ICP/CPP Monitoring

Figure 2: ICP Monitoring Devices

Rationale:       Clinical signs of severely elevated ICP             may never occur             usually a late finding (herniation)       Monitoring improves neurological outcomes   Methods:       Numerous (see diagram)       Variable advantage/disadvantages to each   Purpose:       Early detection of decompensation       Preserve cerebral perfusion       Prevent herniation       Customize/modulate therapies to control ICP   Indications:       Some controversy       GCS 3-8 (ICP>20 in >80% of TBI with GCS<8)       Clinical signs (posturing, cushings triad, etc)       Imaging consistent (slit vents, small cisterns, etc)       Obscured neuro exam and at risk       Risk of elevated ICP

Herniation Syndromes

Figure 3: Various Herniation Syndromes

Subfalcine Herniation

      Cingulate gyrus & related structures herniate laterally under the falx cerebri

      Usually from unilateral mass lesions

      Usually no classic stigmata

Central Herniation

      Downward displacement of brainstem

      Any mass almost anywhere with high ICP (including hydrocephalus / diffuse edema)

      Mild à traction on the abducens nerve (lateral rectus palsy)

      Severe à herniation into foramen magnum (tonsilar herniation) à medulla injury à respiratory arrest, BP instability

Transtentorial/Uncal Herniation

      Medial temporal lobe (i.e., the uncus) herniates inferiorly through tentorial notch

      Causes clinical triad of “blown” pupil, hemiplegia, and coma

            Compression of oculomotor nerve ipsilateral (85% of cases)

                  Initially: dilated & unresponsive pupil

                  Later: impairment of eye movement

            Hemiplegia is often contralateral (compression of ipsilateral corticospinal tract in the midbrain or motor cortex)

            Midbrain distortion leads to decreased level of consciousness and coma

Brain Injury: Multiple Mechanisms of Hypoxic-Ischemic Neuronal Cell Death

Management

Management: Different Models

Opinions differ widely on optimal intracranial hypertension therapy based on

      sustained versus acute increase in intracranial pressure

      mechanism of injury (trauma vs. metabolic vs. infectious)

      determination of cerebral vascular state (hypoperfusion vs. hyperemia vs. vasospasm)

      controversial evidence (e.g., hyperventilation, hypothermia, animal versus human models, etc.)

      how to tailor in setting of specific comorbidities (e.g., ventilation in ARDS, pressors in sepsis, etc.)

Numerous “Schools” of thought:

      ICP Targeted: keep the ICP <15-20 mm Hg

      CPP Targeted: keep the CPP >50-70 mm Hg

      “Lund Concept”: (see below)

       

Figures 4 & 5: ICP increases after various intereventions

Management: Applying Broad Goals in Specific Instances

      ICP < 15-20 mm Hg

            Perhaps lower <10-15 if large skull fractures/defects (avoid herniation)

            Perhaps higher <25-30 if global/metabolic process and other maximized therapies potentially harmful

      CPP > 50-70 mm Hg

            Set an upper limit (excessive CPP can promote cerebral edema where autoregulation is impaired)

            Attention to relative positions of monitoring devices (MAP at heart level, ICP at ear level, Auto-CPP calculations)

            Age-Apropriate targets:

                  Infant 45-55 mm Hg

                  Child 55-65 mm Hg

                  Adult 60-75 mm Hg

      CI > 2.5-3

            Maintain intravascular euvolemia or mild hypervolemia (keep left ventricle full)

            Optimize filling pressures to maximize starling curve of the heart without overly impeding venous return

            Attention to cerebral vascular state: hypoperfusion vs. hyperemia vs. vasospasm

            Careful selection of vasoactive substances from armamentarium

                  Epinephrine: probably ideal for most patients, especially if low CO, low BP

                  Dobutamine: may be optimal for global/metabolic processes, especially if normo/hypertensive

                  β-blockers (labetolol/metoprolol) +/- α2-agonists (clonidine): may be optimal antihypertensives

                        without causing significant cerebral vasodilatation that can lead to elevated ICP

                  Nimodipine: may have role in vasospasm

Intracranial Volume Targeted (“Lund Concept”)

Ways it’s been described:

      Antihypertensive and intracranial volume-targeted therapy

      Physiological volume regulation of the intracranial compartments

Central premise:

      Impaired autoregulation and blood brain barrier occur in the injured brain

      This makes MAP and cerebral capillary hydrostatic pressure driving force behind cerebral edema, and therefore ICP

      Furthermore, supporting the CPP with pressors can promote more cerebral edema

      Therefore, a good CO with normotension and mild vasoconstriction of precapillary cerebral vessels decreases ICP

The volume-targeted “Lund Strategy” has several components

      Reduction of stress response and cerebral energy metabolism (low dose pentothal, sedation)

      Reduction of capillary hydrostatic pressure with systemic antihypertensives (metoprolol and clonidine)

      Reduction of capillary hydrostatic pressure with precapillary vasoconstrictors (low-dose pentathol & ergotamine)

      Maintenance of colloid osmotic pressure and control of fluid balance

      Reduction of cerebral blood volume

What it looks like

      Euvolemia to Hypervolemia

      Normotension using beta-blockers (metoprolol) and alpha-agonists (clonidine)

      Low dose pentothal and dihydroergotamine

      CPP typically near traditional limits, but lower CPP tolerated in preference of antihypertensive therapy

      ICP effectively kept <20 mm Hg most of the time

Outcomes

     Efficacy of the protocol has been evaluated in experimental and clinical studies

     Surrogate physiological/biochemical improvements (lactate/pyruvate ratio in the penumbra zone by microdialysis)

     Non-randomized/non-controlled studies suggest significant mortality benefit

     Subjective clinical experiences favorable

ICP Management: General & Monitoring

      Time is of the essence – the brain tolerates ischemia more poorly than other tissues & injury begets injury

      Multi-pronged approach tailored to primary cause and comorbidities of patient

      Serial neurologic assessments and physical examination with a short feed-back loop is critical

      Continuous cardio-respiratory, ICP, and CPP monitoring

      +/- role cerebral metabolism monitoring adjuncts (micro-dialysis, jugular venous saturation, NIRS)

 ICP Management: Decrease intracranial pressure

      Evacuate mass occupying lesions (e.g., hemorrhage, tumor, abscess, etc)

      Patient Positioning 

                What:       Head up 30 degrees and midline, neck position neutral and non-compressed (e.g., by cervical collar)

                Why:        Enhance cerebral venous outflow and maximize CPP

                Pro:                 Simple, quick, well tolerated

                Con:        Confounding injuries, comorbidities requiring movement (e.g., proning)

      CSF drainage

                What:       Removal of CSF ideally through ventriculostomy (alternately an LP)

                Why:        Decreases “volume” in the compliance equation

                Pro:         Effective, titratable, doubles as monitor, interpretable waveform

                Con:                Invasive, bleeding complications, infectious complications

      Mannitol

                What:       0.5 - 2 g/kg up to Osm of 320

                Why:        Increases intravascular oncotic pressure, rheological benefits, anti-oxidant effects

                Pro:                 Rapid onset, titratable, predictable

                Con:        Intermittent, hypotension, hypovolemia, hypokalemia, duration hours or days, tolerance/rebound (reflection coefficient ~0.9)

      Hypertonic Saline

                What:       5-10 ml/kg 3% NaCl up to [Na] of 145-180 meq/L – may bolus 5-10 ml/kg and start a sliding scale gtt @ 0.5-2 ml/kg/hr

                Why:        Increases intravascular oncotic pressure, volume expander

                Pro:                 Rapid onset, titratable, continuous rx, predictable, high coefficient of reflection (reflection coefficient ~0.95), numerous others

                Con:        Can obfuscate DI/CSW, potential renal function impairment, some concerns for effects on immune function

Craniectomy

                What:       Resect large flap of skull

                Why:        Changes the “volume” part of the compliance equation

                Pro:                 Large sustained ICP reduction

                Con:        Timing critical, surgical risk, tissue herniation through wound, catastrophic Hail Mary

ICP Management: Decrease Cerebral Metabolic Demand

      Sedation & Analgesia

                What:       Benzos, narcs, barbiturates, Lido pETT/IV; possibly premedicate before stimulation; cluster nursing activity; calm environment

                Why:        Decrease CNS metabolic demand, dampen intrinsic catechols

                Pro:                 Easy, quick, reversible

                Con:        Loss of neuro exam, depresses hemodynamics

      Seizure Control

                What:       Agressively treat and consider prophylaxing, numerous choices of ACD (phenobarb, pentothal, dilantin)

                Why:        Decrease CNS metabolic demand

      Barbiturates

                What:       Pentothol 1-5 mg/kg to a level of 10-60

                Why:        Decreased CNS metabolic demand, decreased cerebral blood flow

                Pro:                 Blunts BP and respiratory fluctuations, anticonvulsant, titratable

                Con:        Hypotension, abnormal papillary responses, duration days

      Antipyresis

                What:       Tylenol, paralyzation, cooling measures, caution NSAIDS

                Why:        Metabolic demands increase 5-10% per 1^OC

      Hypothermia

                What:       Pre-existing or induced redection of temperature with paralysis and active cooling measures

                Why:        Hypothermia prior to cerebral ischemic insult protective; induced hypothermia after insult questionable

                Pro:                 Relatively simple, reversible

                Con:        Risks of coagulopathy, arrhythmia, sepsis (usually < 33^OC)

 ICP Management: Supportive and Indirect

      Ventilation: Normoventilate if able, +/- Hyperventilation temporarily if necessary

                What:       pCO₂ 35-40 ideally, but 25-35 mm Hg may achieve needed ICP control (best if transient and minimal)

                Why:        Decrease cerebral blood flow and therefore edema/ICP; hypercapnia blunts CBF autoregulation

                Pro:                 Immediate onset, well tolerated acutely

                Con:        Brain ischemia, hypotension, requires intubation, barotrauma, duration usually hours or less

      Optimize Hemodynamics

                What:       Cardiac Output >2.5-3 (e.g., inotropes, volume); CPP target; good venous return (e.g., vec, low Paw); avoid cardiac depressants

                Why:        generate adequate oxygen/nutrient delivery and waste removal

      Optimize Oxygen Carrying Capacity

                What:       PRBC, Epogen to goal Hb 8-10

                Why:        Deliver adequate O2

                Pro:         Oxygenation / DO2

                Con:                Hb <7-8 can impair DO2; Hb >10-11 can increase viscosity; stored PRBC are less deformable than natural RBC’s

      Glucose Control

                What:       Tight glucose control with prudent dextrose administration and insulin gtt if needed

                Why:        Hypo- and hyperglycemia in the setting of cerebral ischemia leads to enhanced anaerobic metabolism; stablize osmotic variable

                Pro:                 Relatively simple, physiologic

                Con:        Some safety issues with inducing hypoglycemia

      Loop diuretics & Acetazolamide

                What:       Furosemide, Torsemide

                Why:        Decrease CSF production and total fluid overload

                Pro:         quick, simple, reversible

                Con:                Risk of dehydration and impaired CO, electrolyte & acid-base derangements

      Muscle Relaxants

                What:       Vecuronium

                Why:        Stabilize patient, decrease intrathoracic pressure (CVP)

                Pro:                 Easy, quick, reversible

                Con:        Loss of neuro exam, weakness

      Corticosteroids

                What:       Dexamethasone 1-2 mg/kg q6-24h

                Why:        Antiinflamitory that decreases some forms of edema

                Pro:                 Effective on vasogenic edema (tumors, abscesses)

                Con:        Less effective on cytotoxic edema (stroke or hematoma), systemic/immune/gastric side effects

 Other Neuroprotective Strategies to Consider

More widely accepted - Literature generally neutral or is optimistic/supportive

      Magnesium: to levels of 2.5-3 meq/L as a calcium antagonis, vasodilator, anti-vasospasmodic

      Calcium channel blockers (e.g., nimodipine in vasospasm)

      Allopurinol: free-radical scavenger

      Serotonin agonists (e.g., Repinotan)

      Caspase inhibitors: as anti-apoptotic agents

      Neural stem cells

Experimental - Literature highly conflicted or is generally pessimistic

      Carnitine

      Glutamate antagonists / Excitatory Amino Acid (EAA) antagonist

      Anti-inflammatory agents (e.g., Ibuprofen)

      Sodium channel blockers (e.g., dilantin)

      Potassium channel activator

      Sundry free-radical scavengers

      GABA Antagonists

      Opioid Antagonists

      NOS Inhibitors

      Gangliosides

      Neurotrophic factors

 Combination Therapy

      “The whole is greater than the sum of its parts”

      …and yet, one bad ingredient can ruin an otherwise good recipe

Brain Injury is not “All or None”

Neuronal drop-out is fractional: 0-100%

Neuron populations heterogeneous (resilience, metabolic demands, vascular supply, etc.)

Global insult classically leads to

      widespread partial dropout / injury of vulnerable cell populations

      relatively spared territories (e.g., brainstem)

Focal insult classically leads to

      a “core” of hopeless necrosis

      a “penumbra” of neurons of varying injure ranging from dead to salvageable to stunned, to unaffected

Think of brain injury as “irreversible” can be a self-fulfilling prophesy

References