=====Lund Concept===== Lund concept are based on physiological mechanisms for regulation of brain volume and brain perfusion and to reduce transcapillary plasma leakage and the need for plasma volume expanders, involving a "volume-targeted" strategy for [[intracranial pressure]] control. It is based on the premise that the [[blood brain barrier]] is disrupted after [[traumatic brain injury]] and [[cerebral autoregulation]] is impaired; hence, the transcapillary water exchange is determined by the differences in hydrostatic and colloid osmotic pressure between the intracapillary and extracapillary compartments. The Lund concept argues that the only way of inducing transcapillary reabsorption of interstitial fluid is to control the transcapillary osmotic and hydrostatic differences and utilizes a complex combination pharmacotherapy involving β1-antagonist metoprolol, α2-agonist clonidine, low-dose thiopental, dihydroergotamine, and maintenance of colloid osmotic pressure by red blood cell transfusion and albumin administration ((Sharma D, Vavilala MS. Lund concept for the management of traumatic brain injury: a physiological principle awaiting stronger evidence. J Neurosurg Anesthesiol. 2011 Oct;23(4):363-7. doi: 10.1097/01.ana.0000405613.27980.ea. Review. PubMed PMID: 21908990.)). Originated in the University of Lund, Sweden, more than 20 years ago the concept has remained controversial ever since. The [[Lund concept]], directed at bedside real-time monitoring of brain biochemistry by CM showed better results compared to the [[Rosner concept]] CPP-targeted therapy in the treatment of comatose patients sustaining SBI after aneurysmal SAH and severe TBI ((Dizdarevic K, Hamdan A, Omerhodzic I, Kominlija-Smajic E. Modified Lund concept versus cerebral perfusion pressure-targeted therapy: a randomised controlled study in patients with secondary brain ischaemia. Clin Neurol Neurosurg. 2012 Feb;114(2):142-8. doi: 10.1016/j.clineuro.2011.10.005. Epub 2011 Oct 28. PubMed PMID: 22036839. )) ((Liu CW, Zheng YK, Lu J, Yu WH, Wang B, Hu W, Zhu KY, Zhu Y, Hu WH, Wang JR, Ma JP. [Application of Lund concept in treating brain edema after severe head injury]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Oct;22(10):610-3. Chinese. PubMed PMID: 20977845.)). There have been nine non-randomized and two randomized outcome studies with the Lund concept or modified versions of the concept. The non-randomized studies indicated that the Lund concept is beneficial for outcome. The two randomized studies were small but showed better outcome in the groups of patients treated according to the modified principles of the Lund concept than in the groups given a more conventional treatment ((Koskinen LO, Olivecrona M, Grände PO. Severe traumatic brain injury management and clinical outcome using the Lund concept. Neuroscience. 2014 Dec 26;283C:245-255. doi: 10.1016/j.neuroscience.2014.06.039. Epub 2014 Jun 25. Review. PubMed PMID: 24973658. )). ====Goals==== The therapy has two main goals: (1) to reduce or prevent an increase in ICP (ICP-targeted goal) (2) to improve perfusion and oxygenation around contusions (perfusion-targeted goal). The Lund therapy considers the consequences of a disrupted blood-brain barrier for development of brain oedema and the specific consequences of a rigid dura/cranium for general cerebral haemodynamics. It calls attention to the importance of improving perfusion and oxygenation of the injured areas of the brain. This is achieved by normal blood oxygenation, by maintaining normovolaemia with normal haematocrit and plasma protein concentrations, and by antagonizing vasoconstriction through reduction of catecholamine concentration in plasma and sympathetic discharge (minimizing stress and by refraining from vasoconstrictors and active cooling). The therapeutic measures mean normalization of all essential haemodynamic parameters (blood pressure, plasma oncotic pressure, plasma and erythrocyte volumes, PaO(2), PaCO(2)) the use of enteral nutrition, and avoidance of over nutrition ((Grände PO. The "Lund Concept" for the treatment of severe head trauma--physiological principles and clinical application. Intensive Care Med. 2006 Oct;32(10):1475-84. Epub 2006 Aug 2. Review. Erratum in: Intensive Care Med. 2007 Jan;33(1):205. PubMed PMID: 16896859. )). ====Management==== Prevention of brain edema formation to reduce fluid shift from capillaries into brain parenchyma, by preserving capillary colloid osmotic pressure and reducing capillary hydrostatic pressure The improvement of the cerebral microcirculation by the avoidance of arterial vasoconstrictors Preserve osmotic pressure albumin (considered a contra-indication by some based on SAFE trial subgroup analysis) blood products diuretics Reduce hydrostatic pressure metoprolol clonidine thiopentone dihydroergotamine (precapillary vasoconstriction) CPP target if ICP normal aim for 60-70mmHg however, if ICP elevated a CPP of 50mmHg is accepted Vasoactive use avoid dobutamine (cerebral vasodilatation) avoid noradrenaline (cerebral vasoconstriction)