Articles de revues sur le sujet « Parietal heat transfers »

Abstract This work aimed at gaining a detailed understanding of heat transfer when boiling occurs on a heated substrate. More specifically, this work focuses on thermal transfers occurring at wall-fluid interfaces at the transition between natural convection and nucleate boiling regimes in pool boiling experiments. To avoid parasitic effects, the vapor bubble is created at a single artificial nucleation site. The boiling cell is instrumented with sensors for temperature measurement, pressure control, and parietal heat flux measurement. The fluid tested is Fluorinert FC-72. For providing a boiling surface and measuring heat flux, a boiling-meter consisting of a heating resistance, heat flux sensors and two thermocouples is used. This boiling-meter enables heat flux generation, the measurement of both temperature and heat flux, and can be rotated through 360°, enabling the influence of inclination to be studied. The boiling-meter is indented at its center to create a single vapor bubble. Thermal measurements are obtained and studied for different inclination angles between 0° and 180° at the saturation conditions. The results showed the nucleation site’s recurrent pattern of being active and inactive for whatever is the boiling surface inclination. Preliminary results are presented and discussed.

The concept of solar receiver using fluidized particles as heat transfer fluid is attractive from the point of view of its performance but also of the material used. In this concept, the receiver is composed of tubes subjected to concentrated solar radiation in which the fluidized particles circulate vertically. Circulation in the tubes, immersed in a “nurse” fluidized bed, is ensured thanks to a controlled pressure difference imposed on the latter and secondary aeration. This ventilation located at the bottom of the absorber tubes makes it possible to control the fluidization regimes. The latter strongly influence the parietal heat transfers and therefore the performance of the receiver. In order to better understand the conditions of appearance of these regimes and to better identify them, a study at room temperature was carried out with a tube 45 mm in internal diameter and 3.63 m in height. The tube is instrumented with several pressure sensors distributed over its height. More than 170 experiments have been performed exploring wide ranges of particle and aeration flow rates, with and without particle circulation. Signal processing methods, classically used in the scientific literature of fluidized beds, are applied. Combined together, these methods have enabled the identification of bubbling, pistoning (of the wall and axisymmetric), turbulent fluidization and rapid fluidization regimes. The pooling of all this information allows the establishment of a diagram of the fluidization regimes and their transition, showing that the local slip velocity is the key parameter governing the structure of the flow.

The main objective of the study was to investigate the thermal performance of five (open and closed) bicycle helmets for convective and evaporative heat transfer using a nine-zone thermal manikin. The shape of the thermal manikin was obtained by averaging the 3D-point coordinates of the head over a sample of 85 head scans of human subjects, obtained through magnetic resonance imaging (MRI) and 3D-printed. Experiments were carried out in two stages, (i) a convective test and (ii) an evaporative test, with ambient temperature maintained at 20.5 ± 0.5 °C and manikin skin temperature at 30.5 ± 0.5 °C for both the tests. Results showed that the evaporative heat transfer contributed up to 51%–53% of the total heat loss from the nude head. For the convective tests, the open helmet A1 having the highest number of vents among tested helmets showed the highest cooling efficiency at 3 m/s (100.9%) and at 6 m/s (101.6%) and the closed helmet (A2) with fewer inlets and outlets and limited internal channels showed the lowest cooling efficiency at 3 m/s (75.6%) and at 6 m/s (84.4%). For the evaporative tests, the open helmet A1 showed the highest cooling efficiency at 3 m/s (97.8%), the open helmet A4 showed the highest cooling efficiency at 6 m/s (96.7%) and the closed helmet A2 showed the lowest cooling efficiency at 3 m/s (79.8%) and at 6 m/s (89.9%). Two-way analysis of variance (ANOVA) showed that the zonal heat-flux values for the two tested velocities were significantly different (p < 0.05) for both the modes of heat transfer. For the convective tests, at 3 m/s, the frontal zone (256–283 W/m2) recorded the highest heat flux for open helmets, the facial zone (210–212 W/m2) recorded the highest heat flux for closed helmets and the parietal zone (54–123 W/m2) recorded the lowest heat flux values for all helmets. At 6 m/s, the frontal zone (233–310 W/m2) recorded the highest heat flux for open helmets and the closed helmet H1, the facial zone (266 W/m2) recorded the highest heat flux for the closed helmet A2 and the parietal zone (65–123 W/m2) recorded the lowest heat flux for all the helmets. For evaporative tests, at 3 m/s, the frontal zone (547–615 W/m2) recorded the highest heat flux for all open helmets and the closed helmet H1, the facial zone (469 W/m2) recorded the highest heat flux for the closed helmet A2 and the parietal zone (61–204 W/m2) recorded the lowest heat flux for all helmets. At 6 m/s, the frontal zone (564–621 W/m2) recorded highest heat flux for all the helmets and the parietal zone (97–260 W/m2) recorded the lowest heat flux for all helmets.

In this study, the skull bone thicknesses of 150 patients ranging in age from 0 to 72 years were calculated using a novel approach (thermal analysis), and thickness changes were analyzed. Unlike conventional thickness calculation approaches (Beam Propagation, Hildebrand), a novel heat transfer-based approach was developed. Firstly, solid 3D objects with different thicknesses were modeled, and thermal analyses were performed on these models. To better understand the heat transfer of 3D object models, finite element models (FEM) of the human head have been reported in the literature. The FEM can more accurately model the complex geometry of a 3D human head model. Then, thermal analysis was performed on human skulls using the same methods. Thus, the skull bone thicknesses at different ages and in different genders from region to region were determined. The skull model was transferred to ANSYS, and it was meshed using different mapping parameters. The heat transfer results were determined by applying different heat values to the inner and outer surfaces of the skull mesh structure. Thus, the average thicknesses of skull regions belonging to a certain age group were obtained. With this developed method, it was observed that the temperature value applied to the skull was proportional to the thickness value. The average thickness of skull bones for men (frontal: 7.8 mm; parietal: 9.6 mm; occipital: 10.1 mm; temporal: 6 mm) and women (frontal: 8.6 mm; parietal: 10.1 mm; occipital: 10 mm; temporal: 6 mm) are given. The difference (10%) between men and women appears to be statistically significant only for frontal bone thickness. Thanks to the developed method, bone thickness information at any desired point on the skull can be obtained numerically. Therefore, the proposed method can be used to help pre-operative planning of surgical procedures.

Gene transfer to the heart has been accomplished with intravascular administration of adenoviral vectors into the pericardial sac, by increasing the duration of exposure to the adenovirus, would result in gene expression in the pericardium and perhaps myocardium and therefore might provide an alternative method to intravascular administration for gene transfer. We injected a replication-deficient adenovirus (average 1 x 10(12) particles/ml in 3% sucrose; 1 x 10(10) plaque forming units/ml containing cDNA encoding a nuclear-targeted bacterial beta-galactosidase into the pericardial sac of dogs. Samples of the pericardium and heart were examined for enzymatic activity of beta-galactosidase and after histochemical staining with 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside. One day after injection of the adenovirus (1-3 ml), beta-galactosidase activity was highest in the parietal pericardium and left atrial tissue and lower in the right and left ventricles. Histochemical expression of the transgene was predominantly in the visceral pericardium of atria and ventricles and occasionally in the epicardial myocytes, arterioles, and venules. Pretreatment with doxycycline (5 mg) before adenovirus administration increased transgene activity in left ventricles. Thus adenovirus injected into the pericardial sac provides an effective method for gene transfer to the visceral and parietal pericardium over atria and ventricles.

The flow regimes of liquids encountered in engineering practice are mainly turbulent due to their structure, with which the features of such flows at supercritical pressure are considered in the work and some results are compared with similar ones obtained at low Reynolds numbers. Under these conditions, the physical properties of the fluid change sharply in the parietal layer and, depending on the values of the heat flux density and temperature, the area of sharp changes in physical properties can move along the flow cross section. Depending on the influence of these factors, the nature of the fluid flow can change, which affects the patterns of heat transfer and, accordingly, the nature of the distribution of wall temperature. In particular, conditions were identified for the appearance of a primary and secondary improved heat transfer regime. The possibility of the existence of an anomalous behavior of heat transfer during a turbulent flow of aromatic hydrocarbons was revealed, the nature of the distribution of the wall temperature along the length of the experimental tube is examined, and the influence of changes in the thermophysical properties of the substance on it is analyzed. The experimental data for water and toluene with a deteriorated heat transfer mode deviate from the calculated by [Formula: see text]25%. As is known, the flow regime of fluids in engineering practice is mainly turbulent in structure. Therefore, it is very important to study the characteristics of such flows at supercritical pressure and compare some results with similar results obtained at low Reynolds numbers.

Previous studies have characterized the physiological interactions between central nervous system (brain) and peripheral cardiovascular system (heart) during affective elicitation in healthy subjects; however, questions related to the directionality of this functional interplay have been gaining less attention from the scientific community. Here, we explore brain-heart interactions during visual emotional elicitation in healthy subjects using measures of Granger causality (GC), a widely used descriptor of causal influences between two dynamical systems. The proposed approach inferences causality between instantaneous cardiovagal dynamics estimated from inhomogeneous point-process models of the heartbeat and high-density electroencephalogram (EEG) dynamics in 22 healthy subjects who underwent pleasant/unpleasant affective elicitation by watching pictures from the International Affective Picture System database. Particularly, we calculated the GC indexes between the EEG spectrogram in the canonical θ-, α-, β-, and γ-bands and both the instantaneous mean heart rate and its continuous parasympathetic modulations (i.e., the instantaneous HF power). Thus we looked for significant statistical differences among GC values estimated during the resting state, neutral elicitation, and pleasant/unpleasant arousing elicitation. As compared with resting state, coupling strength increases significantly in the left hemisphere during positive stimuli and in the right hemisphere during negative stimuli. Our results further reveal a correlation between emotional valence and lateralization of the dynamical information transfer going from brain-to-heart, mainly localized in the prefrontal, somatosensory, and posterior cortexes, and of the information transfer from heart-to-brain, mainly reflected into the fronto-parietal cortex oscillations in the γ-band (30 −45 Hz).

We examined under the electron microscope samples of parietal peritoneum obtained from nine nondiabetic chronic uremics -six of them on maintenance intermittent peritoneal dialysis, ranging in age from 52 to 82 years -mean 64.4 ± 8.1 years and of nine non-uremic, non-diabetic patients -mean age 40.7 ± 12.2 years. Postcapillary venules and small venules showed areas with several layers of reduplicated basal lamina. Some microvessels showed gaps in basallamina with and/or without focal reduplication. Reduplicated submesothelial basal lamina was found in only one patient. These changes were not observed in the nine non-uremic, non-diabetic controls. To the best of our knowledge, this is the first description in humans of such alterations in the aforementioned locations, which may well be secondary to aging and/or to the intense mesothelial renewal observed in I.P.D. patients. We need to determine the possible influence of these ultrastructural changes on transperitoneal transfer of water and solutes during peritoneal dialysis. The basal lamina of blood vessels may not be of uniform thickness. Human non-diabetic adults show significant increase in capillary basal lamina thickness as one moves from head to foot (1). Those regional variations may be related to differences in venous hydrostatic pressure effective on the capillary bed (1). This paper decribes the first observations of reduplicated basal lamina of microvessels in the parietal peritoneum and of that subjacent to mesothelial cells in elderly, non-diabetic uremic patients.

✓ The authors report a case of Type II odontoid fracture from a frontal impact sustained in the crash of a late-model motor vehicle. They discuss the biomechanical mechanisms of injury after considering patient demographic data, type and use of restraint systems including seatbelt and airbags, crash characteristics, and laboratory-based experimental studies. Multiple factors contributed to the Type II odontoid fracture: the patient's tall stature and intoxicated state; lack of manual three-point seat belt use; obliqueness of the frontal impact; and the most likely preflexed position of the head—neck complex at the time of impact, which led to contact of the parietal region with the A-pillar roof-rail area of the vehicle and resulted in the transfer of the dynamic compressive force associated with lateral bending. Odontoid fractures still occur in individuals involved in late-model motor vehicle frontal crashes, and because this injury occurs secondary to head impact, airbags may not play a major role in mitigating this type of trauma to an unrestrained occupant. It may be more important to use seat belts than to depend on the airbag alone for protection from injury.

The preterm fetus is capable of surviving prolonged periods of severe hypoxia without neural injury for much longer than at term. To evaluate the hypothesis that regulated suppression of brain metabolism contributes to this remarkable tolerance, we assessed changes in the redox state of cytochrome oxidase (CytOx) relative to cerebral heat production, and cytotoxic edema measured using cerebral impedance, during 25 min of complete umbilical cord occlusion or sham occlusion in fetal sheep at 0.7 gestation. Occlusion was followed by rapid, profound reduction in relative cerebral oxygenation and EEG intensity and an immediate increase in oxidized CytOx, indicating a reduction in electron flow down the mitochondrial electron transfer chain. Confirming rapid suppression of cerebral metabolism there was a loss of the temperature difference between parietal cortex and body at a time when carotid blood flow was maintained at control values. As occlusion continued, severe hypotension/hypoperfusion developed, with a further increase in CytOx levels to a plateau between 8 and 13 min and a progressive rise in cerebral impedance. In conclusion, these data strongly suggest active regulation of cerebral metabolism during the initial response to severe hypoxia, which may help to protect the immature brain from injury.

Thermoacoustic instabilities are an undesirable physical phenomenon that can occur in a wide range of combustors such as gas turbines, rocket engines, and boilers. These instabilities are typically loud, vibration-inducing, and can increase parietal heat transfer in the combustion chamber. As a consequence, mechanical fatigue increases and can sometimes lead to a catastrophic failure of the combustor. A well-established formalism to predict thermoacoustic stability is based on network models where the combustor is represented by a sequence of connected acoustic modules. The frequency of the modes appearing inside the combustor are then given by the eigenvalues of a characteristic equation obtained using conservation equations. This approach has been successfully used to predict the stability of a variety of combustors. However, this operation needs to be repeated many times in order to optimise the shape of an unstable combustor at an early design stage. One option to reduce the computational cost of predicting the thermoacoustic stability of a given configuration is to use a data-driven approach as opposed to a physics-based approach. In the former approach, a Machine Learning algorithm is trained to discriminate between thermoacoustically stable and unstable combustors using examples generated by a (physics-based) acoustic network model. The ML model is then able to predict the thermoacoustic stability of an unknown configuration much faster than a traditional acoustic network model and with a very high accuracy. This approach has been validated in a previous study using classical Machine Learning algorithms, but it is restricted to somewhat simple geometries. The objective of this study is to investigate whether Deep Learning architectures can be used to generalise those results to complex geometries with a large number of elements.

Abstract Pituitary apoplexy is a rare endocrine emergency due to acute infarction or hemorrhage of the pituitary gland. It most often involves an underlying adenoma. Precipitating factors include hypertension, major surgery, coagulopathy, or medications. Fulminant liver disease giving rise to a coagulopathy can lead to an increased risk of hemorrhage into the pituitary. A 20-year-old female was transferred from British Overseas Territory for evaluation of fulminant liver failure after presenting with worsening of longstanding abdominal pain and vomiting. She was taking ciprofloxacin and metronidazole for colitis and Tylenol for pain. She denied alcohol abuse, illicit drugs or herbal supplements. Her blood pressure was 107/72 mmHg and physical exam was notable for jaundice. Labs were significant for Alanine Aminotransferase (ALT) 10277 IU/L (n&lt;35 IU/L), Aspartate aminotransferase (AST) 10886 IU/L (n&lt;40 IU/L), total bilirubin 15 mg/dl (n&lt;1.2 mg/dl), alkaline phosphatase 160 IU/L (n&lt;115 IU/L) and INR 4.9 (n&lt;1.3). She was given 100 mg of methylprednisolone. CT head without contrast (WO) completed prior to transfer showed no abnormal findings. The next day, she reported new onset severe headache and diplopia. Bilateral wrist asterixis and worsening lethargy was noted on exam. Ammonia was 278 umol/L (&lt;n 42 umol/L). CT head WO showed a 0.6 x 0.9 x 1.0 cm hyperdense area in the posterior aspect of pituitary gland concerning for apoplexy. Additional labs showed cortisol 11 ug/dL (n&lt;22 ug/dL), ACTH 2.9 pg/mL (n 7.2-63.3 pg/mL), TSH 0.04 uIU/mL (n 0.3-4.5 uIU/mL), free (F) T4 1.4 ng/dl (n 0.6-1.5 ng/dl), FT3 1.2 ng/dl (n 2.4-4.2 ng/dl), FSH 1.8 mIU/ml (n 3.5-12.5 mIU/ml), LH &lt;0.1 mIU/mL (n 2.4-12.6 mIU/ml), prolactin 49 ng/mL (n 5-23 ng/mL), and IGF-1 141 ng/mL (n 109-372 ng/mL). She was managed conservatively with hydrocortisone for secondary adrenal insufficiency and hypopituitarism. With extensive work up, no underlying cause was found for her fulminant hepatic disease. She underwent a deceased donor liver transplant. Perioperatively, she was given 200 mg methylprednisolone which was subsequently tapered to 5 mg prednisone. Postoperative course was complicated by a new right parietal lobe hemorrhage. There was no change in pituitary hemorrhage size. As her FT4 trended down to 0.6 ng/dl, along with suppressed TSH, she was started on 50 mcg of levothyroxine. Upon discharge, she was advised to follow with an endocrinologist and have her hormones revaluated once the acute phase has resolved. Pituitary apoplexy as a consequence of coagulopathy caused by liver failure has not been described before. Although she was given methylprednisolone which can suppress ACTH for up to 48 hours, ACTH deficiency is the most critical endocrine dysfunction and is present in nearly 70% of cases of pituitary apoplexy. Therefore, urgent treatment of secondary adrenal insufficiency is warranted along with thyroid hormone replacement.

AbstractThe posterior parietal cortex (PPC) integrates multisensory and motor‐related information for generating and updating body representations and movement plans. We used retrograde transneuronal transfer of rabies virus combined with a conventional tracer in macaque monkeys to identify direct and disynaptic pathways to the arm‐related rostral medial intraparietal area (MIP), the ventral lateral intraparietal area (LIPv), belonging to the parietal eye field, and the pursuit‐related lateral subdivision of the medial superior temporal area (MSTl). We found that these areas receive major disynaptic pathways via the thalamus from the nucleus of the optic tract (NOT) and the superior colliculus (SC), mainly ipsilaterally. NOT pathways, targeting MSTl most prominently, serve to process the sensory consequences of slow eye movements for which the NOT is the key sensorimotor interface. They potentially contribute to the directional asymmetry of the pursuit and optokinetic systems. MSTl and LIPv receive feedforward inputs from SC visual layers, which are potential correlates for fast detection of motion, perceptual saccadic suppression and visual spatial attention. MSTl is the target of efference copy pathways from saccade‐ and head‐related compartments of SC motor layers and head‐related reticulospinal neurons. They are potential sources of extraretinal signals related to eye and head movement in MSTl visual‐tracking neurons. LIPv and rostral MIP receive efference copy pathways from all SC motor layers, providing online estimates of eye, head and arm movements. Our findings have important implications for understanding the role of the PPC in representation updating, internal models for online movement guidance, eye‐hand coordination and optic ataxia.

Two stages of the creative writing process were characterized through mobile scalp electroencephalography (EEG) in a 16-week creative writing workshop. Portable dry EEG systems (four channels: TP09, AF07, AF08, TP10) with synchronized head acceleration, video recordings, and journal entries, recorded mobile brain-body activity of Spanish heritage students. Each student's brain-body activity was recorded as they experienced spaces in Houston, Texas (“Preparation” stage), and while they worked on their creative texts (“Generation” stage). We used Generalized Partial Directed Coherence (gPDC) to compare the functional connectivity among both stages. There was a trend of higher gPDC in the Preparation stage from right temporo-parietal (TP10) to left anterior-frontal (AF07) brain scalp areas within 1–50 Hz, not reaching statistical significance. The opposite directionality was found for the Generation stage, with statistical significant differences (p &lt; 0.05) restricted to the delta band (1–4 Hz). There was statistically higher gPDC observed for the inter-hemispheric connections AF07–AF08 in the delta and theta bands (1–8 Hz), and AF08 to TP09 in the alpha and beta (8–30 Hz) bands. The left anterior-frontal (AF07) recordings showed higher power localized to the gamma band (32–50 Hz) for the Generation stage. An ancillary analysis of Sample Entropy did not show significant difference. The information transfer from anterior-frontal to temporal-parietal areas of the scalp may reflect multisensory interpretation during the Preparation stage, while brain signals originating at temporal-parietal toward frontal locations during the Generation stage may reflect the final decision making process to translate the multisensory experience into a creative text.

AbstractAuditory stream segregation and informational masking were investigated in brain-lesioned individuals, age-matched controls with no neurological disease, and young college-age students. A psychophysical paradigm known as rhythmic masking release (RMR) was used to examine the ability of participants to identify a change in the rhythmic sequence of 20-ms Gaussian noise bursts presented through headphones and filtered through generalized head-related transfer functions to produce the percept of an externalized auditory image (i.e., a 3D virtual reality sound). The target rhythm was temporally interleaved with a masker sequence comprising similar noise bursts in a manner that resulted in a uniform sequence with no information remaining about the target rhythm when the target and masker were presented from the same location (an impossible task). Spatially separating the target and masker sequences allowed participants to determine if there was a change in the target rhythm midway during its presentation. RMR thresholds were defined as the minimum spatial separation between target and masker sequences that resulted in 70.7% correct-performance level in a single-interval 2-alternative forced-choice adaptive tracking procedure. The main findings were (1) significantly higher RMR thresholds for individuals with brain lesions (especially those with damage to parietal areas) and (2) a left–right spatial asymmetry in performance for lesion (but not control) participants. These findings contribute to a better understanding of spatiotemporal relations in informational masking and the neural bases of auditory scene analysis.

Abstract The present study used resting state MEG whole-head recordings to identify how chronic tonal tinnitus relates to altered functional connectivity of brain’s intrinsic cortical networks. Resting state MEG activity of 40 chronic tinnitus patients and 40 matched human controls was compared identifying significant alterations in intrinsic networks of the tinnitus population. Directed functional connectivity of the resting brain, at a whole cortex level, was estimated by means of a statistical comparison of the estimated phase Transfer Entropy (pTE) between the time-series of cortical activations, as reconstructed by LORETA. As pTE identifies the direction of the information flow, a detailed analysis of the connectivity differences between tinnitus patients and controls was possible. Results indicate that the group of tinnitus patients show increased connectivity from right dorsal prefrontal to right medial temporal areas. Our results go beyond previous findings by indicating that the role of the left para-hippocampal area is dictated by a modulation from dmPFC; a region that is part of the dorsal attention network (DAN), as well as implicated in the regulation of emotional processing. Additionally, this whole cortex analysis showed a crucial role of the left inferior parietal cortex, which modulated the activity of the right superior temporal gyrus, providing new hypotheses for the role of this area within the context of current tinnitus models. Overall, these maladaptive alterations of the structure of intrinsic cortical networks show a decrease in efficiency and small worldness of the resting state network of tinnitus patients, which is correlated to tinnitus distress.

Introduction To describe a unique case of pial arteriovenous fistula presenting as left hemispheric cerebral edema with hemianopsia, sensory change and ataxia. Methods Case report Results Our patient is a 38 year old male with a history of diabetes, hyperlipidemia and congenital deafness with a left cochlear implant who presented to an outside hospital for visual complaints. Non‐contrast CT of the head was negative at that time; he could not obtain an MRI due to his cochlear implant. He developed worsening right hemianopia and aphasia, prompting his transfer to our facility. Upon arrival, repeat imaging was done, including a CTA of the head and neck. This revealed a large region of hypodensity involving the left PCA and distal MCA territories. An MRI was attempted but artifact from his implant obscured visualization of the left hemisphere. Post‐contrast CT was negative for evidence of tumor. CT venogram was negative for veno‐occlusive disease. He complained of worsening headache and demonstrated worsening word‐finding ability. He received100g total of mannitol divided across 3 boluses which improved his symptoms mildly. Over the following days he began to become ataxic and clumsy in the right upper extremity and his headache worsened further and he began to develop focal seizures electrographically localized to the left parietal lobe. Repeat CTA demonstrated expanding hypodensity with marked vascular engorgement in the left hemisphere. He underwent 6‐vessel digital subtraction angiography (DSA) of the head which revealed gross left hemispheric venous congestion with early filling of the left hemispheric venous system by a parasagittal pial ateriovenous fistula believed to be responsible for his hemispheric edema. He was discharged on acetazolamide and acetaminophen for headache management and plans for outpatient follow‐up and potential intervention. Follow‐up DSA revealed improvement in his venous congestion and reduction in the degree of his early venous filling with some symptomatic improvement by medical management. Conclusions Pial arteriovenous fistulae (pAVF) are a rare entity and can present in a variety of ways, with symptomatic intracranial hemorrhage and ischemia being two of the most common. This case illustrates an unusual instance of hemispheric edema initially mistaken for venous infarct caused by a pAVF, and prompts the physician to consider angiography and further exploration when initial workup for cerebral edema and/or venous infarct is initially unrevealing.

Background Eosinophilic granulomatosis with polyangiitis (EGPA) causes inflammation of small blood vessels. EGPA is rare, with an annual incidence of 1 per million, with a mean age of onset of 40‐60 years. EGPA is divided into 2 phenotypes, ANCA‐positive vasculitis type and ANCA‐negative eosinophilia type. There is an overlap between other hypereosinophilic syndromes and EGPA. There are no diagnostic criteria for EGPA, however clinical features of asthma, chronic rhinosinusitis with polyps, eosinophilia, neuropathy, lung infiltrates, and eosinophilic cardiomyopathy or gastroenteritis are supportive. Central nervous system involvement manifests as cerebral infarcts and subarachnoid hemorrhages. Case: Here we present a 53‐year‐old Caucasian female with no past medical history who presented with chest pain and shortness of breath. She reported dyspnea on exertion for 8 months prior, and more recently paroxysmal nocturnal dyspnea and orthopnea, with minimal relief from inhalers. She was noted to have pansinusitis and was started on amoxicillin‐clavulanic acid without improvement. She noted acute right upper extremity weakness. Initial workup showed elevated troponin and a white blood cell (WBC) count of 28.4 with 11.64 eosinophils. CT chest showed bilateral bronchial wall thickening with bilateral nodular consolidative opacities in the right upper lobe and left lower lobe. She was started on a heparin drip. Coronary angiography was negative, and the initial echocardiogram revealed mild circumferential pericardial effusion without tamponade. CT head showed an 11 mm right cerebellar hemorrhage. Heparin was stopped. MRI brain revealed multiple scattered areas of restricted diffusion in bilateral cerebral hemispheres and a right cerebellar hemisphere. CTA head and neck showed normal vessels, and after transfer to our facility, a repeat MRI brain revealed scattered new infarcts in the left parietal and occipital regions. A repeat echocardiogram showed a small loculated pericardial effusion anterior to the right ventricle but no intracardiac shunt. The patient was exposed to wildfire smoke before symptom onset, raising suspicion of fungal infection. The patient underwent fungal evaluation in both serum and sinus aspirate, including beta‐D‐glucan in the serum, which was negative, and a bronchoscopy, which revealed white plaques and nodules with negative fungal and tuberculosis studies. Lumbar puncture revealed an elevated opening pressure of 30 mmHg but otherwise unremarkable infectious studies. Antibiotic therapy included vancomycin, cefepime, and amphotericin, but with consistently elevated WBCs of more than 24 with eosinophilic predominance. Endomyocardial biopsy showed numerous eosinophils. Subsequent endobronchial biopsy showed eosinophilic infiltrates and features suspicious for vasculitis. ANCA and bone marrow biopsy were negative. The primary diagnosis was considered hypereosinophilic syndrome. She was started on pulse dose steroids, and WBC count fell from 24.1 to 11.8 with a decrease in eosinophils from 13.05 to 0.01. Outpatient rheumatology was planned to initiate cyclophosphamide or rituximab. Dual antiplatelet therapy was initiated before discharge. Conclusion Central nervous system sequelae of EGPA are rare, but this diagnosis should be considered in patients with symptoms of sinusitis, elevated eosinophils, and acute stroke, especially without other risk factors. Since ANCA is only positive in about 30‐40% of patients, an early biopsy is needed for confirmation and early treatment with steroids.

Abstract Introduction We describe a 29-year-old gentleman with triple-antibody positive primary antiphospholipid syndrome (APS) who presented with recurrent cerebrovascular thrombotic events despite anticoagulation. He was escalated to rituximab. A pre-rituximab chest radiograph was abnormal resulting in a CT-chest which demonstrated bilateral widespread ground-glass opacities. Carbon monoxide transfer coefficient (KCO) was raised. Lung biopsy showed alveolar haemorrhage, alveolitis, capillaritis and a mixed inflammatory infiltrate consistent with APS. Alternative causes such as infection and malignancy were excluded. This case reflects a complex refractory APS with rare pulmonary manifestations. Management was multidisciplinary and included the use of rituximab to prevent further disease progression. Case description A previously well 29-year-old Asian gentleman presented in late 2015 with multiple right leg deep vein thromboses (DVTs). Rivaroxaban was commenced for six-months. A thrombophilia screen post-treatment demonstrated anti-cardiolipin IgG and IgM levels of > 420 kUnits/litre and 200 kUnits/litre respectively, anti-β2-glycoprotein-I IgG and IgM levels of 163 kUnits/litre and 50 kUnits/litre respectively, and a strongly positive lupus anticoagulant. A follow-up US-Doppler revealed chronic DVTs; apixaban was initiated. Secondary causes of APS were excluded clinically and serologically. Repeat APS antibodies remained strongly positive. In December 2016, he developed multiple APS-driven strokes affecting the occipital lobes, centrum semiovale and cerebellum. Other causes of stroke were excluded. Clopidogrel was commenced and apixaban was changed to warfarin with an INR target of 2.5-3.0. Despite consistently achieving this target he had an acute parietal lobe stroke in May 2017. Consequently, his INR target increased to 3.0-4.0. Hydroxychloroquine and high-dose atorvastatin were also added. In July 2018 he presented with recurrent transient ischaemic attacks. An MRI-head identified a previously unseen chronic temporal lobe infarct. Following a multidisciplinary discussion we changed warfarin to low molecular weight heparin and also planned to commence rituximab. Pre-biologic, his T-spot was positive and his chest radiograph was abnormal. He had no chest symptoms. A CT-chest demonstrated multiple bilateral ground-glass opacities. Pulmonary function tests (PFTs) revealed an elevated KCO (130% predicted). A lung biopsy revealed alveolar haemorrhage, alveolitis, capillaritis and a mixed inflammatory infiltrate consistent with APS. Infection (including tuberculosis), malignancy and granulomatous disease were all excluded. The patient was subsequently treated with high-dose corticosteroids and rituximab. His other treatment for APS remained unchanged. He was also treated for latent tuberculosis with isoniazid. Since this treatment regimen the patient has had no further thrombotic episodes. Moreover, repeat CT-chest and PFTs have both shown significant improvements. Discussion Primary APS is an autoimmune thrombophilic disorder characterised by recurrent arterial and venous thromboembolism, and obstetric morbidity. Deep vein thrombosis and stroke are the most common venous and arterial thrombotic manifestations respectively. Treatment includes the use of anticoagulation such as warfarin. Refractory APS is associated with recurrent thrombotic episodes despite anticoagulation therapy. Our patient developed recurrent cerebral thrombosis despite warfarin and clopidogrel. This continued to occur even after increasing the INR-target. Furthermore, prior to and during each thrombotic episode, our patient’s INR was always within the desired range. We also added secondary treatments for APS including atorvastatin and hydroxychloroquine and these also failed to prevent further cerebrovascular disease. We did not feel changing warfarin to low molecular weight heparin alone was sufficient to prevent further thromboses given the history of optimal INRs. We therefore opted to also add rituximab given its role in preventing further production of B-cell driven autoantibodies via CD20 binding. In addition, our patient had significant APS-driven pulmonary abnormalities which required addressing. Pulmonary embolism and pulmonary hypertension are the most common respiratory pathologies of APS. Rarely APS can also cause pulmonary artery thrombosis and fibrosing alveolitis. Moreover and particular to our patient, it can cause alveolar haemorrhage, alveolitis and pulmonary capillaritis. This occurs via neutrophilic infiltration of the alveolar septum and pulmonary capillary wall, and microthrombi which results in inflammation. Necrosis and loss of capillary integrity then causes disruption of the alveolar-capillary basement membrane resulting in haemorrhage. Remarkably despite the evident APS-driven lung disease in our patient, he was asymptomatic from a chest perspective. Our patient has responded positively to rituximab with improvement in PFTs and CT-chest appearance. Moreover he has had no further thrombotic events. We aim to repeat brain imaging and recheck APS antibody titres to observe the effect of rituximab. Key learning points Excluding pulmonary embolism and pulmonary hypertension, pulmonary disease is an under-recognised manifestation of APS. Rarer lung sequelae include pulmonary capillaritis, alveolitis and alveolar haemorrhage which our patient exhibited. These pathologies require a combination of investigations to diagnose including imaging, PFTs and histopathological biopsy. Most cases of APS respond to first-line treatment with anticoagulation such as warfarin provided INR targets are consistently achieved. Our patient continued to have recurrent thrombotic cerebrovascular events despite anticoagulation, antiplatelet therapy and other treatments. This case raises awareness of a complex refractory APS case which necessitated the introduction of biologic therapy in rituximab. Rituximab is already well-recognised in the treatment of catastrophic APS. We intend by this case to raise awareness of the effectiveness of rituximab in non-catastrophic APS, and its value in treating inflammatory APS-driven lung pathology. We await results for the effect of rituximab on APS-antibodies and whether this has any impact on prevention of disease progression. This case also highlights the importance of a multidisciplinary approach in managing complex cases. We worked alongside other specialities including neurology, stroke medicine, haematology and respiratory medicine to achieve optimal patient care. Conflicts of interest The authors have declared no conflicts of interest.