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Swimming-induced pulmonary oedema (SIPE) is a potentially fatal condition associated with open-water swims. We sought to quantify the contribution of cardiac dysfunction to SIPE. We aimed to assess the incidence of SIPE during an endurance cold water swim. We determined associations between SIPE and changes in cardiac function through a SIPE questionnaire, lung ultrasound (LUS), cardiac biomarkers (N-Terminal pro-B-type natriuretic peptide (NT proBNP) and cardiac troponin I (cTnI)) and transthoracic echocardiograms (TTE). Twenty open-water swimmers (10 males) underwent a TTE, LUS for pulmonary oedema and cardiac biomarkers before, 2-hours and 24-hours after an 8-hour swim. Swimmers had an additional LUS and rated their breathlessness upon leaving the water. Participants with breathlessness and 3 or more B-lines present in two or more LUS views were considered SIPE positive. Five swimmers (25 % of cohort) presenting with post-event breathlessness and evidence of lung water were considered SIPE positive. SIPE had no demonstrable effect on left systolic function (LV ejection fraction, global longitudinal strain [GLS]), diastolic function (left atrial volume, E/e’) and right ventricular (RV) function (RV fractional area change and RV free wall GLS). SIPE was associated with a small increase in troponin post-swim (at 2 hours SIPE+ 32.1 ng/L, SIPE− 12.6 ng/L, p = 0.004: at 24 hours SIPE+ 12.6 ng/L, SIPE− 4.8 ng/L, p = 0.04) but had no impact on NT proBNP. SIPE is common in open-water swimmers following an endurance swim and is identified using LUS. Whilst SIPE was associated with a small increase in post-swim troponin levels, no further evidence of cardiac dysfunction was identified at two hours after the swim to explain the pulmonary oedema.

Space-occupying brain oedema is a potentially life-threatening complication in the first days after large hemispheric or cerebellar infarction. Several treatment strategies for this complication are available, but the size and quality of the scientific evidence on which these strategies are based vary considerably. The aim of this Guideline document is to assist physicians in their management decisions when treating patients with space-occupying hemispheric or cerebellar infarction. These Guidelines were developed based on the European Stroke Organisation (ESO) standard operating procedure and followed the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach. A working group identified 13 relevant questions, performed systematic reviews and meta-analyses of the literature, assessed the quality of the available evidence, and wrote evidence-based recommendations. An expert consensus statement was provided if not enough evidence was available to provide recommendations based on the GRADE approach. We found high-quality evidence to recommend surgical decompression to reduce the risk of death and to increase the chance of a favourable outcome in adult patients aged up to and including 60 years with space-occupying hemispheric infarction who can be treated within 48 hours of stroke onset, and low-quality evidence to support this treatment in older patients. There is continued uncertainty about the benefit and risks of surgical decompression in patients with space-occupying hemispheric infarction if this is done after the first 48 hours. There is also continued uncertainty about the selection of patients with space-occupying cerebellar infarction for surgical decompression or drainage of cerebrospinal fluid. These Guidelines further provide details on the management of specific subgroups of patients with space-occupying hemispheric infarction, on the value of monitoring of intracranial pressure, and on the benefits and risks of medical treatment options. We encourage new high-quality studies assessing the risks and benefits of different treatment strategies for patients with space-occupying brain infarction.

Brain edema, defined as localized or extensive swelling of brain tissue, arises from various pathologies, including trauma, ischemia, hypoxic damage, inflammation (e.g., infection), rapidly growing tumors, and obstructive hydrocephalus. The main types are cytotoxic, vasogenic, and interstitial edema. Cytotoxic edema, typically affecting gray matter, occurs in acute infarction, hypoxic injury, and later stages of cranial trauma. Vasogenic edema, primarily affecting white matter, is associated with tumor growth, infection, early stages of trauma, and any condition disrupting the blood-brain barrier. Posterior reversible encephalopathy syndrome (PRES) is a specific pathology associated with vasogenic edema. Less common are osmotic or hydrostatic edema and brain swelling associated with hydrocephalus. Radiologically, CT scans demonstrate localized or generalized areas of hypodensity with CSF space constriction. Conventional MRI sequences show increased water signal in edematous areas (hyperintensity on FLAIR and T2-weighted images, hypointensity on T1-weighted images) and may reveal underlying causes such as tumors, abscesses, or hemorrhage. Diffusion-weighted imaging differentiates edema types: vasogenic and hydrostatic edema exhibit high ADC values (increased diffusion), while cytotoxic edema shows low ADC values (restricted diffusion). Although CT and conventional MRI cannot directly distinguish between edema types, identifying the underlying pathology can indirectly indicate the type of edema. Diffusion-weighted imaging, by detecting diffusion changes, allows for direct differentiation of edema types. CT scans and conventional MRI baseline sequences are unable to differentiate between edema caused by various factors. However, identifying the underlying cause can help classify the type and cause of brain edema indirectly. Diffusion-weighted imaging techniques enable the differentiation of edema by detecting diffusion restriction or by revealing high signal intensity on ADC maps.

Sepsis is a life-threatening condition characterised by endothelial barrier dysfunction and impairment of normal microcirculatory function, resulting in a state of hypoperfusion and tissue oedema. No specific pharmacological therapies are currently used to attenuate microvascular injury. Given the prominent role of endothelial breakdown and microcirculatory dysfunction in sepsis, there is a need for effective strategies to protect the endothelium. In this review we will discuss key mechanisms and putative therapeutic agents relevant to endothelial barrier function.

BackgroundThere is no accurate, non-invasive measurement to estimate the degree of pulmonary oedema in acute respiratory distress syndrome (ARDS). We developed the Radiographic Assessment of Lung Oedema (RALE) score to evaluate the extent and density of alveolar opacities on chest radiographs. After first comparing the RALE score to gravimetric assessment of pulmonary oedema in organ donors, we then evaluated the RALE score in patients with ARDS for its relationship to oxygenation and clinical outcomes.MethodsWe compared radiographs with excised lung weights from 72 organ donors (derivation cohort) and radiographs with clinical data from 174 patients with ARDS in the ARDSNet Fluid and Catheter Treatment Trial (validation cohort). To calculate RALE, each radiographic quadrant was scored for extent of consolidation (0–4) and density of opacification (1–3). The product of the consolidation and density scores for each of the four quadrants was summed (maximum score=48).ResultsAgreement between two independent reviewers for RALE score was excellent (intraclass correlation coefficient=0.93, 95% CI 0.91 to 0.95). In donors, pre-procurement RALE score correlated with height-adjusted total lung weight (ρ=0.59, p<0.001). In patients with ARDS, higher RALE scores were independently associated with lower PaO2/fractional inspired oxygen and worse survival. Conservative fluid management significantly decreased RALE score over 3 days compared with liberal fluid management.ConclusionsThe RALE score can be used to assess both the extent of pulmonary oedema and the severity of ARDS, by utilising information that is already obtained routinely, safely and inexpensively in every patient with ARDS. This novel non-invasive measure should be useful for assessing ARDS severity and monitoring response to therapy.

Diabetic retinopathy is a frequent complication in diabetes and a leading cause of visual impairment. Regular eye screening is imperative to detect sight-threatening stages of diabetic retinopathy such as proliferative diabetic retinopathy and diabetic macular oedema in order to treat these before irreversible visual loss occurs. Screening is cost-effective and has been implemented in various countries in Europe and elsewhere. Along with optimised diabetes care, this has substantially reduced the risk of visual loss. Nevertheless, the growing number of patients with diabetes poses an increasing burden on healthcare systems and automated solutions are needed to alleviate the task of screening and improve diagnostic accuracy. Deep learning by convolutional neural networks is an optimised branch of artificial intelligence that is particularly well suited to automated image analysis. Pivotal studies have demonstrated high sensitivity and specificity for classifying advanced stages of diabetic retinopathy and identifying diabetic macular oedema in optical coherence tomography scans. Based on this, different algorithms have obtained regulatory approval for clinical use and have recently been implemented to some extent in a few countries. Handheld mobile devices are another promising option for self-monitoring, but so far they have not demonstrated comparable image quality to that of fundus photography using non-portable retinal cameras, which is the gold standard for diabetic retinopathy screening. Such technology has the potential to be integrated in telemedicine-based screening programmes, enabling self-captured retinal images to be transferred virtually to reading centres for analysis and planning of further steps. While emerging technologies have shown a lot of promise, clinical implementation has been sparse. Legal obstacles and difficulties in software integration may partly explain this, but it may also indicate that existing algorithms may not necessarily integrate well with national screening initiatives, which often differ substantially between countries.

BackgroundCarbonic anhydrase inhibitors (CAIs) are frequently used as an initial step to treat retinitis pigmentosa-associated cystoid macular oedema (RP-CMO). Interestingly, it has been postulated that CAIs might reduce outer nuclear layer (ONL) fluid more effectively than inner nuclear layer (INL) fluid due to better access to retinal pigment epithelium basolateral membrane than neurosensory retina. This retrospective cohort study explores if an association between spatial distribution of cystoid spaces in RP-CMO and CAI response exists.MethodsTwo independent graders reviewed pretreatment and post-treatment optical coherence tomography (OCT) images of 25 patients (43 eyes) initiated on topical and/or oral CAIs between January 2013 and December 2014. Documentation included the presence/absence of fluid (and layer(s) involved), external limiting membrane, epiretinal membrane (ERM), vitreomacular adhesion/traction, lamellar/full-thickness macular hole and central macular thickness (CMT)/volume.ResultsINL fluid was found in all study eyes. All 13 ‘responders’ (at least 11% reduction of CMT after treatment) demonstrated pretreatment ONL fluid. In seven patients (four responders and three non-responders), complete clearance of ONL fluid was achieved despite persistence of INL fluid. ERM presence was similar in responders and non-responders.ConclusionIn this study, INL fluid was found to be the most common spatial distribution of RP-CMO. However, patients who were classed as a ‘responder’ to CAI treatment all demonstrated coexisting ONL fluid on their pretreatment OCT scans. This may be explained by CAIs having better access to retinal pigment epithelium basolateral membrane than neurosensory retina. Our study also suggests a minimal impact on response to CAIs by ERM.

AimsDuring diabetic macular oedema (DME), a spectrum of capillary abnormalities is commonly observed, ranging from microaneurysms to large microvascular abnormalities. Clinical evidence suggests that targeted photocoagulation of large microvascular abnormalities may be beneficial, but their detection is not done in a routine fashion. It was reported that they are better identified by indocyanine green angiography (ICGA) than by fluorescein angiography. Here, we investigated the prevalence and ICGA and optical coherence tomography (OCT) features of retinal microvascular abnormalities in a group of patients with DME.MethodsObservational study. The fundus photographs, ICGA and structural and angiographic OCT charts of 35 eyes from 25 consecutive patients with DME were reviewed.Results22 eyes (63%) had at least one focal area of microvascular abnormalities showing prolonged indocyanine green (ICG) staining (ie, beyond 10 mins after injection). In particular, all eyes (n=9) with circinate hard exudates showed foci of late ICG staining. These areas were either isolated globular capillary ecstasies or a cluster of ill-defined capillary abnormalities. They were located at a median distance of 2708 µm from the fovea (range: 1064–4583 µm). Their diameter ranged from 153 to 307 µm. During ICGA, 91% showed increased their contrast and apparent size in late frames, whereas 79% of microaneurysms showed reduced contrast on late frames. OCT angiography was not contributive for the detection of these lesions.ConclusionLate ICG staining revealing large microvascular abnormalities is commonly observed during DME. Because of their specific angiographic and OCT features relative to microaneurysms, we propose to name them telangiectatic capillaries (TelCaps).