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STATE OF THE ART SCHDELHINRTRAUMA
12.01.16 Thomas Brunner, Stv. Leiter Ansthesie/Intensivmedizin 1
STATE OF THE ART SCHWERES SCHDELHIRNTRAUMA Aktuelle Guidelines Evidenz zu aktuellen Therapieoptionen Praktische Aspekte
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SEVERE TRAUMATIC BRAIN INJURY MANAGEMENT AND CLINICALOUTCOME USING THE LUND CONCEPT
L.-O. D. KOSKINEN, a* M. OLIVECRONA a,b ANDP. O. GRANDE c
aDepartment of Pharmacology and Clinical Neuroscience,Neurosurgery, Umea University, SwedenbDepartment of Anaesthesia and Intensive Care, University ofOrebro, SwedencDepartment of Clinical Science in Lund, Anaesthesia andIntensive Care, Lund University, Sweden
AbstractThis review covers the main principles of theLund concept for treatment of severe traumatic brain injury.This is followed by a description of results of clinical studiesin which this therapy or a modified version of the therapyhas been used. Unlike other guidelines, which are basedon meta-analytical approaches, important components ofthe Lund concept are based on physiological mechanismsfor regulation of brain volume and brain perfusion and toreduce transcapillary plasma leakage and the need forplasma volume expanders. There have been nine non-randomized and two randomized outcome studies withthe Lund concept or modified versions of the concept. Thenon-randomized studies indicated that the Lund concept isbeneficial for outcome. The two randomized studies weresmall but showed better outcome in the groups of patientstreated according to the modified principles of the Lundconcept than in the groups given a more conventional treat-ment.This article is part of a Special Issue entitled: Brain com-
pensation. For good?. ! 2014 IBRO. Published by ElsevierLtd. All rights reserved.
Key words: severe traumatic brain injury, Lund concept,management, outcome.
ContentsIntroduction 245Measurement of ICP and CPP 246Treatment of sTBI 247Treatment of ICP 247Blood volume expanders 247
Principles of transcapillary exchange in tissues outside thebrain 248Blood transfusion 249Treatment to improve perfusion 249Osmotherapy 250Lung function 250Anti-stress therapy 251Temperature 251Nutrition 251Drainage of CSF and decompressive surgery 251
Clinical outcome studies 251The Lund concept 251Modified Lund concept 251The Lund concept and meningitis 252
Discussion 252Summary 253References 253
Originally, the Lund concept (LC) for treatment of severetraumatic brain injury (sTBI) was a theoretical approachmainly based on the physiological andpathophysiological principles of brain volume and brainperfusion regulation (Asgeirsson et al., 1994; Grandeet al., 1997; Grande, 2006). The concept aimed at coun-teracting an increase in intracranial pressure (ICP) or toreduce an already raised ICP after sTBI, while improvingcompromised perfusion in and around the contusionareas at the same time. It can be described as an ICP-and perfusion-guided approach. The main componentsof the LC have found support in experimental and clinicalstudies, as described later in this review.
So far, no TBI guidelines have been tested in a largerandomized clinical trial and from that point of view thereis limited high-level clinical evidence for all TBI guidelinespresented today (Muzevic and Splavski, 2013). A specifictherapy therefore must be based on other types of inputsuch as smaller clinical outcome studies including meta-analysis, experimental studies and basal physiologicalprinciples.
Even though different guidelines differ in essentialaspects, the Brain Trauma Foundations guidelines havemoved closer to the LC during the past 10 years, e.g.concerning cerebral perfusion pressure (CPP) and theuse of vasopressors (Bullock et al., 1996, 2000; BrainTrauma Foundation, 2007). In contrast to Brain Trauma
http://dx.doi.org/10.1016/j.neuroscience.2014.06.0390306-4522/! 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
*Corresponding author. Tel: +46-706259701.E-mail address: Lars-Owe.Koskinen@neuro.umu.se (L.-O. D.Koskinen).Abbreviations: ARDS, acute respiratory distress syndrome; CPP,cerebral perfusion pressure; Hb, hemoglobin; ICP, intracranialpressure; LC, Lund concept; MAP, mean arterial pressure; PEEP,positive endexpiratory pressure; sTBI, severe traumatic brain injury;SAH, subarachnoid hemorrhage; TER, transcapillary exchange rate.
Neuroscience 283 (2014) 245255
L.-O. D. Koskinen et al. / Neuroscience 283 (2014) 245255
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L.-O. D. Koskinen et al. / Neuroscience 283 (2014) 245255
Foundation guidelinesin which the ICP-reducing ther-apy should start when ICP is above 20 mmHg (BrainTrauma Foundation, 2007)the LC recommends thatthe therapy should start as early as possible after arrivalat the hospital, in an attempt to counteract the develop-ment of brain edema and to ensure that there is early opti-mization of the perfusion. To our knowledge, no clear sideeffects have appeared with the LC, which means that itcan be given early and to all patients independent ofseverity of the injury and independent of the degree ofautoregulation. The LC has not changed since its intro-duction, except that dihydroergotamin is no longer used.Dihydroergotamin, which reduces ICP via cerebralvenous constriction, was used in the initial version of theconcept in patients with uncontrolled increase in ICP(Asgeirsson et al., 1994). It was withdrawn because ofpossible side effects related to peripheral vasoconstrictionin high doses. For details of the LC guidelines, see;Asgeirsson et al. (1994), Grande (2006, 2011) and
Olivecrona et al. (2007, 2009a,b). A simplified schematicalgorithm of the LC used in the clinical setting is shown inFig. 1.
MEASUREMENT OF ICP AND CPP
Like in other guidelines, monitoring of ICP is an essentialpart of the LC, and the monitoring should be started assoon as possible after the arrival at the hospital. Themethod of ICP monitoring can either be by externalventricular drainage or by an intraparenchymal device. Itis also crucial to monitor the arterial pressure and themean arterial pressure (MAP).
The reference points for MAP and ICP must beidentical when calculating CPP. For example, a headelevation of 15 degrees with the zero-reference point forthe ICP at the external meatus and the zero-referencepoint for the MAP at the heart level gives a difference ofaround 10 mmHg compared to treatment of the patient
Fig. 1. A simplified schematic algorithm of the LC used in the clinical setting. For doses of the pharmacological substances used and otherparameters, see Grande (2006).
246 L.-O. D. Koskinen et al. / Neuroscience 283 (2014) 245255
BLS, BICS, MMM Oxygenation/Ventilation, Kreislaufsupport, Gerinnung,
Thromboseprophylaxe, Ernhrung, Monitoring, ... Sedation Entfernung von Raumforderungen, Liquordrainage Osmotherapie Hypothermie Kraniektomie
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T h e n e w e ngl a nd j o u r na l o f m e dic i n e
n engl j med 370;22 nejm.org may 29, 2014 2121
Critical Care MedicineSimon R. Finfer, M.D., and Jean-Louis Vincent, M.D., Ph.D., Editors
Traumatic Intracranial HypertensionNino Stocchetti, M.D., and Andrew I.R. Maas, M.D., Ph.D.
From the Department of Pathophysiology and Transplantation, Milan University, and Fondazione Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) C GrandaOspedale Maggiore Policlinico both in Milan (N.S.); and the Department of Neu-rosurgery, Antwerp University HospitalUniversity of Antwerp, Edegem, Belgium (A.I.R.M.). Address reprint requests to Dr. Stocchetti at Fondazione IRCCS C GrandaOspedale Maggiore Policlinico, Via F. Sforza 35, 20122 Milan, Italy, or at email@example.com; or to Dr. Maas at the Department of Neurosurgery, Antwerp University HospitalUniversity of Antwerp, Wilrijkstraat 10, 2650 Edegem, Belgium, or at firstname.lastname@example.org.
N Engl J Med 2014;370:2121-30.DOI: 10.1056/NEJMra1208708Copyright 2014 Massachusetts Medical Society.
A n elevation in intracranial pressure can be a medical or surgical emergency. There are many possible conditions that can lead to elevated intracranial pressure on either an acute or a chronic basis (Table 1). In this article, we focus on the increased intracranial pressure that occurs in pa-tients after traumatic brain injury, since this is an area in which there are both physiological and clinical data.
Traumatic brain injury is a medical and social problem worldwide, with an estimated 10 million cases leading to hospitalization or death each year.1 In low- and medium-income countries, in which the use of motor-powered transportation is increasing, the incidence of this condition is rising2 and involves predominantly young men. In contrast, in richer countries, the epidemiology of traumatic brain in-jury is changing because of two main factors: the rate of traffic incidents is decreas-ing owing to successful enforcement of safety laws and preventive measures, whereas the aging of the population makes such injury in the elderly more frequent.2-4
Falls are a frequent cause of injury in older patients, often resulting in contusive brain injury. Elderly patients often have multiple coexisting illnesses and are fre-quently taking a number of medications, including anticoagulants and platelet aggregation inhibitors.4 These medications may contribute to the development of hematomas and hemorrhagic expansion of contu