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Snell et al. Critical Care 2013, 17:241 http://ccforum.com/content/17/5/REVIEWClinical review: The critical care management of the burn patientJane A Snell1, Ne-Hooi W Loh*2, Tushar Mahambrey3 and Kayvan ShokrollahiAbstract Between 4 and 22 of burn patients presenting to the emergency department are admitted to critical care. Burn injury is characterised by a hypermetabolic response with physiologic, catabolic and immune effects. Burn care has seen renewed interest in colloid resuscitation, a PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/12027669 change in transfusion practice and the development of anti-catabolic therapies. A literature search was conducted with priority given to PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17184506 review articles, meta-analyses and well-designed large trials; paediatric studies were included where adult studies were lacking with the aim to review the advances in adult intensive care burn management and place them in the general context of day-to-day practical burn management.leukotrienes, vasoactive amines, platelet activation products and complement allows protein loss into the interstitium. The intravascular (E)-1,2-Di(pyridin-4-yl)ethene colloid osmotic pressure falls and fluid escapes the vascular system. The result is a loss of intravascular fluid, electrolytes and proteins with rapid equilibration with the interstitial compartments. Clinically, this is manifested by hypovolaemia, haemoconcentration, oedema, 2-diamine Methyl 2-(piperidin-4-yl)acetate hydrochloride 7-Nitro-2H-benzo[b][1 reduced urine output and cardiovascular dysfunction. Adequate resuscitation from burn shock is a critical therapeutic intervention in burn management.Introduction Burns are common, with the potential for considerable morbidity and mortality. Almost 29,000 patients were admitted to UK burn services between 2003 and 2007 [1]. Between 4 and 22 were admitted to intensive care from presentation [2] and successful management requires a team approach. Pathophysiology of burn shock Burn injury results in cardiogenic, hypovolaemic and distributive shock. The intravascular volume becomes depleted primarily due to increased capillary permeability and fluid shifts. Above 30 total body surface area (TBSA), only partial compensation can be achieved by fluid resuscitation due Phenyl (4-chloro-3-fluorophenyl)carbamate to a generalised reduction in sodium ATPase activity and disruption of the cellular transmembrane ionic gradient that persists for several days. Microvascular injury secondary to inflammatory mediators such as histamine, bradykinin, prostaglandins,*Correspondence: Will.Loh@gmail.com 2 Department of Neuroanaesthesia and Critical Care, Horsley ICU, The Walton Centre for Neurology and Neurosurgery, Liverpool L9 7LJ, UK Full list of author information is available at the end of the article?2010 BioMed Central Ltd?2013 BioMed Central LtdFluid resuscitation Appropriate fluid management is the foundation of acute burns management. Without early and effective treatment, burns involving greater than 15 to 20 TBSA will result in hypovolaemic shock [3]. Mortality is increased if resuscitation is delayed longer than 2 hours post burn injury [4]. The aim is to prevent the development of burn shock and to minimise disruption to physiologic parameters in the face of ongoing cellular and hormonal responses. Several formulae have been developed to optimise fluid delivery whilst pre.

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