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The Lund Concept


The Lund Concept Does ICP really matter . (or rather who cares about ICP anyway) Our current protocol Maintain cerebral perfusion pressure (CPP) 60 mmHg using ... – PowerPoint PPT presentation

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Title: The Lund Concept

The Lund Concept
  • Does ICP really matter .
  • (or rather who cares about ICP anyway)

(No Transcript)
  • The Lund concept for the treatment of severe head
    injury was introduced in 1990 to 1991 at the
    University Hospital of Lund, Sweden.
  • Conventional guidelines are based on
    meta-analytic surveys from clinical studies
  • maintenance of a relatively high CPP (the
    CPP-guided approach)
  • Lund therapy is a theoretical physiological
  • physiological and pathophysiological hemodynamic
    principles of brain volume and brain perfusion
  • Tx of ICP and maintenance of cerebral perfusion
  • (the ICP and perfusion-guided approach).

The Lund Concept
  • relatively strict recommendations regarding
  • fluid therapy,
  • optimal hemoglobin concentration,
  • lung protection and
  • temperature control, and
  • risks and values of
  • cerebrospinal fluid (CSF) drainage
  • decompressive craniotomy
  • Lund therapy has also been used for the treatment
    of brain oedema in meningitis.

Monro-Kellie doctrine
  • The pressure-volume relationship between ICP,
    volume of CSF, blood, and brain tissue, and
    cerebral perfusion pressure (CPP) is known as the
    Monro-Kellie doctrine or the Monro-Kellie
  • cranial compartment is incompressible volume
    inside the cranium is a fixed volume
  • Blood, CSF, and brain in equilibrium
  • Principal buffers for increased volumes include
    both CSF and, to a lesser extent, blood volume.
  • Compensatory mechanisms- maintains normal ICP for
    volume change lt 100120 mL
  • v.intracranial (constant) v.brain v.CSF
    v.blood v.mass lesion
  • Brain tissue (85), cranial CSF (10), cerebral
    blood (5),
  • spinal CSF is about 75ml - cranial CSF volume

Why do we have CSF?
  • Functions of CSF
  • mechanical
  • maintenance of a constant ionic environment - Ca,
    K, Mg and HCO3 (active) and H and Cl by secondary
  • waste removal
  • acid/base regulation via CO2
  • nutritional and intracerebral transport

Hows it made
  • CSF formation 500ml/day
  • CSF total volume 120ml
  • 70 from choroid plexus
  • (blood vessels projecting into ventricles)
  • - has tight junctions which means ultrafiltration
    (hydrostatic pressure) and secretion are
  • CSF hydrostatic pressure is 5-15mmHg
  • Cilia help move CSF
  • to the 4th ventricle and the foramina Lushka and
  • into the cisterna Magna then
  • into subarachnoid space around cerebella,
  • then further up to basilar cisterns
  • Lateral/frontal cerebral cortex.

  • Reabsorbed via
  • 1. arachnoid villi in sagittal and sigmoid
    sinuses, 90, and
  • 2. spinal arachnoid villi in dural sinusoids on
    dorsal root nerves, 10 
  • reabsorption is via pinocytosis and opening of
    intercellular spaces.
  • rate of reabsorption increases with CSF pressure.
  • resistance to reabsorption is normal until CSF gt
    22mmHg and then it decreases.

The balance
  • CSF formation and reabsorption is in equilibrium.
  • BUT if ICP increases so much that CPP is lt70mmHg
    then CSF formation decreases.
  • If ICPlt7mmHg then minimal reabsorption occurs
  • CSF reabsorption is linear from 7-70mmHg

  • In supine, healthy adults, normal ICP is between
    7 and 15 mmHg.
  • Term - normal ICP 1.5-6 mmHg
  • Young children 3-7 mmHg
  • Adults
  • observational studies ICP 20-25 mmHg -gt much
    poorer outcome from TBI
  • The evidence is even more limited in children,
    but generally
  • Infants lt15 mmHg
  • Younger children lt18 mmHg
  • Older children lt20 mmHg.

Some physiology.
  • Cerebral function is totally dependent on
    oxidative phosphorylation
  • glucose -gt ATP.
  • Brain is 2 of body weight, but uses 20 of
    body's resting oxygen consumption.
  • CBF varies with metabolic rates of the areas of
    the brain.
  • CBF and cerebral metabolism are thought to be
  • Local metabolic factors re coupling are
  • H,
  • K,
  • adenosine,
  • phopholipid metabolites,
  • glycolytic metabolites and
  • nitric oxide.
  • CBF 750ml/min

Whats autoregulation
  • Autoregulation - phenomenon where CBF is kept
    constant over a MAP of 50-150mmHg.
  • gt150mmHg, then CBF passively increases with CPP
    and arterial pressure.
  • CBF increases linerarly by 2-4 for every mmHg
    increase in PaCO2 (between PaCO2 of 20-80mmHg).
  • CO2 diffuses rapidly across BBB, increases H in
    ECF and causes vasodilation.
  • BUT arteriolar tone modifies this effect and
    hence hypotension can abolish ability of cerebral
    circulation to respond to PaCO2 changes.
  • PaO2 - if lt50mmHg then CBF will start to rise and
    doubles by time PaO2 is 30mmHg.
  • Cerebral metabolic rate decreases by 7 for each
    1 degree celsius in body temperature.

More physiology
  • Cerebrovasculature - well innervated by
    serotonergic, adrenergic, cholinergic nerves.
  • Sympathetic activity can cause marked
    constriction of cerebral arteries - ie. in heavy
    exercise can stop high pressure from reaching
    small blood vessels and hence prevent
  • Hypercarbia - get vasodilation.
  • Cerebral steal when decreased blood flow in
    ischaemic area of brain result in hypercarbic
    induced vasodilation in non-ischaemic areas.
  • Conversely,  VC in normal areas of brain from
    hypocarbia can redistribute blood to ischaemic
    areas - i.e. Robin Hood or inverse steal

Last bit of physiology
  • Starling's equation
  • the movement of fluid depends on six variables
  • Capillary hydrostatic pressure ( Pc )
  • Interstitial hydrostatic pressure ( Pi )
  • Capillary oncotic pressure ( pc )
  • Interstitial oncotic pressure ( pi )
  • Filtration coefficient ( Kf )
  • Reflection coefficient ( s )

(No Transcript)
Evidence. Or lack of
  • Recent Chinese study
  • 68 patients, GCS 3-8, severe HI
  • 30 had The Lund Concept.
  • Looked at 28 day mortality
  • Roughly 30 vs 60 (plt0.01)

Evidence or lack of
  • Newcastle Uni UK, 2011 Critical care
  • MA Hamdan1, K Dizdarevic2, 1Newcastle University,
    Newcastle upon Tyne, UK 2Clinical Centre
    University of Sarajevo, Sarajevo, Bosnia and
    Herzegovina, Critical Care 2011, 15(Suppl 1)P342
    (doi 10.1186/cc9762)
  • 60 patients positive, p0.03

  • BBB disrupted after traumatic brain injury
  • 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
  • Induce transcapillary reabsorption of
    interstitial fluid by controlling transcapillary
    osmotic and hydrostatic differences
  • combination pharmacotherapy
  • b1-antagonist metoprolol
  • a2-agonist clonidine
  • low-dose thiopental
  • dihydroergotamine
  • maintenance of colloid osmotic pressure by PRBC
    and albumin

  • Alternatively,
  • RICP -gtreduction of CPP and CBF
  • If persistent may worsen the primary brain injury
    and cause cerebral ischemia
  • Much variability in the practice of Tx of RICP
    and targets for ICP and CPP
  • Methods
  • focus on CPP and CBF Mx as the primary target
  • CPP targeted therapy
  • Uses medications to increase CPP and CBF via
    increasing MAP
  • Alternatively reduce ICP as the primary target
  • ICP-targeted therapy to improve cerebral
  • Lund Concept a specific subcategory of ICP
    control involving a volume targeted strategy

  • ? high CPP -gt improves oxygenation of injured
  • squeezing blood through the swollen brain
  • reduces intracranial blood volume through an
    autoregulatory vasoconstrictor response.
  • improved oxygenation maybe transient in injured
  • capillaries passively permeable to small solutes
  • high perfusion pressure will induce
    transcapillary filtration and exacerbate edema
  • and the autoregulatory response is weak after a
    brain injury.

  • A passive venous collapse (resistance) is
    developed just inside the dura
  • protects brain from change in PV (i.e, head
    elevation or by PEEP)
  • ? ICP from filtration (disrupted BBB) because of
    ? Pc and ? Ponc
  • This ? -gt partly transferred to capillaries with
    ? Pc and further filtration, etc
  • -gt new steady state
  • Hence ICP ? gtgt initial increase in Pc or decrease
    in Ponc that started the filtration.
  • filtration -gt ?? ICP than increase in Pc or
    decrease in Ponc, triggering the filtration.
  • Hence, ? ICP gtgt ? Pc and ?Ponc -gt triggers ? ICP

Passise venous resistance vessel
  • Note
  • slow process taking several hours
  • Vasoconstrictors
  • ? BP but also SEs like
  • ARDS and
  • ? leakage of plasma -gt hypovolemia and general
    tissue oedema
  • inotropes like dobutamine cause cerebral
  • (Lund patients dont get these problems as

The Lund concept ICP
  • Accept a lower CPP than the initial recommended
    70mm Hg -gt avoids vasopressors.
  • Antihypertensive treatment
  • b-1 blockade, a-2 agonists, and ARBs to
    counteract oedema
  • Fluid therapy given in the Lund concept -gt CPP
    will stay acceptable
  • Normalization of reduced Ponc may counteract
    filtration in brain
  • Hence higher CPP can be accepted without inducing
    transcapillary filtration
  • i.e. albumin as the main plasma volume expander.
  • Dihydroergotamine to reduce venous intracranial
    blood volume at significantly RICP
  • (no longer used due to decompressive craniotomy
    being more effective)

Blood volume expanders
  • A ? blood volume -gt ? too low for adequate
    cerebral perfusion, especially in penumbra zone
  • Emphasis on avoiding hypovolemia-induced
    activation of the baroreceptor reflex
  • Conventional guidelines have risk from concealed
  • Crystalloids not used b/c general tissue oedema
    (injured brain with a disrupted BBB)
  • Albumin (? 20 solution) due to its more
    effective absorbing effect
  • beneficial to ? interstitial volume for both
    injured brain and rest of the body.
  • Slow infusion rate of colloid results for longer
  • Hence
  • relatively low arterial pressures,
  • avoidance of vasopressors,
  • maintenance of relatively normal Hb (transfuse
    upto Hb 120 for oxygenation/blood volume)
  • physiotherapy to stimulate the lymphatic drainage

To improve perfusion
  • Perfusion depends on pressure resistance.
  • Brain a relatively low CPP can be compensated by
    an optimal fluid therapy.
  • Confirmed by a microdialysis study on TBI pts
    treated by Lund concept
  • This study showed improved oxygenation, greater
    blood flow, and less tissue degradation, despite
    reduced arterial pressure with antihypertensive
    therapy, by measurement of the interstitial
    lactate/puruvate ratio, glycerol, glucose, and
    glutamate in the penumbra zone.
  • The results can be explained by avoidance of
    noradrenalin-induced vasoconstriction and plasma
    leakage and by avoidance of low hemoglobin
  • These data support the view that adequate blood
    volume is more important for oxygenation of the
    penumbra zone than high CPP.
  • CPP stays in the range of 60 to 70mm Hg in most
    adult patients treated with the Lund therapy
  • Can accept a minimum CPP of 50mmHg if otherwise
    optimal fluid therapy
  • CPP values down to 38-40mm Hg are accepted in
    small children.

  • Not used
  • lack of scientific and physiological support
  • documented side effects.
  • ICP-reducing effect is transient
  • mannitol and urea often has rebound increase in
    ICP some hours after the infusion aggravating the
    brain edema.
  • Mannitol may also be associated with renal
    insufficiency and severe electrolyte
  • Exception
  • Osmotherapy, especially HTS maybe for acute
    control (ED/ambulance)

Lung function
  • The Lund concept includes some specific
    lung-protective measures
  • Vasoconstrictors and high-dose barbiturate
    therapy are associated with pulmonary
    complications in terms of ARDS, pneumonia, and
    high fever - better
  • Positive end expiratory pressure (PEEP) is used
  • reduce atelectasis
  • controversial in head-injured patients due to the
    potential risk of increasing ICP by an increase
    in venous pressure.
  • Experimentally shown that brain in rigid shell-
    variable passive venous outflow resistance,
    provided that the tissue pressure is above the
    venous pressure outside the shell
  • hence moderate PEEP (5 to 8 cm H2O) is safe.
  • Inhalations and moderate bagging (under ICP
    control) are other lung protecting measures
    recommended in the Lund therapy.
  • Avoid crystalloids - plasma volume expanders may
    ? risk of lung oedema.
  • Severe ARDS is very rare in patients with an
    isolated head injury who are treated according to
    the Lund concept.
  • Hyperventilation is not used due to aggravation
    of hypoxia in the penumbra zone

Anti stress therapy
  • Barbituates decrease ICP by decreasing cerebral
    metabolism, CMRO2 and hence CBF and CBV
  • Wake-up tests are not used due to stress effects
    (results in ?ICP) and release of catecholamines
    (may reduce brain perfusion)
  • Heavy sedation
  • midazolam and analgetics in combination with
  • sometimes short-term treatment with a low dose of
  • Sedatives continued until ICP stabilized at a
    normal level and until weaning from the
    ventilator will be successful.
  • A beneficial effect of this sedation regime is
    the lack of epileptic seizures, which means that
    there is no indication of prophylactic
    anticonvulsary treatment.

  • Fever stimulates cerebral metabolism and induces
  • Active cooling not used
  • potential side effects inherent in the
    significant stress and catecholamine release
  • risk of reducing cerebral circulation of the
    penumbra zone.
  • The Lund therapy involves treatment of high fever
  • Steroids (methylprednisolone)
  • Controversial due to SEs (adrenal suppression,
    effects on catecholamine synthesis, decrease NO
  • CRASH trial showed adverse outcome with high dose

Drainage of CSF/decompressive craniotomy
  • Drainage of CSF ? transcapillary pressure in the
    brain due to ? tissue pressure inducing
  • Loss of CSF volume -gtreplaced by more oedema with
    risk of ventricular collapse.
  • The risk can be reduced if the drainage is
    performed from a relatively high pressure level
    and if ventricular volumes are evaluated by
    computed tomography controls.
  • Under such circumstances, CSF drainage is
    accepted in the Lund concept to control a raised
    ICP (only through ventricular drainage),
    especially if there are signs of hydrocephalus.
  • Decompressive surgery in terms of craniotomy and
    evacuation of hematomas and available contusions
    are options in the Lund therapy.
  • lack of studies -gt decompressive craniotomy is
  • SE of craniotomy is strangulation in the cranial
    opening due to herniation.
  • As the protuberance at least partly can be
    explained by transcapillary filtration due to
    loss of counter pressure in the cranial opening,
    antihypertensive treatment, and a relatively low
    CPP, in combination with normal plasma oncotic
    pressure, as favored in the Lund concept, may
    reduce adverse effects of craniotomy.
  • Decompressive craniotomy is the last therapeutic
    measure to prevent brain stem herniation in Lund

Other controversies
  • Prostacyclin to improve microcirculation has been
    recently added
  • General quality of care has improved
  • Local variations in tissue pressure and hence
    perfusion pressure
  • Maybe the injured areas needs a higher CPP, but
    achieving this results in oedema.
  • Reducing catecholamines may prevent their escape
    across BBB which increased cerebral metabolism
    and O2 consumption
  • Is oncotic pressure as important as Lund therapy

  • Basic concept is normalisation of various
  • fluid therapy,
  • Hb
  • lung protection
  • temperature control
  • Potentially
  • cerebrospinal fluid (CSF) drainage
  • decompressive craniotomy
  • Other
  • Normalisation of PaO2, PaCO2, enteral nutrition,
    avoidance of overnutrition

From APIC volume 2, (Antonino Gullo)
Our current protocol
  • Maintain cerebral perfusion pressure (CPP) gt 60
    mmHg using noradrenaline regardless of ICP.
  • Ensure normovolaemia eg. CVP 8-12 mmHg and/or
    ?down lt 5 mmHg
  • Maintain Hb close to 100g/l.
  • Maintain pO2 gt 100 mmHg (check ABG if SpO2 lt 98)
    Maintain pCO2 36-40 mmHg.
  • Monitor ETCO2. continuously if an Evita
    ventilator with capnography is available. Aim for
    ETCO2 30-35 mmHg
  • Sedation 7-14 mls/hr of standard MM for a 70kg
  • Nurse 20-30o head up tilt the whole bed if the
    spine has not been cleared.
  • Ensure that ETT tapes are not causing jugular
    venous obstruction.
  • Control BSL as per unit protocol.
  • Monitor temperature continuously aiming for
    normothermia. Give paracetamol if T gt 37.5oC
  • More aggressive maintenance of normothermia with
    ice can be used at the discretion of the duty
  • Saline or Hartmanns should be used as
    maintenance fluid aiming for Na gt 140 mmol/l.
  • Do not use dextrose solutions.
  • General
  • Early enteral nutrition as per ICU protocol.
  • Stress ulcer prophylaxis ranitidine 50mg tds
  • DVT prophylaxis as per ICU protocol. TEDs and
    calf compressors initially,

Our current protocol
  • Intracranial hypertension needs to be treated
    when ICP gt 20-25mmHg for greater than 5 minutes.
    Aim to control ICP lt 20 mmHg ideally.
  • Ensure basic management measures are in place as
  • Ensure that CPP is maintained gt 60 mmHg with
  • Optimise sedation.
  • morphine/midazolam.
  • Bolus of muscle relaxant
  • Ensure normothermia.
  • Osmotherapy
  • Mannitol If Na lt 155 mmol/l and CVP gt 12 mmHg
  • HTS If Na lt 155 mmol/l and CVP lt 12 mmHg, give
    30ml of 23.4 saline
  • Expect a decrease in ICP within 20-30 minutes.
  • Repeat CT scan to exclude a surgically remediable
    lesion and generally follow the evolution of the

Would I recommend it
  • Physiologically, it makes sense
  • But without adequate evidence and general lack of
    use elsewhere