A 34-year old Hispanic male presented with nausea, vomiting, abdominal pain, and dark urine. Testing revealed elevated transaminases and bilirubin; however, imaging failed to demonstrate cirrhosis or anatomic abnormality. Hepatitis work-up, including testing for viral hepatitis, hemochromatosis, Wilson’s disease, and autoimmune hepatitis, was unremarkable with exception of an elevated Ferritin level of 7089 mg/dL. Genetic testing for hemochromatosis was negative. Medical history was only positive for occasional social alcohol use, and drug toxicology testing was negative. He denied use of energy drinks, herbs, Chinese teas, or muscle milk. He was advised to discontinue alcohol use, which he did, and his symptoms initially seemed to abate.
Six weeks later, the patient developed asterixis, jaundice, and confusion. Follow-up imaging was concerning for rapid onset of cirrhosis or infiltrative hepatocellular carcinoma. He was transferred to our center for further evaluation. On admission, transaminases were elevated with aspartate aminotransferase (AST) 624 U/L, alanine aminotransferase (ALT) 520 U/L and total bilirubin of 34.7 mg/dL. International normalized ratio (INR) remained elevated despite multiple infusions of fresh frozen plasma and vitamin K. Factor Vand VII activities were 18% and < 6%, respectively. Magnetic resonance imaging (MRI) with Eovist contrast demonstrated interval development of heterogeneous, enhancing nodularity with portal venous washout, unlikely to be an infiltrative tumor process.
A full repeat hepatitis work-up was performed (Table ). No definitive cause of acute liver failure could be identified; however, some findings were equivocal. Autoantibody titers demonstrated a positive antinuclear antibody, but no other positive autoantibodies. Evaluation of Wilson’s disease demonstrated normal ceruloplasmin and copper levels; however, 24-h urine copper was elevated. Serum ferritin but not transferrin was elevated.
Liver biopsy was performed and demonstrated submassive necrosis with collapse of the hepatic architecture involving about 70% of the liver parenchyma. Mild lymphocytic inflammatory infiltration and minimal canalicular cholestasis were seen. No viral inclusions or other infectious agents were identified by histology or immunohistochemistry. No evidence of granuloma, tumor, or features of cirrhosis were demonstrated. Periodic acid-Schiff (PAS) stain with diastase was negative for alpha-1 antitrypsin globules. Iron stain showed only mild iron deposition in Kupffer cells and hepatocytes. Quantitative tissue copper was within normal limits (Table ). Findings were felt to be potentially related to drug-induced liver injury.
After extensive questioning, the patient divulged intake of Garcinia cambogia, purchased through the Internet retailor Swanson Vitamins. He imbibed two 80 mg capsules of “Garcinia Cambogia 5:1 Extract” three times daily before meals for five months preceding initial presentation. Since not advised against intake, he continued the supplement after initial presentation. He denied any other medications or supplements and reported no alcohol intake for two months.
The patient’s status declined and his mental status deteriorated. He was listed status 1A for liver transplantation. He received an orthotopic liver transplant from an ABO-identical brain dead donor and has recovered without incident. Histopathologic examination of the explanted liver demonstrated near total hepatic necrosis with massive hepatocellular dropout and mixed inflammatory cell infiltrates, consistent with severe drug-induced liver injury (Figure ).


A previously healthy 67-year-old man from Northern Wisconsin, USA, with a distant history of Hodgkin's disease and subsequent splenectomy admitted to a local hospital during the summer, complaining of the malaise of 2 weeks duration and a single episode of syncope. He reported several days of intermittent fevers with chills, nausea, and vomiting. He described episodes of tick bites on his back a month earlier, and was empirically treated with doxycycline for presumed differential diagnosis of anaplasmosis versus ehrlichiosis. Three days later, he returned to the emergency department with continuing symptoms. At that time, he was febrile to 39°C and tachycardiac with hypotension and tachypnea. Laboratory analysis showed acute renal failure (serum creatinine 2.3 mg/dl, baseline 0.9 mg/dl) and lactate of 3.6 mmol/dl. His peripheral blood smear showed features of B. microti, with a parasitemia of 28.5% []. Blood testing by PCR was negative for Anaplasma spp., Ehrlichia spp., and Borrelia spp. but positive for B. microti. He was given atovaquone and azithromycin before transfer. On arrival to the medical intensive care unit, respiratory status had decompensated, hypoxemia with SaO2 below 90% requiring O2 by nasal cannula, further and he had progressive anemia with evidence of hemolysis (hemoglobin 8.8 mg/dl, lactate dehydrogenase 1608 U/l and total bilirubin 8.5 mg/dl), worsening renal failure (serum creatinine 3.08 mg/dl), and emerging hepatic injury (aspartate aminotransferase 123 U/l, alanine transaminase 72 U/l, alkaline phosphatase 115 U/l, and total bilirubin 8.5 mg/dl). A diagnosis of fulminant babesiosis with impending respiratory failure was made. His pharmacologic treatment was changed to oral quinine and intravenous clindamycin. After a single emergent automated RBC exchange, the parasitemia decreased to 3.1% []. The patient improved significantly within 24 hours of exchange transfusion and was discharged home on day 6 with oral atovaquone, doxycycline, and azithromycin. His blood smear was negative for Babesia 12 days after initial presentation, and he continued antimicrobial therapy for 30 days following his last negative smear. He continues to do well with negative blood smears.


A 45-year-old male presented to our emergency department with a 5 days history of swelling in the right lower limb. Examination of the lower limb demonstrated tenderness and investigations revealed leukocytosis. A diagnosis of necrotizing fasciitis was made. Meanwhile, the condition of the patient deteriorated, and he progressed to septic shock. A right internal jugular venous central line was placed and after initial volume resuscitation and treatment with antibiotics, an extensive debridement was performed. The patient was intubated, placed on mechanical ventilation and inotropic support, and immediately transferred to the Medical Intensive Care Unit (ICU).
A bedside ultrasonography was arranged to assess the fluid and volume status of the patient. Surprisingly, an intraluminal hyperechoic shadow was seen, which raised the suspicion of a missed guidewire [ and ].
An X-ray was ordered which confirmed the position of guidewire, extending from the right internal jugular vein up to inferior vena cava [].
Ultrasound examination of the central venous line revealed the guidewire in its external part.
A left femoral central catheter was inserted immediately, and inotropic infusion pump was shifted to the femoral line. Meanwhile, the right internal jugular line was clamped and successfully removed along with the guidewire. A repeat bedside ultrasound [] documenting the removal of the guidewire.


A 19-year-old male presented to our medical clinic in mid-2009 with complaints of acne, hair loss, and difficulty in getting up from sitting position with evidence of proximal muscle weakness. He had been recently diagnosed with dermatomyositis based on his clinical features of elevated creatine kinase levels, typical skin changes, and electromyography (EMG) pattern consistent with dermatomyositis. His medications at the time included prednisone, methotrexate, folate, and vitamin D. He was sexually active with both male and female partners with inconsistent use of condoms. Subsequently, he had multiple clinic visits between 2010 and 2011 for complaints of sore throat, fever, chills, anal pain, anal itching, and anal discharge. During this time, he was treated for oral candidiasis, scabies infestation, syphilis, and condyloma acuminata. He refused HIV testing, claiming that he was tested negative elsewhere. In early 2012, he consented for HIV testing. HIV ELISA and western blot were positive, with a CD4+ cell count of 182 cells/µL and HIV RNA copies of 1,337,310 copies/mL on diagnosis. He was started on highly active antiretroviral therapy (HAART). After initiation of HAART his CD4+ count gradually increased to 346 cells/µL and HIV-1 RNA copies decreased to 462 copies/mL within 2 months. At this time, he started having frequent flares of dermatomyositis. His dermatomyositis had been fairly well controlled on prednisone and methotrexate before initiation of HAART. He was switched to a combination of prednisone and azathioprine, then with mycophenolate mofetil, all with poor response. In June 2013, he was started on monthly intravenous immunoglobulins (IVIG), to which he initially had a fair response but ultimately required reintroduction of methotrexate and increased doses of prednisone to control the dermatomyositis flares. Despite this regimen, he had another dermatomyositis flare in 2014. In mid-2015, he presented to the emergency department with complains of diffuse muscle pain, chest pain, and shortness of breath on exertion. His last dose of IVIG was a week before presentation. His active medications were prednisone 60 mg daily, methotrexate 40 mg once a week, IVIG once a month, and Atripla. On physical examination, he had mild heliotrope rash on eyes, chest wall tenderness, neck, and proximal muscle weakness on both upper and lower limbs. Critical laboratory findings included creatine kinase of 1,145 IU/L, aspartate transaminase of 400 IU/L, and alanine transaminase of 220 IU/L. Because of the refractoriness of therapy, a muscle biopsy was done which confirmed the clinical diagnosis of dermatomyositis (a and b). He was treated with intravenous methylprednisolone at stress doses with prompt improvement in overall muscle strength. He was discharged to follow up as an outpatient for rituximab therapy. He continues to take HAART and follows up in Infectious disease clinic. At the time of this report, the patient's latest helper CD4 counts was 320 cells/mcL and HIV-1 ultrasensitive RNA <20 copies/mL 02/8/2016. The patient is yet to follow up at the rheumatology clinic.


A 50-year-old male patient presented to our outpatient clinics with complaints of annular skin rashes on his face, and scalp which did not regress with previously administered topical therapies. His lesions emerged 7 years ago for which he consulted to other medical centers. He was then diagnosed as tinea facialis, and granuloma annulare, and treated accordingly. His personal, and family history was unremarkable except for long-lasting complaints of respiratory distress, and coughing. On dermatological examination, multiple archiform, serpiginous, erythematous, annular and partly squamous plaque lesions localized on face, scalp, and inner aspect of the ears were detected (). Direct fungal examination of the material retrieved from lesions could not reveal fungal elements. Histopathological examination of the biopsy material disclosed granulomas containing giant cells localized superficially within the dermis. The lesions were devoid of lymphocytes (naked granuloma) and concomitant necrosis (). On laboratory analysis, ESR, CRP, serum calcium levels, calcium concentration in 24-hour urine, and angiotensin converting enzyme levels were within normal limits, while purified protein derivative test (PPD) result was evaluated as anergic (0 mm). On chest roentgenograms, and thoracic computed tomograms, bilateral hilar lymphadenopathies were detected, and together with clinical, and histopathological findings, diagnosis of stage 1 sarcoidosis was made. Topical steroidal therapy was initiated for the patient with only pulmonary and cutaneous involvement, and he was included in our follow-up protocol.


A 6-year-old boy visited the pediatric outpatient clinic, complaining of unilateral hemifacial flushing and sweating occurring within minutes during or after physical exercise or heat. Over the past 2 years, these episodes had occurred as an isolated symptom without any change in severity. He had an unremarkable birth history and uneventful medical history for trauma or surgery. Additionally, he did not take any medications. None of his family members had similar symptoms. His neurological examination showed normal findings, including normal pupil responses, cranial nerve functions, and muscle stretch reflexes. The rest of systemic examination was unremarkable. His blood pressure and heart rate were normal, and no signs of asymmetric flushing or sweating at rest were noticed. Electrocardiographic findings were within normal limits. Laboratory tests, including the white blood count; levels of hemoglobin, glucose, and electrolytes; and renal, liver, and thyroid function were normal. To objectify hemifacial flushing and sweating, we performed a provocation test (i.e., running for 90 seconds in direct sunlight outdoors). After exercise-induced sweating, there was pale and nearly complete anhidrosis on the right side of the face with compensatory hyperhidrosis and flushing on the opposite side with sharp demarcation (). By using an oil control film, we found that the oil-paper firmly stuck to the left side of the patient's face owing to sweating, but that it immediately slipped off the right side of his face (). On ophthalmological examination, he had mild anisocoria. The right pupil was 1.5 mm in size, while the left pupil was 2.5 mm in size; however, no ptosis, miosis, or enophthalmos was noted, and both pupils responded normally to light and accommodation. Subsequent testing showed no evidence of Horner's syndrome. Magnetic resonance imaging (MRI) was performed to exclude lesions in the cerebrum and cervicothoracic spinal cord, and no abnormalities were noted. In summary, the clinical picture was compatible with idiopathic HS. The child and his parents were explained the benign nature of this condition, and we advised regular follow-ups without medication.


A 13-year-old girl reported to our outpatient department with the chief complaint of discolored upper and lower front teeth. She and her parents revealed that the teeth were discolored right from their eruption into the oral cavity. Her prenatal, natal, and postnatal histories were noncontributory, and she had not visited a dentist before. None of the family members were suffering from this type of problem, and she was the only child in the family. She hailed from a poor socioeconomic background. Her past medical history revealed that she had recurrent episodes of fever and hospitalization in the first year of life, for which she was under antibiotic medication. No abnormalities were detected upon extraoral examination. Intraoral examination revealed dentition corresponding to chronological age.
One of the interesting finding was that DDE were seen on multiple teeth. The distribution of hypoplasia showed a characteristic presentation which was symmetrical, chronological, and presented as a ring-like defect around the tooth (buccal, lingual. mesia, distal) seen in the incisal 1/3rd of 11, 21, 31, 32, 42, cusp tips of 33, 43 []. Demarcated opacities of yellow-to-brown discoloration along with hypoplasia was seen on the occlusal surfaces of 16, 26, 36, 46 []. Presence of localized ring-like hypoplastic defects and hypomineralized enamel of permanent anteriors, first permanent molars, and lower cuspids, as well as natal history confirmed the diagnosis of MIH with linear enamel hypoplasia. Dental fluorosis and amelogenesis imperfecta (AI) were taken into consideration for differential diagnosis. Teeth affected by MIH had well demarcated borders of hypomineralized enamel, in contrast to the opacities of fluorosis which were diffuse. In comparison with the caries-prone MIH affected enamel, fluorosed enamel is caries resistant. Furthermore, the difference between MIH and AI is one of definition. In AI, all teeth are affected and may be detected pre-eruptively on radiograph with a positive family history. In general, affected first permanent molars with MIH are asymmetrical.[]
The clinical situation demanded the restoration of the form and function of the effected teeth. Since the patient was young, it was decided to restore the anterior teeth with composite raters rather than a veneer, followed by the placement of semi-permanent crowns in case of posterior teeth. Oral prophylaxis was done followed by pumice polishing. Pulp vitality test was performed for the affected teeth, which revealed that all the teeth were vital. The initial shade of tooth was noted with the aid of a VITA shade guide (VITAPAN Classical). Written informed consent was obtained from the patient and her parents. Carbamide peroxide and CPP–ACP individualized protocol was used.
Alginate impressions of both the upper and lower arches were realized and working models were obtained with dental stone. Reservoirs produced by placement of spacer material of 2-mm thickness on the buccal and occlusal aspect of hypomineralized teeth, custom made trays were obtained using low density polyethylene plates of 2-mm thickness in a vacuum plasticizer. The reservoir helps patients with bulbous teeth and improves the flow of the material when its viscous.
The trays were customized by using vacuum former and trial was performed to check the fit of the trays. The patient was given a demonstration using the bleaching material (Opalescence 10% Whitening gel, Ultradent Products) []. Instructions such as brushing and flossing the teeth daily before the procedure was explained to the patient. Prior to bleaching, shade was noticed using VITA shade guide (VITAPAN Classical). The patient was instructed to apply the bleaching agent for 4 hours a day, and she was asked to report to the department if there was any postoperative sensitivity. This first step was carried out for 2 weeks in order to obtain an obtrusive esthetic change of the enamel opacities. Post-bleaching the shade was again noted.
The next phase included tooth remineralization using remineralizing agent (CPP–ACP) (GC Tooth Mousse, GC Corporation) inside the trays for 2 hours/day []. CPP stabilizes high concentration of calcium and phosphate that bind themselves to the pellicle and plaque.[] CPP–ACP is a known remineralizing agent, and hence also results in esthetic improvement. This step lasted for 2 weeks in order to obtain a noticeable remineralization of the enamel opacities. Post-remineralization tooth shade was again noted. Shade selection of the composite was done. A bevel on the buccal surface was made with a tapered bur No. 2200 (KG Sorensen, Brazil). The anterior tooth surfaces were acid etched using 35% phosphoric acid for 30 s [], rinsed for 30 s, followed by placement of a two-component adhesive system (AdheSE, Ivoclar Vivadent AG, Schaan, Liechtenstein) [], and the tooth was light-cured for 10 s with an intensity of 1400 mW/cm2 (Radii LED Curing Light, SDI, Australia) []. A highly aesthetic nanohybrid composite resin, IPS-Empress (Ivoclar Vivadent AG), was used to fill the tooth using a combination of incremental and stratified layering technique. The occlusal adjustment was performed with fine and extrafine flame-shaped diamond burs, 3168 F and 3168 FF (KG Sorensen, Brazil). Finishing and polishing of the restoration were performed for dental contouring regularization; for smoothing, resin sanding discs Sof-Lex Pop-On (3M ESPE, USA) were employed followed by multilaminate burs on the buccal surface. For surface smoothness, abrasive silicone-based rubbers were used []. Minimal crown preparation in accordance with the standard crown cutting norms for stainless steel crowns (SSC) was done on all permanent first molars. Number 5 size SSC (3M ESPE) of 16, 26, 36, 46 was found to be adaptive. Contouring was done with Johnsons contouring pliers (API Germany). Margins of the SSC were crimped to increase the retention with no. 800–417 crimping pliers (API Germany). The final fit of SSC was found to be very satisfactory. The SSC were cemented with luting glass ionomer cement (Fuji I) []. Periodic follow-up was done for every 6 months, and the restorations were intact even after 2 years.


A 47-year-old male was diagnosed with malignant melanoma of the scalp in May 2015 at our tertiary care hospital. In reviewing treatment options, he underwent imaging surveillance, including an abdominal computed tomography. This showed a 2.6 cm enhancing mass adjacent to the fundus of the stomach and immediately below the diaphragm [Figure and ]. The radiology differential included a gastrointestinal stromal tumor (GIST), splenule, and metastatic melanoma. The patient had opted to receive biochemotherapy for his primary melanoma, and a biopsy of the perigastric mass was needed to exclude a metastasis. The patient was referred to endoscopy.
Endoscopic ultrasound (EUS) identified a 2.5 cm oval mass in the perigastric space below the diaphragm, without definite involvement of the stomach. These images were suggestive of a lesion arising independently from the gastric wall. Five passes were performed with a 22-gauge Shark Core needle (Medtronic, Dublin, Ireland) to maximize tissue acquisition []. Rapid on-site evaluation (ROSE) was performed by a cytopathologist. After reviewing the first pass, the cytopathologist communicated with the endoscopist to ask if the needle had passed through the liver. The endoscopist confirmed that the needle was not in or near the liver and that it had been passed through the stomach to obtain the biopsy. Small tissue fragments were touched on the slide, and those which did not smear were placed in formalin for the cell block preparation.
Diff-Quik smears of the second fine needle aspiration (FNA) demonstrated flat sheets, single cells, and small clusters of polygonal cells with distinct cell borders, round to ovoid centrally placed nuclei with some size variation, but smooth nuclear contours, open chromatin, and no pleomorphism. Occasionally, prominent nucleoli were identified. Cells had abundant granular cytoplasm which contained some pigments []. The smear findings appeared consistent with hepatocytes. The cell block confirmed this, demonstrating small core fragments of hepatic parenchyma with portal tracts. Immunohistochemistry for arginase-1 confirmed that this was hepatic tissue [Figure and ] and a reticulin stain demonstrated normal hepatic plates (figure not shown). The cytologic and histologic findings, in conjunction with the imaging, were consistent with ectopic liver.


A 43-year-old male patient, with no relevant past medical history, has been admitted to the emergency department after having attempted suicide by shooting a crossbow arrow at his abdomen. He was haemodynamically stable, and fully conscious. The arrow penetrated the epigastric area, without an exit wound, and was left untouched by the emergency team (Fig. ).
A contrast-enhanced CT and 3D reconstructions showed the projectile entering medially at the epigastrium, passing through segment IVb of the liver, progressing to the first part of the duodenum, pancreatic head and finally stopped by the left facies articularis of L4–L5 vertebrae (Fig. A and B). In addition, haematomas were present in the lesser sac, and in the duodenal loop with a shift of the mesenteric vessels to the left. At emergency laparotomy, there was a small amount of free blood in the abdominal cavity. Trustworthy CT findings appeared as a valuable help to surgical procedures. A tactical cholecystectomy was performed, and a cholangiogram demonstrated the absence of bile duct lesion. The arrow was removed by splitting the edge of segment IV of the liver. It was subsequently extracted from the vertebrae with the help of neurosurgeons, and tributaries of a lumbar artery were clipped for haemostasis. Anterior and posterior wounds of the duodenum were closed with interrupted polydioxanone sutures. The gastroenterologist performed an endoscopic retrograde cholangiopancreatography, which showed a complete disruption of the distal part of the Wirsung duct, and a stenting was thus not performed. Prolene interrupted sutures were applied to the anterior and posterior surface lesions of the pancreatic head, and two drains were left locally. A jejunostomy was placed for post-operative enteral feeding.
Post-operative follow-up was complicated by the occurrence of a pancreatic fistula (Fig. ). The patient was kept on octreotide in order to minimize the exocrine pancreatic secretion. A control CT at 4 weeks showed resolution of the fistula and abdominal drains could be removed. Besides, vertebral damage was minimal and presented a favourable outcome. Finally, psychiatric evaluation concluded to schizophrenia.


A 38-year-old male presented to our service with a 10-year history of hair loss evolution. He had AA universalis, with the hair loss affecting the entire integument. Hair loss was associated with dystrophy of the fingernails. Clinical examination showed total absence of the eyebrows, eyelashes, beard, hairs in the trunk, scalp, genitals, armpits, arms and legs. Fingernails were dystrophic, with erythematous blotches (striated lunulae) with regular and superficial pitting and nail fragility (trachyonychia) (fig ). The patient reported nail brittleness (onychorrhexis) and pain in the fingertips leading to difficulty in performing simple tasks and being unable to play the guitar.
Many treatments had been tried previously: oral, topical and intralesional corticosteroids, immunosuppressants such as methotrexate (32.5 mg weekly for 9 months), cyclosporin (200 mg for 6 months and then 300 mg for 3 months) and finally PUVA (oxoralen plus ultraviolet light) therapy. The patient also used diphencyprone, but the drug also caused skin irritation (blisters) even in small doses so that the treatment had to be interrupted. During these therapies, the patient presented some adverse effects, such as weight gain with oral corticosteroids (12 kg in 4 months), hyperglycemia, dyslipidemia and hypertension. Due to the adverse events, all therapies were discontinued.
The patient was then started on tofacitinib as an off-label treatment, with previous consent. Routine laboratory work was performed, including a complete blood count coagulation profile and the following tests and measurements: liver function, purified protein derivative test, HIV test, serology for hepatitis B and C, antinuclear antibodies, thyroid function, lipid profile, blood glucose, erythrocyte sedimentation rate, C-reactive protein, urea and creatinine. All these examination results were within ranges.
Oral tofacitinib was started with 5 mg twice daily. After 1 month of therapy, new hair had emerged in the eyebrow and scalp as well as small eyelashes. After 2 months, the patient had new hair in the beard, scalp, eyelashes and eyebrows. At 4 months, nails started to show increased growth, making them less fragile, and the longitudinal cracking was not so evident anymore (fig ). At 10 months of therapy, there was growth in all fingernails and normalization of the nail plate (fig ). At this point, the patient reported that he resumed his habit of playing the guitar.
Total hair regrowth occurred after 10 months of therapy. Currently, the patient maintains the same treatment, being constantly monitored, and no adverse effects or laboratory abnormalities were observed.


A 43-year-old Caucasian woman presented with a history of recurrent painful subcutaneous nodules at the lower extremities (Fig ). Skin biopsy had revealed lymphocytic lobular panniculitis and led to the diagnosis of erythema nodosum. In addition, the patient had recurrent ulcers of the calves in which biopsies had demonstrated neutrophilic infiltrates without vasculitis, leading to the diagnosis of pyoderma gangrenosum (Fig ). Three months before referral to us, the patient had experienced a new episode of pyoderma gangrenosum, the C-reactive protein (CRP) was 72 mg/L and prednisone had been started (50 mg).
At admission, the patient had multiple ulcers at the calves but was in good general condition. There was no pulse at the left ulnar and radial arteries. The blood pressure was 168/102 mm Hg at the right upper arm, and 117/94 mm Hg at the left upper arm. Magnetic resonance angiography revealed a proximal occlusion of the left subclavian artery (Fig ), and T1-weighted magnetic resonance images showed a circular contrast-enhanced thickening of the wall of the aortic arch and the subclavian artery (Fig ). IgG4 was within normal limits and thrombophilia was excluded. According to the criteria of the American College of Rheumatology, the vasculitis in this woman was classified as Takayasu's arteritis []. Cyclosporine and methotrexate were added to prednisone. After 6 months of immunosuppressive combination therapy, the pyoderma gangrenosum lesions had vanished and the aortic inflammation had regressed.


A 58-year-old Saudi diabetic female presented with left-sided involuntary movements. Unilateral movement was continuous, choreoathetotic, purposeless, non-stereotyped, and involved the face (twitching) and upper and lower extremities. It developed subacutely over 2 weeks. The movement was distressful to the patient and interfered with her activities of daily living and gait, causing recurrent falls. However, it ceased during sleep. She had poorly controlled diabetes for approximately 20 years, and was maintained on oral hypoglycemic agents. She was not on hormone replacement therapy or any other medications to which these symptoms could be attributed. There was no family history of movement disorders, and no clinical features suggestive of connective tissue diseases. Past medical history was of no relevance. Apart from the hemichorea involving the left side of the face and upper and lower extremities, her neurological examination was unremarkable; with normal higher mental function, and normal cranial and sensory nerve examination.
On admission, she was hyperglycemic with a random serum glucose of 30.3 mmol/L, (normal level <6.5 mmol/L); and her glycosylated hemoglobin was 13.5%, normal level=4-6%. Urine was negative for ketones. Expectedly, serum potassium was 5.6 mmol/L (normal level=3.5-5.0 mmol/L), and sodium was 133 mmol/L, (normal level=135-145 mmol/L), but other electrolytes were normal. Her blood count, coagulation profile, liver function tests, vitamin B12, and thyroid-stimulating hormone were all within normal. Lipid profile showed dyslipidemia (cholesterol 9.81 mmol/L, triglycerides 4.61 mmol/L, high-density lipoprotein 1.1 mmol/L, and low-density lipoprotein 6.61 mmol/L). Further workup reinforced the evidence of poor diabetic control; her ophthalmologic examination revealed moderate to severe nonproliferative diabetic retinopathy, and her protein to creatinine ratio was 2000.
A CT scan taken on admission was normal. Non-enhanced brain MRI () was obtained the next day and demonstrated an area of hyperintensity on T1 weighted images; involving the left caudate, putamen, and internal globus pallidus. There was no restriction on diffusion-weighted images (DWI) and the apparent diffusion coefficient (ADC) map was normal. For glycemic control, she was started on an insulin regimen (bedtime insulin glargine and preprandial insulin aspart) with sitagliptin.
Initially she was treated with lorazepam (2-6 mg/day) to control her HH. While lorazepam improved the quality of her sleep, it had no effect on the chorea in her waking hours. Valproic acid (400 mg/day) had no clear effect on chorea and was discontinued due to intolerance. She was then given haloperidol (gradually titrated from 1 mg/day to 8 mg/day) and clonazepam (titrated from 1.5 mg/day to 6 mg/day). She showed clinical improvement after a few days with improvement in her daily activities and gait. Initially, there was more improvement in her lower extremities than upper extremities and the face over a period of 2 weeks. However, she achieved a satisfactory glycemic control, with a fasting serum glucose ranging from 6 to 7.8 mmol/L. With the initiation of neuroleptics and the glycemic control, the hemichorea steadily improved. She was discharged and followed up at an outpatient clinic. Three months later, she was in stable condition and had no recurrence of chorea.


A 57-year-old woman presented with a 2-month history of asymptomatic, steadily growing lesions on her face, neck and shoulders. Her medical history revealed that she was diagnosed with stage IIIa (T3N2M0) gastric SRC adenocarcinoma (SRCC) 12 months prior in an oncology clinic. At that time, she had underwent total gastrectomy and splenectomy. Her surgical pathology reports revealed cancer-free margins and surgery was followed by adjuvant chemotherapy [infusional folinic acid + 5-Fluorouracil (FUFA)] and radiotherapy directed to the gastric lodge. About four months later after the end of the combined chemotherapy and radiotherapy, the patient had noticed several small lumps on her face and shoulders. Since then, these lesions had been consistently growing. At the time of physical examination, multiple asymptomatic skin lesions consisting of two erythematous papules on her forehead, one solitary nodule on the right preauricular area, another one on her right shoulder and two prominent bright red, fleshy nodules on her neck ranging from 1.0×1.0 to 3.0×4.0 cm () were found. An incisonal biopsy was performed from the papule located on the frontal hairline. Histopathological sections showed diffuse dermal infiltration of cells with signet-ring morphology. Immunohistochemical staining were negative for HMB45, CD45, ER, PR, GCDFP-15 stains, lowering the possiblity of an melanoma, a metastatic tumor of hematopoietic origin and a metastatic breast cancer, respectively- and positive for AE1/AE3 and mucicarmine indicating a glandular epithelial origin for the SRCs (). Since the patient was operated in another clinic, original resection material was unavailable to us for a comperative histological and immunohistochemical staining. A working diagnosis for metastatic signet-ring cell carcinoma was made on the basis of the last skin biopsises and patient’s medical history, and the patient was referred to the oncology department for further evaluation. Tests performed by the oncology department, including complete blood count, urea and electrolytes, liver function tests, plasma proteins, tumor markers, chest X-ray, breast, abdominal and suprapelvic ultrasound, bilateral mammography, complete abdominal magnetic resonance imaging, bilateral mammography, upper gastrointestinal endoscopy and colonoscopy, revealed no other internal focus, from which the skin lesions could originate. After the completion of the oncological examination and tests, diagnosis of the patient was established as metastatic cutaneous signet-ring cell carcinoma and she was scheduled for a second round of chemotherapy ().


A 58-year-old male presented to the emergency department neurologically intact, but with a common kitchen knife penetrating the spinal cord at the T11 level. His only complaint was a patchy, vague, and subjective nondermatomal sensory loss in the lower extremities. A computed tomography (CT) image showed that the knife had pierced the right-sided interlaminar space at the T11-T12 level where it fully entered the spinal canal []. All plates were removed from an open Jackson table to allow the patient to be intubated in the supine position. After intubation, the patient was moved back to a stretcher in the lateral position, and a similar turn was utilized to re-position him in the prone position []. Baseline intraoperative neuromonitoring, including motor and somatosensory evoked potentials (MEPs and SSEPs, respectively), was utilized throughout positioning and surgery, and at no point were any significant intraoperative changes were observed.
Subsequent to sterile preparation and draping of the patient, the skin was opened perpendicular to the axis of blade, with care being taken to avoid any undue manipulation. In addition, no electrocautery was utilized during dissection and removal of the knife to avoid potential damage to the spinal cord. The serrated knife was firmly embedded in the T11-T12 laminar bone. An ultrasonic bone cutter was used to create a bone island around the knife, allowing the knife and the surrounding T11-T12 laminae to be removed without traumatic rotational force to the spinal cord. Under microscope visualization, the dural laceration from the knife was extended in order to look for intradural compressive hematoma or vascular injury. Although neither was present, there was a clear laceration of the spinal cord itself. Following copious irrigation, watertight dural closure was performed using running 4-0 Nurolon sutures. In order to minimize infection risk given the foreign body penetration, no adjuvant sealant was used, especially because solid dural closure had been achieved. The patient was placed on antibiotics and received a tetanus shot. Postoperatively, the patient's motor status remained normal, whereas his mild diffuse sensory loss was unchanged. Three months later, the patient continued to have residual sensory deficit, but was fully ambulatory and returned to work.


A 66-year-old male with a history of coronary artery disease, hypertension, and insulin-dependent diabetes mellitus (DM) presented with 2 months of low back pain, left buttock/leg pain radiating down to the calf, and numbness in the L5 distribution. The lumbar magnetic resonance imaging (MRI) revealed mild L4-5 spondylosis with moderate biforaminal stenosis, accompanied by left L5-S1 lateral recess stenosis.
The patient was referred for bilateral selective L4-5 foraminal ESIs utilizing Betamethasone (9 mg per injection) and Bupivacaine under fluoroscopic guidance. There were no immediate post-procedural complications. However, 2 days later, the patient progressively developed a frontal headache, right eye ptosis, and inferolateral displacement of gaze with mild mydriasis of the the right pupil (4 mm OD vs. 2 mm OS), consistent with a right third nerve palsy with partial pupillary involvement []. The right pupil remained sluggishly reactive to direct and consensual light, however, anisocoria was maintained during these maneuvers. Formal ophthalmologic evaluation revealed a stable proliferative diabetic retinopathy with steroid-induced central serous retinopathy, accompanied by blurred vision. MRI and MR angiography (MRA) of the brain were unremarkable. For 3 days following the ESI, the patient's OneTouch glucometer (LifeScan Inc., Wayne, PA) revealed transient elevation in his blood glucose levels []. Daily blood glucose averaged 236 mg/dL vs. 174 mg/dL for the remainder of the month. Within 4 months, the ophthalmoplegia and pupillary dysfunction resolved, and the patient was left with only a mild residual ptosis [].


A 13-year-old boy presented with pain, swelling, deformity and inability to bear weight. He gave a history of a fall on glass pieces while playing 9 days ago. He was asymptomatic for the first 4 days after the fall. Later he developed pain and knee swelling. He was taken to a nearby hospital where X-rays of the knee were done; no abnormality was noticed and was prescribed analgesics. Symptoms worsened after 2 days when he developed deformity of knee and inability to bear weight on the affected side. He was then taken to a different hospital where he was diagnosed to have a foreign body in his knee and referred to our institution for further management. He gave no history of locking or giving away sensation.
On examination, the left knee was in 30 degrees flexion, supra-patellar fullness and mild effusion was noted. An oblique skin laceration of 1x1 cm was noted lateral to the patella (). There was no active discharge from the wound or local raise of temperature. Tenderness was noted around the knee. The skin overlying the knee joint appeared normal. Boy was unable to move his knee due to pain and did not allow us to examine him thoroughly.
Antero-posterior and lateral radiographs of the knee done 5 days prior to admission showed a radio-opaque shadow measuring about 1x1 cm in the supero-lateral quadrant of the knee, residing in the superficial planes, perhaps in the subcutaneous tissues (). This explains the child not having symptoms for the first 4 days. At the time of presentation to our out-patient department freshly taken radiographs revealed radio-opaque shadow in the inter-condylar region of the knee in front of the tibial attachment of the anterior cruciate ligament (ACL) resembling an avulsion of the ACL from the tibial plateau (). With the working diagnosis of foreign body in the knee, the boy was taken up for emergency arthroscopy. MRI scan of the knee was not considered as the history and follow-up events suggested a foreign body in the knee and this would not have changed our management plan.
Under general anaesthesia, the knee deformity was spontaneously corrected suggesting that it may have been due to muscle spasm. Arthroscopy was carried out with the standard lateral and medial portals. About 50 ml of normal looking synovial fluid was drained out. We found a glass piece measuring 1 cm x 1 cm () lying in the inter-condylar notch in the space between the ACL and the lateral surface of the medial femoral condyle. The glass piece was removed () arthroscopically with the help of a small artery forceps by increasing the size of medial portal. The synovium in the supra-patellar pouch, medial and lateral gutter was hyperaemic. There was no obvious damage to menisci or the articular surfaces of the femoral or tibial condyles except for some abrasions (video 1).
A partial tear in the ACL at the femoral attachment with 10-20 % of fibres being involved was noted probably due to the sharp edges of the glass piece (). The cut fibres were trimmed and examined under anaesthesia (, video 2). Anterior drawer, Lachman, Pivot shift and posterior drawer tests were all normal. Varus and valgus stress tests for collateral ligaments were normal. Hence, it was decided not to reconstruct the ACL. The chondral abrasions were smoothened out using a shaver. Joint was thoroughly washed and portals sutured. There was a small tear of 1x1 cm in the lateral retinaculum below the skin laceration, which was repaired. The skin laceration was debrided and sutured.
Wound healed subsequently without any infection. Post-operative radiographs revealed no foreign body in the knee. Post-operatively, the boy was allowed full weight-bearing and knee mobilisation exercises were started. No deformity was noted post-operatively. At the end of 1 year of follow-up, patient had full range of motion with no complaints of instability. He was involved actively in all sports activities. The parents were advised to review in case of any symptoms later. Discussion
Penetrating injuries of the knee are relatively rare. Many of the times, penetrating wounds (i.e., after an accidental fall, road traffic accidents) remain the major cause of foreign body in the knee. Remaining injuries are sustained by missiles shot by machinery for civilian use (e.g., power-gun nails, needles, staples) or by weapons []. Rarely, the cause can be iatrogenic (e.g. arthroscopic instruments for e.g. tip of shaver blades, staples, suture materials, anchors, broken screws used for graft fixation) [, ].
Foreign bodies can be classified as radio-opaque and radiolucent. Metal, glass pieces, and lead objects are radio-opaque and can be identified on X-rays. Objects like thorns, stones, suture material, and bio-absorbable screws are radiolucent and can only be detected by an ultrasound or an MRI []. The presence of a local scar can give a clue to the underlying pathology, as in our case a glass piece had entered from the antero-lateral aspect of the knee joint. Whereas in some cases the cause of uncertain knee complaints especially in children can be due to foreign bodies which penetrated unnoticed into the joint cavity [].
A foreign body in the knee joint is an absolute indication for operation []. Earlier the better, as the amount of intra-articular damage increases with time. A foreign body intruding the knee joint in childhood can go unnoticed initially and can cause symptoms for the first time in adult age []. Fragments can become adherent to the capsule or reside within synovial recesses or bursa without producing any symptoms for a very long time. Symptoms are usually caused by the foreign bodies which are mobile within the knee joint, resulting in meniscal damage or recurrent locking episodes [].
In our case, the glass piece resided in the subcutaneous soft tissue for few days and later migrated into the knee joint to cause symptoms. Late migration of other foreign bodies like bullets, broken arthroscopy probe tips into the knee joint have been reported in literature [, ]. There is also a report of late migration of a glass piece of nearly 1.5 cm in size into the knee joint after remaining in the subcutaneous tissue for 7 years [].


A 68-year-old man presented with sepsis and a two-month history of general malaise and 18kg weight loss. His past medical history includes elective right and left hip replacements, 22 and 14 years ago, respectively. The left hip replacement was complicated with two dislocations, which were both managed with closed reduction and no complications were reported in the right hip. This is on a background of haemachromatosis with no evidence of end organ damage, thoracic shingles with no residual post-herpetic neuralgia, well-controlled gout, osteoarthritis, and a 20-pack /year history of smoking. Physical examination revealed a tender palpable mass in the left lower quadrant. Laboratory findings were as follows: haemoglobin 7.9 g/L; white cell count 8.5 x 109/L; neutrophil 6.29 x 109/L; platelet 625 x 109/L; C-reactive protein 82mg/L. CT of the chest, abdomen and pelvis identified a large left psoas abscess as seen in ().
The psoas abscess was surgically drained and more than one litre of pus was produced. A 24 Fr 3-way catheter was inserted for irrigation of the cavity and a Yates drain was inserted in dependent position for ongoing drainage. The cavity was irrigated with normal saline twice daily, and then reduced to once daily four days post-operatively when the runoff remained clear and there was minimal residual drainage. He was empirically treated with IV Tazocin, and then switched to IV Flucloxacillin three days post-drainage, when sample cultures grew multi-sensitive Staphylococcus aureus (). He was discharged on oral Flucloxacillin 500mg three times a day and was followed up by ‘hospital in the home’ for daily irrigation post-discharge. A CT scan was performed after removal of the catheter to demonstrate resolution of the psoas abscess (). Two months later, a sinus developed at the left inguinal fossa over the site of drainage. This continued to drain despite management by his general practitioner with regular dressings and several courses of oral Cephalexin 500mg BD.
The patient presented again several months later with a one-week history of a painful right thigh mass, which developed after he ‘pulled’ a muscle in his thigh during physiotherapy. He also complained of mild right hip pain on movement. Ultrasound was performed with the provisional diagnosis of a haematoma.
Incision and drainage was performed where 450ml of pus was drained. Cultures grew the same strain of Staphylococcus aureus as from the left psoas abscess (). A sinus formed on the right thigh also, which continued to discharge pus following the procedure. During this admission a sinogram was performed to investigate the persisting sinus from the left psoas abscess drainage site and revealed that it was communicating directly with his left total hip replacement. Interestingly he did not complain of any left hip symptoms. Radiograph of the left hip showed a small lucency at the tip of the prosthesis and below the medial calcar; the prosthesis was otherwise well fixed.
First stage revision of the left hip was performed through a posterior approach with extraction of the infected hip replacement and thorough debridement. Antibiotic impregnated (4g Vancomycin) cement spacer was inserted. Post-operatively, he was treated empirically with IV Vancomycin. The same strain of Staphylococcus aureus was isolated from left hip fluid (), and microbial sensitivity results directed the change of the antimicrobial regimen to IV Flucloxacillin. This was later changed to a two-week course of oral Dicloxacillin and Rifampicin upon normalisation of the inflammatory marker, CRP to 8. Second stage revision of the left hip was performed three months after the first stage using the posterior approach. No sign of infection was noted in the left hip and this was confirmed with culture results ().
MRI of the right hip was performed to investigate the persistent discharge from the right thigh sinus and a fluctuant right buttock mass noted during theatre. A prominent anterolateral right thigh sinus, which extended into the right hip joint could be seen. There was a large erosion posteroinferomedial to the right acetabulum, likely extending from the joint, and a very large posterior collection, mostly deep to the right gluteus maximus. Under local anaesthesia and ultrasound guidance, the right buttock collection was accessed with an 18G needle but only a small amount of blood could be aspirated. The aspirate was sent for culture; no pathogen was grown. This was most likely to represent a solidified uninfected haematoma.
The patient underwent first-stage revision of the right hip two months later. The hip joint was exposed from the posterior approach. Copious amounts of pus was seen and drained. Following thorough debridement, antibiotic impregnated (4g Vancomycin) cement spacer was again inserted. Treatment with IV Vancomycin and oral Ceftriaxone was commenced post-operatively. All specimens collected from the right hip grew the same strain of Staphylococcus aureus as before (), and IV Flucloxacillin 2g TDS was commenced according to susceptibility results. This was switched to oral antibiotics upon discharge.
Eight weeks later when the patient was off antibiotics and his CRP normalized he underwent second stage revision of the right hip. Once again no sign of infection was noted in the joint. He was on IV Flucloxacillin postoperatively, which were ceased when intraoperative samples did not culture any pathogens ().
The patient received a period of inpatient rehabilitation and was discharged 13 days after surgery. Upon follow-up at six months, he remained clinically well and was mobilizing with two crutches. Pathology results were also unremarkable with normal infective and inflammatory markers. Image 3 shows the X-rays as the patient progressed through the various stages.


A 45-year-old female was admitted to our surgical department at the Amir-AL-Momenin Hospital, Semnan, Iran, in May 2012. She presented a 17-year history of lower abdominal and back pain, rectal fullness, pain on defecation, constipation, and symptoms associated with genitourinary obstruction due to a pelvic mass. During her first pregnancy, a cystic pelvic mass had been diagnosed as an ovarian cyst, but the cyst was only drained during the caesarian section. Afterwards, she underwent five additional laparotomies, at first to remove a presumed ovarian cyst and then to treat the actual problem, the retrorectal cyst. The surgeries had been carried out in different centers and even by unprofessional hands. The cyst was not resected completely, and it recurred after each of these procedures. After these unsuccessful surgeries, no other major procedure was done, and the patient was followed with transabdominal ultrasonography approximately every six months. When the patient’s symptoms became unbearable, the cyst was drained through a minimal perineal incision between the coccyx and anus. In the last year, her symptoms did not improve after perineal drainages. It seemed that the cyst was not completely evacuated. A CT scan and MRI studies confirmed two large, separated, noncalcified, unilocular cystic mass lesions with well-defined borders in the retrorectal and retroperitoneal spaces. On a T1-weighted MRI, the lesions were low signal, while on a T2-weighted MRI, the lesions were high signal, indicating fluid content. There were no areas of heterogeneity or irregularity that enhanced with contrast. The retrorectal mass was located in the pelvic cavity behind the rectum and the vaginal canal, compressing and anteriorly displacing the uterus ().
We decided to resect the cysts completely, because the case was so complicated after 19 surgeries (laparotomies and perineal drainage). A team of two general surgeons experienced in anorectal surgery, a urologist, a neurosurgeon, and two anesthesiologists operated on the patient for eight hours.
For complete excision, we used a combined abdominoperineal approach. At first, JJ stents were inserted through cystoscopy to find and protect the ureters during dissection, on account of the massive adhesions and anatomic distortion caused by previous operations. Then the laparotomy was done through a midline incision, revealing a large cystic lesion, adherent to the small bowel and ureters. The mass was carefully dissected and isolated. It seemed to have originated from the left ovary, and it contained clear fluid. The cyst was resected by salpingo-oophorectomy.
The second mass in the retrorectal space was completely apart from the first cyst. Although exceedingly difficult because of adhesions and fibrosis from the previous surgeries, the cyst was dissected with special attention to avoid injuring the rectum, ureters, or pelvic nervous plexus. For complete dissection of this cyst, the operation was continued with a perineal approach. A longitudinal incision was made between the anus and the coccygeal bone, the subcutaneous planes were divided, and the lumbosacral fascia was exposed. The anococcygeal ligament was transected. The retrorectal space was exposed by transection of the fibers of the levator ani. After complete dissection of the cyst, it was removed with a tract that had been created between cyst and skin in the site of the last perineal drainage. The pelvic floor was then reconstructed by suturing the fibers of the levator ani.
Upon histopathological examination, the first specimen consisted of the ovary containing a creamy brown unilocular 9 × 7.5 cm collapsed cyst with a smooth internal surface. The cyst was reported as “ovarian serous cystadenoma.” The second specimen was a unilocular 12 × 6.5 × 8 cm cyst filled with yellow fluid and sebaceous material; the inner aspect of the cyst had a creamy smooth surface. Microscopically, this cyst was lined by stratified squamous epithelium. Also seen were scattered sweet gland-like structures, areas of erosion, granulation tissue formation, chronic inflammation, and fibrosis. The diagnosis was “dermoid cyst.”
Postoperative recovery was complicated by respiratory failure, but eventually the patient improved and was discharged in generally good condition on the twelfth postoperative day. No complications occurred during the 18-month follow-up.


An 83-year-old female patient presented to a rural general practice physician in the north of the republic of Ireland in 1954 with a 13-year history of extreme fatigue, and multiple episodes of transient subacute sensory and motor neurological dysfunction disseminated in time and space. Patient recollection noted that the neurological dysfunction manifested as transient lower and upper limb sensory loss (‘the limb would go dead’), evolving into sensory and motor loss (‘one leg would drag behind as I biked into town’) occurring without warning and with varying anatomical distributions of the limbs both unilaterally and bilaterally (‘at times, I could not stand up at mass for the gospel’). At presentation, she had no significant medical or family history other than fatigue that interfered with her farm chores and headaches in school as a girl. She denied eye symptoms and tremor, bowel and bladder symptoms at that time. The original neurological examination records are not available, but the patient recalls a thorough neurological evaluation with no specific findings at that time.
The patient was examined by the first author in her home in 2014. She was awake, alert and comfortable sitting on the seat of a 4-wheeled walker. She ambulates in a seated position using her lower limbs to propel the walker. Examination of the cranial nerves was unremarkable. Visual acuity was tested with hand motions. The patient was able to read. Corneal reflexes were not tested for patient comfort. The patient's gait was not assessed as the patient was unwilling to ambulate. The examination of the patient's cognition, upper and lower limbs and cerebellum were also unremarkable, while proximal muscle weakness was described; it was not evident on physical examination. Her mood was euthymic and congruent throughout.


A 68-year-old Caucasian female presented with a 2-week history of progressive upper abdominal discomfort which had noticeably worsened in the last 5 days. She first presented to her primary care provider and then came to the emergency department due to persistent pain. The pain was constant, sharp, 9/10 in severity, radiating to her back, slightly worse after eating, and not relieved with over-the-counter pain medications. She endorsed constipation and a mild weight loss but denied any other symptoms.
Her past medical history was significant for hypertension, subclinical hypothyroidism, osteopenia, and cervical spondylosis. Her previous surgeries included small adenomatous colonic polyp removal during a screening colonoscopy, tubal ligation, breast lumpectomy, appendectomy, and an abdominal surgery after swallowing a toothpick 40 years ago. She denied any medications other than lisinopril and over-the-counter ibuprofen. She admitted to active tobacco use (about 10 pack-year), but denied alcohol or illicit drug abuse.
On physical examination, she was tachycardic with a pulse rate of 109 bpm and hypertensive with a blood pressure of 160/110 mm Hg. Other vital signs were in the normal range. Her body mass index was 24. She had moderate epigastric and left upper quadrant tenderness on palpation with mild rebound and voluntary guarding on abdominal examination. Bowel sounds were present. No masses were felt, and there was no distention. The rest of the physical examination was unremarkable.
Initial laboratory tests, including blood counts, metabolic panel, liver function test, amylase, lipase and lactic acid, were within the normal range. Ultrasound of the right upper quadrant was normal. A computed tomography (CT) scan of the abdomen was done with intravenous contrast showing an area of dissection with thrombosis in the proximal SMA beginning just beyond its origin for a length of about 7 cm (Fig , Fig , Fig ).
After careful consideration, no surgical intervention was done, and she was managed conservatively with bowel rest, blood pressure control, and anticoagulation with IV heparin. She was monitored in the Intensive Care Unit. Her symptoms improved with conservative measures. The rest of her hospital course was uncomplicated and the patient was discharged home on warfarin in addition to her outpatient antihypertensive medications.
She was followed up in the surgery clinic at 2 weeks and reported that her symptoms had completely resolved. A follow-up CT showed stable dissection. She had multiple follow-up CT scans which showed a gradual decrease in the size of the dissection.


A 67-year-old man presented with non-ST-elevation myocardial infarction (NSTEMI) and cardiogenic shock. His heart rate was around 120 to 130/min, and his systolic blood pressure was around 70 to 80 mm Hg even though vasoactive agent use. The patient developed pulmonary edema and progressed to profound cardiogenic shock status within 2 hours. Electrocardiography showed diffuse ST-segment depression in precordial leads and Q-wave in inferior leads. His coronary risk factors include hypertension, diabetes mellitus, hyperlipidemia, and smoking. He received intubation and ventilator support due to impending respiratory failure. IABP was set before diagnostic coronary angiography (CAG). CAG revealed severe calcified RCA subtotal occlusion at middle portion, with retrograde collaterals from the distal portion of the left anterior descending artery (LAD) (Fig. A). From the distal LM to the mid LAD, there was a long tubular severe calcified 80% stenosis (Fig. B) and concomitant hypoplastic left circumflex artery (LCX) chronic total occlusion (CTO) without significant collaterals from LAD or RCA (Fig. C). Transthoracic 2-dimensional echocardiography revealed poor left ventricular performance and global hypokinesis with LVEF of 23%. His SYNTAX score (synergy between percutaneous coronary intervention with TAXUS and cardiac surgery) was 43, and the EuroScore (European System for Cardiac Operative Risk Evaluation) was 20 (estimated perioperative mortality rate 20%–38%). The patient and his family refused coronary artery bypass grafting (CABG). Due to unstable hemodynamic condition, ECMO were set up immediately.
Coronary intervention was performed via right transradial (TR) approach because both femoral arteries were used for ECMO and IABP. A 6-French (Fr.) Ikari IL 3.5 guiding catheter (Terumo, Tokyo, Japan) was used for engaging the left main ostium. Tirofiban was used for intracoronary bolus and intravenous maintenance. After advancing a 0.014 Runthrough Floppy wire (Terumo, Tokyo, Japan) to the distal LAD, sequential dilatation was performed using Maverick 2.5 × 20 mm (Boston Scientific, New York, USA) up to 18 atm, NC Sprinter 2.75 × 12 mm (Medtronic, Minneapolis, MN) up to 18 atm, NC Sprinter 3.0 × 12 mm (Medtronic) up to 20 atm, and Quantum 3.5 × 8 mm (Boston Scientific, USA) up to 28 atm. All of these balloons ruptured and long linear dissection occurred. Two drug-eluting stents (DES) Taxus Liberte (Boston Scientific, USA) 2.75 × 28 mm and 3.0 × 32 mm were deployed at mid LAD to distal LM, and subsequently, postdilatation of the in-stent portion up to 30 atm by Quantum (Boston Scientific, USA) 3.0 × 8 mm, 3.25 × 8 mm, and 3.5 × 8 mm balloons. Intra-vascular ultrasound (IVUS) and angiography (Fig. D) revealed that 2 stents were well deployed and well apposed to the vessel wall (Fig. E–H) with retrograde collaterals to the distal RCA.
We performed PCI for the difficult lesion of RCA to complete revascularization due to cardiogenic shock. A hydrophilic wire Pilot 50 (Abbott, Chicago, IL) was successfully advanced to the distal posterior descending artery with a 6 Fr. Ikari IL 3.5 guiding catheter (Terumo, Tokyo, Japan) via the right TR approach. An Ottimo 1.5 × 10 mm balloon (Kaneka, Osaka, Japan) and a Maverick 2.0 × 20 mm balloon (Boston Scientific, USA) were used for dilatation of the lesions from mid RCA to proximal RCA up to 18 atm. Because the RCA was much angulated with an epsilon shape (Fig. A) and linear dissection occurred after balloon angioplasty, we tried to deploy stents from the distal to the ostium RCA but failed. Even though we employed methods such as 2 guidewire technique, balloon anchoring technique, 5-in-6 technique using 5Fr. ST01 catheter (Terumo, Tokyo, Japan), and deep-seating technique to deploy stents (including one drug-eluting stent), but all were unsuccessful when applied separately. Therefore, we proceeded to apply 3 techniques in combination (balloon anchoring technique, 5-in-6 technique, and deep-seating technique) to deploy the first stent Vision 2.75 × 18 mm (short stent) (Abbott) at the most angulated portion (Fig. B) which attributed the success of deploying other 4 stents from the distal to the ostium RCA: pixel 2.5 × 23 mm (Abbott), micro-Driver 2.5 × 24 mm (Medtronic, USA), Vision 3.0 × 28 mm, and Vision 3.5 × 12 mm. After high-pressure dilatation of the in-stent portion, IVUS and angiography (Fig. C) revealed that the 5 stents were well deployed and well apposed to the vessel wall (Fig. D–H).
We removed IABP and ECMO until cardiac contractile function improved to left ventricular ejection fraction over 40 percentage after 1 week. The patient was discharged after 2 months and had survival for 5 years.


The first case involved a 45-year-old female patient who had been admitted to our hospital with the complaint of abdominal pain and nausea. Contrast-enhanced CT showed hypodense cysts (approximately 1 cm in size) in the central portion of the right kidney and macrolobulated hypodense mass (approximately 5.5 × 2.5 cm2 in size) in the subhepatic space accompanied by fat density. Abdominal ultrasound examination showed lobulated cystic lesions (about 64 × 45 mm2 in size), identified in the region adjacent to the lower pole of the right kidney. A gallbladder stone (approximately 5 mm in diameter) was observed in the lumen. The common bile duct and intrahepatic bile ducts were of normal width.
The patient underwent laparoscopic operation. After placing trocars at the appropriate sites and insufflation of the abdomen, the gallbladder was removed. Cystic masses, measuring 9.5 × 4.5 cm2 in the subhepatic space were completely removed ( and ). Pathology reported cysts consistent with lymphangioma. The patient was discharged on postoperative day 7 without any complication. At the one year postoperative follow-up visit, the patient was well, with no complaints or signs of cystic mass at ultrasonography.


Our second case involved a 61-year-old woman who was admitted to our hospital because of abdominal distention and pain. The patient had a history of abdominal hysterectomy and appendectomy. MRI of the abdomen showed a cystic mass (8 × 5 cm2) in the inferior part of the right liver lobe. Laboratory values were normal with a cardiac ejection fraction of 60%. The patient underwent laparoscopic surgery. After placing trocars in the appropriate sites and insufflation of the abdomen, a multicystic mass (8 × 5 cm2) in the lower part of the liver and a few small cysts around the cecum were noticed ().
All cystic masses were completely removed. Pathological result revealed multilocular peritoneal inclusion cysts consistent with benign cystic mesothelioma. The patient was discharged on postoperative day 5 without any complication. At the one year postoperative follow-up visit, the patient was well and ultrasonography showed no sign of cystic mesothelioma.


A 28 year old male while attempting to slaughter a calf holding its head between his thighs accidentally shot himself with bolt gun to right thigh and sustained Grade II open fracture of distal one third shaft of femur (). He had an entry wound measuring 2 cm in length and 1 cm in breadth over anterior aspect of his right thigh ().
The wound was explored and debrided on the day of admission. Wound swab grew Pseudomonas, Proteus and Anaerobes. He was started on intra venous Augmentin. After five days, patient developed fever with chills and rigors. He also had purulent discharge from the wound. Inflammatory markers were raised with C reactive protein of 450. MRI () confirmed there was no collection of pus in the posterior compartment of thigh. He underwent another wound exploration and debridement on fifth day of admission. Pus collection was found in the subcutaneous and sub muscular layers of right thigh. The wound was communicating with knee joint through the supra patellar pouch. Knee was washed out under arthroscopic guidance.
The wound was treated with negative pressure wound therapy. He had a further wound debridement andsecondary wound closure after eleven days of injury and then discharged to home. The limb was immobilized in an above knee cast for four weeks and knee was later mobilized using a knee ranger splint.
He had three weeks of intravenous Ertepenem based on wound swab culture and sensitivity. At 12 months of follow up the wound healed with no signs of infection. He had full range of knee movements.


An 18-year-old female patient presented to our outpatient department with pain in her left knee of 3 years duration. There was a history of fall 3 years ago. She felt pain while walking and while standing up from squatting position. The patient gave no history of locking episodes. On clinical examination, there was no obvious swelling over her left knee. There was no tenderness around the knee except for tenderness over the medial joint line. The patient complained of pain during terminal flexion. There was no laxity in the knee. McMurray test was positive for the medial meniscus. Rest of the examination of the knee was unremarkable.
The patient had already been treated with physiotherapy and occasional analgesics. We decided to image the left knee. The radiographs of the knee revealed no abnormality (). We performed magnetic resonance imaging (MRI) scan of the knee and expected it to show a medial meniscal tear. Initial reporting by the radiologist confirmed a medial meniscal tear without a mention of it being discoid. However, because the body of the meniscus was seen in 4 consecutive sagittal sections of the MRI scan ( and ), we suspected a discoid medial meniscus and got the scan reported again. This time, the radiologist reported it as a torn discoid medial meniscus. We decided to perform arthroscopic partial meniscectomy and meniscoplasty for the patient.
Arthroscopy confirmed a discoid medial meniscus occupying the entire medial tibial plateau (). The anterior part of the discoid meniscus was attached along the anterior cruciate ligament (ACL) (). However, no obvious tear could be visualized (). We then trimmed the lateral edge of the meniscus lying toward the intercondylar region which revealed a large cleavage tear completely restricted to the interstitial part (). We resected the upper and lower flaps till a stable peripheral semilunar rim of meniscus was obtained (). Postoperatively, the patient was started on a physiotherapy protocol to preserve range of motion and muscle strength. Weight bearing was started after pain due to surgery subsided. 2 weeks postoperatively, the patient attained full range of motion and was pain-free even on terminal flexion.


A 65-year-old woman with a recurrent carcinoma of left buccal mucosa, who was earlier operated for tongue cancer with upper neck dissection, had a defect starting from the retromolar area to the lip along with rim excision of the mandible following excision of the left buccal mucosa lesion [Figure and ]. The defect was measured (7.5 cm × 2.2 cm) and then transferred to the lower border of the incision of the lower face-upper neck flap []. The upper, anterior and posterior margins of the marked flap were incised till the depth of the dermis. The ’turned in fasciocutaneous island flap’ was raised at the lower border of the upper cervical flap by subdermal dissection under magnification at the upper border of the island flap up to 1–1.5 cm away from the island. The anterior and posterior ends of the flap were divided. The flap was then turned in, over the mandibular rim into the defect []. The posterior end was sutured to the retromolar region, the lower border of the flap was sutured to the upper cut margin of the defect and the anterior cut end was set in the anterior part of the defect, whereas upper border was sutured with inferior cut margin. It is worthwhile to note that all the direct arterial blood supply including the facial and submental arteries were cut off []. The flap easily set into and healed well [], and the donor site was skin grafted as a precaution to prevent tension on the pedicle (tumour-node-metastasis [TNM] staging: T2, N0, M0). No post-surgery radiation was given. Patient healed well and is recurrence free.


A 30-year-old woman with a post-excisional unreconstructed defect was referred because of a rapid recurrence []. The oncosurgeon did a wide excision and radical neck dissection []. The defect involved a part of the upper lip, buccal mucosa and lower lip. This time the island turnover flap to be raised was anterior starting from the midline. The lower facial skin was detached from the mandible, and the residual mental nerve branches and any arterial twig to the skin were divided [Figure and ]. The flap as marked was divided to the depth of the dermis and 5 mm subdermal dissection was done to create edges for the inner and outer lining [Figure and ]. The flap was turned into cover the buccal defect as well as for the buccal lining of the lip [Figure and ]. The neck side of the incision was closed primarily. The submental zone had a residual defect. This was closed by creating a small z-plasty. The flap showed post-operative congestion and there was a small wound gap [] at the lip but eventually healed well [] (TNM staging: T3,N1,M0). Post-operative radiation was recommended; unfortunately, patient did not undergo radiation. Patient developed metastasis and died after 2 years.


A 57-year-old male came with carcinoma of right buccal mucosa. He underwent radical neck dissection and wide excision. He had a large buccal mucosa defect starting from retromolar region upto lip involving partial loss of right upper lip, lower lip, commissure and part of cheek [Figure and ]. A flap of 4.75 cm × 11 cm length was raised at the lower border of the upper cervical flap from the angle of mandible to the chin []. The island was demarcated and incised, only dermis deep, at the upper border. The subdermal dissection was then carried out up to about 1.5–2 cm upwards at the upper border []. Both anterior and posterior subdermal pedicles were divided to keep about 50% of the central width of the pedicle. The flap was then turned in over the mandible []. The posterior end was stitched to the retromolar defect. The lower border of the flap was stitched to the upper edge of the defect and upper border at the lower edge of the defect till the commissure []. At the commissure, as seen two vertical cuts were made at upper and lower borders up to the dermis []. A subdermal dissection was carried out up to 5 mm under both the edges to create cut edges for mucosa and the skin of the lips. A central undivided portion mimicked the commissure. Then the flap was turned outwards and back from the lip edge to fill the outer defect [Figure and ]. The flap was sutured. Patient received full course of radiation, and the flap survived and the patient is tumour free [Figure and ].


A 55-year-old male came with carcinoma of left lower lip and buccal mucosa [Figure and ]. He received neoadjuvant therapy and was operated with wide excision and upper neck dissection. He had a large defect involving lower lip, buccal mucosa, commissure and a small part of upper lip []. Here, the island flap was raised anteriorly from below the defect []. Anterior part was folded upon itself and turned in [] to create the lower lip including labial mucosa, commissure and to cover the cheek buccal mucosa defect [Figure and ]. Wound dehiscence occurred following early suture removal []. A new incision was taken about 2 cm above the previous incision for reinsetting the flap at the upper border of the defect [Figure and ] and further healing was uneventful. Postoperatively, patient received full course of radiation [Figure and ].


An 18-year-old African-American female came to emergency room after an episode of syncope. She reported progressive swelling of her neck and face for 3 weeks. Her past medical, surgical and family history was unremarkable. She was not taking any medication prior to this hospitalization. She denied smoking tobacco, alcohol abuse or recreational drug use. Physical examination was significant for generalized swelling of neck and face. There was no lymphadenopathy, hepatomegaly or splenomegaly appreciated on examination.
Laboratory evaluation revealed WBC of 10,400/mm3, hemoglobin of 9.4 g/dL, platelets of 378,000/mm3, creatinine of 0.58 mg/dL and lactate dehydrogenase of 368 IU/L (upper limit of normal: 240 IU/L). CT scan showed a 14 × 12 × 10 cm mass in right lung along with liver lesion and multiple small masses in both kidneys. Echocardiogram revealed large, spherical, fixed mass in the right atrial cavity. CT-guided core needle biopsy of lung mass revealed the diagnosis of composite lymphoma with components of PMBCL and focal Hodgkin lymphoma. Needle core biopsies showed two different morphologic processes, and majority of the cores showed an infiltrate of large atypical cells associated with clear cytoplasm and fine fibrosing compartmentalization. Second area of the needle cores showed an infiltrate composed of small lymphocytes, neutrophils and eosinophils with scattered large atypical cells. Immunohistochemical stains also revealed two different patterns; the large atypical cells in the large cell infiltrate were positive for B-cell markers (CD20 and CD79a) and CD23, and negative for CD10 and showed weak expression for bcl-6 and bcl-2. Ki-67 in this subset was 70%. The other subset of cells was positive for CD15 and CD30 with negative to weak expression of PAX-5 (). Bone marrow biopsy showed no involvement with lymphoma.
During her initial presentation, patient developed superior vena cava syndrome due to large lung mass and also found out to have pulmonary embolism. After establishing the diagnosis, patient was started on dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin and rituximab (EPOCH-R) chemotherapy. Patient showed excellent clinical response to treatment and after just two cycles of therapy, her superior vena cava syndrome resolved completely. She was also given CNS prophylaxis with intrathecal methotrexate from third cycle onwards. After six cycles of treatment, PET scan showed no evidence of disease. Patient received a total of eight cycles of treatment with dose-adjusted EPOCH-R. Patient remains in complete remission after completion of treatment.


A male patient in his 40-year-old visited our infectious diseases (ID) outpatient clinic with a chief complaint of multiple body aches, lasting for 2 months. He visited a nearby clinic and was prescribed antibiotic of unknown name to no avail. He disclosed that he had unprotected sex with commercial sex worker (CSW, female) 1 month before the onset of symptoms. He never had such an experience with CSW before this episode. Shortly, after this sex, he started to sweat a lot and underwent HIV test repeatedly at a local Public Health Department. Despite negative HIV test results, he still feared the possibility of HIV infection and visited our clinic.
On physical examination, his vital signs were all normal. There were small lymph nodes palpable on the right posterior neck, but it did not appear pathological. Rest of his physical examination was unremarkable. Laboratory examinations including tests for HIV, hepatitis B, hepatitis C, and syphilis were all negative. He was prescribed amitriptyline and lorazepam PRN, followed by Chinese herbal medicine extracts (Saiko-ka-ryukotsu-borei-to followed by Choto-san). His symptoms improved but still persisted. However, he felt somewhat safe by visiting us and continued to visit our clinic on the regular basis.


A male patient in his 30-year-old visited our ID clinic with a chief complaint of “sputum stuck in his throat” for 2 years. He had been an expatriate in a Middle East country for 4 years. During the stay, he underwent unprotected cunnilingus and penile-vaginal sex with several CSWs (female) for three times. He also disclosed that he used to have sex with CSWs in Japan before staying in the Middle East. Since the last intercourse while in the Middle East, he developed a sore throat and believed that he had acquired STD. He visited a hospital in the Middle East was provided antimicrobial therapy with transient relief of his symptoms, but these with general fatigue relapsed soon. After returning to Japan, he also visited an otolaryngologist and was given some medications without help, and he finally decided to visit our ID clinic.
Physical examination, as well as routine blood tests including HIV, hepatitis B, hepatitis C, and syphilis, was all normal. Throat culture only revealed usual bacterial flora. He was treated with a Chinese herbal medicine (Hange-koboku-to) with the reassurance that no STD is likely. Symptoms improved over several weeks.


A male patient in his 40-year-old presented to our ID clinic with discomfort in throat, low-grade fever, and cough. Three days before the visit, he got acquainted with a diva male and had unprotected sex with him (insertive). This was first ever sex with men ever he had experienced. He was later notified that the man who he had sex with had been infected with HIV on antiretroviral therapy (ART), with good viral suppression.
The patient had history of involuntary dyskinesia and anxiety disorder, and an episode of bowel perforation and had been seen by physicians at the Department of Neurology, Psychiatry, and Gastrointestinal Surgery at our hospital.
On physical examination, he was anxious but did not have any abnormalities otherwise. Routine laboratory workup, including workup for STDs, was all negative.
He was offered antiretroviral medications as postexposure prophylaxis (PEP) as well as hepatitis B vaccines. His symptoms persisted with severe anxiety and had frequent unscheduled appearance to our clinic. After ruling out STDs and providing PEP/vaccines, we referred him to his psychiatrist, and he continued to receive treatment there.


A male patient in his 20-year-old from China visited our ID clinic, with a chief complaint of penile discomfort developed shortly after having unprotected sex with CSW (female) in Japan. After seeing a dermatologist with assurance that there was no skin disorder identified, he decided to visit our ID clinic. He stated that he has both oral and penile discomfort, and he believed that there are abnormal mucous lesions on both. His physical examination was entirely normal, and no abnormality was identified on his skin and mucous membrane, unlike he claimed. Routine blood tests, including HIV, hepatitis B, hepatitis C, and syphilis as well as urine PCR for Chlamydia trachomatis and Neisseria gonorrhoeae were all normal. He was treated with Chinese herbal medicine extract (Hange-koboku-to) with significant improvement of, but not eradication of, symptoms.
We obtained written informed consents from all patients for publication of the current report.


A 39-year old woman presented at the University clinic for obstetrics and gynecology with complaints of a mild low abdominal and pelvic pain, increased frequency of vaginal bleeding and abdominal distension. She was diagnosed with a cystic formation in the right ovary 3 months before her visit at our clinic, since then the cyst was enlarged in size and caused additional symptoms to the patient. She was admitted to our clinic, at the department for operative gynecology for a further examinations and proper evaluation.
Gynecological history of our patient showed that she had her menarche at the age of 13 years, still with regular menstrual cycles and moderate intensity of menstrual bleeding. Her obstetric history revealed that she had two vaginal spontaneous deliveries. On detailed anamnesis she did not report any other medical condition, co-morbidities, previous surgeries or allergies. There was no family history for a malignancy of any type.
On physical examination she had normal vital signs, abdominal palpation showed mildly distended abdomen with a palpable solid mass filling mainly the right side of the pelvic cavity. No abdominal tenderness was observed. Gynecological examinations did not show any irregularities of the vulva, vaginal portion of the cervix, with no evident pathological findings detectable. Bimanual examination revealed palpable tumorous formation, mainly on the right side of the uterine body, with marked tenderness during mobilization.
All the laboratory standard hematological parameters were in referent ranges, blood count, liver function tests, coagulation parameters, urea, creatinine levels and serum electrolytes were in normal limits. Viral serology was negative and tumorous markers, such as cancer antigen 125 and carcinoembryonic antigen, were within their normal values. Cervicovaginal smear showed only inflammation.
The patient was examined with a modern ultrasound Voluson 8, both vaginally and abdominally. Transvaginal ultrasound showed posteriorly dislocated uterus with a total diameter of 5.4cm. Endometrial zone was with a diameter of 1.2cm, secretively changed, with no pathological findings. In front of the uterine body, posterior to the urinary bladder, predominantly on the right side, we detected a large semisolid tumorous formation. It was a large heteroechoic pelvic mass predominantly cystic, with a diameter of 7cmx8cm, septate, filled with thicker fluid in one part. After filling the urinary bladder with saline we excluded a vesical origin of the tumor. Doppler ultrasound study showed marked vascularity, but without pathologically changed Doppler waves. This not so well defined soft tissue lesion seemed to arise from the right ovary, but it had no distinct border with the uterus and it also seemed to spread into the right broad ligament. Left ovary was normal, right ovary was difficult to be properly showed and examined. In differential diagnosis we thought of ovarian tumor or uterine myoma.
Due to the diagnostic dilemma we also performed pelvic computerized tomography (CT). Pelvic CT showed a large tumorous heterogeneous tumorous formation which as localized behind the urinary bladder and in front of the uterus, mostly spread in the right broad ligament. The mass was oval with marked heterodensity, measuring 8.5x7.5cm in size (). Centrally the tissue was solid, with small cystic multilocular and multifocal changes localized peripherally. In the post-contrast CT phase the tumorous formation showed high density in its central parts. The formation makes compression on the other pelvic organs but it does not infiltrate any of them. Uterus and ovaries were detected as normal. The CT did not detect enlarged lymph nodes, lymphadenopathy, or free liquid in the abdominal or pelvic cavity.
Preoperative diagnosis of ovarian cystic tumor was made, although we could not exclude the possibility of degenerative uterine myoma.
Patient underwent surgery with a laparotomy via transverse abdominal incision. During operation, on inspection, we saw large white-yellowish cystic formation right in front of the uterine body, not connected to the right ovary anatomically. Macroscopically I looked like a cystic tumor localized in front of the uterine body, connected to the uterus in a small portion, but spread intraligamentary in a zone of 7cm (, ). The mass was totally extirpated and it was sent to a frozen section. It revealed mesenchymal tissues with highly vascularized structure, totally benign with no signs of malignancy. Due to the patients’ age and obvious benign characteristics of the tumor we did not perform hysterectomy or bilateral salpingo-oophorectomy.
Pathological examination of the operative material detected a well-structured nodule, measuring 8cmx8cm in diameter, with a grayish-white appearance. Macroscopically it as described as a solid tumorous tissue, with wide spread vascular net. It had a soft consistency on its cut surface. Histological examination showed a mixture of spindle-shaped smooth muscle cells, without nuclear atypia, admixed with nests of mature adipocytes. Between these muscle and adipose cells there very numerous vascular elements visible. The lipid cells very all mature, without any lipoblasts. The tumor was highly vascularized, with groups of muscle cells spread among the different sized blood vessels. All of the cells showed only benign characteristics, with no signs of malignancy, but with rare mitosis. Immunohistochemically cells were positive to Vimentin, focally positive to D-100 A4, diffusely positive to Demsin, SMA and Caldesmon, also they showed co-expression to CD100 in focus, while Calmetinin, CK, HMB45, Inhibin and S100 stayed negative. Ki67 showed very low proliferative index (<1%). Based on the above findings, the tumor was diagnosed as a benign vascular lipoleiomyoma.
The patient was hospitalized at our clinic for a total of 16 days, discharged after operation with no complications and in a stable clinical condition.


A 64-year-old female presented with recurrent chest pain and progressive shortness of breath in April 2015. She had a history of asthma and panic attacks. The worsened symptoms triggered a cardiac workup which included cardiac catheterization which showed no obstructive lesions. The findings on echocardiography and CMR in 2015 suggested the diagnosis of HCM (). The patient did not have a family history of HCM, but her father died suddenly at age 48. Her paternal grandfather and two paternal uncles all died suddenly before the age of 40. Genetic testing was negative for pathogenic variants. A serum protein electrophoresis and urine protein electrophoresis were unrevealing. Her breathlessness had improved with a diuretic regimen of low dose furosemide and aldactone with stable volume status. As part of the follow-up, she was re-examined in February 2016, at which time ECG showed low voltage and echocardiography demonstrated restrictive filling pattern. Repeated CMR provided the most important diagnostic information, which is the pattern of abnormal subendocardial late gadolinium enhancement (LGE) suggesting cardiac amyloidosis (). Based on CMR findings, a fat pad biopsy was completed, but negative. A subsequent endomyocardial biopsy was positive for amyloidosis.


A 17-year-old male presented with history of gradually progressive deformity in the back since 3 months and weakness in both lower limbs since 3 days. He had no history of trauma, fever, or similar complaints in the family. There was no significant medical/surgical history. On examination, he had dorsal scoliosis with convexity to the right with angular proximal dorsal kyphosis. His chest was flattened on the right side and the 4th–7th ribs on the right side were absent on palpation. He had non-ambulatory power in his lower limbs (power around the hip and knee was 2/5 and power around ankle and in toes was 3/5) with spasticity and exaggerated deep tendon reflexes. Hypoesthesia below D7 was noted and bowel bladder sensation was preserved. Plantar response was extensor.
An X-ray taken elsewhere 6 months prior to presentation to OPD showed mild scoliosis with few ribs absent on the right side []. Due to suboptimal quality of the X-ray, we could count which ribs were absent. X-ray taken in our OPD demonstrated dorsal scoliosis with convexity to the right side, apex at D6, and Cobbs angle of 41° with angular dorsal kyphosis with apex at D5–D6. The 4th to 7th ribs on the right side were absent with destruction in the lower ribs more as compared to the X-ray taken 6 months back [].
Computed tomography (CT) scan further illustrated the pathoanatomy of the disorder. All X-ray findings were confirmed. Three-dimensional reconstruction showed a complete absence of the right 4th–7th ribs []. There was a severe narrowing of the canal at the apex. In addition, right-sided pedicles and right half of vertebral bodies proximal to the apex showed osteolysis [Figure and ]. There was severe narrowing of the canal at the apex of kyphosis []. Magnetic resonance imaging (MRI) showed stretching and compression of the cord at the apex of the deformity. There was no evidence of abscess/inflammation. Angiography did not reveal any abnormality.
The patient was given zoledronic acid infusion (4 mg) every month. Zoledronic acid was stopped at 18 months and patient was switched to weekly alendronate with a dose of 70 mg per week. He was also given radiotherapy at a dose of 8 Gy (single dose) 2 weeks prior to surgery. This dose was given after consultation with a senior radiotherapy consultant at a tertiary care hospital specializing in cancer treatment.
The patient was taken for surgery in prone position under general anesthesia. Following midline exposure, bilateral T8–T12 pedicle screws were passed. Pedicle screws were passed on the left side from T1 to T3. The right-sided pedicle and body were cystic as confirmed by palpating with a ballpoint probe. Hence, MRI-compatible sublaminar cables were passed from T1 to T3 on the right side. D5 and D6 laminae were soft and were excised. Thorough cord decompression was done. D4 and D5 bodies were excised. The excised bones were sent for histopathological examination. Contoured rod was applied and sequentially tightened. The deformity was fully corrected following fixation. The proximal end of the right-sided rod was bent and the bent part was put between the spinous process of C7 and T1 to provide additional stability.
Bilateral fibulae and cancellous graft from right posterior iliac crest were harvested from the patient's mother after both patient and mother were found to be ABO and Rh compatible in preoperative blood testing. The mother's bone was used as there were chances that the harvested patients bone might get resorbed. Anterior reconstruction was done via posterolateral approach using cancellous bone graft and two pieces of strut fibulae. Posterior fusion was done using two long struts of fibula bridging the laminectomy defect. Additional matchstick graft prepared from remaining fibulae was placed posteriorly []. The wound was closed over a drain.
Histopathology revealed decreased bony trabeculae with irregular vascular formations. The bony trabeculae seemed to be replaced by fibrous tissue. The fibrous tissue demonstrated not only increased number of blood vessels but also the absence of cellular atypia/granulomas. The number of osteoclastic giant cells were increased. The material was negative for any fungal or bacterial organisms. No specific diagnosis was obtained on histology. Due to the unavailability of facility to take microscopic images at our institute, the pathology images could not be provided.
Postoperative X-ray showed full correction of deformity [Figure and ]. The drain was removed on 4th postoperative day. The patient started regaining power on 7th postoperative day and had a complete neurological recovery at 5-week postoperatively. The patient was mobilized with a total contact brace. X-rays at followup showed that resorption of ribs had not progressed. X-ray at 1-year postoperatively showed that alignment is maintained [Figure and ]; however, consolidation of the anterior graft was not seen. A CT scan showed an anterior void and the fibulae had not united with the host bone [].
The patient was taken for surgery in the lateral position and the nonunion site exposed via left transthoracic approach. No rib was excised and the plane between the 5th and 6th rib was utilized to reach the nonunion site. Both fibulae struts were removed and fibrous tissue excised. The mother's tricortical iliac crest bone graft was harvested and used for anterior reconstruction.
At 7-month followup, the patient has no neurological deficit and walks with a total contact brace. Radiographs revealed maintained alignment [Figure and ]. CT showed that anterior strut graft has not resorbed; however, it still has not united with the host bone []. Since patient remained asymptomatic, we have kept the patient on monthly monitoring with X-ray check.


A 50-year-old male presented with sudden headache. At presentation, his Glasgow coma scale was 14 and no lateralizing sign was found. Brain computed tomography (CT) showed a thick subarachnoid hemorrhage in the basal cistern and a hemorrhage on the left frontal lobe and both lateral ventricles. CT angiography revealed an aneurysm at the anterior communicating artery (ACoA). The patient underwent preoperative digital subtraction angiography, which demonstrated a wide necked and bilobulated aneurysm with maximal size of 5.2 mm arising from the left ACoA (). The morphology of the aneurysm in this patient was deemed not amenable to treatment with coil embolization. An emergency clipping of the ruptured ACoA aneurysm was performed. Left side pterional craniotomy was chosen for aneurysm dome avoidance and more favorable view of the aneurysm neck. Brain swelling was moderate and ventricular drain was inserted through Payne's point. Ruptured point of the aneurysm was obliterated by a bayonet type clip. Further dissection of the aneurysm and confirmation of distal tip of the clip was difficult due to the gradually swelling brain and tight adhesions with the surrounding tissues. The patient tolerated the surgery well and showed no neurologic deterioration after surgery. Transcranial Doppler ultrasonography revealed no evidence of vasospasm. The patient's mental status fully recovered with conservative management. Follow-up cerebral angiography, which was obtained on the fourteenth postoperative day showed remnant aneurysm behind the surgical clip (). We recommended repositioning of the clip, but the patient was reluctant to undergo a reoperation. The patient was discharged with no apparent neurological deficit. Follow-up cerebral angiography at 12 months postoperatively showed the remnant aneurysm had regressed almost completely (). A recommendation to monitor the remaining tiny aneurysm with DSA after 12 months was made.


A 55 year old man with cystic fibrosis complained of prominent cough triggered by lying down, bending over, speaking and on rising from the bed. He suffered bloating, erratic bowel habit and mild dyspepsia. He previously had a Nissen fundoplication for airways reflux. His baseline FEV1 was 0.85 litres (25% predicted), weight 68.9 kg and Hull Airway Reflux Questionnaire (HARQ) score of 29 (the upper limit of normal is <13) []. Baseline cough monitoring with the semi-automated Hull Automated Cough Counter HACC [, ] demonstrated an average of 29 cough events per hour. Within 2 weeks of starting treatment with Ivacaftor he felt significant subjective improvement in his cough. This was reflected in the repeat HACC measurement of 9 coughs per hour (Fig. ). The HARQ score concomitantly decreased to 11. FEV1 and weight were unchanged.


An unrelated 35 year old man with cystic fibrosis had similar prominent cough despite Nissen fundoplication. He had baseline FEV1 of 4.64 litres (112% predicted), weight of 63.8 kg, HARQ score of 13 and 76 cough events per hour were observed on cough monitoring. He spontaneously reported a subjective improvement in cough and his cough monitoring improved to 5 cough events per hour (Fig. ). The subjective HARQ score was 9 after one month therapy with ivacaftor. Again there was no spirometric or weight change at his follow up visit.