A 29-year-old man presented himself to the emergency department after noticing that his lips and fingers had turned blue. He had been on a cocaine binge preceding his admission. He estimated that he had been taking at least 14 grams over a period of five days. He felt short of breath on moderate exertion but denied chest pain or any other systemic symptoms. He had been using cocaine regularly for at least ten years, always via the nasal passageways, never injected, and denied taking any other recreational drugs. He was not on any prescription or over-the-counter medications. His only past medical history was of alcohol dependence, though he had not drunk in excess for at least ten months. There was no significant family history.
He was alert and coherent, but slightly anxious. He was apyrexial, his noninvasive blood pressure was 135/96 mmHg, and his heart rate was 85 beats/min. He was tachypnoeic with a respiratory rate of 18/min. There was marked cyanosis of his fingers and lips, and he was, immediately upon arrival in the emergency department, commenced on high flow oxygen. His saturation measured by pulse oximetry (SO2) was 86% on 15 L of oxygen given via a nonrebreathing mask. Arterial blood gasses showed H+ 50.9 nmol/L, pCO2 5.8 kPa, pO2 72.3 kPa, lactate 0.7 mmol/L, bicarbonate 26.0 mmol/L, CO Hb 0.0%. His oxygen saturation on the blood gas (O2 Hb) was 66.6% and his methaemoglobin (Met Hb) level 32.9%. Chest X-Ray, ECG, full blood count, and routine biochemistry were unremarkable.
A diagnosis of methaemoglobinaemia was made, and he received one dose of methylene blue (1 mg/kg) intravenously over five minutes. He was transferred to the high dependency unit where he continued to receive high flow oxygen and was closely monitored.
His methaemoglobin levels, as well as his saturation, improved steadily over the next hours (). He made a full recovery and was discharged home the same evening after review by the local drug addiction liaison service with no further followup.


A 32-year-old female patient presented with the complaint of a recently noticed spacing between the upper front teeth. (Figures –).
The patient noticed the spacing about 1 year before, after which she noticed it to be gradually increasing and associated with intermittent episodes of pus discharge which subsided on taking antibiotics as per advice at a local hospital. There were no associated complaints other than a cosmetic concern from the patient. There was no history of any previous dental treatment. Family history of similar complaints or early tooth loss could not be elicited. The patient was systemically healthy with no relevant medical history.
There were no abnormalities detected in extra oral examination except for a slightly tender and palpable left submandibular lymph node. Full complement of teeth was present. The oral hygiene status of the patient was good as revealed by the oral hygiene index. There was minimal amount of calculus and plaque. There was grade I mobility of 22, 31, 32, 21 and 22. Proximal contacts were lost between the teeth 14 and 13, 13 and 12, 21 and 22 and 22 and 23, 22 and 24 and between lower anterior teeth. There was labial migration and flaring of upper and lower anterior teeth with an evident distolabial migration of 22.
Gingival examination revealed normal color except for the labial aspect of 22 where it was slightly reddish. The margins were of knife-edge contour except for the labial aspect of 22 and 42 where it was bluntly rounded. The gingiva was firm and resilient except in the region on 22 where it was soft in consistency. There was no loss of stippling in the anterior regions. The position of the gingival margin was apical to the CEJ in the labial aspect of 22. There was generalized bleeding on probing, and exudation was present on the labial aspect of 22. All together there were minimal signs of inflammation other than bleeding on probing.
A full-mouth periodontal charting revealed generalized periodontal pockets and clinical attachment loss ().
Pockets were especially deeper in the molar and incisor regions with slightly lesser involvement in the premolar region. The clinical attachment loss ranged from a maximum of 10 mm in the midpalatal aspect of 16 to a minimum of 2 mm in the premolar regions.
An OPG and full-mouth IOPA X-ray were performed which revealed the generalized distribution of alveolar bone loss which was a combination of both horizontal and vertical bone loss (). Routine blood examination results were within normal limits.
Based on the history, examination findings, and the radiographic findings, a diagnosis of generalized aggressive periodontitis was made according to the criteria by AAP 1999 classification.


A 26-year-old male patient presented with the chief complaint of generalized pus discharge from gums which he had been experiencing intermittently for the past 2 years (Figures and ). Pus discharge was associated with bad breath and usually subsided spontaneously after a few weeks. There was no associated complaint other than a generalized mild hypersensitivity to cold and sweet food. He had a history of extraction of lower left posterior tooth due to caries exposure and extraction of lower front tooth due to mobility about 1 year before. There was no history of any other dental treatment.
The patient was systemically healthy, and medical history did not reveal any relevant findings. Family history revealed that the patient's mother had similar complaints of mobility, pus discharge, and spontaneous exfoliation of some teeth following which she consulted a dentist and underwent total extraction by the age of 40. The patient was a nonsmoker, and there was no history of use of any other forms of tobacco.
Extraoral examination revealed bilateral submandibular lymph node enlargement, which was firm, mobile, and nontender.
All teeth were present except for 46, 26, and 41. Tooth 46 was extracted due to caries and 41 was extracted due to mobility. Tooth 26 was grossly decayed with just root stump present. The oral hygiene status of the patient was fair with moderate deposits of calculus and plaque.
Intraoral examination revealed a normal color of gingiva except in the labial aspect of 31, 32, and 33 where the marginal gingiva was slightly reddish. Gingival margins were rounded, and exudation was present in relation to labial aspects of mandibular anterior teeth and maxillary central incisors. There was generalized bleeding on probing and recession in relation to most of the teeth, especially more in maxillary central incisors and mandibular anterior teeth.
There was grade I mobility of 15 and 22 and grade II mobility of 11, 12, 21, 31, 32, 33 and 42. Proximal contacts were lost between maxillary and mandibular anterior teeth with pathologic migration of 11, 21, 31, 32, and 42 and extrusion of 31. Grade II furcation involvement was present with molars and maxillary first premolars. A full mouth periodontal examination revealed generalized deep periodontal pockets and severe generalized clinical attachment loss ().
Severe periodontal destruction was evident with more than 10 mm of clinical attachment loss at multiple sites especially in the incisor and canine regions.
OPG and IOPA X-rays revealed a generalized distribution of periodontal bone loss especially severe in the incisor and canine regions with the molars and premolars affected to a lesser degree (). There was predominantly vertical bone loss in the canine and incisor regions. Routine blood investigations were within normal limits.
A diagnosis of generalized aggressive periodontitis was made according to the established criteria (American Academy of Periodontology, 1999).


A 59-years-old man with nonischemic dilated cardiomyopathy was admitted to the Emergency Department after receiving a shock from his ICD, which was preceded by dizziness. The dual-chamber ICD (Medtronic EnTrust, Minneapolis, MN, USA) was implanted two years earlier for primary prevention of sudden cardiac death. At the time of device implantation, patient was in sinus rhythm with normal PR interval (170 ms) and therefore it was programmed to AAI+ mode (MVP™) at 60 bpm. Therapies were programmed as follows: 1) VT zone at 176 bpm: anti-tachycardia pacing (ATP) (Burst x3, Ramp x2), followed by shock (30J, 35J x3); 2) VF zone at > 200 bpm: shock (30J, 35J, 35J x4) with ATP During Charging™.
Device interrogation currently demonstrated normal function. Two episodes of ventricular arrhythmias were logged by the device, both of them in the VF zone. The first one terminated spontaneously and no therapies were delivered. The second episode occurred the following day and was terminated after a shock. In the present case, both episodes can be explained by the same mechanism.
shows the dot plot and cardiac electrograms (EGMs) during the episode treated with shock. In the beginning, patient rhythm was atrial pacing (AP) with intrinsic atrioventricular (AV) conduction and ventricular sensed events (VS). However, some VS events occurred before AP, indicating premature ventricular complexes (PVCs). Suddenly, there is an increase in the ventricular rate to a CL of 170-240ms, which fell into the VF detection zone and was successfully treated with a 30J shock. The EGM before the tachycardia episode shows a device pacing initially in AAI mode. This is inferred form the fact that the AV interval is longer than the programmed sensed AV interval (160ms). The first AP beat is followed by a VS event, representing normal AV conduction. The second and third beats are PVCs with retrograde atrial conduction (AR). According to the MVP algorithm, after a PVC, AP is inhibited and a new ventriculo-atrial escape interval is started. After these PVCs, the absence of intrinsic atrial activity resulted in an AP beat. The sequence of couplets of PVCs, separated by a long pause was the responsible for a short-long-short (S-L-S) sequence, which triggered VT.


An 84-year-old woman was admitted to our hospital due to fever, abdominal pain and nausea, in May, 2011. At the age of 81 she has been diagnosed as Churg-Strauss syndrome and has been treated by prednisolone (7.5 - 10 mg/day). After the steroid treatment started, she developed steroid-induced diabetes, and her diabetes has been treated by premixed insulin (insulin lispro mix 50/50, 14 units before breakfast and 6 units before dinner). On the admission, her body temperature was 37.9 oC and blood pressure was 154/95 mmHg. Physical examination revealed pain and muscular defense in her abdomen. Her body weight was 43 kg and height 148 cm (BMI 19.6 kg/m2). Fasting plasma glucose level (150 mg/dl) and hemoglobin A1C level (6.8%; normal range, 4.3 - 5.8%) were elevated. Laboratory data showed increased leukocyte counts (23,600/μl). Serum levels of asparatate aminotransferase (73 U/l; normal range, 10 - 40 U/l), alkaline phosphatase (374 U/L; normal range, 115 - 359 U/L), γ-glutamyl transpeptidase (61 U/L; normal range, < 30 U/L) and C-reactive protein (15.1 mg/dl; normal range, 0 - 0.3 mg/dl) were significantly elevated. Abdominal ultrasound showed enlarged and distended gallbladder containing debris, and thickness of the wall of gallbladder (). Abdominal enhanced computed tomography (CT) also revealed enlarged gallbladder and thickness of the gallbladder wall, and ascites around gallbladder, however, CT did not show a conical structure connecting the gallbladder to the liver (). From abdominal ultrasound and CT findings, leukocytosis and her history of diabetes and steroid use, we diagnosed her as having peritonitis due to acute bacterial cholecystitis or perforation of gallbladder, and she was referred to the department of Surgery. Abdominal operation revealed the necrosis of gallbladder by torsion due to a floating gallbladder (). The perforation of gallbladder wall was not detected.


A previously healthy 25-year-old-Asian woman was referred for evaluation of an enlarging, painless, subcutaneous mass located intergluteal fold. It was clinically diagnosed as a pilonidal cyst by previous examiner. She could remember that a mass had been present in this region for 2 years. During the 2-year period the mass had slowly increased in size from less than 0.5 cm to over 2.5 cm in diameter. During the past few months, the mass had become tender and sometimes making it uncomfortable to sit down. There was no history of urinary or faecal problems. Physical examination revealed a 2 × 3 cm sized, solid, mildly tender, mobile mass over the coccyx. It was well circumscribed proximally but not in distally on palpation. Neurological examination was normal.
Magnetic resonance imaging (MRI) revealed a 6 ×3 cm well-circumscribed subcutaneous mass located over the coccyx. This tumor was comprised of two ovoid mass and there was no direct invasion to the coccyx (). Ultrasonography (USG)-guided needle biopsy was performed and microscopic examination showed a myxopapillary ependymoma. Computed tomography (CT) scanning of the thorax and abdomen demonstrated no evidence of lung or liver metastases. Isotope bone scanning revealed no evidence of skeletal metastases.
The mass was completely excised. Intraoperatively, the lesion was seen near the tip of the coccyx and well-circumscribed. It was composed of two ovoid but contiguous masses, the larger 3.0 × 2.5 × 1.5 cm, and the smaller 1.2 ×1.0 ×0.8 cm (). The histology of the specimens again confirmed a myxopapillary ependymoma (). Her postoperative course was uneventful and no adjuvant therapy was offered.
During 2 years of follow-up no local recurrence or metastasis were detected, with chest radiography and abdomino-pelvic MRI ().


A 35 year old female patient presented to the ENT out patient department of the Lok Nayak Hospital, Delhi, with chronic nasal obstruction, excessive sneezing, nasal discharge and frontal headache since several months. Nasal obstruction was of gradual onset, non progressive, more on the left side than right. Nasal obstruction did not respond to standard medical treatment and was of recurrent nature. The nasal discharge was intermittent, purulent and nonfoul smelling. There was no history of hemifacial pain, ear discharge, ear ache, nasal trauma or previous nasal surgery. No history of any allergies to drugs or food products was present. Systemic history was uneventful.
On examination the nose showed external parrot beak deformity and there was mild external deviation of the nose to the right. Nasal septum was deviated to right inferiorly, and towards left superiorly. There was Candal deviation to left. Nasal patency was decreased on the right side and Cottle's test was positive. No sinus tenderness could be elicited.
Differential leukocyte count of the patient showed eosinophilia suggesting an allergic etiology and the Non Contrast CT PNS revealed a deviated nasal septum towards right, bilateral concha bullosa, mucosal thickening in left frontal recess, left anterior ethmoidal air cells and right sphenoidal sinus and bilateral inferior turbinates. Near total opacification in both maxillary sinuses with blocked osteomeatal units were seen (). There was no bony erosion or invasion on CT scan. The major CT feature of allergic sinusitis is the presence of a soft tissue mass within the involved sinus, seen on unenhanced studies (). Failing any improvement on medical therapy, bilateral fibreoptic endoscopic sinus surgery with septoplasty was planned under GA and the biopsy was excised and sent for fungal culture.
Both Gram staining of the impression smears of the tissue crushed between two sterile slides and 10% KOH preparation showed the presence of fungal hyphae. Biopsy material was inoculated on a set of Sabouraud dextrose agar with and without antibiotics and one tube of each set was incubated at 22°C and 37°C respectively. On the 5th day of incubation, a black colored wooly growth was seen in all four tubes. The LPCB preparation of the growth showed phaeoid septate hyphae with internodal branching and macroconidia with alternate septations similar in morphology to Alternaria, but the presence of verrucose, muriform macroconidia borne from short geniculate conidiophores showing 2-3 transverse septa and 1-2 longitudinal and/ or oblique septation indicated towards Ulocladium spp. A slide culture was done and the absence of chains of macroconidia ruled out Alternaria spp. and confirmed the fungi to be Ulocladium botrytis morphologically ().


A 57-year-old Greek man was referred to our facility with pain, hemorrhage and a gangrenous smell due to a so-called wound on his penis. A physical examination revealed the complete absence of his penis and a large chasm in the lower abdominal wall, which made it possible to see parts of the lower pelvis, such as the spermatic cords, the destroyed basis of the corpora cavernosa and the residual stump of the urethra. The scrotum and the testicles were stiff and were possibly invaded by the cancer. In the chasm margins, we could detect hemorrhagic and necrotic areas (Figure ). The inguinal lymph nodes were palpable, hard and mobile. Our patient was in a good general condition and his body temperature was normal. From his medical history, he had discovered a lesion in his inner prepuce 18 months before. He had requested medical advice at a private health center concerning that lesion. According to his recollection, a biopsy had been taken and he was diagnosed as having penile cancer (this biopsy could not be found, as he did not ask for a copy of it at the time and the private health center failed to track our patient's data as he was never hospitalized there). The physicians at the time suggested he should undergo a partial penectomy, but he refused and stopped seeking medical treatment.
The lesion slowly progressed, eventually involving the whole penis. He could not specify the exact time his penis sloughed off completely. He was not circumcised. Standard laboratory test results showed that his values were within normal limits except for a small rise in white blood cell count (14,750 cells/μL) and microcellular anemia (hemoglobin = 9.8 g/dL, hematocrit = 31.2%). A chest X-ray did not show any remarkable findings. An abdominal computed tomography (CT) scan showed lymph nodes of a pathological size and number, bilateral in the iliac vessels and inguinal areas as well as an erosion of the pubic bone (Figure ). We proceeded with a chest CT scan, which did not show any distant metastases or lymph nodes. On the first day of his hospitalization, we obtained biopsies from the chasm margins and identified a poorly differentiated SCC. The clinical staging was T4N3M0 and our patient was treated with chemotherapy and regional radiotherapy. We also performed a bilateral cutaneous ureterostomy, with a Gibson incision in order to protect the corroded tissues from further urine impregnation (Figure ). From a combination of regional radiotherapy and bilateral cutaneous ureterostomy, total dryness of the wound was achieved. During his extended hospitalization, he presented with deep vein thrombosis in the right shin vein and seizures that were attributed to small ischemic brain strokes after a brain CT scan. Debulking and flap coverage of the wound was not considered possible, firstly because of deep vein thrombosis, epileptic seizures and his poor general condition increased the risk from operation and secondly the size of the chasm combined with very poor vascularization of the region (a topical angiography was performed). Gradually, our patient developed depression, denial of feeding and loss of weight. He died 18 months after his first admission and six months after his last follow-up admission to our clinic.


In June 2008, a 57-year-old male was found drifting in the sea at 08:07 a.m. The seawater temperature was 12°C. Emergency medical technicians confirmed his cardiac arrest at the port at 08:28 a.m., and his electrocardiogram showed asystole. He was brought to our emergency department (ED) at 08:51 a.m. A core body temperature of 22.0°C was registered in the rectum, and his pupils were fixed and dilated (Figure ). Although we continued standard CPR with tracheal intubation and external rewarming using warmed infusions and radiant heat, the patient's temperature remained at 22.8°C 30 min after arrival. In addition, sputum comprising massive bubbles resembling seawater was evident in his endotracheal tube. Because he had been in cardiac arrest for at least 90 min, we were stumped about whether to continue resuscitation or not at that time. However, we found that spontaneous slight gasping breathing without a pulse and chest compressions appeared at 09:24 a.m. We then decided to apply CPB (cannulated from right femoral vessels) for rewarming and circulation because we suspected that the cause of his cardiac arrest was severe accidental hypothermia rather than hypoxia due to drowning. After we started CPB at 09:55 a.m., although his electrocardiogram showed asystole at first, it changed to ventricular fibrillation (VF) of low amplitude as his temperature rose, and its amplitude slowly increased. His condition changed from VF into sinus rhythm without defibrillation at the time point when his temperature reached 26.7°C (10:22 a.m.). Soon, movement of his limbs appeared, the size and reactivity of the pupils became almost normal, and spontaneous breathing became adequate. Aspiration of a large amount of seawater was suspected from the thoracic radiography (Figures , ). However, head CT showed no hypoxic changes such as diffuse swelling at that time (Figure ). CPB was discontinued at 01:25 p.m. because of his hemodynamic stability with catecholamine treatment, which was started at 34°C. After neurological rehabilitation, he was discharged without any neurological deficits on day 32.


A 65-year-old man was referred on April 2010 to our surgical department with histologically documented metastatic thyroid carcinoma on biopsy samples taken from a pathological fracture of his left femur. He had already undergone orthopedic stabilization of the fracture followed by adjuvant radiotherapy. Staging work-up with Computed Tomography (CT) documented a tumor in the right lobe of the thyroid, multiple cervical supraclavicular and axillary lymph-nodes, multiple bone metastases and liver metastasis (Figure ). Aspiration biopsy cytology of the neck and axillary lymph nodes showed malignant thyroid follicular epithelium-derived cells. Levels of serum thyroglobulin and anti-thyroglobulin antibodies were 102815,0 ng/mL and 727,4 IU/ml, respectively.
We treated the primary thyroid tumour with a near-total thyroidectomy including central plus right neck dissection and the addition of right axillary lymph node dissection.
On gross pathological examination, the thyroidectomy specimen weighted 74 g; the right lobe was enlarged, measuring 7.5 × 3.5 × 3 cm. The cutting surface showed a solid nodule, 3.8 × 2.5 cm in size at the apex of the right lobe. Microscopic examination of the thyroid tumor showed a follicular neoplasm with two growth patterns: micro- and macrofollicular areas alternating with predominantly cribriform and solid/insular areas. A thick, fibrous capsule was still evident around the nodule although it was completely invaded by the tumor; extensive vascular invasion, within and beyond the tumor capsule, was also observed.
Histologically, the cuboid neoplastic cells had eosinophilic cytoplasm; a striking feature was represented by their frequent cytoplasmic vacuolization, with formation of "signet ring cells" having prominent cytoplasmic vacuoles with eccentric nuclei. Colloid-like material was found in micro-macrofollicular areas; focal mucoid secretion within glandular lumens and inside the "signet ring" cells too was highlighted by mucicarmine and Alcian-blue staining; 7/22 cervical lymph nodes, 5/23 axillary lymph nodes showed massive infiltration/total substitution by a follicular cell derived carcinoma with three peculiar cell types: 1) cylindrical, eosinophilic cells with apical snouts, arranged in follicle-like structures; 2) oxyphilic cells with abundant granular cytoplasm and strong nuclear pleomorphism; 3) cuboid cells with vesicular, round nuclei with deeply eosinophilic nucleoli, nuclear pseudoinclusions and a focal papillary growth pattern were also evident. Immunohistochemistry was performed using a peroxidase-antiperoxidase complex method. Neoplastic cells, both in the primary thyroid tumour and in the lymph node metastases, showed intense and diffuse staining for thyreoglobulin (TG) and thyroid transcription factor (TTF-1), while carcino-embryonic antigen (CEA) and CD15 stainings were negative. In areas with solid growth, p53, bcl2 and E-cadherin were intensively expressed, and a Ki 67 staining ratio of > 10% was found. A diagnosis of poorly differentiated follicular carcinoma with "signet ring cells" and Hürthle- cell features was made (Figure ).
The disease stage according to the AJCC criteria was IVc. The patient received 260 mCi of 131I in May 2010 and 260 mCi of 131 I in October 2010. Radioiodine whole body scan performed after completion of treatment still detected multiple metastatic lesions (Figure ). One year later, the patient is alive with persistent, stable disease and, on a background treatment with levotiroxine 150 mcg per day; TSH approaches 0.5 uIU/mL and thyroglobulin has lowered to 44.000 ng/ml.


Our patient was a 41-year-old Caucasian woman who presented to our Rheumatology clinic for evaluation of progressive exercise intolerance, fatigue, diffuse myalgias, arthralgias and difficulty sleeping. The pain primarily involved her entire back and arms, and she reported multiple tender points all over her body. On the basis of her symptoms, our patient had also been diagnosed with fibromyalgia, and was treated with multiple different medications without any relief.
Her other medical history included hypothyroidism, cervical disc disease, hypertension and Raynaud's disease. Notable family history included breast carcinoma and hypertension in her mother, and lymphoma in her father. Her medications at presentation included lisinopril 5 mg daily and levothyroxine 25 μg daily. Other pertinent medications she had previously used included pregabalin, amitriptyline and gabapentin. Her physical examination results were normal except for mild tenderness to palpation along her upper and lower back, and shoulders.
Significant laboratory results included creatine kinase (CK) = 325 U/L (normal range 0 to 150 U/L), normal comprehensive metabolic panel (CMP) and complete blood count (CBC), liver function tests and thyroid functions tests. A six-minute walk test revealed a normal resting lactic acid = 1.6 mmol/L, and an elevated post-six-minute-walk lactic acid = 5 mmol/L (normal result < 2 mmol/L). Her ammonia levels were normal at rest and after six-minute walk (14 μmol/L and 38 μmol/L respectively; normal 0 to 40 μmol/L). A muscle biopsy was performed for biochemical evaluation, which revealed several abnormalities including decreased levels of citric acid synthase (49% of normal), cytochrome c oxidase (53% of normal), succinate dehydrogenase (72% of normal), and nicotinamide adenine dinucleotide (NADH) dehydrogenase (73% of normal), thereby demonstrating a defect in the mitochondrial respiratory chain. Genome sequencing was performed, which revealed multiple POLG1 polymorphisms (C-T polymorphism at 2254, and G-T polymorphism at 3708) and several mitochondrial genome polymorphisms (1438 A-G, 3992 C-T, 14365 C-T, 14582 A-G, and 4042 A-G).
Our patient was started on a compound of Co-Q10 200 mg, creatine 1000 mg, carnitine 200 mg and folic acid 1 mg to be taken four times a day. She gradually showed significant improvement in her symptoms over a course of several months.


An 84-year-old Asian man was admitted to hospital for dyspnea and was found to have a large, recurrent right-sided pleural effusion. This was the third time our patient presented with an effusion since the initiation of rifampin, isoniazid, pyrazinamide and ethambutol (RIPE) therapy for presumed extrapulmonary TB. Nine months prior to this presentation, our patient underwent a screening colonoscopy with a biopsy that reportedly yielded a single granulomatous, acid-fast stain-positive, but TB culture-negative lesion. No anti-TB treatment was initiated at that time. The purportedly acid-fast stain-positive specimen could not be located subsequently for re-review. A repeat colonoscopy with biopsy at six months demonstrated no granulomas or other evidence of TB. There was no radiographic evidence of pulmonary TB and interval sputum cultures were negative, as was a serum QuantiFERON-TB Gold test. Nevertheless, our patient was started on RIPE combination therapy.
Four weeks after the initiation of this regimen (two months prior to the episode described in this report), our patient complained of dyspnea, cough and weakness. He was admitted to hospital with the initial right-sided pleural effusion presentation (Figure ). Thoracocentesis yielded exudative, culture- and stain-negative pleural fluid (Table ). Our patient was given a presumptive diagnosis of a paradoxical tuberculous effusion and discharged on a tapering course of systemic glucocorticosteroids while he continued on RIPE therapy. Two months later, he was re-admitted with a similar clinical picture. A further liter of exudative fluid was removed by repeat thoracocentesis (Figure and Table ).
Two weeks later, a re-accumulated pleural effusion led to the admission we report (Figure ). Our patient underwent a video-assisted thoracoscopic surgical biopsy. The pleural fluid again demonstrated a lymphocytosis with benign cytology and an adenosine deaminase assay yielded a value of 23.8 units per liter (Table ). Multiple pleural biopsies demonstrated inflammation without any well-formed granulomata. All cultures of pleural fluid and biopsies were TB negative. Our patient's pleural fluid, which had not been tested serologically on previous thorocenteses, manifested a low complement with a total complement activity (CH50) of 10, but was antinuclear antibody (ANA) negative. The serum ANA titer, however, was elevated to 1:160 with a speckled pattern, while a serum antihistone assay was negative. The isoniazid was discontinued, although rifampin and ethambutol were continued to complete a nine-month course as recommended by the infectious disease subspecialty consultants. There have been no further pleural effusions over two years of follow-up.


A 57 years old Caucasian male presented with recurrent nausea, vomiting, abdominal pain and diarrhea for the past 1 - 2 years. Patient stated he had multiple episodes of retching and bilious vomiting in the past 24 hours, with one episode of hematemesis 2 hours before coming to the emergency department. He had no prior episodes of hematemesis.
He described his abdominal pain as diffuse, was occasionally sharp initially, with residual dullness which slowly resolved over 24 - 36 hours. The pain was not associated with food, and not relieved or worsened with bowel movements. His stool had been of regular caliber, color and consistency, and he had approximately 1 bowel movement daily.
His history dated back approximately twenty years ago when he started complaining of dyspepsia. He was treated at an outside hospital for H. Pylori, and remained relatively well controlled until seven years prior to admission when he started to notice discrete episodes of malaise, followed by 1 day of loose watery stools, then another day of intense bouts of bilious but non bloody emesis (up to 30 episodes a day) which would leave him with (usually) dull abdominal pain that gradually resolved over the next 2 days.
Besides associated flushing and diaphoresis with the diarrhea, he could not state any triggers or associated symptoms. He endorsed a 20 lb weight loss in the past year. No constitutional symptoms, such as heartburn, dysphasia, odynophagia, bright red blood per rectum or steatorrhea were found.
His past medical history was significant for an incidental discovery of a renal mass on MRI (magnetic resonance imaging) two years previous, with eventual left nephrectomy for renal cell carcinoma (RCC) soon after discovery. He also had a history of ‘gastroenteritis’, hyperlipidemia, and chronic back pain.
The patient’s medications included Omeprazole 20mg QDay, Gabapentin for CBP, Loperimide Q8 hours prn loose stools, Psyllium husk BID for constipation, and PRN vicodin for chronic back pain. He had no known drug allergies. Family history was pertinent for a mother with Crohn's disease and a sister with migraines. The patient denied tobacco, alcohol, and drug use.
On physical examination, patient’s vitals were normal and stable. He appeared as a thin male in no apparent distress, but looking fatigued. His abdomen was flat with a visible well-healed nephrectomy scar at the left lower quadrant. Bowel sounds were present in all 4 quadrants. All other parts of the physical exam were within normal parameters. Complete blood count, basic metabolic panel, liver function tests, and coagulation markers returned in the normal ranges. Urine analysis was clear with a pH of 7 and nitrite and leukocyte esterase negative.
Imaging included a CT (computed tomography) of the abdomen/pelvis on six months prior that was read with questionable findings of ‘probable wall thickening of colon and possible distal ileum, raising possibility of inflammatory bowel disease or an infectious process.’ Also a left renal lesion was seen.
An esophageal gastroduodenoscopy (EGD) on four months prior revealed a 5cm hiatal hernia, acid reflux esophagitis, and cobblestone appearance of stomach of unclear clinical significance. Biopsy results showed mucosa without significant pathological change in most of the stomach with minimal reactive gastropathy in the antrum.
Colonoscopy four months prior showed colonic mucosa without significant pathologic changes and lymphoid mucosa. A tubular adenoma polyp was seen at 40 cm of the colon, a tubular adenoma polyp at the cecum, and a rectal hyperplastic polyp. Histopathological features in these biopsies were not commensurate with a diagnosis of inflammatory bowel disease.
A current EGD showed a hiatal hernia with a Mallory Weiss tear. A Schatzki ring was present.


A 50-year-old woman presented to Ophthalmic Emergency Department with sudden onset proptosis and decreased vision in her left eye of 2 hours duration. She had history of systemic hypertension and was on atenolol 100 mg daily. She had no history of trauma or any ocular disorder.
On ophthalmologic examination, the right eye was normal but the left eye had no light perception, intraocular pressure (IOP) of 50 mmHg, profound relative afferent pupil defect, severe proptosis, frozen eye, subconjunctival hemorrhage and periorbital ecchymosis (). A prominent bruit was heard over the globe. Intravenous mannitol was initiated and lateral canthotomy was performed to control the raised IOP.
Orbital computed topography (CT) scan revealed proptosis, a dilated superior ophthalmic vein, enlarged orbital muscles, and intraocular hemorrhage (). Magnetic resonance angiography (MRA) and selective carotid angiography showed a high flow arteriovenous shunt (). The patient was then transferred to the neurosurgery department for further management, but she refused to undergo surgery because of possible complications. Therefore, she was recommended to undergo manual carotid compression. Two months later, she had mild proptosis and congested conjunctival vessels, but visual acuity was unchanged at no light perception ().


A 50-year-old African American man with sickle cell disease (SCD), transfusion-associated iron overload and stage III chronic kidney disease was admitted to our hospital with fever, shortness of breath and tachypnea. He was found to have bilateral lung crackles, leukocytosis and bilateral basilar infiltrates on chest radiography. Our patient reported a 15-pound weight loss and an increased frequency of bone pain over a period of six months. His medications included hydroxyurea and deferasirox. He was treated for painful sickle crisis and community-acquired pneumonia with analgesics, oxygen and antibiotics. He showed an initial improvement in clinical condition. He received repeated blood transfusions for his worsening anemia but did not show a subsequent increase in his hematocrit. His refractory anemia workup did not support any active bleeding or hemolysis. His reticulocyte count was 1.2% and his parvovirus B19 antibody assay was negative. A peripheral smear showed anisocytosis and Howell-Jolly bodies, but no schistocytes.
Our patient deteriorated four days after admission, with drowsiness, disorientation and slurred speech. A physical examination was unrevealing and a neurological examination showed no focal deficits. His electrolytes, blood urea nitrogen, creatinine, blood and urine cultures and brain imaging were indeterminate. His serum ammonia level was 81 μmol/L; he was started on lactulose with no clinical response. His opioid medications were decreased and he was given naloxone without improvement in his mental status. By the seventh day, he was stuporous. His family began to consider a 'comfort measures only' goal of care.
This case was a diagnostic quandary. To decipher the cause of the refractory anemia, bone pain and change in mental status we focused on the surprising finding of a serum anion gap (AG) of zero (Table ). His outpatient AG over the last six months had been between three and four. Further testing revealed that he had decreased serum albumin (2 g/dL), elevated serum protein (12.6 g/dL) and increased gamma globulin (7.5 g/dL). Immunofixation showed an immunoglobulin G monoclonal protein with kappa light chain specificity. Bone marrow analysis revealed 70% plasma cells, confirming the diagnosis of multiple myeloma (MM) (Figure ). He was treated with dexamethasone (Decadron) and melphalan hydrochloride and made significant improvement, returning to his baseline functional status within 14 days.


Our patient was a 35-year old Caucasian woman with CP of unknown etiology. Her main complaint at the time of the consultation was severe chronic abdominal pain refractory to narcotic pain medication. Additionally, she was experiencing nausea and vomiting. Her pancreatic function was normal, with a hemoglobin A1C level of 5.4% and basal C-peptide level of 1.3 ng/mL. The history of her present illness was significant for several episodes of recurrent pancreatitis over the past six years after undergoing an open cholecystectomy with subsequent removal of a retained common bile duct stone by endoscopic retrograde cholangiopancreatography (ERCP). Her past medical history was also significant for psoriasis and heavy alcohol consumption, which likely contributed to the subsequent development of CP, although she reported abstinence for the past year.
At the time of her admission, an ERCP was performed and demonstrated the presence of a previous sphincterotomy and a dilated common bile duct of approximately 11 mm without filling defects. A stricture of her main pancreatic duct was observed at the level of the ampulla of Vater; dilatation of the remaining portion of the pancreatic duct was present. An endoscopic ultrasound was performed and revealed sonographic changes consistent with mild CP (2.5 mm pancreatic duct, heterogeneous parenchyma) according to the Cambridge classification []. Magnetic resonance cholangiopancreatography and computed tomography of her abdomen were also performed and demonstrated findings consistent with those observed in the ERCP. Given the young age of our patient, we gave priority to surgical therapy to avoid additional endoscopic procedures. After discussing the various therapeutic options with our patient, she chose an RA-PPPD, for better drainage of the distal pancreas and pain relief. Additionally, in consideration of her young age and the future unknown fate of the pancreatic remnant, our patient was offered AIT to preserve endocrine function.
After induction of general anesthesia, our patient was placed in the lithotomy position, with slight reverse Trendelenburg, and her abdomen was prepared and draped in the usual sterile fashion. Trocars were placed as indicated in Figure . The Da Vinci robotic surgical system (Intuitive Surgical, Inc. Sunnyvale, CA, USA) was docked into position, with a viewpoint from our patient's head. We mobilized the right colonic flexure, exposed the second portion of her duodenum and completed mobilization of the pancreatic head. The pancreatic head was enlarged and fibrotic. Next, her hepatic hilum was dissected, her common hepatic artery was exposed and her right gastric artery was ligated. The origin of her gastroduodenal artery was prepared with a vessel loop but not divided (Figure ) to preserve the blood supply to the head of the pancreas. The dissection of her gastrocolic ligament was completed, exposing the inferior border of her pancreas and the pancreatic neck. The neck of her pancreas was prepared and her superior mesenteric vein was widely exposed. Next, the pylorus was prepared; her right gastroepiploic artery and vein were divided. The first portion of her duodenum was divided 2 cm distal to the pylorus using a stapling device. The first loop of her jejunum was transected using a stapler device as well. Her duodenum was retracted, exposing the uncinate process. Subsequently, her common bile duct was transected and the dissection was conducted in the neck of her pancreas, dividing the pancreatic neck with the Harmonic scalpel. Her pancreatic duct was enlarged, measuring approximately 3 mm to 4 mm. The dissection proceeded cautiously until the entire head of her pancreas was connected only to her gastroduodenal artery and superior pancreaticoduodenal vein. Immediately before the transection, a small Pfannenstiel incision was made; a hand access device (Lap Disc, Ethicon, Cincinnati, OH, USA) was inserted with the aim of preserving the pneumoperitoneum. At this point, her gastroduodenal artery and superior pancreaticoduodenal vein were clipped and divided (Figure ). The specimen was placed in an endobag and extracted immediately through the mini laparotomy previously performed. Her pancreas was flushed with University of Wisconsin solution on the back-bench and brought to the islet isolation facility in a sterile bag on ice for processing.
In the interim, the reconstruction phase of the operation was initiated. A pancreaticogastrostomy was performed. Next, a retrocolic end-to-side hepaticojejunostomy was created with the first loop of her jejunum. The last anastomosis was an end-to-side two layer pylorojejunostomy, 40 cm distal to the hepaticojejunal anastomosis. Once the reconstruction was completed, her inferior mesenteric vein was dissected and canulated with a 16-gauge canula in preparation for the islet cell infusion.
The islet isolation procedure was conducted as previously described []. In brief, the pancreatic duct was canulated and injected with a purified collagenase solution (Serva, Heidelberg, Germany). The pancreas was cut into small pieces and placed into a modified Ricordi digestion system. Under microscopic control of repeat samples, the digestion was stopped by dilution and cooling as soon as 50% of the islets were free from the exocrine tissue. The digest was collected and washed under repeat centrifugation. After a quality assessment the islet preparation was placed into several syringes and brought into the operating room. The islets were successfully infused into the portal stream and her inferior mesenteric vein was subsequently ligated (Figure ). To conclude, two Jackson Pratt #10 drainages were placed - one adjacent to the pancreatic anastomosis and one underneath her liver.
Our patient tolerated the procedure well. The weight of the resected pancreas portion was 47 g, after trimming of non-pancreatic tissue. Fifteen milliliters of tissue containing 134,727 islet equivalent (IEQ; 2867 IEQ per gram of pancreas or 2449 IEQ per kilogram of the recipient body weight) were collected. The viability of the tissue was 97%, as measured by propidium iodide and cytogreen fluorescent staining. The operation lasted six hours and thirty minutes, with an estimated blood loss of 200 mL. Our patient was maintained on an intravenous insulin drip during the first two days after the operation. She was subsequently transitioned to 4U to 6U of long-acting insulin daily. Our patient's recovery was uneventful; her C-peptide level on the eighth postoperative day was 2.2 ng/mL. She was discharged home on the ninth postoperative day with pain improvement and was maintained on low dose insulin. During her last follow-up 45 days after the surgery, she was normoglycemic without any insulin injection and reported complete resolution of her pain.


A 16-years-old female presented with a history of severe abdomino-pelvic pain, which increased lasting 2 to 7 days with each of her menstrual cycles, hindering her daily activities.
Gynecologic history indicated menarche at 13 years of age, followed by 3 years of irregular menses.
The patient denied any recent abdominal trauma, abnormal vaginal bleeding, nausea, vomiting or diarrhea.
A bimanual physical examination indicated a right-sided cystic and tender pelvic mass, movable, mildly tender to palpation. The medical staff recommended further evaluation such as US, which showed the absence of right kidney and the possibility of uterine anomaly; so Magnetic Resonance Imaging (MRI) was performed in order to evaluate the possible genito-urinary anomaly.
The MRI examination was performed on a 1.5 Tesla MR clinical scanner (Siemens, Avanto Erlangen Germany). The patient's mother gave her informed consent for MRI exam. Images were acquired on multiple planes with T1-weighted (TR 714 ms; TE 12 ms) and T2-weighted Turbo Spin Echo (TR 5530 ms; TE 150 ms) sequences; fat-suppressed T2-weighted TSE images (TR 6810 ms; TE 150 ms), Flash3D T1-weighted (TR 5.2; TE 2.5) and HASTE sequences (TR 700; TE 89). A contrast agent was not used as it was not considered necessary.
MRI imaging showed a uterine-vaginal anomaly consisting of didelphys uterus and double vagina, one of which was obstructed (Figure ); consequently, there was accumulation of fluid exhibiting a signal intensity similar to methaemoglobin in the right uterus (slightly dilated, 14 mm diameter of the lumen) and in the right obstructed vagina (which appeared to be considerably dilated, 43 × 34 × 35 mm).
In the right ovary an expanding mass of 31 mm was hyperintense on T1-weighted images and mildly hypointense or hyperintense on T2-weighted images (Figure ). The mass was characterized by a typical "shading" sign (Figure ) and exhibited features compatible with an endometriosic cyst; there was mild fluid in the pouch of Douglas.
There was no evidence of an expansive process in the left ovary. The extension of examination to the upper abdomen revealed right renal agenesis and apparent compensatory hypertrophy of the left kidney (Figure ).


A 15-years-old woman presented with severe abdominal pain that occurred since the patient achieved menarche at 14 years of age; the patient also had irregular menstruation with severe dysmenorrhea and she reported that the pain worsened immediately prior to menstruation and improved with menstrual flow.
Upon physical examination, the findings were non-specific, with the exception of lower abdominal tenderness, arising from the pelvis, mildly tender to palpation. A gynecologic examination did not reveal any anomalies of her external genitalia or hymen.
So, MRI was then performed, using the same sequences protocol employed for Patient 1.
Contrast agent was not given and the patient's mother provided informed consent to perform MRI exam.
MRI indicated a uterine-vaginal malformation consisting of didelphys uterus communicating with a double vagina, of which the right vagina was obstructed (Figure ). Consequently, there was a collection of fluid that exhibited a high signal intensity on T1 fat-saturated sequences, referred to as methaemoglobin, both in the right uterus (slightly enlarged: 18 mm diameter), and in the right obstructed vagina (which appears to be highly dilated and thus compressing the bladder, 60 × 65 × 76 mm) referred to hematocolpos (Figure ).
There was no evidence of an expansive process in the ovaries, but the extension of the examination to the upper abdomen showed right renal agenesis and apparent compensatory hypertrophy of the left kidney (Figure ).


A 13-years-old female presented with severe abdominal pain. She reported that the pain had begun a few months earlier and had subsequently worsened over the past several weeks. The pain worsened immediately prior to menstruation and then improved once menstrual flow began. The patient also reported worsening constipation and denied problems with urination, nausea, vomiting or diarrhea.
The patient underwent menarche 2 months prior with menses exhibiting 3 to 4 days of very light flow. Physical examination did not reveal any alteration of her external genitalia. A previous sonography revealed a solitary left kidney as well as probable unicornuate uterus.
MRI examination confirmed an unicornuate uterus with a left single horn open into a normal vagina and a controlateral non-communicating rudimentary horn that contained material with a signal intensity similar to methaemoglobin (Figure ).
The ipsilateral Fallopian tube was characterized by fluid sero-mucinous distension (Figure ). In the right paramedian side, at the level of the Douglas, posterior to the ideal point of continuity between uterus and rudimentary horn, there were some adjacent nodules most likely of endometrial etiology (14 mm, 38 mm in total) (Figure ). In addition, a moderate rate of pelvic fluid was present.
The extension of the examination to the upper abdomen showed agenesis of the right kidney with compensatory hypertrophy of the left one and a left renal artery with a larger lumen, most likely of functional significance.
This is, evidently, another kind of MDA, different from the HWW syndrome, showing an association with uterine anomaly type IIb with renal aplasia, whereas HWW syndrome displays an association with Ia vaginal anomaly with a III uterine anomaly and renal aplasia.


A 40-year-old female was found to have a 3.5 cm cyst at the body of the pancreas on ultrasound during a routine health screening. She had 2 previous laparoscopic procedures for pelvic inflammatory disease and excision of ovarian cyst.
A CT scan showed a complex cyst with septations measuring more than 3 cm and subsequent endoscopic ultrasound followed with fine-needle aspiration showed a multiloculated hypoechoic cystic lesion located at the body of pancreas with high Ca 19-9 of 148.2 U/mL (n.v. ≤ 37 U/mL), (), suggestive of cystic mucin-producing neoplasm. She subsequently underwent spleen-preserving distal pancreatectomy via single-port approach.


A 4-year-old male patient was brought to the pediatric dental clinic of a public teaching institution for dental treatment. The child had no relevant medical history.
During clinical and radiographic examinations, extensive carious lesions were observed in the deciduous second molars. Because of the patient's poor oral hygiene, the final restorations were not placed until the patient's oral environment had improved. Temporary restorations were placed in the decayed teeth using glass-ionomer cement and the caregiver was instructed about her child's oral hygiene and dietary habits in order to control caries-promoting risk factors.
Unfortunately, the patient did not show up for treatment for 10 months, and when he returned there was irreversible pulp damage in the lower right primary second molar. As a result, a pulpectomy was performed, and the root canals were filled with iodoform-based paste. Because of extensive coronal destruction involving the occlusal, buccal, and lingual surfaces, the treatment of choice was biologic restoration using a deciduous molar crown obtained from the tooth bank at the same institution ().
After 12 months, a clinical followup of the provisional restorations was carried out. Upper right primary second molar, which had been restored with glass-ionomer cement, was treated with a formocresol pulpotomy and class I restoration with photoactivated resin composites (TPH; Dentsply, Rio de Janeiro, RJ). The other temporary molars were restored in a direct way with resin composite. Clinical visits took place every 3 months and radiographs taken every 6 months to observe the patient on a routine basis and to reinforce the caregiver's and patient's oral health preventive practices.
Five years after finishing the treatment of the lower right primary second molar, even though there was partial resorption of the root canal filling material, we did not observe any periapical lesion or clinical evidence of unsuccessful endodontics. The same applies to the upper right primary second molar, after 4 years after pulpotomy. At that time, we decided to clinically evaluate those endodontically treated teeth having the most extensive restorations. We compared the results with others obtained at the beginning of treatment (baseline). Four evaluation approaches were used: FOTI, clinical evaluation based on USPHS criteria, radiographs, and SEM (JEOL JSM 5310-SEM).
After dental prophylaxis, transillumination was performed using a photoactivating device (Heliomagic HD; Vigodent, Rio de Janeiro, RJ). The FOTI scores were established according to the shadow produced on the tooth-restoration interface according to the index created by Santos et al. []. The FOTI criteria were 0 (no shadow on the interface), 1 (fine shadow restricted to the enamel), and 2 (shadow reaching dentine). After this analysis, dental restoration failure was observed. This finding was further confirmed by the similarity between baseline and final results. Clinical evaluation () using USPHS criteria was performed by one trained investigator, and the results are shown in . shows absence of microleakage according to follow-up radiographs of the 2 restorative techniques. Finally, shows the restoration interface of 2 teeth using an SEM. To perform this task, a Xantopren impression was transferred in epoxy resin for replication. These replicas were gold sputtered and then studied in the SEM. Although no microleakage was observed in the dental elements, a small gap was found in the tooth restored with composite.


A healthy fifty-two-year-old Bangladeshi man was referred via general practice to the author's ENT outpatient service due to a short history of odynophagia, and an oropharyngeal foreign body sensation, together with a history of impacted fish bone in his throat. He presented previously in Accident and Emergency with the same symptoms, when a “foreign body” of his right tonsil was diagnosed. He denied dysphagia, dyspnoea, otalgia, or other sinister symptoms. However, exploration of his social history confirmed a moderate smoking pattern and a positive history for chewing betel nuts. Clinical examination did not reveal any fish bones but instead yielded a large tonsillolith ulcerating through the right noninflamed palatine tonsil. Specifically, the protruding lesion appeared hard, mobile, well-delineated, nontender, and yellowish white in colour. Fibreoptic appraisal of the upper aerodigestive tract did not reveal any malignancy and there was no palpable neck lymphadenopathy. No fish bone was evident on lateral neck X-ray, but a uniform calcification of tonsillar area overlapping the mandibular ramus was seen ().
A right tonsillectomy was carried out with a mid-tonsillar incision over the right tonsil with removal of the tonsillolith at a submucosal level (Figures and ). Postoperative recovery was uneventful. The specimen was submitted for histological examination: macroscopically, the tonsillolith was irregular and whitish yellow in colour and measured 2.5 × 2 centimetres; microscopically, the tonsillar tissue showed some chronic inflammation with no signs of malignancy.


A 85-year-old Caucasian man presented to our department in 2011 with a 4-year history of swelling on the mandibular angle of both sides. After initial slow and continuous growth, the masses now showed an accelerated enlargement in the last months, he indicated.
In 2004 the patient had suffered from a carcinoma in situ of the right auricle that was treated by photodynamic therapy alio loco. At that time neither ultrasound nor a CT-scan showed any cervical masses. Follow-up care did not reveal any local recurrence of the carcinoma. In 2007, there had already been detected two enlarged lymph nodes of unknown dignity on the left (2.4 cm) and right (1.4 cm) angle of the mandible by ultrasound examination. The performed CT-scan classified the lymph nodes unspecific with a diameter of 1.6 cm on both angles of the mandible. During follow up, ultrasound was performed twice a year and showed no further enlargement of the lymph nodes. In the year 2011 ultrasound detected a mass on the left side of 3.5 cm and two masses of 1.5 and 1.6 cm on the right side, respectively. Due to their appearance they were classified as suspect lymph nodes. CT-scan paralleled these findings of suspect lymph nodes on both sides of the mandible (3.2 cm left, 1.8 cm right). The masses showed a defined border and an uptake of the contrast medium (Figure ). No further masses or lymph nodes in the parotid glands or the neck were detected. Therefore the patient was submitted to our department in order to perform a lymph node biopsy.
The patient was a non-smoker. He reported no pain, facial or trigeminal disorders. B-symptoms, a stay abroad and the presence of domestic animals were denied. Furthermore, the patient suffered from coronary heart disease, cardiac arrhythmia, barrett esophagus and hypertension.
Physical examination in our department showed soft, painless solid masses at the left and right angle of the mandible which were moveable to the skin and the deeper tissue. Ultrasound revealed two round-ovoid-shaped nearly fused lymph nodes in the left regio IIA cranial to the bifurcation of 16 and 15 mm in the maximum diameter, respectively. No vessels could be detected inside the lymph nodes, the regular lymph-node anatomy with hilum and cortex was absent. The internal echo was increased with interspersed hypoechoic areas. The borders of the lymph nodes were widely well-defined and they displayed a dorsal sound-enhancement. A very similar lymph node was found in the right regio IIA which measured 18 mm in the maximum diameter (Figure ). Thus, to exclude metastatic tumor growth in the three lymph nodes we decided to excise them in toto without prior FNAC.
Therefore, the patient underwent a selective lymph node excision on both sides in general anesthesia without any complications. Histological examination revealed oncocytic benign epithelial cells and mixed lymphoid cells consistent with Warthin's tumors in three cervical lymph nodes (Figure ). On the left side there were two lymph nodes with a diameter of 1.5 cm each and on the right side the diameter of the mass was 3.2 cm.
The patient recovered from the operation very soon and showed no signs of recurrence during follow up so far.


A 18-year-old male patient reported to our center with a chief complaint of pain and swelling of the left maxilla since 6 months. On extraoral examination, there was a diffuse bony swelling of the left maxilla which was slightly tender on palpation. Intraoral examination revealed bicortical expansion of the left maxillary alveolar ridge with the swelling extending from left first premolar to the first molar which was roughly elliptical in outline and nontender (). The swelling was hard in consistency and measured approximately 3∗2 centimeters in greatest dimension. No mobility of the teeth in the region was elicited and there was obliteration of the buccal vestibule. Mucosa over the swelling was normal with absence of any ulcerations or sinus discharge. There were no other secondary changes involved like paresthesia or cervical lymphadenopathy.
Radiographic examination revealed a well-circumscribed, radio-opaque lesion mixed with areas of radiolucency. The lesion was roughly round to oval in outline and measured around 3∗3.5 cm in diameter. The periphery of the lesion was surrounded by a well-defined radiolucent rim (). There was no reactive bone forming rim at the periphery. Radiographically, the lesion was extending from distal surface of canine root anteriorly to the mesial surface of second molar posteriorly. Superiorly, the lesion was invading into the maxillary sinus and the inferior extent was almost till the alveolar ridge ().
Incisional biopsy was performed under local anesthesia. Access to the lesion was gained through a buccal crevicular incision. A diagnosis of benign bone tumor was then made based on the histological, radiological, and clinical findings. Complete excision of the tumor mass was planned under general anesthesia. Under strict aseptic precautions, complete excision of the tumor was performed through a buccal vestibular incision extending from canine to the second molar (). Intraoperatively, the tumor was not very vascular and as it was well circumscribed which facilitated in toto excision (). Complete hemostasis was achieved and primary closure was performed. The specimen was sent for histopathological examination which confirmed the diagnosis of benign osteoblastoma. shows vascularized fibrous connective tissue with bony trabeculae lined by numerous osteoblasts and scattered osteoclasts. Epitheloid like osteoblasts are present in some areas. Resorption of the trabeculae by multinucleated osteoclasts and prominent reversal lines are observed.
There were no specific complaints postoperatively, and the patient was discharged 5 days postoperatively. The patient was disease free without any recurrence during the follow-up period.


An 83-year-old Caucasian woman was admitted to the Department of Orthopedics with a chief complaint of progressive kyphosis, which had worsened over the previous six months. The patient complained of a progressive dysphagia and had lost approximately 20 kg over the previous six months. Posteroanterior and lateral chest radiographs (Figures and ) demonstrated a mediastinal homogenous opacity partially filling the left hemithorax and causing tracheal displacement. She was then referred to our department for further investigation.
A physical examination revealed marked prominence of the left hemithorax. This region was dull to percussion and did not move with respiration. The intercostal spaces were bulging, and no breath sounds were heard on the left. The right hemithorax was clear and moved well with respiration. The remainder of the physical examination was unremarkable. Her general condition was good. Physical examination of the heart as well as an electrocardiogram (ECG) revealed no abnormal findings. Routine laboratory tests were within normal limits. Liver and renal function was very good.
The presence of a giant tumor was confirmed by computed tomography (CT) (Figure ) (size 2 × 20 × 11 cm). The CT scan showed that the tumor caused bilateral lung compression and tracheal and esophageal displacement. No fluid accumulation was seen. A CT-guided fine needle aspiration identified the mediastinal mass lesion as a possible thymoma.
The patient subsequently underwent radical surgical excision of the tumor (Figure ) via median sternotomy.
The total weight of the excised tumor was 2550 g (Table ) [-]. Histological examination showed a thymoma [B1 according to the World Health Organization (WHO) classification, CD3(+), CD5(+), CD1(+), keratine(+), CD20(-) and CD30(-)]. The tumor was macroscopically and microscopically completely encapsulated (Masaoka stage I).
The patient was extubated in the operating room and then taken to the intensive care unit for two days of postoperative monitoring. The rest of her postoperative recovery was uneventful, and she was discharged on the tenth postoperative day.
Two years after the operation, the patient currently shows significant improvement of her posture, no pulmonary discomfort, and she has regained 20 kg of weight. Follow-up CT scans revealed no evidence of disease (Figure ). Her trachea and esophagus were returned to their anatomical location, the lungs were fully expanded and the mediastinum had returned to its normal width.


SM. A 48-year-old white female presented for evaluation of possible laser vision correction.
Descriptions of her eye findings: 20/20 best corrected vision, normal intraocular pressure, simple myopia, normal cornea thickness, normal pupil size, and normal topography. The significant ocular findings: chronic bilateral optic disk edema for ten years.
In the consideration for the selection of either PRK or LASIK as the procedure for this patient, it is necessary to search relevant evidences to support the decision.
PRK and LASIK are laser eye surgery procedures intended to correct a person's vision to reduce dependency on glasses or contacts.
In PRK, the surgeon removes the outer layer of epithelium with various techniques, then an excimer laser ablates and reshapes corneal tissue. Anesthetic drops are used to reduce pain. LASIK uses a microkeratome device or a femtosecond laser under suctioning to increase intraocular pressure to about 65 mmHg up to 100 mmHg for 45 second to cut epithelium and stroma to a thickness of 100–180 microns, and then, an excimer laser ablates corneal tissue under the epithelial/corneal tissue flap [].
PRK is an excellent alternative when LASIK is not an option. It is suitable for those with less corneal tissue, because it can preserve more corneal tissue. There will be no complications of stromal flap in PRK. Unlike LASIK, it does not require pressure suction on the eye ball. Nevertheless, the drawbacks are more discomfort than LASIK in the first 24 hours after procedure, it requires more healing time than LASIK, trauma may cause complications after surgery, and long-term outcomes are not as well established as older corrective procedures such as LASIK [].
LASIK is appropriate for people who have more corneal tissue. The benefits are less discomfort than PRK, almost no pain, 20/20 vision or better is typically achieved by the first day, corneal haze is very rare, immediate clear vision, and follow-up enhancements are easier if needed. However, the drawbacks are contraindicated with thinner corneas, flap may dislodge with trauma, increases higher-order aberrations (HOA), nonsmooth flap may lead to astigmatism, flap may result in scars, and postoperational treatment is needed in approximately 5% of patients [].
A search strategy was developed to search evidence in the literature to support the decision in the selection of the better procedure for this patient.
The search was conducted over Pubmed, Medline and Cochrane Library. 1492 articles were found, and 5 papers were selected for this case report. Pubmed had 83 articles, and none was selectedfrom Cochrane library review.
There were three observational case reports and two experimental studies (see Tables and ).
LASIK-induced optic neuropathy by Cameron et al. [] clearly described the case of a subject with a previously normal optic nerve who developed bilateral optic neuropathy after LASIK surgery []. The neuropathy manifested with visual field defects. Valid test such as complete eye exam with detailed evaluation of the optic nerve, detail medical history, stereodisc photographs, GDx nerve fiber analyzer, was used rigorously to confirm the diagnosis associated with LASIK pre-op and post-op. Other possible causes of optic neuropathy were also carefully ruled out. The author concluded that optic nerve neuropathy is a dangerous complication of LASIK. It may be due to barotrauma or ischemia from elevation of intraocular pressure by the suction ring during the LASIK procedure. Lee et al. and Montezuma et al. also reported similar cases with the same conclusion [, ]. Lee et al. even reported two cases that experienced chronic disc edema pre-op similar to this case pre-op []. The two cases he reported had LASIK and suffered acute visual loss. Nevertheless, the experimental parallel control trial of Lester demonstrated no statistically significantly different measurement between before and after a compression of 100 mmHg to the eye for 45 second (as in suction ring pressure of LASIK procedure) in the mean RNFLT (retina nerve fiber layer thickness). This quantitative study showed that the acute increase in intraocular pressure during LASIK did not significantly change the thickness of retina nerve fiber layer in normal eyes []. Furthermore, Hamada conducted a prospective consecutive study of 53 normal eyes to compare the RNFLT before LASIK and after LASIK. He concluded that transient extreme elevation of intraocular pressure (IOP) during LASIK does not affect RNFLT in normal myopic eyes for at least one year after surgery [].
There were two case reports and one case series. Although these are poor-quality studies and rank near the bottom of hierarchy of evidence, these cases provide valuable insights and warning for potential sight-threatening conditions.
The two experimental studies were appraised according to the CASP framework.
Both studies have a clear focus: P: patients undergoing refractive laser surgery I: LASIK (will receive 100 mmHg of pressure for 45 seconds during the procedure) or 100 mmHg of pressure for 45 seconds. O: change in RNFLT (retina nerve fiber layer thickness).
These were not randomized trials but were prospective consecutive cases.
Participants were appropriately allocated to intervention. The groups appeared equivalent (all normal eyes) and had low risk of selection bias with strong internal validity.
It was not possible to “blind” due the nature of intervention. However, the outcome measures are objective that will reduce the threat to internal validity.
All the participants in these two studies were accounted for at the conclusion. The follow-up rates were 100% that increase both the internal and external validity.
The data collection and the follow-up were done in the same way. (This increases internal validity.)
The power calculations were not mentioned in the either of the two studies. It is a decrease of external validity. However, Hamada's [].Study may have enough power with 53 participants for a single outcome measurement.
The result showed no statistically difference in RNFLT (retina nerve fiber layer thickness) before and after the application of pressure (100 mmHg) to the normal eye ball during LASIK or for the experiment for 45 seconds in 2 minutes, one month, 7 month, and 13 month.
No confidence interval was reported in the two studies.
The internal and external validities were good in the studies for using locally.
Since glaucoma patients are contraindicated for LASIK surgery and it is a rare to see patients having sick optic disc desire laser refractive surgery, there are neither systematic reviews nor randomized control studies available as reference for this case. Furthermore, the alternative laser refractive procedure such as PRK is available for those suspicious cases; most surgeons will choose the alternative way to avoid catastrophic result.
The two experimental studies showed no statistically difference in RNFLT (retina nerve fiber layer thickness) before and after the application of pressure (100 mmHg) to the eye ball during LASIK or for 45 seconds in normal eyes. It revealed the safety of LASIK to normal eyes with the application of 100 mmHg pressure for 45 seconds during surgery by quantitatively measuring the change of nerve fiber thickness using scanning laser tomography or nerve fiber analyzer (laser diagnostic technology).
All the cases that report with abnormal optic nerve showed severe vision decrease due to LASIK. The case series of Lee had two identical conditions of this case (optic disc edema) and suffered severe vision loss after LASIK. However, in Cameron's case with normal optic nerve before operation, there was development of optic neuropathy after LASIK.


A 3-year-old male child born of nonconsanguineous marriage to a 28-year-old mother and a 32-year-old father by caesarean section was referred for evaluation for delayed development and abnormal facial features. There was a history of three spontaneous abortions. One pregnancy was terminated in late second trimester of gestation as the fetus was found to have multiple congenital anomalies on antenatal ultrasound. Exact cause of abortions could not be determined as chromosomal analysis of fetuses was not done, although TORCH screening of mother was negative. Antenatal, natal, and immediate postnatal history of the child described was not significant. After the age of three months, the parents noticed a lag in development along with abnormal facial features. Developmental assessment at the time of presentation revealed global delay. The child achieved neck holding at 12 months, sitting at 18 months and independent standing at 24 months of age. He had jargon speech with only few intelligible words. He was not able to feed himself. His weight was 11.0 kilograms (less than 5th percentile for age), height 75 cm (less than 5th percentile for age), and head circumference was 47 cm. Dysmorphic facial features included prominent forehead, large prominent ears with prominent antihelices, deep-set eyes, hypertelorism, bilateral corneal opacities, broad nose, thick everted lips, and high-arched palate. Orthopedic anomalies included camptodactyly of second through fifth fingers, mild scoliosis, short metatarsals, and deep plantar and deep palmar creases (). X-ray spine showed mild scoliosis and posterior open neural arch defect in upper dorsal vertebra. Abdominal ultrasound, echocardiography, and cranial neuroimaging did not reveal any congenital anomaly of internal organs.
In view of presence of facial dysmorphism, musculoskeletal abnormalities, developmental delay, and history of recurrent loss of pregnancies, we got his karyotype done on peripheral lymphocytes, which revealed trisomy 8 mosaicism (47, XY, 6 + 8 [15]/46, XY [15]) (). Chromosomal analysis of parents showed normal karyotype.


A 41-year-old male was referred for blurred disk margins and possible papilledema from his optometrist. He was visually asymptomatic. He had been seen in a hematology-oncology clinic one month prior for swollen groin lymph nodes that were noted to be reactive, but of unknown etiology. He had not had any previous STDs, genital lesions, penile discharge, or rash.
On exam, visual acuity was 20/25+ OD and 20/20− OS. Ishihara color plates were 11/11 OU. He had a trace afferent pupillary defect OS. Intraocular pressures were 12 OD and 18 OS. He had asymmetric disc edema, greater in the left eye. Optical coherence tomography showed a retinal nerve fiber layer (RNFL) average thickness of 188 microns OS with concentric circumferential elevation and an average RNFL thickness of 118 OD with inferonasal elevation ().
Brain MRI and MRV with and without contrast were unremarkable, without mass lesions or venous occlusion. He underwent a lumbar puncture which showed a normal opening pressure of 18 cm H2O, normal protein, and glucose, and 72 white cells/mm3, predominately lymphocytes. Within 2 weeks of presentation, he developed headaches and eye pain, especially when bending over. Repeat examination showed worsening disc edema in the right eye and enlargement of the blind spot on visual field testing. Because his presentation was not consistent with papilledema, orbit MRI was performed, which showed increased optic nerve sheath fluid, especially posterior to the globes () and contrast enhancement of the optic nerve sheaths. Since the clinical and imaging findings appeared consistent with optic perineuritis, he was tested for secondary causes. He tested positive for syphilis with a rapid plasma reagent (RPR), with a titer of 1 : 128. FTA-ABS measured for confirmation was also positive. HIV testing was negative. He was placed on IV Penicillin 3,000,000 Units every 4 hours for 14 days. Repeat testing two weeks after antibiotic treatment showed marked improvement in both his symptoms and the extent of disc edema (). Visual field testing also improved after antibiotics, with resolution of the enlarged blind spot ().


A 69-year-old woman presented with a 14-month history of intermittent fornication in the distribution of the left mandibular (V3) division of the trigeminal nerve. MRI scan identified a presence of an ill-defined, diffuse lesion, involving cortex and subcortical white matter of the left occipital and parietal lobes extending into the frontal lobe, with only slight mass effect and relative preservation of underlying anatomy with no postcontrast enhancement. The MRI features were suggestive of low-grade diffuse glioma or gliomatosis cerebri. After five months time follow-up MR scan with MRS (1.5 T Siemens Avanto) using 2D CSI and single voxel (SV) technique (TE of 135 ms, TR of 1500 ms) was performed. The analysis of MRS findings was done using the standard software provided by the manufacturer. The MRI scan again confirmed the presence of extensive signal abnormality, which unchanged in size from the previous scan (). The MRS (SV and CSI) through the abnormal areas was extensively assessed but showed no alteration in choline and N-acetyl aspartate (NAA) peaks compared to normal brain tissue and was entirely within normal limits (Figures and ).
The patient presented six months later with 2 weeks history of partial seizures, involving the right upper and lower limbs. Repeat cranial MRI scan revealed significant progression of the lesion into the occipital region and an increase in the mass effect. An area of enhancement in the left parietal lobe was also present, measuring 19 × 18 mm (). The patient subsequently went on to have a biopsy. The pathology confirmed the presence of glioblastoma multiforme (GBM).


A72-year-old woman with a history of gravida 10, para 10 was referred to department of Obstetrics & Gynecology of Taleghani Hospital. She had a pelvic mass that was from 2 months before, and was admitted to a local hospital complaining of dyspnea. Her medical history had included hypertension since 4 years ago and her other medical history had been normal. In physical examination, she had a top normal size uterine and palpable mass in lower side of abdomen. No lymphadenopathy was detected in auxiliary, supraclavicular or inguinal regions. In paraclinical examination, chest imagings showed massive pleural effusion on right side (Figures and ). The cytological evaluation for the pleural fluid showed inflammatory cells infiltration and no malignant changes had been detected. Then a chest tube was inserted for the patient to reduce the volume of pleural effusion. The pleural fluid culture for anaerobic and other organisms and its direct smear for Mycobacterium Tuberculosis were negative.
Her transvaginal ultrasonography showed multilocular cystic-solid mass on her right ovary measuring 53 mm in diameter, with a 6.8 mm internal septae and 19 mm mural nodule. The low-resistant pattern on the right ovarian artery was in favor of malignancy (RI = 0.61). There was also free intraperitoneal fluid in pelvic cavity. The sonographic figure of her mass declared a case of serous cystadenocarcinoma.
Then an abdominopelvic CT scan with IV and Oral contrast was performed (Figure ). The results showed a multicystic pelvic mass with irregular calcified mural nodules, measuring 95*120 mm in size that seemed to be an ovarian cancer. After checking the Tumor markers, the CA125 was higher than normal range (607.4 Units/ml).
CA19-9 = 62.72
CA125 = 607.4
CEA = 1.92
Inhibin A < 0.1
The patient went through operation. Her abdominal cavity had about 700 cc of free fluid sent for cytological examination. The uterine and left ovary was normal. There was a 9 cm-diameter mass on her right ovary with vegetative lesions on its surface that was resected and sent for the frozen section.
The result of frozen study was granulosa cell tumor. Therefore, the abdomen was explored and no other involvement was detected. Omentectomy was performed which was intact. The hysterectomy and bilateral salpingo-oophorectomy was performed for the patient. The permanent pathological report was struma ovarii (Figure ). The uterus, left ovary and fallopian tube were histologically unremarkable and the cytological evaluation of the ascitic fluid showed no evidence of malignant cells.
The patient recovered normally and went to home on the fifth postoperative day. After three months of surgery, no evidence of ascites and pleural effusion was detected and the serum level of CA 125 was in the normal range (9.3 Units/ml); 12 months following the surgery the CA125 level is 12.5 Units/ml, and there is neither pleural effusion in chest X-ray (Figure ) nor ascites or mass in abdominopelvic ultrasonography. The patient is healthy and TSH level is 1.6 micIU/ml.


A 33-year-old man was admitted to our hospital because of generalized weakness, emaciation and anorexia 12 years after massive small bowel resection. Our patient underwent massive small bowel and ileocecal resection because of small bowel volvulus 12 years ago. An end-to-side anastomosis was performed between his proximal jejunum and his ascending colon, with only 40 cm of his small bowel remaining. Subsequent bowel rehabilitation therapy, which included enteral nutrition with dietary fiber, recombinant human growth hormone and glutamine, was instituted for four weeks []. Our patient was weaned from total parenteral nutrition (TPN) and had a normal diet up to the present.
One month ago, our patient developed diarrhea and weight loss of 7 kg with no obvious predisposing cause; he felt weak, anorexic and dizzy, and became progressively cachexic. Urinary volume was reduced, while stool volume was increased. On admission, our patient's body weight was 36 kg, body mass index (BMI) 12.2 kg/m2, heart rate 80 beats per minute (bpm), blood pressure 70/50 mmHg, and respiratory rate 18 bpm. He was oriented and cognitively intact. Pitting edema appeared in his lower extremities. An abdominal examination revealed previous surgery scarring, thin skin, a scaphoid abdomen, and negative shifting dullness. A chest X-ray showed a high density shadow of a nodule outside his right upper lung, considered to be rib calcification. A lower limb X-ray and ultrasound of both kidneys and ureters were normal. An ultrasound of his gallbladder showed gallbladder atrophy. An electrocardiogram showed normal sinus rhythm with T wave changes (II/III/avF/v4-6 flat, inversion), with incomplete right bundle branch block. All laboratory values are presented in Table .
Our patient was diagnosed with severe malnutrition and was supported by blood transfusion, parenteral nutrition (500 kcal/day), fluid, electrolyte, trace element and multi-vitamin supplementation (one ampoule each of Soluvit® and Addamel® daily), along with thiamine 100 mg intravenously prophylactically. Our patient's physical strength improved after these treatments, and pitting edema of the lower extremities decreased. Within 24 hours, our patient presented with profound fatigue and flaccid weakness of all four limbs. His heart rate was 98 bpm, respiration was normal, but biochemical investigation showed severe hypophosphatemia 0.05 mmol/L (Table ), hence a clinical diagnosis of RFS was made, and immediately the patient was transferred to the intensive care unit (ICU) for closer monitoring. Parenteral and enteral nutrition were interrupted and intravenous supplementation with phosphate polyfusor (120 mmol on the first day, then 60 mmol per day intravenously or enterally for five days) was initiated, along with enteral and parenteral multi-vitamins and trace elements (two ampoules each of Soluvit®, Vitalipid® and Addamel® daily for two days, thereafter one ampoule of each daily). He also received a once daily intramuscular dose of Vitamin B12 0.1 mg and thiamine 100 mg. In addition, a hydrocortisone injection 100 mg was given to prevent adrenal insufficiency on the fifth day. A plasma transfusion was given to expand blood volume because blood pressure fell to 97/60 mmHg temporarily.
On the seventh day, our patient had numbness of his limbs, diarrhea and dyspnea. At the same time, a chest X-ray indicated right middle lobe pneumonia. Respiratory muscle weakness was considered to be the reason, and an emergency tracheotomy with mechanical ventilation was done, and sputum aspiration was regularly performed. Anti-diarrhea (diphenoxylate 1 pill three times a day by mouth), anti-infection (moxifloxacin 0.4 g/day intravenously), and antacid (omeprazole 40 mg intravenously twice daily) therapy were given immediately.
On the ninth day, when his blood chemistry became normal, enteral nutrition was resumed at 500 kcal/day and increased gradually. On the twelfth day, total enteral nutrition was well tolerated with improved pulmonary symptoms, and our patient was successfully weaned from mechanical ventilator support. Subsequently, he received recombinant human growth hormone therapy (10 u/d) and total enteral nutritional support for one month and recovered uneventfully with a weight of 45 kg (gain of 9 kg) and a BMI of 15.2 kg/m2.


A 3 day-old male neonate was brought to medical attention by his parents who complained of inability to see his eyes since birth, mucopurulent discharge and excessive tearing (). The baby had developed a fever 24 hours before presentation. Antenatal care had been uneventful, there was no maternal genital infection, delivery was normal vaginal and there was no report of birth trauma.
The baby was slightly febrile (temperature, 38.5°C) and without jaundice. Ocular examination revealed a purulent discharge, moderate conjunctival injection and massive chemosis in both eyes (). Both upper lids were everted and the eyeball could not be seen without a speculum. No systemic abnormality was detected.
A diagnosis of bilateral congenital lid eversion with possible neonatal sepsis was made. Pediatricians were consulted and the patient was treated as a case of neonatal sepsis with intravenous cefuroxime. The eyes were treated with tobramycin ointment, padding with 5% hypertonic saline-soaked gauze dressing and frequent application of methylcellulose gel. By the eighth day of admission, the chemosis resolved (), the eyelids became well-apposed and fever subsided. Dilated funduscopy with 0.5% tropicamide eye drops revealed normal fundi in both eyes.


A 4 day-old boy () presented with protrusion of the left eye of 4 days’ duration. The right eye did not open spontaneously, but seemed otherwise normal. No discharge was reported. Pregnancy had been uneventful and delivery was vaginal and spontaneous. There was no history of maternal genital infection or birth trauma.
There was no history of fever or convulsions and pediatric assessment revealed no abnormalities. The left upper lid was everted with gross conjunctival injection and chemosis, but there was no discharge. Mild upper lid eversion, and mild conjunctival injection and chemosis of the right eye were also present. Both globes were otherwise normal.
The left eye was treated with tobramycin ointment, methylcellulose gel and padding with gauze dressings soaked in 5% hypertonic saline. The right eye was treated with only tobramycin ointment. The left upper lid needed to be repositioned twice. Complete resolution was achieved by the tenth day of admission (). Dilated funduscopy with 0.5% tropicamide eye drops showed normal fundi.


A 4 hour-old male neonate was referred from a private hospital immediately after birth to the emergency room of our eye clinic with fleshy protrusion of the lids and inability to open both eyes since birth (). Pregnancy had been uneventful, labor was not prolonged, and delivery was spontaneous and vaginal. The perinatal period had also been uneventful. There was no history suggestive of genital infections in the mother. There was no eye discharge, nor had any traditional eye medication been applied.
Pediatric assessment revealed no abnormality. Ocular examination revealed bilateral everted upper lids, exposed and chemotic conjunctiva covering the eyeballs and tense lids, but normal cornea and anterior chamber depths in both eyes.
The parents refused admission on financial and social grounds; he was therefore treated on an outpatient basis. Treatment consisted of daily eye cleansing, application of gauze dressings soaked with 5% hypertonic saline over the chemotic conjunctiva, chloramphenicol ointment, and padding. During follow up, he developed a mild serous discharge and ciprofloxacin eye drops were commenced every two hours. Ten days later, the baby achieved complete eye opening in both eyes (). Dilated funduscopy with 0.5% tropicamide eye drops disclosed normal fundi.