Critical care : the official journal of the Critical Care Forum
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Pleural effusion (PLEFF), mostly caused by volume overload, congestive heart failure, and pleuropulmonary infection, is a common condition in critical care patients. Thoracic ultrasound (TUS) helps clinicians not only to visualize pleural effusion, but also to distinguish between the different types. Furthermore, TUS is essential during thoracentesis and chest tube drainage as it increases safety and decreases life-threatening complications. ⋯ Moreover, TUS can help diagnose co-existing lung diseases, often with a higher specificity and sensitivity than chest radiography and without the need for X-ray exposure. We review data regarding the diagnosis and management of pleural effusion, paying particular attention to the impact of ultrasound. Technical data concerning thoracentesis and chest tube drainage are also provided.
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An exaggerated, dysregulated host response to insults such as infection (i.e. sepsis), trauma and ischaemia-reperfusion injury can result in multiple organ dysfunction and death. While the focus of research in this area has largely centred on inflammation and immunity, a crucial missing link is the precise identification of mechanisms at the organ level that cause this physiological-biochemical failure. Any hypothesis must reconcile this functional organ failure with minimal signs of cell death, availability of oxygen, and (often) minimal early local inflammatory cell infiltrate. ⋯ Arguably, these processes may offer protection against a prolonged inflammatory hit by sparing the cell from initiation of death pathways, thereby explaining the lack of significant morphological change. A narrow line may exist between adaptation and maladaptation. This places a considerable challenge on any therapeutic modulation to provide benefit rather than harm.
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Circulatory shock is a common syndrome with a high mortality and limited therapeutic options. Despite its discovery and use in clinical and experimental settings more than a half-century ago, angiotensin II (Ang II) has only been recently evaluated as a vasopressor in distributive shock. We examined existing literature for associations between Ang II and the resolution of circulatory shock. ⋯ Intravenous Ang II is associated with increased BP in patients with cardiogenic, distributive, and unclassified shock. A role may exist for Ang II in restoring circulation in cardiac arrest.
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The acute respiratory distress (ARDS) lung is usually characterized by a high degree of inhomogeneity. Indeed, the same lung may show a wide spectrum of aeration alterations, ranging from completely gasless regions, up to hyperinflated areas. This inhomogeneity is normally caused by the presence of lung edema and/or anatomical variations, and is deeply influenced by the gravitational forces. ⋯ Although most of the literature on VILI concentrates on the possible dangers of tidal volume, mechanical ventilation in fact delivers mechanical power (i.e., energy per unit of time) to the lung parenchyma, which reacts to it according to its anatomical structure and pathophysiological status. The determinants of mechanical power are not only the tidal volume, but also respiratory rate, inspiratory flow, and positive end-expiratory pressure (PEEP). In the end, decreasing mechanical power, increasing lung homogeneity, and avoiding reaching the anatomical limits of the 'baby lung' should be the goals for safe ventilation in ARDS.
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Recent advances in technology and better understanding of mechanisms underlying disease are beginning to enable us to better characterize critically ill patients. Instead of using nonspecific syndromic groupings, such as sepsis or acute respiratory distress syndrome, we can now classify individual patients according to various specific characteristics, such as immune status. This "personalized" medicine approach will enable us to distinguish patients who have similar clinical presentations but different cellular and molecular responses that will influence their need for and responses (both negative and positive) to specific treatments. ⋯ We will also increasingly be able to conduct trials in groups of patients specifically selected as being most likely to respond to the intervention in question. This has already begun with, for example, some new interventions being tested only in patients with coagulopathy or immunosuppressive patterns. Ultimately, as we embrace this era of precision medicine, we may be able to offer precision therapies specifically designed to target the molecular set-up of an individual patient, as has begun to be done in cancer therapeutics.