title: Lund concept for the management of traumatic brain injury: a physiological principle awaiting stronger evidence.
abstract: The "Lund concept" involving a "volume-targeted" strategy for intracranial pressure control originated in the University of Lund, Sweden, more than 20 years ago and has remained controversial ever since. 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. Although improved outcomes compared with historical controls and other institutions have been reported with treatment strategies based on the Lund concept by a few nonrandomized studies from various Swedish neurological centers, the protocol has never been subjected to a randomized trial and has not been evaluated outside Sweden. It deemphasizes the effect of secondary cerebral ischemia and contradicts the common treatment goal of cerebral blood flow optimization by augmentation of cerebral perfusion pressure. In fact, good evidence exists against the use of many individual components of the Lund therapy in traumatic brain injury. In the absence of strong evidence to support it, the Lund concept is unlikely to gain acceptance elsewhere.
authors: Departments of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA.
authors: Deepak
authors: D
authors: Sharma
authors: Monica S
authors: MS
authors: Vavilala
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists / Q000627:therapeutic use; D058671:Adrenergic beta-1 Receptor Antagonists / Q000627:therapeutic use; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D001812:Blood-Brain Barrier / Q000502:physiology; D001930:Brain Injuries / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy*; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D005334:Fever / Q000150:complications / Q000188:drug therapy; D006706:Homeostasis; D006801:Humans; D007427:Intracranial Pressure / Q000187:drug effects / Q000502:physiology*; D008991:Monitoring, Physiologic; D009997:Osmotic Pressure; D013256:Steroids / Q000627:therapeutic use; D013548:Sweden
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D058671:Adrenergic beta-1 Receptor Antagonists; D047228:Angiotensin II Type 1 Receptor Blockers; D013256:Steroids