A 56-year-old female patient suffering from dry cough, continuing after upper respiratory tract infection, was referred to pulmonary diseases clinic by the attending physician for the suspicion of malignancy because of abnormal findings on chest radiography, consisting in a left lung lower lobe mass with lobulated contour that included cystic areas, and a right lung lower lobe mass in the paravertebral region on thorax CT scan. The patient had no complaint except dry cough. Her medical history was unremarkable, there was no history of previous disease, chronic cough and sputum production, hemoptysis, chest pain, shortness of breath or recurrent pulmonary infections.
The physical examination revealed a BP of 110/60 mm Hg; pulse rate : 72 beats/min; respiration rate : 16 breaths/min; and body temperature : 36°C. Respiratory system examination revealed decreased breath sounds in left lower lung and a systolic murmur was heard in the medial part of the lower zone. Other physical examinations and laboratory findings, including complete blood count and C reactive protein, were normal.
The patient's chest CT was evaluated by a radiologist, and the mass lesions in the CT scan were thought to be compatible with a PS, but that examination was considered insufficient to confirm the diagnosis. Then, chest CT angiography was performed. It showed abnormal tissue compatible with bilateral PS in the posterobasilar lower lobes bilaterally with heterogeneous internal structure, including cystic areas, and two aberrant feeding arteries branching from celiac truncus with venous drainage to the pulmonary veins (Figures
,
). The echocardiographic evaluation was normal. The patient was recommended surgical treatment for the bilateral intralobar PS, but she refused, so that a clinical follow up is ongoing.


A 56-year-old right-handed female office worker presented to the emergency department with marked pain and limitation of movement to both shoulders subsequent to a fall down a flight of stairs at home. Minor bruising was noted around both shoulders. There were no neurovascular deficits. No other injuries were obvious on clinical examination. Plain film radiographs demonstrated bilateral proximal humeral fractures (). The patient had no significant past medical history of note.
A CT scan confirmed bilateral four-part proximal humerus fractures (). Open reduction and internal fixation with threaded pins and tension band suture was undertaken on the dominant right side. Seven days later, surgery on the left was performed. As a satisfactory open reduction could not be achieved, a replacement hemiarthroplasty was performed (). The postoperative course was uneventful. At the two year followup, the patient reported an oxford shoulder score of 58/60 on the fixed right side and 57/60 on the replaced left side. The patient had an abduction of 150° bilaterally and near normal external rotation (). Though there was little difference objectively, the patient expressed a preference for the shoulder which had been treated with internal fixation, stating that “it feels more natural and secure.”


Mrs. T was a 67-year-old woman who had no past history of physical disease and had no psychiatric family history. In June 2008, she experienced depressed mood, decreased energy, anxiety, agitation, and insomnia, and she visited a psychiatric clinic. She was diagnosed with MDD. She took milnacipran (30 mg/day), but her depressive symptoms became more serious gradually without a change of the medication around December 2008. She completely lost interest in her leisure activity. In April 2009, she developed physical symptoms such as a respiratory discomfort. She was examined in many physical hospitals, but no abnormal results were found. She developed hypochondriacal delusions and delusions of poverty gradually. Her appetite decreased, and her body weight was decreased by 12 kg in a year.
She was admitted to a regional psychiatric hospital in May. She had severe agitation and complained, “I cannot breathe.” It was difficult for her to keep still, and she wandered about the hospital ward. She was treated sequentially with fluvoxamine (100 mg/day), amitriptyline (30 mg/day), sulpiride (50 mg/day), and augmentation olanzapine (10 mg/day), but it was impossible to use adequate doses because of her strong apprehension in regard to psychotropics. Finally, the neuroleptics and antidepressants were discontinued, and minor tranquilizers were prescribed, but her agitation did not improve. In October, paroxetine monotherapy (40 mg/day) was started, and she was transferred to us in November 2009.
Severe anxiety, agitation, depressed mood, decreased energy, loss of appetite, decreased body weight, insomnia, hypochondriacal delusions, and delusions of poverty were noted, and she fulfilled the DSM-IV diagnostic criteria for MDD with psychotic features. Total score on the 17-item Hamilton Rating Scale for Depression (HRSD) was 31. The physical examination and neurological examination revealed only low body mass index of 16.6. The blood examination revealed only anemia (hemoglobin 11.4 g/dL). An electrocardiogram, electroencephalogram, and brain MRI revealed no abnormalities.
ECT was done because she had severe depressive symptoms with psychotic feature. Anesthesia consisted of atropine sulfate (0.25 mg) intravenously with propofol (0.9 mg/kg) by intravenously bolus. Succinylcholine (0.9 mg/kg) was given intravenously as a muscle relaxant after induction of anesthesia. Thymatron IV system was used, and bifrontal brief pulse ECT was performed twice a week. The seizure threshold was determined by the half-age method. Paroxetine (40 mg/day), zolpidem (10 mg/day), and bromazepam (4 mg/day), those she had been taking at the previous hospital, were continued.
Confusion persisted soon after awakening from anesthesia at the initial ECT session. 30 minutes later, she failed to respond to our calling and fell into a substupor. Concurrently she developed autonomic symptoms, including pyrexia (38.6°C), tachycardia (160/min), elevated blood pressure (160/70 mmHg), and severe hyperhidrosis, and neurological symptoms, including severe generalized rigidity, palpebral and labial myoclonus, tremors of all limbs, and generalized hyperreflexia. Her total score on the Serotonin Syndrome Scale (SSS) [, ] was 20, and she was diagnosed with the serotonin syndrome. Except for leukocytosis (12,250/μL) and anemia (hemoglobin 9.9 g/dL), the blood examination revealed no abnormalities, including serum creatinine, blood urea nitrogen, creatinine phosphokinase, or electrolytes. The electroencephalogram revealed no paroxysmal abnormalities. In the same day, all oral medication including paroxetine was discontinued. Fluid administration was started under general management. Flunitrazepam (2 mg) was administered intravenously, and the neurological symptoms and autonomic symptoms were alleviated, but the benefit lasted only about 2 hr. The symptoms were gradually alleviated subsequently, and 24 hr later all vital signs except the pyrexia became normal. 48 hours later, the symptoms of serotonin syndrome including pyrexia and substupor resolved completely.
We continued the discontinuation of paroxetine, and performed the second ECT session 5 days after the initial session. We performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of serotonin syndrome were observed. Finally, her MDD remitted. The time-courses of the total scores on SSS and HRSD are shown ().


A 39-year-old Japanese woman consulted a doctor because of back pain, and UPJO was detected after an examination. She was referred to our department and agreed to undergo laparoscopic surgery. A renogram showed that the function of her left hydronephrotic kidney was maintained to some extent, and surgery was thought to be effective. However, CT data revealed that the network of arteries and veins was very complicated. Therefore, we decided to use our simulator before surgery, and our patient agreed.
CT data were saved in the DICOM (Digital Imaging and Communications in Medicine) file format. CT was performed with slices of 1mm in thickness from the chest to the pelvis, and its DICOM file was reconstructed to obtain three-dimensional (3D) volume data. The reconstructed organs were shaped with 3D mesh by using computer graphic techniques. After 3D conversion, the data were transmitted to our simulator, and relations and locations of organs were set. Fibrotic tissue and fat were added appropriately around the organs, and reconstruction of the body was completed (Figure
).
During the simulation, we first placed the camera and trocars on the body surface and obtained a virtual view of the abdominal cavity. When we changed the position of the trocar, the virtual view of the abdominal cavity also changed. Thus, we could choose a better position of the trocar in this pre-operative simulation. There were four renal arteries, two renal veins, and one gonadal vein that bifurcated in the middle. The lumbar vein was not important during surgery and therefore was not depicted.
During surgery, we chose the right flank position and four trocars. The pneumoperitoneum pressure was 10mmHg. We approached the retroperitoneum from the lateral aspect of the descending colon. We found the gonadal vein and ureter and then reached the renal hilum. We found an anonymous vein that tightened the ureter. We removed the target vein and ureteral stenosis and performed a dismembered pyeloplasty after placing a ureteral stent. The pathological finding was fibromuscular tissue, which was thought to be the cause of the UPJO. Operative and pathological findings showed that ureteral stenosis occurred not only because of the crossing vein but also because of endogenous stenosis. Our patient was discharged from our department without complications. After surgery, there were still four renal arteries, two renal veins, and one gonadal vein; the status of the lumber vein remained unknown because the lesion was outside the target area. The locations of the arteries, veins, ureter, and UPJO were almost the same. However, the anonymous vein, which tightened the ureter and ran dorsal to it on the simulator, ran ventral to it during surgery (Table
).


Case 1: A 28-year-old male patient referred to Department of Oral Medicine and Radiology with a complaint of decay in the upper left back tooth for one year. The patient presented a history of defective speech and lisping from childhood.
On general examination the patient was moderately built and nourished. There was no relevant medical and family history.
On intraoral examination no abnormalities were detected in the palate. The uvula was inspected after flattening the tongue with the dental mirror. Cleft involving the uvula bifurcated from three-fourths to its total length was detected (). A provisional diagnosis of isolated bifid uvula was made (Type D) according to Meskin et al classification 1964.


Case 2: A 42 year-old male referred to us with decayed teeth in the upper and lower jaws. The patient had difficulty in speech and swallowing from childhood due to an abnormally small tongue. He had no other relevant medical history. No other abnormalities were detected during general physical examination. Intraoral examination revealed presence of multiple root stumps in the maxillary and mandibular arches. The tongue was hypolastic, around 2 cms long antero-posteriorly and 1 cm wide. The tongue surface was devoid of papilla and movements were restricted in all directions. Lingual frenum was absent, and the floor of the mouth was pinkish in appearance and leathery. The mandibular arch was v-shaped. The palate was high arched with collapsed maxillary arch. Uvula and faucial pillars were ill-developed. The palate showed complete absence of uvula ().


Case 3: A 24-year-old man referred to the outpatient department, with the chief complaint of difficulty in swallowing. He denied any history of trauma but gave us the history of tonsillectomy three years ago.
Clinical examination showed incomplete elevation of the soft palate on the right side. There was absence of gag reflex and uvular deviation to the right was seen (). No facial palsy, diplopia, nor any evidence of motor weakness or sensory deficit was present. A provisional diagnosis of uvular deviation to the right secondary to glossopharyngeal nerve palsy was made.


A 60-year-old woman was admitted to our clinic with swelling in the left eye. On physical examination; exophthalmus, subconjunctival hemorrhage and restricted eye movements due to a mass localized in the medial side of the orbit were observed. The bulbus oculi was displaced to the anterior and lateral parts of the orbit. On CT examination, a homogeneous soft-tissue mass with regular contours causing minimal expansion in the medial orbit wall was observed at the intraconal region of the left orbit. The mass containing a few small punctate calcific foci () had dimensions of 4.5 × 4.5 centimeters. On MRI examination, the mass was isointense with the muscle on T1-weighted images () and showed moderate and heterogeneous contrast enhancement after intravenous contrast material injection (). It was heterogeneously hypointense with the muscle on T2-weighted images. The mass was found to cause medial displacement of the medial rectus muscle and anterior and lateral displacement of the bulbus oculi ().
After biopsy by an endoscopic transnasal and transorbital approach (), the microscopic evaluation was performed. Hematoxylin and eosin stain demonstrated the homogeneous and amorphous amyloid matrix (). The lesion showed positive interaction between crystal violet and amyloid accumulation (). Abdominal ultrasound, electrocardiogram, chest radiography, thyroid function and serum immune electrophoresis tests were normal. Routine blood chemistries, complete blood count, erythrocyte sedimentation rate, antinuclear antibodies, serum angiotensin-converting enzyme, rheumatoid factor and urine laboratory tests were also normal. Rectal biopsy was negative. No finding of systemic amyloidosis was determined during the laboratory investigation and the diagnosis was notified as localized amyloidosis. After 8 weeks following a course of oral prednisone, the lesion was stable. The patient reported mild clinical improvement.


The patient is a 29 year-old woman who initially presented to her physician at the age of 25 with uncontrolled hypertension and hypokalemia. To control her blood pressure, multiple medications were required, with only minimal effect in establishing blood pressure control. Additionally, she had recurrent low potassium levels (less than 2.5 mEq/L) requiring large amounts of oral potassium chloride per day (120 MEq/day). Family history was significant for a deceased mother who had kidney failure at a young age from uncontrolled high blood pressure. Because of these above findings, she was sent to an endocrinologist for workup of secondary causes of hypertension.
The initial labs indicated possible PA by measuring plasma aldosterone concentration (PAC), plasma renin activity (PRA), and calculating an aldosterone-to-renin ratio (ARR) (PAC = 8.0 ng/dL, PRA = 0.1 ng/ml/h, ARR = 80 measured at 10 pm with potassium of 2.6 mEq/L). She was on multiple medications (labetalol and verapamil) at the time including spironolactone. Repeat labs indicated PAC = 16.0, PRA = 0.06, ARR = 267 measured at 10 am with potassium of 3.0 mEq/L, these labs were done after 6 weeks off of spironolactone. Of note, we had her take extra potassium tablets to obtain near-normal potassium levels before repeating these studies. Confirmation of PA was done by 2 liter saline infusion test over 4 hrs, where pre-infusion values showed a PAC/PRA ratio of 28/0.3 and post-infusion values showed a PAC/PRA ratio of 14/1.2 (potassium was 3.2 mEq/L at time of test, patient was off spironolactone for over 2 months prior to this test). Evaluation for other secondary causes of hypertension ruled out pheochromocytoma, Cushing’s syndrome, and renal artery stenosis.
During this period, she had dedicated adrenal imaging by both CT (3/23/2010) and MRI (7/13/2010) scan. These studies demonstrated normal adrenal glands, without evidence of nodules or hyperplasia (done 2 years after initial diagnosis, at age 27 years old). Adrenal venous sampling (AVS) was then performed to determine if lateralization of the aldosterone secretion to one adrenal gland occurred. However, the first AVS sampling was technically not successful. This procedure was subsequently repeated over the coming years twice more, and both times the serum potassium levels prior to the procedures were normal. While both procedures were technically successful, the results were difficult to interpret. These studies are highlighted in Table
.
Through the subsequent few years, the patient had multiple admissions to emergency rooms. Her presenting symptoms for these visits were mostly related to severe headaches, a symptom that developed when her blood pressure was uncontrolled. Some of these emergency room visits led to hospital admissions for further management of her uncontrolled blood pressure and/or hypokalemia. On one of the most recent admissions, we reimaged her adrenal glands (10/17/2011) and found a left adrenal adenoma (2.3 × 1.4 cm, less than 10 Hounsfield units on non-contrast CT images), a finding not previously observed approximately 1 year ago by CT scan and MRI (Figure
). Considering her history, the authors discussed with her the pros and cons of left adrenalectomy and informed her that this is the likely source of excess aldosterone, though it could not be guaranteed. Due to her poor quality of life, which included multiple medications, intolerance to high dose potassium supplements, recurrent headaches and multiple hospital admissions, she decided to go forth with surgery. Pathology revealed adrenal cellular proliferation consistent with adrenal cortical adenoma. Post-operatively, she did well, and her blood pressure returned to normal limits on two anti-hypertensives. Aldosterone levels on post-operative day one were undetectable. She has maintained a normal blood pressure in the subsequent year on these two medications, including normal potassium levels off potassium supplementation on repeat blood studies. It has been 9 months since the operation, and at last visit, her blood pressure medications were decreased and one of these two medications will likely be able to be stopped altogether.


Our patient, AH, is a right-handed 49-year-old female who presented with a headache and visual disturbances following a venous thrombosis that led to secondary haemorrhage. Orthoptic investigation confirmed a small bilateral right superior visual field loss which mildly improved over the first three months after stroke (see of the ). Speech production, comprehension, and repetition were normal. No other deficits were apparent in the patient at 4 years after stroke. Structural MRI identified a large lesion in the left occipito-temporal region. Automated lesion identification () showed that AH’s lesion covered a cerebral volume of 41 cm3 (a volume roughly equivalent to that of a golf ball). This lesion extended in MNI space from −22 mm to −66 mm in the x-axis, from −88 mm to −30 mm in the y axis and from −28 mm to +10 mm in the z axis ().
The left occipito-temporal damage severely impaired the patient’s ability to read. Her writing was relatively preserved as examined with a written picture description task at 5 months after stroke (see of the Supplementary material). When making errors in the written picture description task, the patient subsequently made self-corrections consistent with a diagnosis of alexia without agraphia. Her comprehension of short familiar written words was preserved (see example of her performance during a semantic association task in of the Supplementary material). She was better able to read short rather than long words (see below for details) and often named individual letters prior to producing the whole word (consistent with a “letter-by-letter” reading strategy). Below we report the assessment of her reading that was conducted nearly 4 years after her stroke (46 months) at the time of the fMRI study. In each task, stimuli were presented in point 18 Times New Roman font, with stimulus presentation managed by E-Prime software (; Psychology Software Tools, Inc., PA-Sharpsburg). Experiments were conducted on a Toshiba laptop computer and vocal reaction times were recorded using an attached voice-key.
Each letter of the alphabet (26 lower-case and 26 upper-case) and the numbers 2 through 9 were presented three times each in a pseudorandom order. The patient correctly named 76/78 lower-case letters, 76/78 upper-case letters and 24/24 numbers. Her errors (e.g., /b/ identified as D on one trial and /d/ on another; and E identified as F) were typical of those made by pure alexic patients (). The mean response times for naming individual letters was 570 ms after removing trials in which the voice-key failed to trigger and outlier values that exceeded two standard deviations from their condition mean ().
AH was presented with a total of 160 words that manipulated the factors of length (three, five, seven, nine letters) and frequency (high, low). Words were presented in pseudorandom order. The patient made a total of six errors, which were distributed across the various experimental conditions. Correct RTs were analysed by means of a two-way ANOVA treating each RT as an independent subject with the factors being length (three, five, seven, nine) and frequency (high, low). The results demonstrated main effects of length (F(3, 139)=24.129, p<0.001) and frequency (F(1, 139)=11.692, p=0.001) and a significant length×frequency interaction (F(3, 139)=2.66, p=0.05) (see for details). The effect of frequency (low>high) was only significant for nine-letter words (t(36)=2.635, p=0.012). In summary, the patient showed a word length effect requiring approximately 280 ms per letter, consistent with the letter-by-letter reading strategy that typically follows LvOT damage (). However, a word length effect of 280 ms per letter is moderate (e.g., ) and AH was still able to read three letter words in approximately 1 s. This suggests that AH had some preserved parallel letter processing abilities despite the loss of her LvOT (). During the scanning sessions (see below) she was given an average of 1.5 s to read each 3–6 letter word; this relatively fast presentation rate encouraged the patient and controls to read as rapidly as possible while minimizing the likelihood that the patient would adopt an overt letter-by-letter reading strategy.
The patient was presented 160 nonwords that varied in length (three, five, seven, nine) and nonword ‘familiarity’ (familiar, unfamiliar). ’Familiar’ nonwords included items such as toredom, meeking and hospile that are only one letter away from a real word, whilst smazung, twavcla and clajelb were amongst the ‘unfamiliar’ nonwords because they were not orthographically close to real words. Items were presented in pseudorandom order. Reading accuracy was analysed by means of a log-linear analysis, with factors of length (three, five, seven, nine), nonword familiarity (familiar, unfamiliar) and accuracy (correct, incorrect). Results demonstrated significant interactions between length and accuracy (χ²(3)=13.206, p=0.0042), reflecting improved reading of shorter nonwords compared to longer nonwords (three-letters=33/40, five-letters=28/37, seven-letters=30/39, nine-letters=18/38), and between familiarity and accuracy (χ²(1)=7.733, p=0.0054), demonstrating significantly better reading of ‘familiar’ nonwords (63/78) than ‘unfamiliar’ items (46/75). Correct RTs were analysed by means of a two-way ANOVA, with factors of length (three, five, seven, nine) and nonword familiarity (familiar, unfamiliar). There were reliable main effects of length (F(3, 96)=47.304, p<0.001) and familiarity (F(1, 96)=24.019, p<0.001) but no significant length×familiarity interaction (F(3, 96)=1.669, n.s.), see for details. The main effect of familiarity was a consequence of significantly faster naming for familiar (3094.7 ms) compared to unfamiliar (4131.7 ms) nonwords. This effect of familiarity indicates the influence of lexical and/or sublexical knowledge on nonword decoding.
The patient was tested on a set of 150 words used by Mechelli and colleagues to explore how neuronal interactions within the reading system are influenced by word type (). Words varied in length (between 4 to 9 letters in length) and they included (i) 75 regular words with typical spelling-sound correspondences (e.g., cult, shock, fact, chill), and (ii) 75 exception words with atypical/inconsistent spelling-sound correspondences (e.g., folk, debt, doubt, cough). Words were visually presented for 3 s with a stimulus onset asynchrony of 4 s. All words were matched for number of letters, number of syllables, bigram frequency, familiarity, imageability, and written frequency that ranged from 1 to 447 (per million) with a mean of 40.8 and a standard deviation of 66.48; for more details see (). For regular words, the patient was able to read 48 out of 50 (96%) of words with 4–6 letters in length and 18 out of 25 (72%) of words with 6–9 letters in length. All errors were null responses except for “enigma” which she said “elephant”. For exception words, the patient was able to read 41 out of 50 (82%) of words with 4–6 letters in length and 15 out of 25 (60%) of words with 6–9 letters in length. All errors were null responses except for “myth” which she said “my” followed by “th”and for “parachute” which she said “para” followed by “sh” (i.e., regularization errors). In sum, irrespective of word length, the patient successfully read 75% of exception words that were visually presented for 3 s.
Given unlimited presentation time, the patient was able to name 70/76 pictures from the Birmingham Object Recognition Battery (BORB) (). Under speeded conditions (a triad of three pictures per 4.5 s) the patient’s performance was only 48% over a total set of 32 triads of pictures of familiar objects. This is consistent with previous studies of patients with LvOT damage, although picture naming can appear to be normal at unlimited exposure durations, errors occur when exposure duration is reduced ().
As detailed above, the patient’s reading was not consistent with either phonological or surface dyslexia. Rather, the patient’s reading followed, in an exaggerated way, the same pattern that would be expected from normal subjects. Reading difficulty was more apparent for unfamiliar nonwords and words with atypical spellings when compared with words with typical spelling (e.g., ).


A 28 year-old-man presented with progressive pain and swelling on the left thigh for 2 weeks prior to admission associated with intermittent fever. This pain started off as a deep boring pain associated with rest pain and night pain. It progressively got worst till he was unable to bear weight on the affected limb and was bound to a wheelchair. In addition to that, he also experienced constitutional symptoms such as loss of appetite and loss of weight. He denied history of cough, night sweats, haemoptysis or recent contact with tuberculosis patients. There were no recent skin or soft tissue lesions in him or any of his household contacts. No exposure to healthcare settings or any hospital interventions were elicited within the past one year. There was no previous medical history and he had not received antibiotic treatment in the past 3 months.
Our patient is a civil servant who worked temporarily in Sabah, a state in East Malaysia. He is an avid deer hunter and 2 weeks prior to his clinical presentation he went deer hunting with a hunting partner and caught 3 deer from a forest in Tawau, a small town located at the south-east coast of Sabah. There was extensive direct contact with the deer carcass as he slaughtered the deer with a meat saw, skinned it, cut the deer meat into pieces and cleaned it up. They then cooked the deer meat and consumed it. Neither he nor his hunting partner had any food-poisoning symptoms after eating the meat. A few days after this hunting venture, the patient flew back to his family-home located about 1800 km from Tawau and was brought to the hospital by his family members as he was experiencing severe pain on his left thigh. According to our patient, his hunting partner also experienced fever and lower leg pain at about the same time as him. Unfortunately, we could not obtain any further history regarding his hunting partner as our patient lost contact with him once he left Tawau.
Apart from deer, he was not exposed to any other animals including companion animals. He is a regular smoker; however he does not use intravenous drugs and had no history of acupuncture, trauma, recent travel abroad or involvement in recreational activities like river rafting, diving or contact sports. He is single and denies homosexual behavior.
His vital signs on admission revealed a temperature of 38.7°C, heart rate of 90 beats/min and blood pressure of 120/78 mmHg. His left thigh was warm and tender with a deep ill-defined swelling measuring 20 cm by 8 cm. There were no discharging sinuses or other skin or soft tissue lesions noted. His left knee movement was restricted due to pain; however there was no swelling or tenderness of the knee joint. There was no inguinal lymphadenopathy and neurological and vascular testing was unremarkable. His lungs were clear both clinically and radiologically and examination of other systems was unremarkable.
Plain anteroposterior radiography revealed an osteolytic lesion with erosion of cortex and periosteal reaction involving the mid-shaft of the left femur (Figure
). A magnetic resonance imaging done (MRI) showed involvement of the mid-shaft of left femur with surrounding circumferential soft tissue involvement (Figure
). The technetium-99 m bone scan showed isolated uptake of the left mid and distal femur (Figure
). A provisional diagnosis of osteosarcoma was made based on the radiological findings.
Initial blood investigations revealed leukocytosis (17.7 × 109/L) with 86% neutrophils, normal haemoglobin and platelets. The C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were both markedly elevated at 45.6 mg/dL and 140 mm/hour respectively. All other blood investigations were normal. Blood cultures were taken on day of admission and we proceeded to a needle biopsy. Three days later, both blood and bone biopsy cultures grew MRSA.
Patient was immediately commenced on intravenous vancomycin 1 gram bd, based on antibiotic sensitivity results. An incision and drainage was performed for the left thigh abscess and the cultures of pus also yielded MRSA. Management of the patient was complicated by a pathological fracture of the distal third of left femur sustained during an incision and drainage when a manipulation under anaesthesia was performed at the same time for the stiff knee (Figure
). The fracture was managed with skin traction. Meanwhile, histopathological examination of the bone biopsy revealed acute on chronic suppurative inflammation with no evidence of granulomas or neoplastic cells. Ziehl- Neelsen stain did not reveal acid-fast bacilli and fungal stains were negative. A transthoracic echocardiogram done showed no evidence of valve vegetation, excluding the possibility of infective endocarditis. Ultrasound of abdomen did not reveal abscesses or other abnormalities. Placement of a peripherally inserted central catheter (PICC) line was done for long term antibiotics administration. Hepatitis B and HIV screening were performed and both were negative.
One month after initiation of treatment, the patient finally showed some improvement. His leukocytes, ESR and CRP demonstrated a downward trend and were 10.2 × 109/L, 125 mm/hour and 9.1 mg/dL respectively (Table
). At about the same time, the patient developed swelling and tenderness of his left knee and a knee arthrotomy and washout was performed, the knee aspirate too grew MRSA with similar antibiogram as the previous isolates. Subsequently, fusidic acid was added to vancomycin. Following this, the temperature started to settle. Vancomycin level monitoring was regularly done to evaluate drug toxicity and vancomycin was continued till discharge.
Patient was discharged on day 73 of admission with fusidic acid 500mg tds and rifampicin 300 mg tds and was advised non-weight bearing. At 2 weeks post-discharge follow-up, the leukocyte counts, ESR and CRP were 6.8 × 109/L, 93 mm/hour and 2.6 mg/dl respectively. It took 6 months for the ESR and CRP to normalize, indicating active inflammation; requiring 6-months of anti-MRSA therapy. During the subsequent months, the left thigh pain had improved substantially and patient was able to ambulate. Patient was back to work and was able to perform his daily activities without limitations within one year. At 2-year follow-up, he had full function of his left lower limb and there was no evidence of relapse.
Antimicrobial susceptibility testing (Oxoid Ltd, Bastingstoke, UK) was performed and interpreted by the Clinical and Laboratory Standards Institute (CLSI) disc diffusion method.
Characterization of SCCmec types and detection of pvl gene was performed using conditions as previously described
[]. Detection of 20 other virulent genes; sea, seb, sec, sed, see, seg, seh, sei, sej (enterotoxin genes); eta, etb, etd (exfoliative toxin genes), tst (toxic-shock syndrome toxin gene), efb (extracellular fibrinogen binding protein), fnbA, fnbB (fibronectin binding protein), cna (collagen-adhesin gene), hlg (γ-hemolysin genes), ica (intracellular-adhesin gene) and sdr (putative-adhesin gene) was performed by multiplex PCR using GoTaq DNA Polymerase (Promega Madison Wis, USA) following conditions previously described
[-]. Typing of staphylococcus protein A (spa), mec-associated dru and multilocus sequence type (MLST) was performed using established protocols as described by web-based electronic database (
;
;
), whereas typing of accessory gene regulator (agr) group was performed as previously described by Moore and Lindsay
[].


A one-day-old male newborn was referred to our hospital due to an imperforate anus. He was born vaginally after an uneventful pregnancy, apparently full term, with a birth weight of 1800 gr and an OFC of 29 cm, both far below the 2nd percentile. His nonconsanguineous parents are healthy as are his 5 siblings. Dysmorphic features were immediately noted: hirsute forehead, synophrys, bushy and arched eyebrows, long eyelashes, depressed nasal bridge, thin upper lip with down-turned corners, long philtrum, and micrognathia (). Furthermore, generalized hirsutism was seen (), as well as clinodactyly of the left fifth finger (), limited elbow extension, and coronal hypospadias. The imperforate anus was confirmed. He had a weak sucking reflux and a weak cry.
Chest X-ray and echocardiography were normal. Abdominal ultrasound revealed moderate right-sided hydronephrosis, while the left kidney could not be visualized.
A colostomy was performed. He was discharged in a fair condition after 2 weeks and regular followup was initiated.
Venous blood was sampled, and DNA was sent to the Netherlands (DNA Diagnostic Laboratory, Department of Clinical Genetics, Amsterdam Medical Centre, Amsterdam). Sequence analysis of the NIPBL gene revealed a heterozygous nonsense mutation (c.3445C>T), leading to a premature stop codon in the protein (p.Arg1149X), thereby confirming the clinical diagnosis of CdLs.


A 33-year-old woman came from the outskirts of Danzhou city, Hainan province, China. In April 2010, she reported an 11-month history of recurrent diarrhea associated with colicky pain. The watery diarrhea had persisted since May 2009, occurring about three to four times daily. She also experienced weight loss of 12.5 kg. She was admitted to an outpatient clinic and one hospital in Danzhou. Since May 2009 to March 2010, the patient was given a treatment of checking diarrhea. The detailed diagnosis, treatment and lab investigation of her diarrhea were not clear. In April 2010, because her symptoms could not be relieved, she was admitted to People’s Hospital of Hainan province in Haikou, China. Clinical examination showed moderate dehydration; pallor; a soft, nontender, nondistended abdomen; and marked pitting edema of the lower limbs. The liver and spleen were not enlarged.
Serum total protein and albumin levels were low (47 and 14 g/L, respectively), and proteinuria was not detected (Table 1). A chest radiograph and abdominal ultrasound did not disclose any specific abnormalities. Gastroscopy showed hyperemia, edema, and superficial erosions in the gastric antrum.
In April 2010, stool examinations were quickly performed several times through direct smear method by the laboratory of the hospital, and nothing was found. In May 2010, Stool examinations were carefully performed 9 times through direct smear method and brine flotation by the Department of Parasitology of Hainan Medical College. Eggs (0–1 eggs/10 ×40 microscopic fields) that were elongated and peanut-shaped with flattened bipolar plugs and striated shells (43.7 × 14.6 μm) were observed as shown in Figure
. The eggs were identified as those of C. philippinensis. Adult male C. philippinensis (1.6 × 0.1 mm) was also found in the stool samples. In addition, cysts of Entamoeba coli were found.
The patient reported eating sashimi of two raw Misgurnus anguillicaudatus loaches every day from March to April in 2009 to treat a 7-year history of constipation. One month later, the diarrhea associated with colicky pain emerged and persisted. She had no travel history outside the residence town in the time before falling ill. All other family members did not eat the fish, and were healthy without any diarrhea. The patient was given a 30-days course of albendazole (400 mg/day). The patient left the hospital at the fifth day of treatment. Till now, the patient had an uneventful and stable recovery through telephone follow-up visit.


A 19-year-old woman was referred to our hospital with complaints of productive cough and massive hemoptysis. One month earlier she had been admitted to a hospital in the northern province of the country with symptoms of fever, weight loss, and bloody sputum. A computed tomography (CT) scan was performed and showed cavitary lesions with nodules in both lungs. Medical therapy for pulmonary infection consisting clindamycin and ceftriaxone was started, but did not respond well to the treatment after 3 weeks. So bronchoscopy was performed which reported an acute severe bronchitis. Culture of bronchoalveolar lavage specimen was negative after a 7-day inoculation and the transbronchial lung biopsy (TBLB) showed pulmonary angiitis granulomatosis compatible with Wegener's granulomatosis. Also antinuclear antibody test (ANA) was positive (1/640) but anti-dsDNA was negative. She was referred to our hospital for a complementary workup.
The patient was a young housewife originally from north Iran. Her illness started 30 days ago with fever, night sweats, weakness, and weight loss of four Kg, that followed with productive cough and hemoptysis, about 20 cc of blood in her sputum for 3 times. She had a normal delivery 5 months ago with a normal infant. She is a nonsmoker, without any history of recent travel or drug abuse. She had no significant medical history except an episode of pyelonephritis when she was 6 years old, recurrent oral aphthous ulcers, and multiple episodes of common cold in the last two years. She had four healthy, living siblings and her parents were not related. Her aunt had pulmonary tuberculosis twenty years ago.
On admission she was dyspneic and febrile with oral temperature of 39°C. Her blood pressure was 110/60 mm Hg, heart rate was 120/min, and respiratory rate was 20/min. Physical examination was unremarkable except pectus excavatum and bilateral course crackles along with rhonchi in right hemithorax. Peripheral blood leukocyte count was 16300/μL with 65% neutrophil, 10% lymphocyte, 11% monocyte, and 14% eosinophil (total eosinophil count: 2282/μL); hemoglobin and platelet counts were 8.6 mg/dL and 552 × 109 per liter. The erythrocyte sedimentation rate was 125 mm/h. All results of biochemical tests were normal. Also c-ANCA, p-ANCA, anti-PR3 IgG, and anti-MPO IgG were negative.
A chest X-ray was done and showed cavitary lesions and nodules in both lungs. Direct smear of sputum for acid fast bacilli was negative three times. Ciprofloxacin and meropenem were started but no improvement was seen in her condition.
The thorax CT scan was performed and showed biapical cavitary lesions and intracavitary soft tissue projection in the left lung. Also scattered nodular infiltration with a large mass-like consolidation was seen in the right lower lobe. Right hilar and subcarinal adenopathy there also reported ().
Bronchoscopy was done which showed a necrotic obstructive mass at the right middle bronchus. No bacterial or fungal agents were isolated from sputum and bronchoalveolar lavage (BAL) fluid. Histopathological study showed filamentous septated hyphae with acute angle branching, without any evidence of granuloma or necrotizing vasculitis. Galactomannan assay index of serum was highly positive (10 ng/mL). Voriconazole was added to her treatment.
Aspergillus fumigatus was isolated from the culture of tissue specimen. Bronchoscopy was repeated for the removal of obstructive mass. Distal to it, a lot of necrotic material was discovered (). Voriconazole was changed to Itraconazole 200 mg t.i.d after seven days of treatment. Brain CT scan was performed and was normal.
The patient's immune system was assessed. Ranges of the immunoglobulins were normal. The nitroblue-tetrazolium (NBT) test was 0%. Also the dihydrorhodamine 123 (DHR) assay confirmed the diagnosis of chronic granulomatous disease (CGD).
Patient's symptoms improved gradually, fever stopped, and she did not have any episodes of hemoptysis at all. Therapeutic dose of Itraconazole was continued for four months, after that it was prescribed as 100 mg once daily concomitant with Trimethoprim-sulfamethoxazole as prophylaxis up to now. Also at the follow-up visits there was no sign of recurrent infection. Screening of the other members of the family was negative for CGD.


A 36-year-old male patient reported to the Department of Conservative Dentistry with a chief complaint of caries with 37 and food impaction in relation to 37 and 38. Clinical and radiographic examination () revealed caries on the distal aspect of 37 encroaching into the pulp space with resorbed distal root and a mesioangular impaction of 38. Involved second molar tooth (37) was nonrestorable and was indicated for extraction. Impacted third molar 38 was a sound, mature tooth without caries and was found to be ideal for transplantation. The mesiodistal dimensions of 37 and 38 were suitable for transplantation.
After taking the complete medical history and explaining the risks and benefits of the procedure to the patient, an informed consent was taken. Patient was prescribed 1000 mg Amoxycillin one hour before surgery to prevent infection and 400 mg of Ibuprofen was prescribed to prevent post-treatment pain. 37 and 38 were extracted atraumatically () without damaging the buccal and lingual cortical plates. Root canal therapy for 38 was completed extra-orally within 30 minutes using ProTaper NiTi rotary files. Care was taken to prevent any damage to periodontal ligament (PDL) cells by holding the tooth at cementoenamel junction, and the roots were kept moist with sterile gauze soaked in coconut water during access cavity preparation. During biomechanical preparation and obturation of the root canals, the roots were wrapped with sterile gauze and were submerged in coconut water in a sterile dappen dish. Access cavity was restored with high copper silver amalgam. Alveolar socket of 37 was widened using surgical bur in a slow speed hand piece, under copious saline irrigation and 38 was transplanted into 37 socket. Suturing was performed with silk thread to stabilize the soft tissues and the transplanted tooth. Nonrigid intraradicular occlusal splinting with malleable orthodontic wire and composite resin was done from 35 to 37 (). Postoperative IOPA radiograph revealed radioopaque object in the interdental area of 36 and transplanted tooth. This could be a fragment of amalgam restoration of 37 that may got impregnated into the tissues during intraradicular groove preparation for splinting. The patient was instructed to perform daily mouth rinsing with 0.12% Chlorhexidine gluconate, twice a day for seven days, Amoxicillin 500 mg thrice daily, Metronidazole 400 mg thrice a day, and Etrobax 120 mg twice daily for 5 days were prescribed.
Sutures were removed after a week and healing appeared satisfactory. The patient was reviewed after 1 week, 1 month, 2 months, 6 months, and 1 year. Non rigid splinting was removed after 2 months. Patient was asymptomatic during recall visits. Clinical examination demonstrated absence of mobility and masticatory dysfunction.The occlusion was found to be normal. There were no signs of loss of attachment. Percussion test did not produce the characteristic metallic sound of ankylosis. At the 1-year followup, radiographic examination revealed healing of the site (). There were no signs suggestive of root resorption or other pathological processes and revealed normal periodontal attachment. At the end of 1 year, bone growth around the transplanted tooth was considered satisfactory.


A 30-year-old Caucasian female presented with a two-week history of central abdominal pain and distension, vomiting, and increased frequency of bowel motion. There had been no weight loss or history of foreign travel. She was known to have coeliac disease diagnosed at age two. She was compliant to gluten-free diet. There was no history of drug allergy, asthma or skin eczema. Abdominal examination showed sign of ascites. There were no stigmata of chronic liver disease. The rest of the systemic examination was also within normal limits. A summary of her laboratory investigations is presented in . Computed tomography of the abdomen and pelvis showed large volume ascites and prominent small bowel loops (Figures and ). There was no evidence of a pelvic or peritoneal mass. A diagnostic paracentesis revealed straw-coloured ascites. Analysis of the ascitic fluid is summarized in . Oesophagogastroduodenoscopy () showed multiple areas of erythematous patches at the superior duodenal angle close to the second portion of the duodenum. Colonoscopy and biopsies of colonic and terminal ileal mucosa were normal. Histological examination of duodenal mucosa revealed Marsh 3a villous atrophy consistent with coeliac disease although no previous biopsies were available for comparison ().
Jejunal mucosa showed dense infiltration of eosinophils on the lamina propria (30/HPF) (Figures and ). There was no histological evidence of an enteropathy-associated T-cell lymphoma, granuloma, or malignancy. Unfortunately, the endoscopist did not obtain oesophageal and gastric biopsies.
Laporoscopic examination showed no evidence of underlying intra-abdominal malignancy. After excluding the possibilities of malignancy, parasitic disease and an autoimmune disorder, eosinophilic gastrointestinal disorder was diagnosed. This diagnosis was based on the presence of peripheral eosinophilia, eosinophilic ascites, and eosinophilic infiltration of the proximal duodenum and jejunal mucosa.
The patient was started on intravenous hydrocortisone 100 mg four times a day with rapid resolution of her symptoms and eosinophilia. She received three days of intravenous hydrocortisone and was converted to a reducing dose of oral prednisolone 40 mg per day for four days. This was reduced to 20 mg per day for four days, 10 mg per day for three days, 5 mg per day for five days, then 2.5 mg per day for seven days, and stop.
However, the length of steroid treatment was greatly influenced by the development of steroid-induced psychosis. The patient was eventually admitted for psychiatric treatment following discharge. Her psychosis had resolved upon discontinuation of steroid and did not require long-term antipsychotic treatment. A repeat computed tomography of the abdomen and pelvis three months after discharge from hospital showed resolution of the ascites and small bowel wall thickening (Figures and ).


On May 2010, a 79-year-old man was hospitalized for severe postprandial abdominal pain, nausea and vomiting. His medical history revealed a HCV-related mild non-progressive chronic hepatitis (diagnosed in 1985; Child-Pugh class A), never treated with anti-HCV therapy. He had a normal body weight (BMI: 25), and did not present any other risk factor for thrombosis, such as smoking, alcohol intake or diabetes mellitus. Furthermore, his family history was negative for bleeding or clotting disorders. Since 1996, he was under treatment with lisinopril/hydrochlorothiazide (20/12.5 mg/day) for hypertension. Fifteen days prior hospitalization, he was placed under treatment with indomethacin (100 mg/day) for back pain. After 11 days of indomethacin therapy, the patient started to complain of dyspepsia and abdominal pain, which worsened rapidly leading to his hospitalization.
At admission, physical examination revealed a tractable and painful abdomen. The patient reported a past sporadic use of anti-inflammatory non-steroidal drugs (NSAIDs) and no previous indomethacin intake. Blood tests showed increased neutrophil count and alanine aminotransferase, as well as moderate reductions of platelet count, activated partial thromboplastin time (aPTT) and antithrombin III. However, the prothrombin fragment F1+2 was not assessed, and therefore a clear information about the status of thrombin generation in this patient could not be obtained. Notably, all these parameters were within their normal ranges on a previous assessment, performed about 2 months earlier (i.e. 45 days before starting indomethacin), during a scheduled visit for monitoring his liver function and general health condition. Relevant laboratory parameters, recorded before and throughout the hospitalization, are summarized in Table
. Abdominal ultrasonography displayed: liver with regular margins and fine heterogeneous structure; ascites involving all quadrants; increase in the diameter of portal vein (17 mm). Both ascites and portal vein ectasia had not been detected on recent past follow-up ultrasounds. Based on leukocytosis, the clinicians hypothesized a bacterial infection, and started a treatment with ciprofloxacin (1000 mg/day). In addition, indomethacin was discontinued, as its possible involvement in the pathogenesis of abdominal symptoms was suspected.
On day 4, a follow-up abdominal ultrasound confirmed previous findings and displayed diffuse small bowel distension, without colonic involvement. An upper digestive endoscopy did not reveal erosions, ulcerations, mucosal dysplasia or gastro-esophageal varices. On day 5, a virological blood screening was performed: cytomegalovirus (CMV) IgM index was negative, while IgG levels were positive, suggesting a past infection; anti-HCV antibody, anti-HCV IgM and HCV core antigen were positive; screening tests for hepatitis B virus were negative. A CT-scan of chest and abdomen, with intravenous contrast medium, revealed: massive thrombosis of portal trunk; partial thrombosis of left portal vein branch and superior mesenteric vein; mild ascites and ileal distension, with parietal thickening; mild lymphadenopathies in the hepatic hilum, celiac trunk and intercavo-aortic region; and no sign of cancer or suspected lesions. A diagnosis of PVT was then made, and a treatment with fondaparinux (7.5 mg/day) and antithrombin infusion (2000 UI) was started.
On day 7, a decrease in protein C (30%, reference range 72-146%) and protein S (30%, reference range 70-140%) was detected. However, both parameters had never been altered in past assessments. A genetic screening did not show relevant mutations. Treatments with intravenous antithrombin and oral ciprofloxacin were discontinued. On day 11, a follow-up abdominal CT scan, with contrast medium, displayed the persistence of thrombosis in portal trunk, left portal vein branch and superior mesenteric vein, with a reduction of intestinal distension and ascites. Moreover, an abdominal Doppler confirmed an almost complete PVT. Throughout the hospitalization, the patient had some episodes of red bloody stool excretion, which were ascribed to his venous stasis.
On day 15, the severity of postprandial pain decreased significantly, and the patient was discharged. After discharge, he remained on fondaparinux for 12 days, and then he was switched to warfarin with the goal of maintaining the international normalized ratio within the therapeutic range of 2–3. Thirty days later, a follow-up ultrasound did not show appreciable signs of PVT. At 2 years from discharge, several follow-up visits have shown that the patient persists on a stable mild liver disease and he has not experienced further thrombotic events.


A 5-year-old male patient reported with the chief complaint of discolored upper front teeth. There was no relevant medical or dental history. On intraoral examination, dental caries was present in 51, 52, 61, 62, 74, 75, 84, and 85. An accessory cusp like projection was seen in relation to the lingual surface of 82 which extended from the cervical region to almost two-thirds of the incisal edge suggestive of a talon cusp (). Intraoral periapical radiograph was taken in relation to 82 which not only confirmed the presence of a talon cusp in 82 but also revealed the presence of permanent tooth buds of 31, 32, 41, and 42 with no abnormal finding (). The patient had no clinical problems associated with the presence of the talon cusp. Hence, no treatment such as grinding or reduction of the talon cusp was done. Restoration of the carious teeth was done and topical fluoride was applied. The patient was asked to report after every three months for review.


A 43-year-old male presented to our emergency department with complaints of elbow injury. The patient was wake boarding in the ocean and subsequently fell into the water. In order to break his fall, he threw his arms out in front of him. After the event, he noted pain in both elbows and noted decreased strength in both elbow extensors. He noted the right elbow to be worse than the left. The patient also noted a “knot” near the elbow on the right that was not present prior to the event. Furthermore, the patient denied loss of consciousness, no neck pain, and any other complaints. On social history, the patient is a healthy police officer, who does not take any medications and does not smoke or does illicit drugs.
On physical exam, the patient's vital signs were unremarkable with a normal temperature, pulse, respiratory rate, and blood pressure. The patient's physical exam was completely normal except for his extremity exam. The patient had normal radial pulses and normal capillary refill. He also had a normal sensory exam to pinprick and light touch. Motor exam revealed normal 5/5 flexor strength in bilateral upper extremities. Inspection revealed preserved lateral triceps head integrity, tension during extension on both sides, and swelling near the elbow which were thought to be tendon attachments. On formal extensor motor exam, the patient was barely able to overcome gravity on both the right and left sides. He was noted to have minimal engagement of the medial and long heads of both triceps. The examination was noted to be difficult due to the bilateral nature of the injury and the inability to compare the affected sides.
Bilateral plain radiographs of the elbow were ordered. The right elbow radiograph showed an avulsion fracture of the right olecranon with no dislocation. The left elbow radiograph was the same, showing an avulsion fracture of the left olecranon. Orthopedic surgery was consulted and they requested magnetic resonance imaging of both upper extremities. The MRI of the left elbow showed an avulsion fracture at the distal triceps insertion, with 2.6 cm proximal retraction of the triceps tendon. In addition, there was an ulnar collateral ligament was noted to strip off the corresponding tubercle. The MRI of the right elbow demonstrated an acute rupture of the triceps tendon with an avulsion fracture of the olecranon. There was no dislocation noted. Orthopedic surgery subsequently placed bilateral long arm splints on the patient and he was discharged from the emergency department (Figures , , , , , and ).
He was subsequently seen by orthopedic surgery as an outpatient and successfully had each triceps tendon sutured to bone bilaterally, with no complications. The patient successfully resumed his career as a police officer with no limitations.


A 47-year-old man with a history of hypertension presented with fever, dyspnea, and chest discomfort for one day. He denied any other medical history, including HIV infection. On arrival in the emergency department, his body temperature was 38°C, and blood pressure was 207/125 mm Hg. Physical examination was unremarkable. The laboratory findings were as follows: white blood cell 14300/mm3 with predominance of neutrophils (89.8%) and C-reactive protein 213 mg/L (normal reference < 6 mg/L). Cardiac enzyme, arterial blood gas analysis, renal function, and electrolytes were within normal range. Chest X-ray did not show pneumonia patch, and urinalysis did not reveal pyuria. Computed tomography (CT) of chest and abdomen showed an aortic intramural hematoma from the arch to suprarenal level (). Intravenous ceftriaxone (2 g every 12 hours) was administered under the impression of infected aortic aneurysm after collection of two sets of blood culture. Two days later, cultures of blood grew K. pneumoniae which is only resistant to ampicillin. Because he continued having intermittent pyrexia, antibiotic was switched to ceftazidime (2 g every 8 hours) and gentamicin (80 mg every 8 hours). Thereafter, the patient's fever gradually subsided, and repeat blood cultures were negative. On the 20th day, sudden onset of fever (39°C) recurred, and hypotension developed. Repeat CT showed progressive dilated aorta and enlarged intramural hematoma (). Emergency operation with aortic grafting was performed, but the patient's condition gradually deteriorated, and the patient died eight days after surgery. The repeated blood culture on hospital day 20 and the specimen of excised aorta all grew K. pneumoniae. All of the K. pneumoniae isolates have the same antibioticgram, which is only resistant to ampicillin. The pathology report disclosed atherosclerosis, necrotizing inflammation, organized hematoma, and bacterial clumps in the aortic wall, which are compatible with mycotic aneurysm. Finally, the diagnosis of K. pneumonia-related mycotic aneurysm was confirmed.


A 61-year-old woman was found confused on her floor by paramedics after they were called by concerned neighbors, who had not seen her for five days. Upon arrival to the emergency department (ED), the medics reported seeing no unusual circumstances in her residence but relayed that she had been “acting odd” at a neighborhood party five days prior. The patient was unable to provide any information secondary to her altered mental status. Initial vital signs in the ED were a temperature of 36.6°C, a pulse of 94/min, respiratory rate of 18/min, a blood pressure of 134/59, and O2 saturation of 96% on 4 L O2 by nasal cannula placed in the field. Medications found in the home by EMS included rosuvastatin, nadolol, albuterol inhaler, citalopram, and a lidocaine patch. The above medications for a medical history of hypertension, hyperlipidemia, asthma, bipolar disease, and chronic back pain were confirmed by telephone with her daughter. She had a partial gastrectomy for a peptic ulcer eight years prior and had been sober from alcohol for five years. Physical exam revealed a lethargic uncooperative patient with incoherent verbalization who withdrew only the right upper extremity from noxious stimuli. She had icteric sclera, mild jaundice, and dry mucus membranes. There were no topical medication patches in place. The stool was negative for occult blood, and chest and abdominal exam were unremarkable. There was no nystagmus, and the remainder of her neurologic exam was limited by her inability to participate.
Suspecting neurological, metabolic, or toxicologic catastrophes, a CT-head and full complement of laboratory tests were ordered. The CT-head showed no acute abnormality. Hematologic studies revealed a white blood cell count of 3,600/mm3, a platelet count of 138,000/mm3, and a hemoglobin level of 15.5 g/dL. Electrolytes were normal except for a blood urea nitrogen (BUN) of 53 mg/dL (normal 7–20 mg/dL). Her initial creatinine level was 0.7 mg/dL, and her GFR was 90. Other lab results included a lactate of 2.7 mmol/L (0.4–2.2 mmol/L), an INR of 3.07, a troponin T of 0.04 ng/mL (normal <0.01 ng/mL), and a creatine kinase of 531 U/L (24–170 U/L). Serum toxicology levels were normal, with acetone present but less than 10, and an acetaminophen (APAP) level of 3 mg/L (10–20 mg/L). Transaminase levels were initially delayed and returned one hour later with elevation of the aspartate aminotransferase (AST) level up to 1240 U/L (0–34 U/L), alanine aminotransferase (ALT) to 1450 U/L (0–34 U/L), and alkaline phosphatase (AP) of 238 U/L (30–130 U/L). Potassium and ammonia levels were unavailable due to hemolyzed blood samples. Direct and indirect bilirubin levels were 5.8 mg/dL (<0.2 mg/dL) and 9.3 mg/dL (<1.2 mg/dL), respectively. Urinalysis was dark with a specific gravity of 1.018, moderate bilirubin, moderate ketones, and no evidence of infection. The electrocardiogram was normal except for a premature atrial complex. A chest X-ray was normal. No prior records were available for comparison.
The patient was given 2 L of normal saline based on a clinical exam consistent with dehydration. Intravenous NAC treatment was initiated to treat acute liver failure. The normal APAP level did not contradict the NAC use, but pointed to a possible etiology for this patient's liver failure. She was admitted to the intensive care unit and evaluated by the liver transplant team. An ammonia level drawn 12 hours after presentation was 70 μmol/L (11–35 μmol/L), and she demonstrated asterixis as her mental status cleared. A complete 20-hour IV NAC regimen was completed, and lactulose given PO, and the patient recovered without serious sequelae. An ultrasound of the liver showed minimal evidence of fatty infiltration but revealed no sonographic evidence of cirrhosis. At discharge five days later, her AST had decreased to 96 U/L, her ALT to 212 U/L, and her AP to 174 U/L. Her bilirubin levels remained high at direct of 13.3 mg/dL and total of 17.7 mg/dL, but the INR had normalized to 1.27. After return of mental capacity, the patient denied relapse of her sobriety from alcohol and endorsed taking “a lot of Tylenol” four days prior to presentation. She refused to comment on the specific quantity or her motivation for taking the pills.


A 75-year-old Caucasian female presented to the Internal Medicine Department with high fever, diffuse abdominal pain, and pseudodiarrhea. After thorough clinical and laboratory testing, ileus was diagnosed and the patient was admitted to the department. She did not recall any history of malaise, fatigue, night sweating, weight loss, or preceding trauma. Her past medical history revealed a left hip hemiarthroplasty, 5 years ago, due to a subcapital femoral fracture.
On admission, she had fever (38.2°C) attributed partially to a urinary tract infection as well as to the infected knee joint. Pseudomonas aeruginosa was isolated from urine cultures. After administration of appropriate antibiotic therapy, the patient's body temperature returned to normal. However, despite the initial treatment of the ileus, consisting of enemas, correction of fluid and electrolyte imbalance, and administration of appropriate antibiotics and analgesics, the patient continued to experience diffuse abdominal pain, flatulence, and pseudodiarrhea. Lumbar pain and sciatica were added to the clinical picture. The clinical examination of the right lower limb revealed a positive Lasègue sign at 45° as well as reduced muscle power, sensation, and tendon reflexes. At this stage, cauda equina syndrome was considered to be the most probable diagnosis. However, few days later, the patient became feverish again (38.5°C) and had dyspnea and profuse watery diarrhea. The patient's general condition started to rapidly deteriorate. Blood cultures revealed an anaerobic organism, and parenteral nutrition was administered along with a triple scheme of antibiotic therapy (teicoplanin, netromycin, and ciprofloxacin). Two weeks later, patient's right knee joint became reddish, hot, and edematous while palpation revealed crepitation. Emphysematous cellulitis of the knee was diagnosed at this stage. Surgical debridement was immediately performed, revealing a seropurulent wound discharge. E. coli and Enterococcus were isolated from the obtained cultures. Despite the thorough debridement and the appropriate adjustment of the antibiotic therapy (penicillin, vancomycin, and amikacin), the patient remained febrile and the surgical wound purulent. A new wound culture revealed Pseudomonas aeruginosa and E. coli, while a blood culture revealed a gram-negative microorganism. The patient's general condition continued to deteriorate with dyspnea, tachypnea, cyanosis, Hippocratic face, and decreased level of consciousness. Radiologic examination of the right femur demonstrated the presence of gas between the muscles and subcutaneous tissue (). Within 24 hours from the last deterioration, under epidural anesthesia, the anterolateral surface of the right thigh was dissected. Approximately 2 liters of pus were drained from the space between the muscles and the totally detached fascia, and thorough mechanical fluid lavage and tissue debridement were performed. Purulent fluid resembling diarrhea along side with gas bubbles was observed while the surrounding tissues were necrotic (). Since fecal discharge and gas bubbles were seen coming out of the greater sciatic foramen, during provoked coughing, a fistula between the intestine and the wound was suspected to be the cause of the patient's condition. A general surgeon performed a rectal digital examination and recognised a rectal perforation 5 cm proximal to the anal ring. Radiologic examination of the pelvis by means of a gastrografin enema revealed the presence of a recto-femoral fistula treated surgically with an emergency sigmoidostomy (Figures and ). During the next 19 days, mechanical lavages were routinely performed and appropriate antibiotic treatment was administered. On the 20th postoperative day, the distal end of the surgical wound was closed.


A 30 year old single unemployed man was presented to our out-patient psychiatry clinic because of a recurrence of the psychotic episode. The patient did not have any comorbidity with medical diseases or substance abuse disorders in the past. Recurrence of the psychotic episode was due to the self-discontinuation of quetiapine secondary to recurrent priapism. He was diagnosed with paranoid schizophrenia since 10 years ago. His main symptoms included delusions of control, persecutory delusion, and auditory hallucination. His symptoms were relatively controlled. He had several recurrences and all of them were associated with drug discontinuation due to the patient's lack of compliance. He did not have any major stressors before recurrences. He was under treatment of first- and second-generation antipsychotics. He developed drug-induced Parkinsonism several times which was resolved with dose-adjustment and anti cholinergic therapy. The patient experienced priapism secondary to use of some antipsychotic medications like risperidone, olanzapine, clozapine and finally quetiapine. The diagnosis of priapism was confirmed by a urologic consult. All medical causes of priapism were ruled-out by a thorough urological history and physical examination. To prevent priapism, we substituted the combination therapy of lithium and sodium-valproate for control of psychotic symptoms. After six months he again experienced psychotic symptoms. Then, we started a low-dose quetiapine (25mg per day, gradually increased to 100mg per day). After 2months of this regimen, he experienced a 6- hour-long painful priapism. It was resolved with diazepam use without any surgical intervention. Despite reducing the quetiapine dose to 25mg per day, he experienced priapism every 4–5days. Astonishingly, he did not experience priapism with accidental cigarette smoking. As mentioned above, the patient did not have a history of substance abuse disorder. He accidentally and adaptively smoked cigarette to get rid of priapism. After a two-week challenge test of smoking cessation, he re-experienced priapism again. After all the challenges and even though smoking is considered a maladaptive behavior to get rid of the side effects, the patient decided to keep on smoking while consuming quetiapine. He has not been complaining of priapism since then. Patient signed a consent form for publication of this report.


A 47-year-old male presented to the emergency department (ED) complaining of nausea, vomiting, diarrhea, stomach pain, and constant hiccups for three days. He had attributed his symptoms to having the flu and had been self-medicating with DayQuil and NyQuil without relief. The nausea and vomiting were not associated with eating or drinking and emesis was described as nonbloody and nonbilious. His past medical history was significant for previously treated tuberculosis. He denied any medications, allergies, or past surgeries. He lived alone and denied any current use of alcohol, tobacco, or illicit drug use but endorsed prior abuse of alcohol, cocaine, and marijuana. He was an unemployed construction worker with no recent travel.
Review of systems revealed increased fatigue over the prior 4-5 days, an estimated 30 pound unexpected weight loss over the past three months, peeling of palms and recent upper respiratory infection symptoms, but was otherwise negative.
Upon arrival, his vital signs were as follows: oral temperature 97.3°F, blood pressure 123/78, heart rate 72, respiration rate 20, and an oxygen saturation of 96% on room air. He was noted to be persistently hiccupping, although in no acute distress and generally well appearing. Examination of the ENT, neck, chest, and cardiovascular system were within normal limits. Abdominal exam was soft and exhibited normal bowel sounds. There was mild epigastric tenderness to palpation, no guarding, no rebound, and no masses. Rectal exam revealed guaiac positive stool. He was noted to have mild desquamation of his palms bilaterally.
ED laboratory results were significant for WBC 28 K/cumm, hemoglobin 12 gm/dL, hematocrit 32%, and platelets of 84 K/cumm. Sodium was 125 mmol/L, bicarbonate 20 mmol/L, BUN 121 mg/dL, and creatinine 5.3 mg/dL. An ED visit 4 years prior demonstrated a creatinine of 1.0 mg/dL. Bilirubin was 4.9 mg/dL, AST 185 IU/L, ALT 93 IU/L, and ALP 158 IU/L. The urinalysis revealed 11–20/HPF WBCs, positive nitrates, and many bacteria but was otherwise negative. A KUB X-ray was obtained demonstrating a 1.2 × 0.7 cm rounded opacity overlaying the expected course of the left ureter.
The patient was administered normal saline IV fluids and chlorpromazine 25 mg IV with temporizing affect of the hiccups. A workup for postobstructive uropathy was initiated, including a renal ultrasound which showed mild left hydronephrosis with a proximal 1.1 cm ureteral stone ().
Urology was consulted and a CT IVP was obtained. In addition to prior findings of hydronephrosis and a 1.1 cm ureteral stone, a subcapsular fluid collection concerning for an abscess was noted overlying the left kidney (). The patient was started on empiric IV ciprofloxacin and admitted to the Internal Medicine service. An emergent percutaneous nephrostomy tube was placed.
During the patient's hospital admission, he was converted to an oral antibiotic regimen which initially responded well to therapy. It was noted, however, that the patient continued to experience persistent hiccups. A subsequent increased leukocytosis and recurrent fever prompted a repeat CT IVP which demonstrated another left subcapsular fluid collection concerning for abscess. A second percutaneous nephrostomy tube was placed and an additional course of IV antibiotics started, with subsequent resolution of the patient's hiccups and normalization of his renal function. He was discharged in good condition 3 days later and subsequently lost to followup.


A 47 years old male transported to the Emergency dept. of our hospital after a car crash. At the arrive in ER the patient was shocked with a bi-lateral pneumothorax, multiple rib fracture (II-III-IV-V-VI) with flail-chest on the right side (Figure ), haemo-peritoneum and an exposed fracture of the right femur. Bilateral thoracic drains were immediately positioned and the patient was then transferred to the theatre for an explorative laparotomy and liver packing. Two days after the packing have been removed and the flail-chest (III and IV ribs) was fixed with titanium devices. The femur fracture was temporarily treated with external fixator. Ten days after the intervention the postoperative course was complicated by a biliary fistula treated with ERCP and biliary endo-prosthesis positioning. During the ICU recovery the patients developed ARDS and chest wound infection. Blood samples and chest wound cultures demonstrated infection by Aspergillus Fumigatus and Pseudomonas Aeruginosa MRSA respectively. The antibiotic treatment have been immediately addressed. 21 days after the intervention the patient have been re-operated for hemorrhagic shock from erosion of the right internal mammary artery by the rib margin. Surgical haemostasis was necessary. Free segment of the III and IV ribs were removed. Due to the infection titanium devices were removed too and the defect (7×8 cm) was repaired using a biologic mesh (CollaMend®, 18×23 cm) fixed to the thoracic wall with PDS-0 interrupted suture (Figure ). 9 days after the second intervention a thoracic-abdominal CT-scan was performed (Figure ). It documented no thoracic pathologic findings, satisfactory post-surgical results and a left hepatic artery post-traumatic pseudo-aneurism treated with angio-embolization. Femur fracture was then definitively treated with endomidollar pin positioning. Chest wound infection was treated with medication and healed completely in four weeks (Figure ). 18 months after the discharge the patient is well and with documented no respiratory impairment.


A 36-year-old male patient visited the local hospital for the chief complaint of discomfort of the upper abdomen. An appendectomy was performed under the clinical diagnosis of acute appendicitis. During the operation, a tumor was observed in the colon. The operation was aborted because of an inability to remove the tumor. Two days later, a computed tomographic (CT) scan of the abdomen revealed the mass arising from the ascending colon. The regional enlarged lymph nodes and metastases in the liver were noted (Figure ).
The patient was transferred to our hospital for treatment. Tumor markers, including carcinoembryonic antigen, cancer antigen 19–9 (CA 19–9) and CA 125, were in the normal range. His serum beta human chorionic growth hormone (β-HCG) level was 3.38 mIU/ml. A colonoscopy revealed a yellow tumor in the colon (Figure ) and endoscopic biopsy findings suggested a poorly differentiated adenocarcinoma. After two days, a colectomy was performed. The tumor located in the ascending colon measured 4 cm × 5 cm and penetrated the serosa and the mesocolic fat, with 12 adjacent enlarged lymph nodes. The pathologic findings showed that the tumor invaded the serosa of the intestinal wall and was composed of syncytiotrophoblastic cells, cytotrophoblast-like cells and intermediate trophoblastic cells. Necrosis and hemorrhage were also noted in the mass. Immunohistochemical staining was positive for HCG and negative for cytokeratin 7, cytokeratin 20, villin, caudal type homeobox 2, α-fetoprotein and CD30 (Figure ). Metastasis was found in the liver and in eight of the excised lymph nodes.
Systemic chemotherapy using bleomycin, etoposide and platinum was performed. Chemotherapy engaging etoposide phosphate 100 mg, cisplatin 30 mg, bleomycin 18 mg was initiated. The β-hCG level increased from 3.38 to 10,000 mIU/ml after the first course of chemotherapy, and CT showed another mass in the liver. After three cycles of chemotherapy, his β-hCG level remained high. Because of the progression of disease, the patient and his family abandoned other alternative regimens of chemotherapy.


A 48-year-old Chinese male visited his local hospital in May 2010 with a gradually enlarged and ulcerated erythematous plaque on his right knee. The patient stated that the lesion had been presented on the extensor side of his right knee for approximately 6 months and treated with a steroid ointment initially. However, the lesion gradually enlarged and ulcerated, and a new skin nodule presented with pain during the last few months. As a result, the patient was referred to our hospital for examination and treatment. Physical examination showed 8.0 cm×6.0 cm well-defined ulcerated plaque on the extensor side of his right knee. A solitary nodular mass, measuring 1.5 cm in diameter was also found near the large ulcerated lesion (Figure ). There was no weight loss and no palpable lymphadenopathy or organomegaly. The laboratory results, including blood count, differential, liver and renal function, were within the normal range. A clinically presumed diagnosis was squamous cell carcinoma of skin. Surgical resection of the skin lesion without preoperative skin biopsy was performed. After diagnosis, the patient underwent polychemotherapy according to a CHOP protocol (cyclophosphamide, doxorubicin, oncovin, and prednisone) for six cycles. The skin ulcerated lesion regressed and the nodule became smaller in size. The patient was on a regular follow-up period for 12 months after chemotherapy. The bone marrow examination was performed 6 months after chemotherapy, but there was no abnormality found. Since there was a possibility of multiple organs involvement, the patient was referred to a whole body positron emission tomography/computed tomography (PET/CT) study to search the potential secondary tumor, but no abnormality was found. During the period of follow-up, there was no sign of recurrence of tumor and lymph node enlargement.


A 69-year-old Tunisian female with no family history of auto-immune disease. She had a history of hypertension and was explored 4 years prior to admission for transient arthralgias and arthritis. At age 69, she experienced photosensitivity, malar rash and diffuse discoid lesions in her trunk and face for which she visited our hospital. She also reported weight loss of approximately 3 kg in the last three months. She had no history of drug abuse or significant alcohol consumption prior her admission. The physical examination showed synovitis of the wrists. Her general state of health was regular, eupneic. Cardiovascular and respiratory examinations were within the normal range. The patient had no previous laboratory tests. On admission, her initial laboratory tests were as follows: erythrocyte sedimentation rate at 45 mm/1st hour associated with hyper-γ-globulinemia 20 gr/l. Her leukogram showed lymphopenia 850/mm3, and platelets were normal. Creatinin and urinalysis are normal. The autoimmune profile confirmed a strong positivity of Antinuclear antibodies (ANA) with titre 1:400 and anti-double-stranded DNA (anti-dsDNA) at 115 UI/ml with normal serum complements. The patient was non-reactive for the following antibodies: anti-La; anti-cardiolipin; lupus anticoagulant; anti-SM; anti-RNP; anti-SCL-70; and anticentromere, rheumatoid factor and autoantibodies against citrullinated protein. Serology for VDRL was negative, hepatobiliary enzyme and lactate dehydrogenase levels were within normal range. Therefore, presence of 6 of 11 American College of Rheumatology criteria (photosensitivity + malar erythema + positive ANA and anti-dsDNA tests + hematologic abnormalities including lymphopenia + arthritis) allowed the diagnosis of SLE. The patient was treated with Chloroquine (200 mg/day). The patient showed improvement of her general state of health, and weight gain. No aggravation of SLE was observed. However one year later, she developed liver dysfunction. The patient was referred to gastroenterology unit. On physical exam, skin rash involving her face was observed. Abdominal examination revealed neither hepatosplenomegaly nor pruritus. Laboratory investigations revealed a normal complete blood count and urinalysis. His erythrocyte sedimentation rate was at 60 mm/1st hour while C-reactive protein was within normal range. Concentrations of both serum cholesterol and triglyceride are normal. Blood creatinine clearance 80 mL/min and there was no proteinuria. Aspartate aminotransferase 92 IU/L (normal range: 8–38); alanine aminotransferase 87 IU/L (normal range: 4–44 IU/L) (2 times above the normal limit), total bilirubin 0.9 mg/dl; alkaline phosphatase 107 IU/L, gammaglutamyl transpeptidase 42 IU/L and lactate dehydrogenase 230 IU/L are at normal range. Antimitochondrial antibodies (AMA) were positive (1:164), with positive anti-E2 fraction. The antinuclear antibody was positif as well as anti-dsDNA. Negative results were seen for anti-smooth muscle antibody and anti-centromere antibody. Serologic makers for hepatitis B and hepatitis C viruses were negative. Abdominal echo showed no fatty change of the liver and no abnormality of the bile ducts. Biochemical liver tests and AMA results are compatible to PBC. However, liver biopsy is required to give information on the stage of PBC. Microscopic examination reveals a focal florid duct lesion characterized by a portal lymphocytic infiltrate and epitheloid cells that are centred on interlobular ducts with evidence of destruction (Figure ). These lesions are associated with a lymphocytic cholangitis and a portal inflammation containing conspicuous plasma cells and numerous lymphocytes (Figure ). No granuloma was found in lobule. These findings led to a diagnosis of stage I PBC according to Scheuer’s classification. Based on the hematology and liver-tissue results, as well, she was diagnosed with asymptomatic PBC. Treatment with ursodeoxycholic acid (600 mg daily) was started. The transaminase levels normalized with one month. The patient has not complained liver dysfunction. She was followed up regularly with stable health.


An 82-year-old male was admitted to our hospital on October 5, 2011, with a 2-week history of right-sided flank pain and abdominal fullness. An abdominal sonogram revealed a huge liver mass and the patient was then admitted to our gastrointestinal (GI) section. The patient had a history of well-controlled chronic obstructive pulmonary disease (COPD), hypertension and benign prostate hyperplasia. The patient had herniorrhaphy 1 year earlier and had received amlodipine, tamsulosin and PRN ipratropium/albuterol turbu-haler. The patient had no known allergies and had smoked half a pack of cigarettes per day for 40 years, after which the patient quit for 20 years.
Laboratory data revealed the following: white blood cells, 52,310 cells/μl with 46.3% neutrophils and 45.4% eosinophils; 13.3 g/dl hemoglobin and 242,000 cells/μl platelets; renal functional insufficiency with 36 mg/dl blood urea nitrogen (BUN) and 1.4 mg/dl creatinine; a routine stool test revealed no evidence of parasite infection; immunoglobulin E level was 99.1 IU/ml and the levels of tumor markers in the blood, including carcinoembryonic antigen (CEA; 6.47 ng/ml) and cancer antigen (CA) 19-9 (49.81 U/ml), were elevated.
On admission, crackles were heard in the right lower lung field. Abdominal palpation revealed mild epigastric tenderness without muscle guarding. A chest radiograph revealed an ill-defined mass lesion ∼5 cm in size in the right middle lung zone (). Computed tomography of the chest revealed a right middle lung lobe mass and multiple variable-sized nodules in the two lung fields. Computed tomography of the abdomen demonstrated several peripherally enhancing lesions in the lobes of the liver. Magnetic resonance imaging of the brain revealed no evidence of metastasis. Whole-body bone scan revealed multiple bone metastases. Biopsies of the liver and lung mass were performed and pathology revealed poorly differentiated adenocarcinoma of the lung, positive for thyroid transcription factor-1 (TTF-1; ). Definitive oral-targeted therapy was advised if epidermal growth factor receptor (EGFR) abnormality was present due to the patient’s end stage and old age.
The patient was discharged following completion of the staging work-up and waited for the result of the EGFR analysis. One week later, the patient was readmitted for cognitive disturbance and shortness of breath. On arrival, the patient was noted to be agitated and disoriented and had disorganized speech. Physical examination revealed diffuse wheezing over all lung fields. Pitting edema was noted on the legs. The peripheral white blood cell count had increased 4-fold over a week (168,800 cells/ml), with a proportional increase in eosinophil counts (55.2%). Elevated potassium (5.6 mmol/l), uric acid (13.8 mg/dl), creatinine (2.7 mg/dl) and lactate dehydrogenase (LDH; 420 U/l) levels were also noted. Chest radiography demonstrated diffuse infiltration and ground glass opacities over the two lung fields in addition to the previous finding (). Brain computed tomography presented no special findings. Bone marrow biopsy was performed, which revealed reactive bone marrow hypercellularity with a markedly high eosinophil count (). The average percentage of eosinophils was 39%, compared to 1–5% in normal bone marrow. Chromosomal analysis demonstrated normal karyotype. Immunohistochemical analysis using the monoclonal mouse anti-human IL-5 antibody (R&D Systems, Minneapolis, MN, USA) demonstrated that IL-5 was specifically expressed in tumor cells (). Lung cancer-associated paraneoplastic eosinophilia and acute renal dysfunction were diagnosed.
The patient was treated with hydration and allopurinol to control extreme hyperuricemia. Due to the old age and weak condition of the patient, anticancer treatment was not provided. Since eosinophilia-related organ damage was suspected, hydroxyurea and corticosteroid were administered to reduce the number of eosinophils. The white blood cell count was reduced significantly after 9 days of treatment to 65,500 cells/μl with 23% eosinophils (). The patient’s conscious state, kidney function and blood cell count improved following treatment. However, the dyspnea persisted and the patient acquired pneumonia 4 days after the second admission. The family refused further treatment and intervention due to the poor prognosis. The patient succumbed to healthcare-acquired pneumonia with severe sepsis due to Pseudomonas aeruginosa, 10 days after admission.


A 25-year-old primipara patient was admitted to hospital at 32 weeks of pregnancy due to a headache for 1 month and blurred vision for 20 days. The patient was in the third trimester of pregnancy. Ultrasonography (USG) showed a single intrauterine live pregnancy with occiput presentation. A magnetic resonance imaging (MRI) scan showed a left frontoparietal mass (size: 6x5x5 cm) with peripheral enhancement (), with a shift of the median line.
After multidisciplinary consultation with the neurosurgery, obstetrics and anesthesiology departments, the initial decision was to delay the neurosurgery until after delivery. The patient and her family agreed with this strategy. The decision was made to treat the patient with dexamethasone to control the cerebral edema and accelerate fetal lung maturity. However, the patient’s visual acuity rapidly worsened. Therefore, the patient was scheduled for a CS and neurosurgical resection of the tumor under general anesthesia at 34 weeks’ gestation.
A live 1,900-g female was delivered 6 min after the skin incision. The neonate’s Apgar score at 1 min was 8 and after 2 min, the Apgar score sharply decreased to 3. The neonate was resuscitated immediately with intermittent positive pressure breathing and 0.04 mg naloxone was administered intramuscularly 5 min later. The Apgar score returned 8. The neonate was then admitted to the neonatal intensive care unit.
Oxytocin (10 units) was administered i.v. to improve the uterine contraction. Following delivery, the neurosurgical resection of the tumor was performed uneventfully. The patient recovered quickly from anesthesia without any neurological deficit and was extubated in the operating room.
The pathology laboratory revealed an astrocytoma, which was WHO grade III. The positive expression of glial fibrillary acidic protein (GFAP), CD34, p53, Olig-2, vimentin and isocitrate dehydrogenase-1 (IDH-1) were observed by immunohistochemical staining techniques. The patient was discharged 7 days after surgery. Adjuvant therapy was initiated 2 weeks after surgery. The patient completed radiotherapy and chemotherapy by taking temozolomide for 6 months post-craniectomy. The mother remained in a good condition and the baby was observed to develop normally throughout the 12-month follow-up period.


A 42-year-old, gravida 4, para 3, patient was hospitalized at 34 weeks’ gestation due to a severe headache and vomiting for 15 days. The patient was admitted to the Xuanwu Hospital and was hemodynamically stable, with bilaterally reactive pupils. The patient’s previous obstetric history included three full-term pregnancies with two vaginal births and one CS. A physical examination confirmed weakness in the faculty of memory, indifference of facial expression and a Glasgow Coma Scale score of 13/15. An MRI scan showed a right frontal lobe tumor with an intratumoral hemorrhage (), causing a significant midline and brain shift toward the left side. Obstetric USG showed a single intrauterine live pregnancy with breech presentation which was concordant with its gestational age. The patient was otherwise healthy and denied any previous history of disease. The laboratory results were within the normal ranges. Due to the presence of an intratumoral hemorrhage, termination of the pregnancy was recommended. Following mannitol and steroid infusion, the patient was taken to the operation room for CS followed by neurosurgical resection of the tumor.
CS and craniotomy in the supine position were performed under general anesthesia. A healthy 2,450-g female was delivered by CS 5 min after the skin incision. The female neonate had an Apgar score of 9 at 1 min and 10 at 5 min after delivery and was taken to the neonatal intensive care unit for observation.
Ten units of oxytocin were administered intravenously to improve the uterine contraction after clipping the umbilical cord. The obstetrician massaged the uterus regularly to improve uterine tone during the neurosurgical procedure, which was performed uneventfully. At the completion of craniotomy for resection of the brain tumor, the patient was extubated while fully awake in the operating room and then transported to the intensive care unit.
The pathology laboratory reported an anaplastic oligodendroglioma, WHO grade III. Immunohistochemistry of the tumor cells revealed positive p53, IDH-1 and Ki-67 (40%) expression and partially positive GFAP, CD34 and EMA expression. The patient was discharged 8 days after surgery. The patient received radiotherapy 25 times and treatment with chemotherapy using temozolomide was administered in another hospital.
At follow-up 6 months after discharge, the mother was observed to have an adequate condition and the newborn was observed to be in a good neurological and behavioral state of development.


A 16-year-old boy sought treatment with the chief complaint of proclined upper and lower anterior teeth. To fulfill the objectives of the patient we decided to go for fixed orthodontic appliance therapy along with extraction of all first premolars. All the first and second molars were banded. Upper and lower bonding was done. Patient's followup was done for three months. After that the patient reported to the clinic a complaint of ingestion of some part of the appliance. On examination it has been noticed that second molar band in the upper right side was missing. In search of missing band we did abdominal X-ray. The swallowed band was found in the upper abdomen () with no associated features of perforation or peritonitis. As the patient was asymptomatic we decided to manage him conservatively and use the wait and watch strategy. He was advised to soft diet and laxatives and was admitted for observation. His stools were checked after each act of defecation.
The patient was reevaluated after 72 hours; there had been no passage of molar band along with stool since admission. Repeat abdomen X-ray showed the molar band in the same position as it was in the previous X-ray; this was suggestive of impaction within the gastrointestinal tract. We decided to perform an endoscopy evaluation and attempt endoscopy retrieval of the molar band. At endoscopy it was noted to be in the distal part of stomach and molar tube hook was impacted in the mucosa. Using endoscopic grasper, the molar band was grasped, gently pulling it out of the gastric mucosa fold. The molar band was retrieved along with endoscope (). After retrieval of the molar band repeat X-ray was done to rule out bowel perforation and it was normal (). He was discharged after one day.