A neglected organ in multiple organ failure – ‘skin in the game’? S. E. Pischke 1,2 , H. Haugaa 1 and M. Haney 3 1 Department of Anaesthesiology, Division of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway 2 Department of Immunology and K.G. Jebsen IRC, University of Oslo, Oslo, Norway 3 Anesthesiology and Intensive Care Medicine, Ume  a University and the University Hospital of Ume  a, Ume  a, Sweden Correspondence S. E. Pischke, Department of Anaesthesiology, Division of Emergencies and Critical Care, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, 0027 Oslo, P.b. 4950 Nydalen, 0424 Oslo, Norway E-mail: s.e.pischke@medisin.uio.no Conflict of interest The authors report no conflict of interest Funding None doi: 10.1111/aas.12823 In a recent issue of this journal, Drs. Koskela et al. investigated immunological changes in the skin in sepsis patients. 1 They obtained fluid from non-injured skin by applying vacuum and collected the fluid of the resulting blisters. This can remind one of the images from the recent summer Olympic games where a number of ath- letes had undergone the alternative medicine treatment of ‘cupping’. Although samples were collected in this study from healthy looking skin, index cytokines for sepsis severity were increased in septic patients in comparison to healthy controls. Interestingly, concentration of many cytokines was higher in skin blister fluid than in blood from sepsis patients. Sepsis is defined in the new sepsis guidelines as ‘life-threatening organ dysfunction caused by a dysregulated host response to infection’ and diagnosed by an increase of two points or more in the now renamed Sepsis-related Organ Failure Assessment (SOFA) score. 2 Thus, it is acknowl- edged that sepsis affects the whole organism and not only compartments. However, the SOFA score does not include the biggest organ in the body, which is the only organ that has always direct contact with the environment, the skin. Skin has a finely balanced homeostasis to ensure protection of the body and allow growth of protective commensal bacteria, which is each individual’s microbiome. 3 Thus, skin is a large and vulnerable organ. Extensive skin injury poses an immediate threat to the patient and a considerable challenge to the intensivist. It is widely recognized that there are high mortality rates associated with toxic epidermal necrolysis and extensive burn injury. At the same time, almost every intensive care patient shows sign of disturbed skin homeostasis, resulting in high-risk for pressure ulcers and prolonged wound healing. In the affected skin, the micro- biome is changed, that is, pathogenic bacteria like S. aureus dominate and increase the risk for systemic infections leading to sepsis and poor outcome. 3,4 Disturbed skin homeostasis during septic shock may result from ischaemia/reperfu- sion injury caused by dysfunction of the micro- circulation in addition to blood flow diversion from the periphery to central organs. 5 Ischae- mia/reperfusion injury is known to cause activa- tion of the innate immune system with subsequent cytokine production resulting in increased skin vulnerability. 6 Additionally, stressors like catecholamines, acetylcholine and glucocorticoids, all produced in vast amounts during sepsis, have been shown to affect the dermal microbiome, resulting in impaired Acta Anaesthesiologica Scandinavica 61 (2017) 5–7 ª 2016 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd 5 EDITORIAL