounding hyperintense T2-weighted and fluid-attenuated-inversion-recovery (FLAIR) signals compatible with edema (). The enhanced rim demonstrated a hypointense T2-weighted signal. The internal contents of the lesion were hyperintense on T2-weighted and FLAIR signals with corresponding restricted diffusion. These imaging findings were highly suggestive of a brain abscess.
Stereotactically guided drainage was applied immediately to the patient. Five milliliters of foul-smelling, purulent fluid was aspirated. The patient was initially started on vancomycin, ceftriaxone, and metronidazole after cultures were obtained. Streptococcus mitis grew in these cultures, and so the antibiotic coverage was appropriately narrowed.
The patient subsequently underwent transthoracic echocardiography (TTE) and transesophageal echocardiography with agitated-saline contrast agent injected into the right arm; the results were unrevealing. A CT scan of the chest was performed with contrast agent on postoperative day 13 due to a transient episode of hypoxia, which revealed an incidental finding of an anomalous connection between the left brachiocephalic vein and the left superior pulmonary vein. No PAVMs were noted.
Diagnostic cardiac catheterization via the left basilic vein confirmed the anomalous venous connection and the presence of a predominantly left-to-right shunt based on measurement of the oxygen saturation. TTE with agitated saline injected into the left arm this time demonstrated the passage of a large amount of bubbles into the left side of the heart. The patient recovered well after abscess drainage and was discharged to a rehabilitation facility with plans for close follow-up, and eventual percutaneous closure of the anomalous connection.


A 27-year-old male presented with complaints of progressive thickening of facial skin for past 5 years. Thickened forehead skin subsequently developed deep transverse furrows []. Associated broadening of fingers and toes with painless clubbing of nails were noticed []. Recurrent episodes of pain and swelling over knee and ankle joints had occurred over the past 1 year, for which he was prescribed steroid and non-steroidal anti-inflammatory medications causing symptomatic relief. There were no significant complaints pertaining to cardiac respiratory or gastrointestinal systems, any history of fever or recent weight loss. No other member of his family exhibited similar complaints.
On examination, the patient showed coarse facial features with increased facial skin thickness, seborrhoeic hyperplasia, deepening of nasolabial folds and furrowing of forehead skin into multiple transverse folds. Scalp skin showed furrows oriented parallel to the sagittal plane, with normal hair distribution and no fixity of skin to the underlying calvarium [].
On investigation, his haemogram, blood counts, erythrocyte sedimentation rate, peripheral smear, platelet counts, liver and renal function tests and serum electrophoresis were within the normal limits. Serum uric acid value was 4.8 mg/dl. Anti-nuclear antibody and rheumatoid factor were negative, with elevated C reactive protein value of 41.6 mg/L. Human growth hormone assay showed 1.34 ng/ml using chemiluminescence immunoassay method. Age and sex matched insulin-like growth factor 1 level was also within normal limits.
X-rays of long bones showed minimal skeletal changes with periosteal reaction involving diaphysis of fibula, without any evidence of joint effusions []. Magnetic resonance imaging showed diploic space enlargement in calvarium indicating marrow hyperplasia []. Sella turcica and pituitary glands were visualised normally. Skin biopsy showed increased pilosebaceous structures and minimal increase in perivascular and periappendageal inflammatory infiltration. Bone marrow biopsy showed minimal erythroid hyperplasia.
A frontal rhytidectomy through a browlift incision, with dissection into forehead in the subgaleal and subfrontalis planes was done. A spindle shaped excision of scalp skin and frontalis muscle behind hairline was performed. Skin was sutured without excessive tension, frontalis muscle was repaired with tacking sutures to periosteum. This procedure caused considerable improvement in his forehead furrows, though he is expected to require revision surgeries in future with progression of the disease [].