29 research outputs found

    Acute neurological deficit with submassive pulmonary emboli

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    Pulmonary embolism (PE) is frequently encountered in the emergency department. Syncope, often as a consequence of impending haemodynamic collapse, is associated with increased mortality. While loss of consciousness owing to cerebral hypoperfusion and reduced left ventricular preload is a common cause of collapse with large volume PE, other syndromes can also cause neurological deficit in thromboembolic disease. Here, we describe a case of a woman in her 60s, presenting to the emergency department with features of high-risk PE. During clinical examination, the patient collapsed and became unresponsive with a Glasgow Coma Scale of 4/15 despite normal haemodynamics. Neurological signs were noted and CT revealed evidence of a large territory cerebral infarction. Further cardiovascular investigations identified a grade 4 patent foramen ovale. We describe a challenging case of established venous thromboembolism complicated by paradoxical embolism, highlighting the importance of thorough clinical examination and investigation and discuss the current evidence base of treatments.</jats:p

    Improved oxygenation following methylprednisolone therapy and survival in paediatric acute respiratory distress syndrome.

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    BackgroundMethylprednisolone remains a commonly used ancillary therapy for paediatric acute respiratory distress syndrome (PARDS), despite a lack of level 1 evidence to justify its use. When planning prospective trials it is useful to define response to therapy and to identify if there is differential response in certain patients, i.e. existence of 'responders' and 'non responders' to therapy. This retrospective, observational study carried out in 2 tertiary referral paediatric intensive care units aims to characterize the change in Oxygen Saturation Index, following the administration of low dose methylprednisolone in a cohort of patients with PARDS, to identify what proportion of children treated demonstrated response, whether any particular characteristics predict response to therapy, and to determine if a positive response to corticosteroids is associated with reduced Paediatric Intensive Care Unit mortality.MethodsAll patients who received prolonged, low dose, IV methylprednisolone for the specific indication of PARDS over a 5-year period (2011-2016) who met the PALICC criteria for PARDS at the time of commencement of steroid were included (n = 78).OSI was calculated four times per day from admission until discharge from PICU (or death). Patients with ≥20% improvement in their mean daily OSI within 72 hours of commencement of methylprednisolone were classified as 'responders'. Primary outcome measure was survival to PICU discharge.ResultsMean OSI of the cohort increased until the day of steroid commencement then improved thereafter. 59% of patients demonstrated a response to steroids. Baseline characteristics were similar between responders and non-responders. Survival to PICU discharge was significantly higher in 'responders' (74% vs 41% OR 4.14(1.57-10.87) p = 0.004). On multivariable analysis using likely confounders, response to steroid was an independent predictor of survival to PICU discharge (p = 0.002). Non-responders died earlier after steroid administration than responders (p = 0.003).ConclusionsAn improvement in OSI was observed in 60% of patients following initiation of low dose methylprednisolone therapy in this cohort of patients with PARDS. Baseline characteristics fail to demonstrate a difference between responders and non-responders. A 20% improvement in OSI after commencement of methylprednisolone was independently predictive of survival, Prospective trials are needed to establish if there is a benefit from this therapy

    In Oxygen Saturation Index before and after steroid therapy in survivors and non- survivors.

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    Mean and 95% CI calculated using a multi-level linear regression model with OSI (log transformed) as the dependent variable, days post admission as the fixed effect variable, and patient identifier as the random effect variable.</p

    Kaplan-Meier plot of all-cause mortality in days after commencement of steroids and 95% confidence interval (shaded areas) by responder / non-responder to steroid status.

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    The analysis was adjusted for age, PIM-3 score, PELOD, admitting unit, prior steroid use, immune compromise, prematurity, direct/indirect PARDS phenotype (direct/indirect) and infection/non-infection as independent variables in a Cox proportional hazard model, and demonstrates that death occurred earlier in ‘non-responders to steroid therapy (p = 0.003).</p
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