Critical Evaluation of the Lund Concept for Treatment of Severe Traumatic Head Injury, 25 Years after Its Introduction

Abstract

When introduced in 1992, the Lund concept (LC) was the first complete guideline for treatment of severe traumatic brain injury (s-TBI). It was a theoretical approach, based mainly on general physiological principles—i.e., of brain volume control and optimization of brain perfusion and oxygenation of the penumbra zone. The concept gave relatively strict outlines for cerebral perfusion pressure, fluid therapy, ventilation, sedation, nutrition, the use of vasopressors, and osmotherapy. The LC strives for treatment of the pathophysiological mechanisms behind symptoms rather than just treating the symptoms. The treatment is standardized, with less need for individualization. Alternative guidelines published a few years later (e.g., the Brain Trauma Foundation guidelines and European guidelines) were mainly based on meta-analytic approaches from clinical outcome studies and to some extent from systematic reviews. When introduced, they differed extensively from the LC. We still lack any large randomized outcome study comparing the whole concept of BTF guidelines with other guidelines including the LC. From that point of view, there is limited clinical evidence favoring any of the s-TBI guidelines used today. In principle, the LC has not been changed since its introduction. Some components of the alternative guidelines have approached those in the LC. In this review, I discuss some important principles of brain hemodynamics that have been lodestars during formulation of the LC. Aspects of ventilation, nutrition, and temperature control are also discussed. I critically evaluate the most important components of the LC 25 years after its introduction, based on hemodynamic principles and on the results of own an others experimental and human studies that have been published since then.

Intracranial pressure elevation alters CSF clearance pathways

“…However, fluid exchange across this barrier is still a combination of hydrostatic and osmotic forces [21,23] which are taken into account to estimate the effective capillary pressure ( p cap ) used in our model. where the hydrostatic capillary pressure p cap,h = 35 mmHg [73], the reflection coefficient σ = 1 [74], the oncotic blood pressure π cap = 25 mmHg [74], and the oncotic tissue pressure π PVS is set to 40% of π cap (10 mmHg) [74], resulting in p cap = 20 mmHg . Note that the contribution from the electrolytes to the osmotic pressure, both on the vascular and interstitial side, is not included and thus assumed to be equal and constant.…”

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

“…Therefore, the management of TBI focuses on the control of intracranial pressure (ICP) and maintenance of adequate cerebral perfusion, oxygenation, and metabolism attempting to limit secondary injury progression [26][27][28]. Mortality rates have decreased in the last decades, largely due to improvements in trauma systems and supportive critical care [29]. Yet, case fatality rates in severe TBI have not decreased significantly since 1990 [30], remaining with an outstanding mortality, because up to 50% of the patients will still die and nearly all survivors will present some degree of sequelae [3,4,6,[31][32][33].…”

Vasopressor Therapy and the Brain: Dark Side of the Moon

“…Brain injury leading to elevated ICP will reduce CPP if blood pressure remains identical. During severe brain injuries, vasopressors will maintain MAP but may also induce extreme vasoconstriction in the injured zones of the brain, lowering blood flow in these regions, thereby potentially worsening cerebral injuries (108). Optimal blood pressure strikes a delicate balance between transcapillary hydrostatic and oncotic forces and acceptable cerebral perfusion pressure (108).…”

“…During severe brain injuries, vasopressors will maintain MAP but may also induce extreme vasoconstriction in the injured zones of the brain, lowering blood flow in these regions, thereby potentially worsening cerebral injuries (108). Optimal blood pressure strikes a delicate balance between transcapillary hydrostatic and oncotic forces and acceptable cerebral perfusion pressure (108). Only one study in sepsis assessed ICP without finding any evidence of intracranial hypertension (109).…”