We report on a 55 year old male patient with a history of severe aortic valve stenosis, ectasia of the aorta ascendens (48 mm) and reduced left ventricular function. He underwent prosthetic valve replacement with a mechanical valved conduit (St. Jude Medical Conduit CAVG 29 mm) in 2003. Anticoagulation was started with phenprocoumon. Implantation of a cardiac pacemaker (Medtronic Kappa KDR 503) due to atrioventricular block III° was necessary five days after initial heart surgery.
The patient presented to the emergency department in 03/2013 with a new sleep-onset weakness of the left arm and difficulties to speak. Emergency cranial computed-tomography (CCT) revealed ischemic brain lesions in the territory of the right middle cerebral artery. Neither atrial fibrillation nor valvular lesions or carotid artery stenoses were detected, when the patient was evaluated for causative mechanisms. Rehabilitation was finally completed with minimal residual neurological symptoms. Five months later, the patient was readmitted with fatigue, febrile temperatures, headache, nausea and progressive left-sided weakness and dysarthria. CCT scans after readmission showed signs of the preceding ischemic stroke in the territory of the right middle cerebral artery and new signs of progressive embolisation in the territory of the left middle cerebral artery with haemorrhage. C-reactive protein (CRP) was now 59 mg/l (ref. <5 mg/l) and the erythrocyte sedimentation rate (ESR) was 45 mm/h (ref. 0–30 mm/h). Sequentially obtained blood culture samples (5 of 5 sets) were positive for Staphylococcus epidermidis resistant to oxacillin (MRSE) (see Table ). In line with additional minor DUKE criteria, predisposition, febrile temperatures and septic emboli, the definitive diagnosis of infective prosthetic valve endocarditis (PVE) was made. Antiinfective treatment with vancomycin plus rifampicin was started and the patient was transferred to a tertiary university medical center providing immediate facilities for cardiosurgical and neurosurgical interventions. The initial bedside transthoracic echocardiography on admission revealed no signs of valvular masses suggestive for vegetations, a moderate mitral regurgitation was noted. Evaluation via transesophageal echocardiography 48 h later showed a filiforme (7x4mm) mass at the prosthetic aortic valve and a perivalvular dehiscence of the mechanical valved conduit. Fortunately, at this time no surgical intervention was required.
In 11/2013 the patient developed progressive clinical signs of heart failure on the basis of severe mitral regurgitation, on transesophageal echocardiography destruction of the aortic-mitral continuity was noted, which made a mitral-valve repair intervention impossible. Urgent prosthetic valve replacement was successfully performed (St. Jude Medical MJ-501 33 mm). Histopathological samples showed signs of low grade chronic inflammation. Tissue samples from the surgical site and swab specimen from the left ventricular outflow tract (LVOT) were culturepositive for S. epidermidis (MRSE). In conclusion, new prosthetic valve material had to be inserted into a non-sterile situs despite antiinfective pretreatment and sterile bloodcultures. A curative approach seemed from that particular time on all but impossible and the patient was discharged with cotrimoxazol plus rifampicin as a timely indefinite oral suppressive treatment. Seven months after mitral valve replacement, in the context of a rising CRP and progressive fatigue, breakthrough bacteremia was detected. The MRSE strain isolated from sequential bloodcultures displayed now resistance against rifampicin (see Table ). Bloodstream negativity was achieved after prolonged treatment with daptomycin plus clindamycin. From the infectious disease perspective, the presence of this now isolated “difficult to treat” MRSE strain, together with lacking surgical options to remove or revise prosthetic material resembled a palliative situation, since there were no substances for effective oral suppression therapy left. The main concern however, was that in the near future the progressive destruction of the periprosthetic tissue between the aortic and mitral valve (Fig. ) might result in a fatal valve complication or progressive embolization to the brain. Regarding the lack of curative options, salvage OHT was discussed as a measure of last resort. During the pretransplant workup, prostate cancer (pT3a, pN0 (0/27), R1, L0, V0, M0; Gleason Score 3 + 4 = 7a) was diagnosed and the patient was delisted for OHT due to apparent malignancy. Radical prostatevesiculectomy was performed with adjuvant radiotherapy, after an interdisciplinary tumorboard decision. Twelve months later, under oral antiinfective suppressive therapy with moxifloxacin and clindamycin, the patient developed febrile temperatures with MRSE bacteremia – now displaying resistance against clindamycin and all fluoroquinolones. Fortunately, bloodstream negativity could be induced again with a prolonged course of daptomycin on an outpatient basis (OPAT). Finally, the patient was reassessed for OHT under stable conditions, bloodculture negativity and in line with oncological transplant requirements – 28 months after the first diagnosis of infective PVE, the patient was successfully transplanted. In the peri-transplantion period and for four weeks post-transplantion the patient received daptomycin plus fosfomycin. Bloodcultures remained sterile at any time and in particular after ending antiinfective treatment. He is now under close follow-up doing well (6 months post-OHT). Histopathological examination of the explanted organ and prosthetic material showed clear evidence of chronic active IE. Tissue specimen from aortic tissue were conclusive positive for Staphylococcus epidermidis on broadspectrum 16 s-PCR. From the isolated tissue samples the mecA gene encoding for oxacillin resistance was amplified.


A 21-hour old newborn male, born at a gestational age of 41 weeks and weighing 3.14 kg, presented with respiratory distress. Chest radiograph showed right diaphragmatic hernia and complete opacification of the right hemithorax with displacement of mediastinal structure to the left hemithorax (Fig. 1). The patient was intubated and put on oscillatory mechanical ventilation; dobutamine and dopamine were also started. After initial stabilization, the patient underwent repair of right CDH via a right supra-umbilical transverse incision. At operation, there was an 8cm wide posterolateral defect of the right hemidiaphragm, with the liver herniated into and filling most of the right hemithorax. The diaphragmatic defect was enlarged to the liver was delivered back to the abdomen. During reduction, it was noted that the severely hypoplastic right lung was fused to the dome of the liver (Fig. 2). No distinct plane between the liver and the lung could be established while dissection. The patient developed severe bradycardia during surgery; therefore, decision was made to partially fermeture the diaphragmatic defect. We closed the vast majority of the diaphragmatic defect postero-laterally, leaving enough space medially for the fused lung and liver. Postoperative course remained stormy and patient succumbed to progressive pulmonary failure.


An 11-year-old female patient was referred to the clinic of Endodontics and Operative Dentistry at Damascus University, Dental School with a chief complaint of pain in the right mandibular second premolar. Vitality, percussion and palpation tests of the mandibular second premolar and adjacent teeth revealed its negative response and positive responses of adjacent teeth to pulp vitality tests. An evaluation radiography revealed the presence of secondary caries under an old composite restoration on the immature second premolar. All the tests were done using Endo-Frost (Coltène-Whaledent, Langenau, Germany) (). The final diagnosis was pulp necrosis of the immature tooth.
Local anesthesia was administrated by infiltration of mepivacaine (Mepivacaine HCL 3%, Alexandria, Egypt). The tooth was isolated using a rubber dam and the access cavity was prepared. The canal was initially irrigated with a 5.25% NaOCl solution. The working length was established radiographically and confirmed with an apex locater (J. Morita USA, Inc., Irvine, CA, USA). The canal was irrigated with the needle inserted 2 mm shorter than the working length, using 17% ethylenediaminetetraacetic acid (EDTA, Dia-Prep Plus, Diadent Group International Inc., Chongju, Korea) for 1 min to remove the smear layer, without damaging the stem cells present in the periapical area []. The canal was then irrigated with saline, followed by irrigation with 5.25% NaOCl for 3 min, saline and then 2% chlorhexidine for 5 min. Finally, the canal was irrigated with saline and dried using sterilized paper points. A #20 K-file (Dentsply Maillefer, Ballaigues, Switzerland) was then used to irritate the apical tissues gently and invoke bleeding in the canal. The bleeding was stopped 2 mm below the CEJ level and left for 10 min to allow clottting.
A mixture of Biodentine (BD, Septodont, Saint Maur des Fosses, France) was applied according to the manufacturer’s instructions and placed over the blood clot using endodontic pluggers. After 15 min, a light-cure glass ionomer restoration (GC Fuji II LC, GC Corp, Tokyo, Japan) was placed, and the patient was scheduled for follow-up (). Six months later, the teeth were double-sealed with permanent filling materials (3M ESPE, FiltekTM Z250, Universal Restorative, USA). The patient was recalled after 6, 12, and 24 months for clinical and radiographic examinations, which showed complete root maturation, with intact supporting soft tissues, without a sinus tract, pain, or swelling ().


A 78-year-old woman visited our hospital with a fever over 38° and for evaluation of her painful, swollen and palpable purpuric skin eruptions on her lower legs (Fig. a). Physical examination revealed swollen and punctate purpuric eruptions on her both lower legs. Laboratory examination showed normal leukocyte count of 8400/μl and elevated C-reactive protein level at 6.33 mg/dl (normal, <0.14 mg/dL). A skin biopsy specimen taken from a purpuric lesion on her leg revealed that neutrophil-rich leukocytoclastic vasculitis in upper dermis with extravasation of red blood cells into the dermis (Fig. b). Direct immunostaining shows IgA deposition surrounding small vessels in upper dermis. Based on the clinical course and laboratory examination, we diagnosed her skin eruption as an anaphylactoid purpura exacerbated by cellulitis. After the treatment with oral methyl-prednisolone 10 mg per day and cefazoline 2 g per day, her eruption improved remarkably in 2 weeks.
When cellulitis re-emerged on her lower legs, a generalized purpuric eruption reappeared on her upper arms, legs and lower abdomen (Fig. c). Laboratory examination showed a leukocyte count of 10,900/μl with neutrophillia (8262/μl) and elevated C-reactive at 10.77 mg/dl. Based on the clinical course and laboratory examination, we again diagnosed the eruption as anaphylactoid purpura, following cellulitis. The patient was treated with antibiotic, sulbactam/ampicillin 3 g per day and methyl-prednisolone 30 mg per day. After these treatment, her cutaneous inflammatory reaction and purpuric skin eruption rapidly subsided.


The patient is an 11-year-old male with attention deficit hyperactivity disorder (ADHD) who presented with an unintentional 20 lb. weight loss that was initially attributed to ADHD medication. Exam was notable for cervical lymphadenopathy. Laboratory workup showed leukocytosis with left-shifted granulocytes (WBC 210,000 cells/μL; 65 % neutrophils, 6 % bands, 5 % lymphocytes, 3 % monocytes, 2 % eosinophils, 3 % metamyelocytes, 13 % myelocytes, 2 % promyelocytes, 1 % blasts), normocytic anemia (Hgb 10.8 g/dL, MCV 92 fL), elevated LDH (1,858 U/L), and elevated uric acid (7.0 mg/dL). Abdominal CT scan showed splenomegaly.
A bone marrow study revealed hypercellular marrow (>95 %) with increased myeloid cells at all stages of maturation, increased eosinophils, scattered basophils, few erythroid progenitors, so-called dwarf megakaryocytes, and sea-blue histiocytes (Fig. ). Blasts were <5 % morphologically. Flow cytometry identified a population of atypical CD3+ MPO- TDT+ T lymphoblasts (9 % of total events). IHC of the bone marrow core biopsy confirmed these latter findings, showing individual and clusters of CD3+ TDT+ T lymphoblasts comprising ~10 % of overall cellularity and 20–30 % of cells in restricted areas (Fig. ).
RT-PCR from peripheral blood was positive for the BCR-ABL1 p210 transcript. Cytogenetic analysis of the bone marrow showed 46,XY,t(6;9;22)(p22;q34;q11.2)[]/46,sl,inv(3)(q21q26.2)[], confirming the presence of a variant three-way translocation generating the BCR-ABL1 fusion. The presence of a subclone (11 of 20 cells analyzed) with inv(3)(q21q26.2) suggested disease progression. Following identification of this inversion and validation of a novel MECOM antibody, combined IHC for MECOM and CD3 was performed on the bone marrow core biopsy. Interestingly, the CD3+ population and the MECOM-overexpressing population were non-overlapping (Fig. ), indicating the T lymphoblastic transformation was independent of the acquisition of inv(3)(q21q26.2).
Based on these findings, a diagnosis of CML with T lymphoblastic transformation was rendered. The patient was started on hydroxyurea and allopurinol, followed by single-agent treatment with imatinib (500 mg daily). Repeat bone marrow studies on day 25 of treatment showed restoration of trilineage hematopoiesis and normal cellular morphology, with abnormal T lymphoblasts comprising 1 % of total cellularity by flow cytometry. Subsequent to this study, he was transitioned from imatinib to dasatinib (100 mg daily) due to the development of oral ulcers, and continued to improve clinically on TKI alone. A third bone marrow biopsy and aspirate at day 54 showed 0.02 % T lymphoblasts. Peripheral blood quantitative RT-PCR analysis at three months showed a 1.4 log reduction of BCR-ABL1 transcripts (4.3 % IS units) (Table ). Despite this response to TKI monotherapy, a matched unrelated stem cell donor was identified and transplantation is scheduled given the high-risk features of his disease.


A 20-year-old Caucasian male presented to the cardiac clinic for evaluation of chest pain and elevated blood pressure. His chest pains were sharp, occurred randomly, and were mostly nonexertional. He also had an abnormal EKG demonstrating nonspecific ST/T wave changes (see ). His past medical history was unremarkable. He is a smoker and drinks alcohol socially and denied illicit drug usage. An echocardiogram performed in the office was normal, with the coronary arteries arising from the appropriate cups.
A cardiac computed tomography angiography (CCTA) was performed revealing anomalous origin of the right artery from the left coronary cusp. The proximal portion had an acute-angle take-off with an intramural course with a 70–80% stenosis. The vessel also coursed between the aorta and pulmonary arteries (see ).


A 36-year-old man was referred after failure of internal fixation to an open fracture (Gustilo–Anderson IIIA) of the distal meta-diaphysis of the left femur 5 months earlier. This initial injury was managed by emergency debridement, irrigation and distal femoral locking plate fixation. At presentation with the non-union, the patient had healed scars with no evidence of sepsis. The painful non-union was evident clinically and associated with a varus deformity of the femur in the region of the fracture site.
Local and systemic staging confirmed the patient to be smoker with no other co-morbidities. Radiographs displayed a broken locking plate and a femoral non-union with a 12° varus and 5° procurvatum deformity (Fig. ). Knee motion was reduced, with a passive range of motion from full extension to 50° flexion. No evidence of infection was found after routine biochemical investigation and confirmed after intra-operative sampling.
Surgery consisted of plate and screw removal through an exposure along the entire length of the plate followed by circular external fixator application (TL-Hex, Orthofix SRL, Verona, Italy) using the ‘rings first’ method. Proximal fixation consisted of three hydroxyapatite coated half pins secured to a 5/8th ring and an arch. Distal fixation consisted of one 1.8 mm tensioned transverse wire and two hydroxyapatite half pins secured to a full ring (Fig. ). The non-union site was left undisturbed, and no bone graft used.
After a latency period of 7 days, gradual correction was achieved over 6 days. This included 5 mm of distraction at a rate of 1 mm per day to facilitate reduction. Final anatomical alignment in the coronal and sagittal plane was confirmed on radiographs. Functional rehabilitation was encouraged with the assistance of a physiotherapist during the correction and consolidation phases. Full weight bearing was allowed from the first post-operative day. Pin track care followed our standard protocol and included twice daily cleaning with an alcoholic solution of chlorhexidine [, ].
The only complications encountered during the treatment period were minor pin track infections. One half pin developed a Checketts and Otterburn stage II infection that responded to oral antibiotics []. The tensioned wire developed a stage III infection at a late stage of treatment. The wire was removed without further complications.
Radiographs confirmed solid union with exuberant callus formation after 13 weeks. The external fixator was removed when painless weight bearing on a dynamized frame was achieved. At last follow-up, 9 months after frame removal, no deformity had occurred at the union site and knee range of motion had improved at full extension to 90° flexion (Fig. ).


A 57-year-old woman with no past medical history presented at our emergency department (ED) with 1 day of posterior neck pain, followed by weakness in her left upper limb and both lower limbs, and inability to pass urine since that morning. There was no history of trauma to the head or spine. Two weeks prior to the ED visit, she experienced severe neck ache and consulted a chiropractor, who performed manipulation and needle acupuncture of her back, with relief of her initial symptom.
On examination, the patient was afebrile, with a blood pressure of 116/55 mmHg, a pulse rate of 108 beats per minute, a respiratory rate of 18 breaths per minutes and an oxygen saturation of 97 % in room air. Palpation of her abdomen revealed a bladder distended to the level of the umbilicus. Neurological examination disclosed weakness of the left upper limb and spastic paraparesis. Power in the right upper limb was full. There was also decreased sensation from the level of the neck downwards but with sparing of the right upper limb. A lax anal tone was obtained on digital rectal examination.
X-rays of the cervical and thoracolumbar spine showed disc narrowing at the C5/C6 and C6/C7 levels, and grade 1 spondylolisthesis of L4 on L5. The white blood cell count was 30.13 × 109 cells/L (normal range, 4–10 × 109 cells/L) with neutrophilia, and the C-reactive protein and erythrocyte sedimentation rate levels were 391 mg/L (0.2–9.1 mg/L) and 119 mm/h (3–20 mm/h), respectively. Her procalcitonin level was 2.4 μg/L (<0.5 μg/L).
Magnetic resonance imaging (MRI) of the spine showed multiple spinal abscesses in the posterior epidural space from C5 to T1 and from L4 to L5. The former measured 0.7 × 1.3 × 5.1 cm, displacing the cervical cord anteriorly and compressing it at C7-T1, with a high T2 signal intensity in the cord (see Fig. ). There was also a high T2-TIRM signal in the C6-7 vertebral bodies and intervening disc with abnormal enhancement, in keeping with osteomyelitis and discitis. This was also seen in the lumbar spine (see Fig. ).
In the lumbar spine, another collection measuring 0.4 × 1.2 × 3 cm was noted in the right posterior epidural space along the right lamina of L4/L5. Together with a disc bulge, this compressed the thecal sac and cauda equina (see Fig. ).
She was admitted to the orthopaedic surgery high dependency unit, and intravenous (IV) antibiotics were commenced. Surgical decompression of the spinal cord and drainage of the epidural abscesses was performed early the next day. Blood cultures and intra-operative fluid cultures grew pan-sensitive Staphylococcus aureus. Following advice from the infectious disease specialist, the patient completed 6 weeks of IV penicillin G. Repeat blood cultures taken 1 week after initiation of antibiotics were negative.
Post-surgery, she underwent intensive physical therapy for a month, after which she was discharged independent without aid in the community. A follow-up MRI scan performed 4 months later showed resolution of all the abscesses.
A spinal epidural abscess (SEA) is a pyogenic infection of the potential space between the vertebral body and dura mater of the spine. Although rare, their incidence has been rising gradually over the past decade, possibly due to increasing intravenous drug abuse, an ageing population with multiple comorbidities and more frequent use of spinal instrumentation.
SEAs can be either primary or secondary. Primary SEAs result from haematogenous spread of pathogens from a distant focus to the epidural space, while secondary SEAs occur after spinal trauma, injections, surgery or direct inoculation of a pathogen into the epidural space [].
In a literature review of 40 studies published from years 2000 to 2013 [], the most common symptoms and signs reported in SEA were neck and back pain, fever and neurological deficits. Altered mental state and incontinence were also documented. However, presentation can be ambiguous and variable, resulting in delayed diagnosis. The most common predisposing factor is diabetes mellitus. Others include alcoholism, renal failure, intravenous drug abuse, chronic inflammatory conditions, bacteremia and previous spinal intervention.
The neuroimaging study of choice is MRI. It visualizes soft tissues as effectively as computed tomography (CT) myelography, with a comparable sensitivity for SEA. It also provides superior identification of perimedullary lesions with no risk of introducing pathogens into the thecal sac. MRI is able to differentiate between SEAs and other spinal lesions such as subdural abscesses and tumours. The classical description of an SEA on MRI is the collection in the epidural space which is iso- or hyperintense on T1 images which enhances with gadolinium contrast, and a T2 image with a non-homogeneous and hyperintense signal [].
A systematic review of 12 studies published after 1999 [] reported S. aureus as the most common causative pathogen, followed by Streptococcus species.
SEA formation following acupuncture is rare, and a literature search yielded only seven such cases between 1998 and 2015, summarized in Table . There is variability in patient profile, clinical presentation, spinal level of involvement, causative organism and treatment.
Acupuncture is an early form of medical intervention that originated in China thousands of years ago and continues to be practised today, especially in Asian countries. Studies report its clinical benefits for chronic painful musculoskeletal disorders, headaches and hypertension. Major complications are uncommon, with an incidence of 0.55 per 10,000 individual patients in 12 prospective surveys []. The most common infection is hepatitis B (>60 %) due to transmission via contaminated needles. Only three cases of spinal infection were reported in this review.
Treatment of SEA includes antibiotics for systemic manifestations and surgery for local disease control. One literature review of 28 case series acknowledges that SEAs are rare, with significant variation in their causes, anatomical locations and rate of progression, making it difficult to build a strong evidence base to stratify patients to the most effective treatment algorithm [].
However, there is relative consensus that patients with acute or progressive neurological deficit, progressive deformity, spinal instability, or disease progression despite antibiotics require surgical intervention [].
When surgery is required, a posterior laminectomy is the most common approach. Less invasive methods of surgical evacuation include CT-guided needle aspiration, hemilaminectomy and interlaminar fenestration, which report promising results. For extensive SEA, suction irrigation catheters passed through end- or intermediate-level laminectomies or multilevel unilateral fenestrations may be performed to avoid a multilevel laminectomy [].
Based on the best available evidence, medical management should be considered in the following patients []:Those who are unfit for surgery (medically unstable, serious comorbidities) Complete paralysis for >48 h without significant concern for an ascending lesion (surgical risks likely to outweigh the chance of functional recovery) Risk factors for failure of medical treatmentDiabetes mellitis Bacteremia White blood cell count >12.5 × 109 cells/L C-reactive protein >115 mg/L Ring enhancement of lesion on MRI Methicillin-resistant S. aureus infection
Although the period of antibiotic therapy is debatable, this should last at least 4 weeks because studies have shown a 25 % rate of relapse in patients who were treated for less than 4 weeks [].
The patient and treating physician should bear in mind that even in the absence of risk factors, there is no guarantee that medical treatment will not fail and that the patient will not require surgery eventually. The risk of failed medical management has been reported to be between 8.3 and 17 %. The best predictor of post-operative neurological outcome is preoperative neurological status [].


A 13-year-old girl presented with deteriorating school performance for 2 years with repetitive impulses to touch others inappropriately and believing that there is a devil living inside her body for a duration of 6 months.
She has had normal developmental milestones and average school performance for 2 years back. Over the past 2 years, she had inattention, lack of interest in school work, and deteriorating school performance. During the 6 months prior to presentation, she had poor sleep, had become irritable, and had developed grandiose delusions, claiming that she had attained nirvana. She also had bizarre delusions with somatic hallucinations, believing that a devil was residing inside her and feeling this devil's movements. She had episodes of aggression and attributed these to the devil, which was consistent with a delusion of control. There were no mood symptoms. Over this period, she had obsessional impulses to perform certain acts of sexual nature. A diagnosis of schizophrenia with obsessive compulsive symptoms was made and she was commenced on risperidone 2 mg at night and escitalopram 20 mg in the morning.
Over time, she showed poor response to medication and started refusing to go to school as she believed her classmates were talking about her. She started acting out on her obsessional impulses and tried to touch her classmates inappropriately. She displayed odd behaviors such as putting match sticks in her dog's mouth and sleeping on the roof.
On mental state examination, she was disinhibited evident by her behavior during the interview where she made inappropriate sexual advances towards the interviewer. Her speech lacked prosody. Her mood was flat. She had persecutory delusions and ideas of reference regarding her classmates. She had obsessional impulses to touch others inappropriately, which she resisted minimally. There were no perceptual abnormalities. Her verbal fluency was reduced. Other frontal lobe functions measured by categorical fluency, proverb interpretation, Luria 3-step test, go/no-go test, and written sequencing were normal. Parietal and temporal lobe functions measured by left-right orientation, clock drawing test, and drawing reproduction and memory measured by recall of 5-item address were normal. Nonverbal IQ measured by TONI-3 (Tests of Nonverbal Intelligence-3) was normal. Physical examination revealed bradykinesia, but no rigidity, hyperreflexia, or reduced muscle power. There were no abnormal movements, cerebellar signs, or sensory deficits. Examinations of the cardiovascular, respiratory systems, and the abdomen were unremarkable.
Her investigations revealed the following. Full blood count, blood picture, and erythrocyte sedimentation rate done with a view to detect any underlying inflammatory conditions including autoimmune disorders were normal. Tests for thyroid function were done to rule out psychiatric manifestations arising due to thyroid dysfunctions. Both free thyroxine and thyroid stimulating hormone were normal (free thyroxine 1.12 ng/dL and thyroid stimulating hormone 3.87 IU/L). Electroencephalography recorded in the alert state was normal for the age. An eye referral excluded the presence of Kayser-Fleischer rings. Cerebrospinal fluid lactate done to exclude mitochondrial diseases was normal. Computerized tomography brain showed an asymmetrically dilated 4th ventricle, with a cerebrospinal fluid filled cleft connected to right sigmoid sinus, bisecting cerebellar hemispheres which were poorly formed (). Appearance was consistent with a Dandy-Walker syndrome variant.
Risperidone was increased to 2 mg twice daily and escitalopram continued at the same dose. Over 6 months of treatment, her psychotic symptoms, disinhibition, and obsessions showed partial response and she continued to have odd behaviors with deterioration of school performance. The option of changing the antipsychotic to olanzapine or quetiapine was discussed with the patient and her family. However, they preferred continuing the current medication due to the higher incident of side effects of weight gain and sedation associated with these medications. In addition, commencing a newer antipsychotic such as aripiprazole, which is not available in the government sector in Sri Lanka, was considered, but family was unable to afford it. Neurology opinion was sought and it was decided that no active surgical interventions were indicated at this stage.


A 59-year-old woman with follicular lymphoma was initially treated with six cycles of chemotherapy and prednisolone. After 2 months, the patient had received a total of 1350 mg of prednisolone and was on her fourth cycle of chemotherapy. She fell from bed and sustained a blow to her left shoulder. She complained of pain in her left shoulder and was examined on the same day. The shoulder was swollen with tenderness over the ACJ. Radiographs showed an ACJ dislocation with a distal clavicle fracture and CP deformity (). Three-dimensional computed tomography (3D-CT) reconstruction clearly showed a small CP bone fragment at the CCL insertion site (). We diagnosed the patient with a CP avulsion fracture. She was treated nonoperatively in a sling for 3 weeks, followed by progressive range-of-motion exercises. One month after her injury, the patient's shoulder functioned normally without pain.


A 35-year-old African American female with no prior history of coronary artery disease and no significant family history presented with sudden onset of exertional chest discomfort with radiation to the back. The patient became unresponsive shortly after arrival to the emergency department and was subsequently found to be in ventricular fibrillation-cardiac arrest (V-fib). The patient was in V-fib for 6 minutes, with conversion after electrical cardioversion and subsequent development of PEA-arrest for a total of 4 minutes. Repeat EKG after return of spontaneous circulation demonstrated inferolateral STEMI (). The patient received tenecteplase and heparin prior to urgent transfer to the catheterization laboratory. Left heart catheterization showed 99% thrombotic occlusion of mid-distal LAD (Figures and ). Two overlapping drug eluting stents (Xience RX 2.5 mm and Xience RX 2.75 mm) were placed in the distal LAD, and TIMI III flow was achieved (). Due to severely decreased ventricular function with ejection fraction of 10–15%, the patient received ventricular support with an Impella, with discontinuation soon after secondary to hemolysis. Further evaluation revealed positive toxicology screen for amphetamines. Pertinent laboratory results for possible autoimmune causes of the acute myocardial infarction were negative, including antinuclear antibody (ANA), ribonucleoprotein antibody (RNP), RA latex turbid, anti-chromatin IgG antibodies, SSA (Ro) and SSB (La) antibodies, and double stranded DNA antibody (dsDNA).
The patient's cardiac function recovered with medical management. Subsequent transthoracic echocardiograms revealed improved ejection fraction to 60–65% after 11 days and a new finding of left ventricular apical thrombus. The patient received anticoagulation with intravenous heparin, as well as continuous treatment with dual antiplatelet therapy with aspirin and clopidogrel.
The patient remained in the coronary care unit (CCU) for a total of 17 days. CCU course was further complicated by development of pulmonary edema with diffuse alveolar hemorrhage and developing MRSA and pseudomonas pneumonia.
Due to the need for prolonged mechanical ventilation, the patient received a tracheostomy and continued to improve in terms of her pulmonary function while treated with antibiotics for ventilator-associated pneumonia. Her neurological status improved significantly, and on interview, she denied any use of Adderall, amphetamines, or illicit drugs that could have precipitated this event. She reported that recently she had increased her level of physical activity in order to lose weight and was supplementing such efforts with the addition of a natural weight loss dietary supplement.


A 75-year-old Japanese man who had no history of thrombosis or thromboembolism underwent resection of his right upper lung lobe for adenocarcinoma of localized adenocarcinoma without distant metastasis, 2 years previously. Chemotherapy and radiation therapy were not performed. After the operation, periodic follow-up CT was undertaken every 6 months and fluorodeoxyglucose-positron emission tomography (FDG-PET) was performed after 1 year of operation in order to check for recurrence of lung cancer, and the results showed no recurrence or distant metastasis and no abnormality of the thoracic aorta or unexpected mural thrombus (Fig. ). However, an aortic thrombus was incidentally detected in the descending aortic arch 1.5 years after the primary operation (Fig. ). At that time, the patient was apparently healthy, with a body temperature of 36.2 °C, blood pressure of 122/68 mmHg, heart rate of 76 bpm, and peripheral oxygen saturation of 96 % in room air. Laboratory data showed slightly elevated D-dimer, decreased plasma protein-C activity, and normal liver function and lipid profile (Table ). Lupus anticoagulant or anticardiolipin antibody was not detected and the patient stopped smoking at 60-year-old (Brinkman index 800). Although the cause and significance of decreased protein-C activity was not fully understood, we started anticoagulant therapy for aortic thrombosis using warfarin. Follow-up CT showed the aortic thrombus was gradually regressing and was eliminated completely after 6 months of anticoagulant therapy without major complications (Fig. ). Then, anticoagulant therapy was terminated without recurrence of aortic thrombus and plasma protein-C activity was recovered within normal range (72 %).
Aortic thrombosis is a rare disease which can cause distal embolism, but can also be detected incidentally in asymptomatic cases [, ]. Although aortic mural thrombus associated with abnormal aortic disease, such as aortic aneurysm and aortic dissection, is often seen, a thrombus in an apparently healthy aorta is very rare, since the aortic blood flow is too fast for clotting and the formation of a growing thrombus [, ]. Virchow’s triad for thrombogenesis, featuring hypercoagulability, blood flow stasis, and vessel wall injury, is known to be important in thrombus formation, however the concept is generally adopted for thrombosis in veins and/or small arteries []. On the other hand, thromboembolism complicated with atrial fibrillation is well-known, but arrhythmia cannot be the etiology of local thrombus of the aorta. Thus, the detailed mechanism of the etiology of aortic thrombosis is not well understood [, ].
In the present report, we describe a case of aortic thrombosis which was seen in an apparently healthy man in a postoperative state after lung cancer surgery with decreased protein-C activity. Although hereditary protein-C deficiency is well known to be associated with recurrent thrombosis [, ], this patient and his family did not have episodes of thrombosis. Moreover, the protein-C activity was recovered within normal range after termination of anticoagulant therapy. Protein-C deficiency is often seen in the acute phase of thrombosis and in patients undergoing anticoagulation therapy, since protein-C and protein-S are vitamin K-dependent glycoproteins that are massively lost in such conditions [, ]. Thus, the contribution of protein-C deficiency to the development of aortic thrombosis, while possible, is not clear. Present case is in contrast to several recent reports of aortic thrombosis which were associated with malignant disease, hematological disorders, and chemotherapy-related thrombosis, especially in relation to cisplatin-based chemotherapy [, ]. Actually, the background of our previously reported case of aortic thrombosis included malignant lymphoma and related chemotherapy [].
The therapeutic strategy for aortic thrombosis is controversial, however, the main strategy is conservative pharmacotherapy [–]. There is no definitive evidence as to the antithrombotic therapy to be selected or the appropriate duration of such treatment in the case of aortic thrombosis. Therefore, we chose warfarin therapy for 6 months in accordance with the standard therapy in the case of venous thrombosis. After termination of the warfarin therapy, the recurrence of aortic thrombosis has not been confirmed more than 6 months. Another strategy is surgical therapy, which is particularly useful for symptomatic cases with distal thromboembolism, and combined therapy may also be selected occasionally [–]. We selected conservative pharmacotherapy since signs of distal thromboembolism were not evident. However, recently the technique of aortic stent graft treatment has been dramatically improved, allowing an alternative treatment choice for aortic thrombosis, especially in emergency cases or in unfavorable conditions [].


In November 2013 a 67-year-old female with negative familiar history for any type of tumor lamented asthenia, mental confusion, memory disturbances, dizziness, decreased vision and partial right homonymous hemianopsia. These symptoms gradually worsened over a period of a few days. The patient was referred to us for observation accusing the above symptoms and she underwent a complete neurological investigation. The results of the investigation excluded a deficiency in the cranial nerves and an Magnetic Resonance Imaging (MRI) scan was requested. A pre-operative MRI was performed which highlighted an expansive lesion altering the signals at the left temporal lobe and the left posterior occipital lobe (Fig. ). The presence of oedema determined compression of the occipital horn of the lateral ventricle. Moreover, extensive alteration of the signal from the left temporal, occipital and posterior parietal lobes, with swollen appearance of the parenchyma and resulting compression on the occipital horn were reported. The lesion was mainly located in the left occipital region showing a circular, ring-like distribution of the contrast.
A ring contrast-enhanced lesion localized in the left occipital region with intralesional hypointensity are not pathognomonic for glioblastoma. At the same time the site, the compression on the ventricle, the oedema and the persistent symptoms made the patient a candidate for surgical intervention to remove the lesion tissues. The initial patient’s performance status according to the Eastern Cooperative Oncology Group (ECOG) was classified as ECOG = 1. During the pre-operative phase, as well as the routine blood tests, a sample of peripheral blood in EDTA was taken for analysis of the CTCs. Peripheral blood sample is collected to detect CTCs. We used whole peripheral blood pre-treated with a red cells lysis solution (Fig. ) and in parallel we performed gradient procedure (Fig. ) as previously reported []. The reported dot plots in Fig. ) vs ), confirm that the gradient phase is enriched in CTCs Vimentin positive (Vimentinpos) as previously demonstrated for other type of tumors [, , ].
After 14 days of CTCs expansion, the chambers were eliminated and the adherent cancer cells were fixed with Cytofix aerosol preparation for pathological analysis. The pathologist diagnosed an high grade astrocytic tumor due to neoplastic cells with gemistocytic pattern and nuclear atypia, in Haematoxylin and Eosin (H&E) stained slide (Fig. ).
In December 2013 the patient underwent a bulk resection of the lesion: a left parietal-occipital craniotomy was performed and no complications were found after surgery. Post-surgery recovery was satisfying, the management of the patient during the post-surgical phase did not present significant problems; antioedema and antibiotic therapies were administered and the patient recovery time was 10 days. The patient was dismissed 10 days after surgery. The clinical symptoms disappeared except for the persistent right homonymous hemianopsia. The cancer tissue excised during surgery was analysed by a pathologist (Fig. ).
The pathologist diagnosed a multiform glioblastoma due to neoplastic tissue with severe atypical astrocyte proliferation in presence of mitosis and microvascular proliferation. This diagnosis was confirmed using immunohistochemistry techniques.
The specialists advised adjuvant “whole brain” radiotherapy. Total radiotherapy dose was 60 Gy delivered in 30 consecutive days associated with temozolomide.
The patient tolerated the antitumor therapy well without showing modification of the initial performance.
In January 2014 a second peripheral blood sampling for CTCs isolation was performed. The cytological analysis of the resulting slide highlighted the persistence of CTCs in the peripheral blood, with an increased concentration of 7 CTCs-Vimentinpos/ml, compared to the first blood sampling (4,5 CTCs-Vimentinpos/ml).
After 9 month of apparent wellness and clinical benefit, in October 2014 the patient returned to us complaining difficulty in maintaining a standing position, urinary incontinence and further reduction in vision that led to complete hemianopsia. A brain MRI revealed a recurrence of the tumor which showed as an irregular area with increased absorption of the contrast. In particular, T2-hyperintense and T1-hypointense highlighted perifocal oedema in left parietal-temporal-occipital area. The ipsilateral occipital horn appeared partially dislocated, while the hippocampal cortex, the hippocampus and the midbrain appeared dislocated to the left, with a slight shift of the midline (Fig. ). The patient was treated with anti-oedema agents, mannitol and cortisone to reduce the symptoms. Only in February 2015 the patient agreed to undergo surgery to excise the relapsing lesion. The surgeons carried out a second surgical resection of the left parietal-occipital lesion. Conditions of the patient in the post-surgical phase were complicated by the formation of a fistula containing liquid on the operation site. Anti-oedema and antibiotic therapies were administered. The histopathologic examination was diagnostic for a recurrence of a glioblastoma. The patient’s general state of health began to worsen and she died in March 2015.


In May 2015 a 31-year-old man presented with a one-month history of headaches associated with phonophobia and photophobia, dizziness and short term memory deficits. On admission, he was somnolent and disoriented. He had bilateral papilledema and left homonymous hemianopsia.
Laboratory examinations showed 14500/mm3 white blood cell count, 558 UI/Lactate dehydrogenase (LDH). Cerebrospinal fluid analysis showed high values in proteins and glucose whereas the cytology was negative. Computed Tomography (CT) scans showed a cystic expansion entrapping the temporal horn of the left lateral ventricle with an extensive periventricular hypodensity area and controlateral dislocation of the ventricular system.
Preoperative imaging demonstrated that the primitive lesion displayed a high density on CT scans. Contrast-enhanced MRI showed a T1-hypointense and T2-hyperintense lesion. The signals were significantly enhanced by the contrast (Fig. ).
The patient was advised to undergo stereotactic biopsy procedures. During the pre-operative phase, a blood sample was collected for CTCs detection. The resulting slides were analysed by the pathologist who suspected a lymphoma for the morphology of neoplastic cells highlighted by H&E staining (Fig. ). The patient underwent CT scans with and without contrast for the upper abdomen, the lower abdomen and the thorax. Scans confirmed that the lymphoma was exclusively localized in the intracranial area. In this case, the CTCs were not characterized for mesenchymal antigens as reported for the first case. Given the cytological analysis and neuroimaging data, diffuse large B-cell lymphoma diagnosis was directly confirmed by immunostaining for CD20 on tissue biopsy specimen. Therapy with high doses of corticosteroids resulted in a nearly complete disappearance of the primary lesion and improvement in the patient’s general state of health. We made a stereotactic biopsy of the primary temporal lesion and stereotactic placing of external ventricular shunt by a ventricular catheter positioned into the left temporal horn. The patient responded well in the post-operative phase and recovered within 3 days of surgery whilst continuing the anti-oedema therapy. During the second post-operative day there was an appreciable improvement in clinical symptoms. The neurological deficits completely disappeared after the therapy. Follow-up CT scans showed adequate decompression of the temporal horn and disappearance of the ventricular low-density area. The midline shift disappeared as well.
In the following days the patient underwent a whole body fluorodeoxyglucose (FDG)-positron emission tomography (PET) that, despite its spatial and biological limits of resolution, showed no areas of pathological increase in glucose metabolism in the body regions examined. FDG-PET brain did not recognize areas of significant alteration in glucose metabolism in various cortical, subcortical and subtentorial districts. These data confirm that the lymphoma is primitive and exclusively of the brain.
On histopathological examination of the surgical specimen (Fig. ), the initial hypothesis of a brain lymphoma was confirmed, revealing a CD20pos large B cell lymphoma with high proliferation index (Ki67 Positivity) greater than 70 %. Subsequently, the patient was referred to our medical oncology outpatient clinic where he was followed carefully. The external ventricular shunt was removed because of the high risk of infection. Chemotherapy cycle was prescribed with the following scheme: rituximab 375 mg/mq on day 1, methotrexate 3500 mg/mq on day 2, cytosine arabinoside 2 gr/mq doses twice daily on day 2,3, thiotepa 30 mg/mq on day 4 (weight 78 kg, height 178 cm, body surface area 1,9 mq, total dose rituximab 700 mg, methotrexate 6650 mg, cytosine arabinoside15,2 g, thiotepa 60 mg). Treatment was generally well tolerated by the patient and currently (follow up after 8 months MRI in Fig. ) the patient’s general condition are good.


A 42 year old diabetic woman from North Western Province of Sri Lanka presented with abdominal pain, vomiting and intermittent fever for one month. She had recurrent skin abscesses 6 months before presentation which was treated with incision and drainage and a short course of antibiotics for which there was only partial improvement. Three months before presentation to us she was found to have multiple liver abscesses which were aspirated in a local hospital. The aspirate grew “coliforms” resistant to gentamicin and sensitive to ceftazidime. She was treated with cefuroxime, meropenem, co-amoxyclav and metronidazole; further identification of the organism was not done at the local hospital.
On presentation to us she had high fever and tender hepatomegaly. Her body weight was 40 kg. Rest of the examination including nervous system was normal.
Her full blood count showed leukocytosis [15.7×109/L] and granulocytosis [11.3 × 109/L], ESR was 100 mm in the 1st hour and C-reactive protein was 98.4 mg/L. Ultra sound scan of abdomen showed multiple liver and splenic abscesses.
Presence of recurrent multiple liver and splenic abscesses in a diabetic patient who had recurrent skin abscess in the past made us consider melioidosis in the differential diagnosis. Intravenous meropenem 2g eight hourly was started empirically and aspirate was sent with a sample of serum to Faculty of Medicine, University of Colombo which serves as the National Reference Laboratory, to confirm the diagnosis. There the aspirate yielded pinpoint colonies on blood, chocolate and Macconkey agar after overnight incubation. Since biochemical panels are not very accurate in diagnosis of Burkholderia pseudomallei, isolate was subjected to PCR which confirmed the diagnosis.
Serum antibodies to melioidin antigen using an in-house indirect haemagglutination (IHA) test based on that described by Alexander et al. with antigen prepared from local strains of B.pseudomallei [] were positive at a titre of 1:10240.
After confirmation of melioidosis intravenous meropenem was continued. However after a week of treatment the disease course was complicated by bilateral lower limb weakness which progressed over the next 4 days. Her lower limbs were flaccid and deep tendon reflexes were absent. There was no sensory sign or bladder/bowel involvement. Cerebro-spinal fluid analysis showed protein of 114.5 mg/dl, glucose 62 mg/dl, white cells <10 mm9/L and red cells < 10 mm9/L. MRI scan of the brain was normal. The nerve conduction study showed evidence of severe peripheral neuropathy with axonal degeneration; compatible with a primary axonal type inflammatory neuropathy such as acute motor axonal neuropathy or acute sensory motor axonal neuropathy.
A diagnosis of Guillan-Barre syndrome was made based on Brighton case definition (Table ) () and she was treated with 4 cycles of plasmapharesis on alternate days for which there was marked improvement of neurological deficit.
With intravenous meropenem patient further improved and her ESR and CRP became normal. Repeat ultrasound scan of abdomen showed reduction of the size of liver and splenic abscesses.
Eradication therapy with cotrimoxazole 1920 mg 12 hourly and co-amoxyclav 625 mg 8 hourly was started on the seventh week and overlapped with intravenous antibiotic for further two weeks. Patient was discharged to outpatient clinic after two weeks of oral antibiotics with a plan to continue them for12 weeks. At the end of 12 weeks she had no residual neurological weakness and there was no sign of a relapse.


A 68-year-old male patient was admitted to our hospital with chest pain for 6 months and lower limb fatigue for 1 month. There had been no obvious cause for the onset of back pain 6 months ago. This pain was particularly evident at night and had become more severe and accompanied by lower limb fatigue 1 month previously. He had received no anti-TB therapy before admission. X-rays, MRI and CT of spine, routine blood tests, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) concentrations and hepatorenal function were examined. He had a white blood cell count was 5.7 × 109/L, ESR 87 mm/1h, CRP concentration 21.4 mg/L and normal hepatorenal function.
The patient consented to publication of data concerning his case.
Physical examination showed hypesthesia below the rib arch, Grade 1 lower limb muscle strength and Frankel Grade C neurological function. It also showed increased muscular tone in the lower limbs, knee and ankle hyperreflexia and positive sign for ankle clonus.
X-ray films showed collapse of the T8 vertebrae and T7–8 intervertebral space. CT scan showed destruction of T7, T8 and the intervertebral space and sequestrum formation, especially on the left side. A paravertebral abscess was limited to T7 and T8 without an obvious gravitation abscess. The height of the T8 vertebral body was markedly reduced and the dural sac and spinal cord severely compressed by an abscess posterior to the vertebral body.


A forty-three-year-old female with no significant past medical history underwent an uncomplicated, laparoscopic umbilical hernia repair. She had no prior history of lower urinary tract infections, urinary dysfunction, or incontinence. Preoperative computed tomography with intravenous (IV) and per os contrast of the abdomen and pelvis demonstrated normal bilateral kidneys and ureters, with no pelvic abnormalities. Preoperative serum evaluation demonstrated normal renal function with an estimated GFR of 134 mL/min.
A 16 French (Fr) Foley catheter was placed preoperatively without difficulty. Intraoperative details were uncomplicated and the patient received 1200 cc of intravenous fluids. On postoperative day one, her bladder catheter was removed and spontaneous voiding occurred.
On postoperative day two, the patient developed an intestinal ileus and reported inadequate pain control at incision sites that required morphine dosed at 4 mg IV q6 hours. Over the next two days, the patient's ileus had resolved, illustrated by tolerance of regular diet along with passing of flatus and bowel movements. On postoperative day four, the patient complained of dysuria, urinary hesitancy, and right flank pain. Vitals at the time were heart rate of 93 bpm, BP of 138/86 mmHg, respiratory rate of 22, and febrility at 38.2 degrees Celsius. Physical exam elicited a soft but distended abdomen with right costovertebral angle (CVA) tenderness. Significant laboratory values included an increase in white blood cell count to 17,000 and creatinine rise from 0.7 to 5.5 mg/dL. A bladder scan showed a volume of ~600 cc. Thereafter, the patient was catheterized and had a postvoid residual (PVR) of 800 cc.
A renal ultrasound demonstrated moderate right hydroureteronephrosis with a complex perinephric fluid collection. Further evaluation with computed tomography (CT) of abdomen and pelvis without contrast showed severe right-sided hydronephrosis, a perinephric fluid collection, and a dilated ureter down to the level of the bladder. At this time, our differential diagnosis included acute pyelonephritis, obstructive nephrolithiasis, and iatrogenic injury.
The patient underwent urgent cystoscopy and retrograde pyelogram that demonstrated severe hydroureteronephrosis and a severely tortuous ureter (). Attempts to catheterize the right renal collecting system were unsuccessful secondary to a proximal ureteral tortuosity. The patient then underwent a percutaneous nephrogram where a stiff guidewire was successfully passed into the bladder by interventional radiology (IR) and allowed for placement of an indwelling 8 Fr double-J ureteral stent (Figures and ). At the end of the procedure, a diversionary 8 Fr nephrostomy catheter was placed into the renal pelvis.
The patient tolerated these procedures without difficulty. On postprocedure day one, the patient's WBC and serum creatinine had normalized. The patient's pain had resolved and her percutaneous nephrostomy tube was capped and removed by IR following stable serum creatinine. The patient was discharged with a bladder catheter and the indwelling stent. The patient has since resumed normal voiding and her ureteral stent has been removed.


A 12-year-old boy presented to Tangerang district hospital, on 12 February 2015. Tangerang is a suburb in coastal area in the Jakarta metropolitan, consists of both agriculture and business areas. A large river crosses the middle of the town; and some areas are commonly flooded during the rainy season. Dengue and typhoid fever are endemic in this area; whereas sporadic outbreaks of influenza H5N1 have been reported since 2005 []. This boy had fever for three days (38.0 °C, on admission to the hospital), headache, fatigue, and muscle pain. The patient was alert and anicteric, with blood pressure of 110/70 mmHg, pulse 100 min, and respiratory rate (RR) of 22 min. Complete blood count showed anemia (7.5 mmol/L), thrombocytopenia (68,000 µL), neutrophilia (84 %), elevated absolute neutrophil count (ANC) (6048 µL), and normal leukocyte count (7200 µL). Based on these findings, a diagnosis of dengue hemorrhagic fever grade I was made; and the patient received supportive treatment with intravenous fluid, acetaminophen, and omeprazole.
On the third day of hospitalization, due to persistent fever, thrombocytopenia (20,000 µL), leukocytosis (15,000 µL), decreasing hemoglobin (5.4 mmol/L), and jaundice (total bilirubin/TB 82 µmol/L); the clinical team conducted additional tests which were blood smear and Coomb’s tests for Evans syndrome, dengue NS1 and IgM antibodies, HAV and HCV antibodies, HBsAg, and serum transaminases. All tests, except increased of AST (371 U/L) and ALT (120 U/L), were negative. On the fifth day of hospitalization, the patient appeared septic with oliguria, continued icterus, and RR of 26/min. The clinicians requested rapid IgM test (SD®) for leptospira which came back positive. Biochemistry showed increased of TB (366 µmol/L), AST (660 U/L), ALT (179 U/L), BUN (11.1 mmol/L), and creatinine (442 µmol/L).
Leukocytosis and thrombocytopenia were persistent; and metamyelocytes were detected in blood smear. Blood cultures were negative. Interview with the family member revealed that the patient played in flood water near his house a week before illness. Treatment with ceftriaxone 70 mg/kg twice a day was commenced and continued for 14 days.
On the eighth day of hospitalization, the patient’s renal function declined (BUN 20.35 mmol/L, creatinine 503.8 µmol/L); and he became anuric with decreased consciousness (Glasgow Coma Scale/GCS = 7). While waiting for the availability of the intensive care unit (ICU) room for intubation, as required by the hospital standard procedure, the GCS improved in the following day. The patient was hemodialysed on the 10th and 12th day of hospitalization.
After hemodialysis, laboratory parameters began to improve; and on the 21st day of hospitalization, the patient was clinically improved and renal function became normal. The patient was discharged although he was still anemic (Hb 5.5 mmol/L), had TB of 82.4 µmol/L and c-reactive protein (CRP) of 1.2 mg/dL. His hemoglobin and bilirubin returned to normal three weeks after discharge.
With the parents’ consent, serial plasma and serum were stored and later tested to confirm leptospira infection. Leptospira IgM rapid test (SD®) was positive in the samples on the first, fifth, and 20th day of hospitalization, and one week after discharge. The micro-agglutination test (MAT) assay was conducted in the leptospira reference center at Kariadi Hospital, Semarang on serum samples from the first, 10th, and 20th day of hospitalization. The titer for Leptospira serogroup bataviae increased from <1:20 (on the first day and 10th day) to 1:640 (on the 20th day).
Retrospective tests on plasma samples during admission were negative for dengue NS1, dengue IgM, and Salmonella typhi IgM. However, several biochemistry parameters were slightly elevated, which were direct bilirubin (13.7 µmol/L), AST (123 U/L), ALT (53 U/L), BUN (4.0 mmol/L), creatinine (123.8 µmol/L), creatinin-kinase (CK) (326 U/L), CRP (30.5 mg/dL), amylase (125 U/L), and lipase (98 U/L). Serial hematology and biochemistry profiles are described in Fig. .


A 70-year-old male, with history of hypertension, dislipidemia, and hyperuricemia, presented to our institution with a one-year long history of progressive and intense lower lumbar pain causing great limitation of daily activities. Physiotherapy or medication was ineffective. The patient reported a palpable mass on this region for years but with neither symptoms nor size progression. He had no constitutional or neurologic symptoms. On examination, there were tenderness over the central and left paraspinal area and a fixed palpable mass of size approximately 7 × 5 cm, hard in consistency, and no pulse. The pain aggravated with flexion, extension, and rotational trunk movements. Neurologic examination was normal. Radiographs showed a bony mass protruding posteriorly, apparently from the L5 vertebra. CT scan showed a 7 cm long well-limited mass with an apparent cartilage cap arising from the spinous process of L5. It was lateralized to the left with adjacent paraspinal muscle compression (). Under general anesthesia, the tumor was marginally resected along with the L5 spinous process through a posterior approach (). Histologic examination has shown a specimen composed of trabecular bone with focus on bone marrow covered by lobules of cartilaginous tissue, without cellular atypia, consistent with osteochondroma (). After surgery pain was completely relieved, and neurologic function was normal. At one-year follow-up there was no evidence of local recurrence or symptoms.


A 70-year-old Caucasian man with no prior medical history suffered a pelvic trauma after being run over by a truck, sustaining an anterior-posterior compression pelvic injury. Primary stabilization with pelvic external fixation and damage control was performed in another institution. Twelve hours after the accident, the patient was admitted to our emergency department.
The patient was hemodynamically stable and responsive, complaining of pain on the lateral and posterior regions of the left buttock, accompanied by left ankle extension weakness. Physical examination revealed a truck wheel-shaped bruise on the left thigh, scrotal hematoma, and swelling (). Left ankle extension showed active movement against gravity, with some weakness against resistance. Arterial pulses were intact, but sensory and motor deficits were consistent with left sciatic nerve palsy. Pelvic radiographs and computed tomography showed a traumatic disruption of the pelvic girdle without bony injury. Left sacroiliac dislocation and pubic symphysis diastasis were still evident despite the external fixation ().
Admission laboratory results showed increased levels of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), suggesting muscle death and tissue damage. He subsequently lost left ankle flexion and extension, suggesting sciatic nerve palsy. One hour after his arrival and considering the clinical findings, diagnosis of GCS was made and urgent fasciotomy was indicated.
Prior to the surgery, an intracompartmental pressure of 46 mmHg was measured in the gluteus maximus compartment, confirming the diagnosis of gluteal compartment syndrome. Urgent fasciotomy was performed to decompress the three muscle compartments of the gluteal region (gluteus maximus, gluteus medius/minimus, and the fascia lata) (). Vaccum assisted closure was applied for wound management.
Before surgery, the patient developed acute kidney failure with anuria along with increased serum values of urea and creatinine, requiring hemodialysis after the procedure. Once the patient was stable, open reduction and internal fixation by anterior and posterior approaches were performed. Laboratory markers (urea, CPK, Cr, and LDH) returned to normal values within the following month, after which the patient was discharged. Three months after initial trauma, the patient recovered normal kidney function but continued with sciatic nerve palsy. At one-year follow-up, the patient persists with neurological deficit according to the Medical Research Council (MRC). He had 1/5 strength with testing of the anterior tibialis, musculus peroneus longus, and musculus peroneus brevis.


A nine-year-old boy with unilateral cleft lip and palate was referred to the Department of Orthodontics of Mashhad University of Medical Sciences (Iran). At the beginning of the treatment, study models, panoramic radiograph and lateral cephalogram as well as facial and intraoral photographs were taken. The patient presented with a concave facial profile, anterior cross bite (overjet: -4mm), and bilateral posterior cross bite. Cephalometric analysis showed skeletal Class III malocclusion with maxillary hypoplasia and steep mandibular plane angle (). He had no medical problems.
Treatment Procedures:
Initially, a W-arch expander constructed from a 0.9 mm stainless steel wire was cemented on the molars. This device was activated 3 mm/month to overcorrect the posterior crossbite. Next, two L-shape miniplates (General implants, GmbH Deutschland, Germany) were placed at the zygomatic buttress under local anesthesia by a maxillofacial surgeon and fixed with three miniscrews, the distal ends of the miniplates were exposed through the attached gingiva between the upper first permanent molars and second premolars to control vector of elastic traction. In the mandible, two L-shape miniplates (General implants, GmbH Deutschland, Germany) were placed under local anesthesia and were fixed by three miniscrews. The terminal ends of the miniplates were exposed between the lower central and lateral incisors. The ideal position for the insertion of the miniplates was evaluated using a panoramic radiograph in order to avoid damage to the roots of the adjacent teeth and mental foramen.
Four weeks after the placement of the miniplates, their mobility was checked by the surgeon and orthodontic latex elastics (3/16′′ heavy size on both sides-American Orthodontics, Sheboygan, USA) were attached to the hooks of the miniplates to generate approximately 100 g of force on each side.
The patient wore a tightly fitting and well-retained lower removable appliance in order to disclude the upper and lower jaws during maxillary traction. The patient was instructed to wear the removable appliance full-time except for eating, contact sports, and tooth brushing; he was also told to replace the elastics every day (). The traction force was doubled after 1 month, and the final 250g of force per side was reached after 2 months. Skeletal and soft tissue analyses were performed on pre-treatment and post-treatment cephalograms (,).
Treatment Results:
After four month of active treatment, a positive overjet and a significant improvement in the patient’s profile were achieved (). Post-treatment cephalo- metric tracing of patient 1, showed a favorable increase of 4° and +4.5 mm in ANB and wits appraisal, respectively. (). Also, soft tissue analysis of the patient revealed a favorable forward movement of the upper lip (). Minimal movements of the upper and lower incisors were observed (). Pre- and post-treatment cephalometric superimpositions on the anterior cranial base are showed in .


The second case was an eleven-year-old boy with bilateral cleft lip and palate. Similar to case 1 clinical and radiographic examinations were performed. The patient presented with concave facial profile, anterior cross bite (overjet: -5 mm), anterior open bite (overbite:-7 mm), and posterior crossbite. This case also showed skeletal Class III malocclusion due to maxillary hypoplasia and steep mandibular plane angle (, ).
Treatment Procedures:
All the treatment steps were similar to the case 1.
Treatment Results:
After four month of active treatment a significant improvement in the patient’s profile was achieved. The anterior open bite was also reduced significantly (). The over jet of the patient was increased from -5 to 0. In this case, the ANB angle and wits appraisal favorably increased by 3° and +3 mm, respectively (). Also, soft tissue analysis of the patient revealed a favorable forward movement of the upper lip().Minimal movements of the upper and lower incisors were observed (). Pre- and post-treatment cephalometric superimpositions on the anterior cranial base were demonstrated in .


In January 2016, a man in his early 40s returning to Italy from a two-week stay in Haiti developed fever (38.5 °C) and pruritic maculopapular rash on his trunk and arms that fully resolved after three days. The patient, who reported mosquito bites in Haiti, had an unremarkable past personal medical history. Laboratory analyses, performed at day 3 after symptom onset, showed blood cell count and liver function tests within the normal range. Testing for dengue, chikungunya and ZIKV infection, according to previously described methods [], demonstrated the presence of ZIKV RNA in plasma and urine at 175 copies/mL and 25,600 copies/mL, respectively, and ZIKV-specific IgM but not IgG antibodies. Dengue virus (DENV) IgG antibodies were also detected by ELISA, but they represented cross-reacting antibodies induced by previous vaccination against yellow fever virus, as confirmed by virus neutralisation assays; DENV IgM, DENV NS1 antigen and chikungunya virus IgM and IgG were negative. Sequencing of the full ZIKV genome was obtained directly from a urine sample collected at diagnosis (GenBank KX269878), which demonstrated over 99.6% nucleotide sequence identity with ZIKV strains circulating in Haiti (GenBank KU509998 and KX051563).


A 65-year-old Chinese man was admitted to our hospital with a complaint of upper abdominal distention. There was no positive sign on physical examination. Tumor markers including carcino-embryonic antigen, carbohydrate atigen 19-9, alpha fetoprotein, and prostate specific antigen were normal. Abdominal enhanced computed tomography (CT) scan revealed a 5.4 × 4.1 cm2 irregular soft tissue mass in the space between the liver and stomach (Figure A). In the arterial and venous phase, the mass enhanced gradually (Figure B and C). The magnetic resonance imaging (MRI) showed the mass had long T1 and T2 signal, and the diffusion-weighted imaging (DWI) revealed a high signal of the mass (Figure D–F). Histopathological examination of endoscopic ultrasonography (EUS)-guided fine needle biopsy revealed malignant tumor cells (Figure ). No evidence of distant metastasis was identified. Complete tumor resection and lymphadenectomy were performed. The protocol for the surgical resection was decided together by the patient and a multidisciplinary team from different departments including hepatobiliary surgery, radiology, and chemotherapy.
Grossly, the tumor was situated in the lesser omental bursa and measured 9.0 × 5.0 × 4.5 cm3 (Figure A). The inside of the tumor presented grayish-white color with necrosis (Figure B). Frozen section during the operation revealed that it was a malignant tumor with epithelioid and mesenchymal components.
Histologically, the tumor showed biphasic differentiating. The first component was epithelium cells that arranged like cancer nests. Meanwhile, the second component revealed a sarcomatous growth pattern (Figure A). Immunohistological study indentified the tumor components by specific labeling techniques. Final diagnosis of carcinosarcoma was confirmed by hematoxylin and eosin (H&E) staining and immunohistochemical analysis showing positive p63, pan-cytokeratin (CK), vimentin (VIM), CD99, and Bcl-2 (Figure B–F). Postoperation diagnosis of the patient was primary carcinosarcoma of the lesser omentum without lymph node metastasis.
Two months after the operation, the MRI showed a 1 cm mass in the left liver (Figure C) with enlarged lymph nodes in the retroperitoneal area; metastasis was considered. The patient refused a second operation and instead received chemotherapy. The chemotherapeutic protocol (epirubicin 28 mg continuous intravenous infusion 24 hours d1–3 and ifosfemide 2 g d1–3, q3w) was scheduled as 1 time per month and lasted for 6 months till the end. After the chemotherapy regimen, the hepatic MRI showed that the left liver metastases disappeared completely (Figure D). Three months later, a hepatic MRI showed no recurrence in the patient's liver. The patient is still alive without any signs of recurrence during 3 years of follow-up.


A 43-year-old Caucasian male was referred to the nephrology clinic at Overton Brooks VAMC by his primary care practitioner, in November of 2002 for management of his chronic kidney disease. He was asymptomatic. His BP was well controlled at 115/83 mmHg. He was morbidly obese with a body mass index (BMI) of 46, chronic kidney disease stage 4 (MDRD GFR of 16 ml/min), non insulin dependant diabetes mellitus, hypertension, coronary artery disease status post stent placement and hyperlipidemia. His medications included nifedipine, fosinopril, atenolol, rosiglitazone, furosemide, simvastatin, aspirin, glyburide and calcium carbonate. Laboratory results: Serum creatinine 4.3 mg/dl, BUN 54 mg/dl, normal electrolytes, serum calcium 8.8 mg/dl, serum phosphorus 4.9 mg/dl, random urine protein 292 mg/dl, random urine creatinine 49 mg/dl, urine protein/creatinine ratio of 5.9, hemoglobin A1c 7% and hemoglobin 13.9 g/dl. Patient was educated about the course and prognosis of his kidney disease and advised diet and exercise for weight loss. He was referred for arterial-venous fistula placement for providing renal replacement therapy in future. Over the next 6 months the patient failed all conservative methods of weight loss including the use of orlistat. His morbid obesity posed a major contraindication for enrolling him for kidney transplantation. He agreed to the surgical therapy option for treating his obesity. He was referred for bariatric surgery in June 2003.
After the bariatric surgery in September 2003, he had lost 60 pounds at 6 months (BMI 37). He was able to discontinue all his oral hypoglycemic agents maintaining a hemoglobin A1c of 6.2% and required only one anti-hypertensive medication to achieve the recommended target blood pressure reading. His BUN and creatinine has remained at 22 mg/dl and 4.6 mg/dl respectively. The patient is being followed at regular intervals and over the course of the next eight months has lost an additional 30 pounds (BMI 32), a total weight loss of 90 pounds since the bariatric surgery. His serum creatinine has remained stable at 4 mg/dl, BUN 37 mg/dl, random urinary protein 99 mg/dl, random urinary creatinine 121 mg/dl, urine protein/creatinine ratio of 0.8 and hemoglobin A1c 5.1%. The inverse creatinine to time plot as shown in figure clearly demonstrates the stabilization of the renal function 15 months following his weight loss surgery. The patient was being evaluated for pre-emptive renal transplantation and because of his previous history of coronary artery disease he underwent a left heart catheterization study in March 2005. Unfortunately, despite all precautions he developed radio-contrast induced nephropathy and had to be initiated on renal replacement therapy. He currently remains on dialysis and is awaiting a renal transplantation, which would not have been possible without his weight loss.


A 40-year old female patient was referred to our emergency department because of an intended overdose with 200 mg diazepam, 400 mg temazepam, and 2250 mg sertraline.
Her main complaints were fatigue and drowsiness. Blood pressure, pulse rate, and auscultation of the heart and lungs were normal. The patient was treated with sodiumsulfate and charcoal and was admitted to the intensive care unit for continuous control of vital signs. Routine laboratory studies (hematology, chemistry) were normal. Plasma levels of diazepam and temazepam were elevated, 1155 ugr/l (normal: 125 – 750 ugr/l) and 1710 ugr/l (normal: 300–900 ugr/l, respectively). Plasma levels of sertraline and desmethylsertraline were 174 ug/l (normal 20–55 ug/l []) and 276 ng/l, respectively.
Her ECG upon admission (upper panel of the figure) shows a sinus rhythm (77 b.p.m.) without conduction disturbances. QT interval in lead V2 was 370 ms. We used the Bazett method (QT time divided by the square root of the RR interval) to calculate the corrected QT (QTc). QTc at admission was 420 ms and negative T-waves were found in leads V1–V3. A second ECG, taken one day after admission (lower panel of the figure), showed a markedly prolonged QT interval with deepened negative T waves in leads V1–V3. QT interval was 520 ms in V2, at a heart rate (HR) of 63 b.p.m (QTc 525 ms). An old ECG (august 2002) showed a sinus rhythm with a HR of 63 b.p.m and a QT interval in lead V2 of 370 ms (QTc 373 ms; ECG not shown).
After 4 days the patient was discharged to a psychiatric hospital because the risk for another suicide attempt was deemed high by the psychiatric consultant. After discharge, the patient underwent further out-patient cardiac evaluation. Echocardiography revealed no structural heart disease. On exercise electrocardiography, patient reached 88% of her maximum HR – no abnormal ST-segment changes were observed. Hereafter, the use of sertraline was resumed in a dose of 50 mg twice daily under guidance of her psychiatrist. Control ECG revealed a normal QT interval (not shown).


A previously healthy 46-year old man on no medications was diagnosed with a Clark Level 5 malignant melanoma on his left shoulder following resection of a mole under local anesthetic. The lesion was subsequently reported as a melanoma and three weeks following his resection, before he could undergo a metastatic work-up, he presented to hospital with nausea, vomiting and right upper quadrant pain. He did not appear toxic, he was afebrile, and physical examination was unremarkable but for a tender right upper quadrant and hepatomegaly. Laboratory investigations demonstrated leukocytosis, modestly elevated liver enzymes, and lactic acidosis. Computed tomography scanning revealed marked hepatomegaly with an extensive infiltrative process and ultrasound demonstrated normal bile ducts. Baseline imaging of his abdomen was planned for staging, however it was not conducted prior to his presentation to hospital.
On day two of his admission the patient deteriorated with respiratory failure requiring endotracheal intubation and mechanical ventilation. He had oliguria, and hypotension refractory to fluid resuscitation. Rapidly progressive multi-system organ failure developed with anuria/azotemia requiring continuous renal replacement therapy. Liver failure ensued as evidenced by coagulopathy refractory to plasma infusions and by progressive transaminitis and hyperbilirubinema. He developed distributive shock requiring maximal pressor support. There were significant biochemical derangements including hyperkalemia, acidosis, hyperphosphatemia, hyperuricemia and hypocalcemia. Hemodialysis was commenced to rectify the hyperkalemia and acidosis that was refractory to continuous renal replacement therapy. An aggressive resuscitative and treatment approach was undertaken to allow confirmation that the liver lesions were melanoma and not a potentially treatable infection or lymphoma. An ultrasound guided transjugular biopsy of the liver was performed in the intensive care unit. Based on a frozen section diagnosis of malignant infiltration of the liver, high dose corticosteroid therapy was commenced. The patient continued to deteriorate despite maximal physiologic support and palliative measures were instituted after discussion with the next-of-kin. He succumbed to his illness on day-4 of admission. Autopsy revealed >80% liver infiltration by melanoma (Figure ), a diagnosis verified by an immunohistochemical phenotype of S-100 and HMB-45 positive cells (Figure ).


A 40-year-old woman received excision of a superficial spreading melanoma from the rima ani with a safety margin of 3 cm (Clark-Level IV, tumor thickness 1,82 mm). Lymphatic drainage was detected to both inguinal basins and both excised sentinel lymph nodes were unaffected. None of the staging examinations including computer tomography (CT) of the brain, chest, abdomen and pelvis, as well as lymph node sonography revealed any signs of tumor manifestation. The medical history of the patient was otherwise unremarkable and she was not on any medication. There was no family history of hypertension, heart disease or pulmonary disease. Because of the high-risk nature of the melanoma, the patient started long-term adjuvant therapy with IFN α2b (5 × 10 million U. s.c. per week for 4 weeks followed by 3 × 10 million U. s.c. per week).
After 30 months of IFN α2b treatment the patient reported increasing dyspnea on exertion and afebrile non-productive coughing accompanied by sudden malaise and edema of the lower legs. Electrocardiography showed sinus tachycardia (120 /min) and right axis deviation. A chest x-ray showed signs of right ventricular dilatation and pleural effusion on the right side; no pneumonic infiltrates were seen. Abdominal sonography revealed a significant amount of ascites. The patient was diagnosed with decompensated right heart failure and was therefore hospitalized. Initial investigations with transthoracic echocardiography showed right ventricular hypertrophy and dilatation (Figure ), PAH with a calculated systolic pulmonary artery pressure (PAPsyst) of 80 mmHg and tricuspid insufficiency grade II-III with morphologically normal valves (Figure ), a reduced right ventricular ejection fraction of 40%, a hypokinetic right ventricle and pericardial effusion without signs of tamponade. Laboratory work-up showed slightly increased levels of d-dimers and liver enzymes, while inflammatory markers were within the normal range. There were no signs of vasculitis, hypercoagulability or rheumatologic disorders. A high-resolution CT of the chest revealed no signs of pulmonary embolism, alveolar or interstitial lung diseases, but signs of PAH with a widened central pulmonary artery (40 mm), right ventricular dilatation (> 80 mm), regurgitation of contrast medium into liver veins, a circular pericardial effusion and a 300–400 ml pleural effusion of the right side.
Diagnostic right heart catheter revealed a PAPmean of 56 mmHg (PAPsyst 87 mmHg), a pulmonary vascular resistance (PVR) of 1.128 dyn × sec × cm-5, an impaired cardiac index and a 3 fold increased total peripheral resistance. Testing of pulmonary vasoreactivity showed a reduction of PAPmean from 56 mmHg to 26 mmHg with the PDE-5-inhibitor sildenafil (Table ).
Therefore, treatment with 3 × 25 mg sildenafil per day was initiated. No side effects occurred. After one month, tricuspid insufficiency improved to grade I-II. After six months right ventricular hypertrophy and dilatation were reduced. Because of the 2 documented cases of patients with PAH due to therapy with IFNα2 where PAH was reversible half a year after termination of IFNα2 [,] we attempted to terminate sildenafil under control of hemodynamic monitoring. PAPmean increased promptly to 57 mmHg. In this context we could verify the same effectiveness for therapy with vardenafil in comparison to sildenafil. Reduction of PVR was higher in vardenafil vs. sildenafil (Table ); therefore the therapy was switched from sildenafil to vardenafil 10 mg twice daily. 24 months after onset of PAH the patient felt fine and resumed working. Vardenafil is still necessary to lower her PAP as demonstrated with transthoracic echocardiography: after pausing vardenafil for two days the PAPsyst increased about 40 mmHg, but decreased again 120 minutes after administration of vardenafil. The heart diameter is steadily decreasing (right ventricular outflow tract from 39 to 27 mm and right atrium from 60–65 to 36–44 mm). Regarding the melanoma she remains relapse-free.


On October 6, 2004, a 31-year-old Korean male was admitted to the hospital with a fever, chills, general fatigue, cough, dyspnea, night sweats, and a weight loss of 2 kg, all of which he had experienced over the previous four weeks. The patient had smoked half a packet of cigarettes per day for the past 10 years and had been diagnosed four years previously with adrenoleukodystrophy. During August and September of 2004, the patient travelled to Corona, California. The symptoms began while at this location, and he was subsequently treated for bacterial pneumonia at an area hospital. However, his symptoms worsened rapidly and he returned to Korea.
On admission to the hospital, the following vital signs were observed: temperature, 37.8°C; blood pressure, 130/70 mmHg; pulse, 92 beats/min; and respiratory rate, 24 breaths/min. A clinical examination revealed a moderately ill-appearing male with multiple, encrusted, erythematous, papular nodules on the face and trunk. There were no other remarkable findings on examination. Laboratory tests revealed leukocytosis with eosinophilia (white blood cell count 23,460 cells/μl; eosinophils 22%), an increased erythrocyte sedimentation rate (100 mm/h), and increased levels of C-reactive protein (24.7 mg/dl). A chest X-ray (CXR) and computerized tomography (CT) scan revealed tiny, multiple nodules in both lung fields (Figure , top). Sputum acid-fast bacillus stain and tuberculosis culture were both negative. The patient underwent a bronchoscopy and a skin punch biopsy. The biopsy revealed the presence of a chronic granuloma with thick-walled, mature spherules containing endospores. A subsequent skin tissue culture grew Coccidioides immitis. The patient's serum complement fixation (CF) titre was 1:16, and a serum coccidioidal immunodiffusion test for IgG antibody was negative. (All coccidioidal CF antibody testing was carried out at the laboratory of Lynn A. Cheryk, Mayo Clinic, Minnesota, USA). Cerebrospinal fluid (CSF) showed no evidence of meningitis.
The patient was diagnosed with diffuse coccidioidal pneumonia with skin involvement and was treated with amphotericin B deoxycholate (total dosage, 1970 mg; ~1 mg/kg) for 40 days (day five to day 45 of hospitalization). However, the patient still complained of night sweats and a cough. Physical examination revealed a persistent fever (temperature of 38.6–39°C) and no improvement of the skin rash. His general condition progressively deteriorated. The patient developed a right pleural effusion and miliary shadows on the CXR did not improve. A follow-up CF titre performed on day 27 of hospitalization had increased to 1:64. On day 45 of hospitalization, the therapy was changed to caspofungin (initially 70 mg and then 50 mg/day, given intravenously) and fluconazole (400 mg/day, given orally). Sixteen days after the combination treatment (day 60 of hospitalization), a CXR revealed a reduction in both the miliary nodes and the pleural effusion. The patient improved initially, developing only occasional fevers. Forty-nine days after the combination therapy, the patient's peak body temperature fell below 38°C, and the dyspnea had subsided. The serum CF antibody titre had decreased to 1:8. However, the cough remained. By day 125 of the combination treatment, the patient had defervesced, and all of his respiratory symptoms subsided. Although some skin lesions still remained on his face, most were nearly resolved. The serum CF antibody titre was undetectable, and on day 131, caspofungin therapy was discontinued. The patient was subsequently treated with only fluconazole at a dose of 400 mg/day. There were no drug-related side effects noted from the use of the caspofungin and fluconazole. On day 194, his follow-up CF antibody titre increased to 1:256. However, the patient did not experience respiratory symptoms, develop a skin rash, or develop abnormalities on CXR. A follow-up examination five months following completion of the combination treatment revealed minimal residual nodules visible on CXR and CT scan (Figure , bottom). The patient's CF antibody titre was 1:128. As of September 2005, the patient was clinically healthy and without any respiratory symptoms and/or fevers. However, he is still receiving suppressive treatment with fluconazole.


A 25 year old male patient was admitted with a diagnosis of Eales' disease and a non-resolving vitreous hemorrhage involving the left eye of 2 months duration. Ultrasound evaluation of the posterior segment revealed findings consistent with an organized vitreous hemorrhage and incomplete posterior vitreous detachment. Transconjuctival sutureless pars plana vitrectomy was planned using the Bausch and Lomb 25G vitrectomy system. Per-operatively, sleeve for the infusion line was first placed in the inferotemporal quadrant transconjunctivally using the 25 G trocar. After inserting the infusion line through the above sleeve, two more sleeves for the endo illuminator and vitreous cutter were made using the 25G trocar transconjunctivally. Vitrectomy was started using high cut rates (1500 cuts/min) and suction of 500 mm Hg. A fibrovascular frond was noted attached to the disc, which had to be diathermised. To accommodate a conventional unimanual bipolar diathermy probe a localized peritomy was made and the superonasal sclerotomy was enlarged using a 20 G MVR blade. The frond was diathermised, endolaser pan retinal photocoagulation was completed and the conventional sclerotomy was closed using 6-0 vicryl mattress suture placed at a depth of about 75% of the scleral lip. Vitreous was well cleared from this wound opening using the vitrectomy probe around the edges of the sclerotomy before closure. The sleeves of the remaining two 25 G sclerotomies were removed and the overlying conjunctiva was slightly massaged in that area. No wound leak was noted at the end of the procedure. Postoperatively intraocular pressure of 10 mm Hg was recorded.
Ultrasound biomicroscopy (Paradigm model P40) of the sclerotomy sites was done on day 2 postoperatively and again repeated on day 7 and day 14. The port sites were identified at the 20G site by the color of the vicryl suture and at the 25G site by the distortion of the overlying conjunctival vasculature. On day 2, we observed a wide gape at the site that had been enlarged to accommodate the diathermy probe using a 20G MVR blade. In contrast to this, the other two sites wherein sleeves were placed transconjunctivally using the 25G trocar showed only a mild gape (figure ). While significant gape continued to persist at the subsequent evaluations on day 7 and day 14 only at the port that had been enlarged, the other two ports showed only a minimal gape of the internal lip (figure 2). In addition, we also observed some vitreous incarceration at one of the 25 G sclerotomy sites.


A 63-year-old right-handed woman attended her local hospital with a left hemiparesis of sudden onset 24 hours after a RTA. Her motor vehicle had collided with a parked vehicle. There was neither loss of consciousness nor any definite head or whiplash injury. Within a further 24 hours she developed right leg weakness. Computed tomography (CT) brain scan revealed a small low-density area in the right fronto-parietal region only; a CT scan of her cervical spine was normal. Given her progressive triplegia, immediate transfer to our centre was made, to exclude cervical spinal cord injury.
Initial assessment revealed her to be orientated with fluent speech. However, she had evidence of cognitive impairment with an inappropriate jovial affect, poor cognitive estimates and concrete thinking, bradyphrenia and was unable to provide a reliable history. Additional history was obtained from her husband and family. There was no preceding history of cognitive decline but some reduced self-care and hygiene, weight loss of approximately 8 kilograms over three months, and altered bowel habit. Her family had witnessed three episodes of left arm monoparesis, lasting between minutes and 1–2 hours, in the 48 hours preceding her accident. Twenty-four hours after her accident she developed a dense left hemiparesis of sudden onset.
She consumed less than 2 units of alcohol per week, was an ex-smoker, and had no other past medical history of note. She had a family history of ischaemic heart disease.
General examination was unremarkable and she was in sinus rhythm. Neurological examination revealed impaired volitional saccades to the left, but normal targeted saccades. Snout and palmomental reflexes were present. Mild left sided visuospatial dysfunction was present. No sensory inattention was demonstrated. She had a dense left hemiparesis (MRC grade 0 arm and leg) and mild right leg monoparesis (MRC grade 4). Deep tendon reflexes were brisk bilaterally, and both plantar responses were extensor. There was no sensory level.
Formal neuropsychological assessment later confirmed specific difficulties with visual memory, executive functioning and perceptual/constructional abilities.
Urgent brain and cervical spine MRI, revealed an ischaemic lesion in the right fronto-parietal region but no structural cervical cord pathology. Diffusion weighted images were not obtained. A repeat MRI brain scan, 8 days after the onset of left hemiparesis showed additional infarction in the distal left anterior cerebral artery territory.
Comprehensive serial blood tests revealed the following abnormal results (normal ranges and units in brackets): white blood cell count between 11.6 and 13.9 (4 to 11 × 109/L), C-reactive protein between 17.8 and 49.5 (< 8 mg/L), erythrocyte sedimentation rate between 54 and 65 (5 to 15 mm/h), total serum cholesterol 5.7 (<5 mmol/L), carcinoembryonic antigen (CEA) 15.7 (0 to 3.5 ng/mL). Carotid ultrasound examination revealed a right internal carotid artery (ICA) stenosis >85%, whilst all other vessels were normal. Routine cerebrospinal fluid examination was normal. CTA neck confirmed the right ICA stenosis, but no significant left ICA disease. CTA circle of Willis (CoW) showed the right A1 anterior cerebral artery (ACA) segment to be dominant, the left A1 ACA segment to be absent, and an anterior communicating artery (AcoA) aneurysm (Figure ). The remainder of the CoW was considered to be normal. A transthoracic echocardiogram demonstrated no cardiac embolic source. A colonoscopy revealed a rectal tumour, confirmed on biopsy to be a moderately differentiated adenocarcinoma.
Pharmacological treatment included aspirin, pravastatin and perindopril. She also received care from a multi-disciplinary rehabilitation team including physiotherapy. By 10 days after the onset of the left hemiparesis, improvement was noted in all of her deficits, and by 18 days she was regaining power in the left hand and wrist. She was transferred back to her referring hospital for management of her rectal tumour.
The neurological formulation at discharge was one of symptomatic right internal carotid artery stenosis and embolic stroke. It is possible that the RTA was a complication of left-sided visuospatial dysfunction. The subsequent presentation is consistent with multiple bilateral embolic strokes, secondary to CoW variation.


Mr. Ortiz, a 45-year old Bronx resident, was convicted of burglary in June 2005 []. A review of medical records during Mr. Ortiz' trial revealed that he was also Hepatitis C positive and that he had persistently low platelets for several years, irrespective of a fluctuating CD4+ level/HIV viral load. Although aware of his HIV infection since original diagnosis in the late 1990's, Mr. Ortiz was unaware of his hepatitis status until his trial when review of his records revealed a positive Hepatitis C test from a hospital visit after his most recent incarceration and shortly before his arrest on the burglary charge for which he was convicted. Mr. Ortiz reports regular medical care during his prior incarcerations, including diagnosis and treatment of his HIV but recalls no mention of liver disease []. This finding led Mr. Ortiz's defense team to seek further medical evaluation. Testimony by a consulting gastroenterologist was presented during the sentencing phase of the trial and identified Mr. Ortiz as having advanced Hepatitis C with platelets too low for biopsy []. Mr. Ortiz reports having used IV drugs 10–15 years prior to his recent trial which is consistent with the observation that approximately 70% of person's co-infected with HIV and Hepatitis C become infected via IVDU []. Given the slow progression of hepatitis C, even allowing for a hastened disease course in the setting of HIV infection, it is likely that Mr. Ortiz became infected at least ten years earlier. Over this period of time, Mr. Ortiz was known to have HIV and was being intermittently treated for HIV infection.
Aside from never learning of his Hepatitis C while incarcerated, another example of the burdens that the CJS may impose on individuals such as Mr. Ortiz is bias in sentencing. Because of his multiple criminal convictions, the Bronx District Attorney asked that the presiding Judge sentence Mr. Ortiz to a lengthy prison term as a 'persistent felony offender'. This rarely used statute allows a Judge to impose a sentence of 15 year to life, as opposed to whatever sentence would normally apply for their individual conviction []. In this case the burglary charge (even with the prior offenses) could have brought Mr. Ortiz as little as a 2 to 4 year sentence. Instead, the Judge held that Mr. Ortiz was a persistent felony offender and sentenced him to 15 years to life, noting that the "Extensive medical testimony and other evidence established that it is questionable whether, even if I sentence him merely as a second felony offender to the minimum sentence of 2 to 4 years, he would still be alive at the expiration of his sentence" (see ). He went on to explain that "Given his weakened state, any assertion that the Defendant is a serious threat to the public as a burglar is really not credible. However, if released, he may well return to the life of a street addict, thereby endangering the public health through the exchange or sharing of dirty needles." This despite the fact that during this trial, no evidence was introduced about Mr. Ortiz currently or recently using intravenous drugs. Other trial testimony available to the Judge indicates that Mr. Ortiz had last reported intravenous drug use over a decade before his trial. Yet the Judge concluded that incarceration in a state prison would provide "a setting that will ensure that he takes his medications on schedule, and without resort to the use and sharing of dirty needles" [].