4Monroe-Kellie Doctrine An increase in the volume of any of the contents within the intracranial vault must be met with a decrease in the volume of another or the intracranial pressure will increaseV (vault)= V (CSF) + V (brain) + V (blood) + V (other)First described over 200 years ago.
5Intrinsic Compensatory Mechanisms Brain- noneCSF- redistributed into compliant paraspinal CSF spaceBlood- venous blood forced into internal jugular veinsWhen compensatory mechanisms are exhausted, ICP rises more rapidlyEventually, the compensatory mechanisms are exhausted and a sharp rise in ICP will occur.A normal ICP does not indicate where in the pressure volume curve we are.
6CBF via auto-regulation Maintains CBF via auto-regulation over wide range of MAP by altering resistance of cerebral blood vesselsThis insures supply of oxygen and metabolic substrates to neurons are unalteredICP > 20 has been shown in both adult and pediatric studies to be associated with increased morbidity and mortalityIschemia, disrupted BBB, inc ICPMaximally DilatedIschemia
7Loss of auto-regulation CPP = MAP – ICPMinimal CPP is age variantInfants 50 mmHgChildren 60 mmHgAdults 70 mmHgA good starting target CPP is 40 mmHg.The Peds CCM recommendations from 2003 are to maintain at least that as two pediatric studies showed increased mortality below that level.However, adults studies show better survival with a CPP > 65. Thus, it is likely that the goal CPP is age related.The target would be discussed in conjunction with neurosurgery, but likely it will increase as the patient gets older.
8Maintaining Adequate Brain Oxygenation Hypoxia results in vasodilation therefore increasing CBF and potentially worsening ICPAnother way of maintaining good oxygenation is to attack it from the consumptive endDecrease cerebral metabolismKeep patient adequately sedatedIn extreme cases, use a pentobarbital induced coma
9Etiologies of elevated ICP Increased ICP can occur with any CNS pathology that results in a spaceoccupying mass lesion, edema (osmotic, vasogenic, cytotoxic), or obstruction toCSF flow. Some common etiologies include:• Trauma: epidural, subdural bleeds, contusion, hematomas, diffuse axonalinjury, intraventricular hemorrhage• Infection: meningitis, encephalitis, cerebritis• VP shunt malfunction• Mass lesion: tumors, AVM• Metabolic: hepatic encephalopathy, DKA• Vascular or embolic disease, stroke with subsequent edema or mass effect
10Icp monitors and waveforms Intraventricular monitoringadvantage of accuracy, simplicity of measurement, and the unique characteristic of drainage of CSF.disadvantage is infection, up to 20 percent of patients, hemorrhageIntraparenchymal (thin electronic or fiberoptic transducer)Advantages include ease of placement, and a lower risk of infection and hemorrhage (<1 percent) than with intraventricular devicesDisadvantages include the inability to drain CSF for diagnostic or therapeutic purposes and the potential to lose accuracy (or "drift") over several days, since the transducer cannot be recalibrated following initial placementDrift- . One group found only a small (1 mmHg) drift in a group of 163 patients ; however, a second report found that readings varied by >3 mmHg in more than half of the 50 patients studied .
11Interpreting ICP waveforms: A waves Interpreting ICP waveforms: A waves. The most clinically significant ICP waveforms are A waves, which may reach elevations of 50 to 100 mm Hg, persist for 5 to 20 minutes, then drop sharply - signaling exhaustion of the brain's compliance mechanisms.A waves may come and go, spiking from temporary rises in thoracic pressure or from any condition that increases ICP beyond the brain's compliance limits.Activities, such as sustained coughing or straining during defecation, can cause temporary elevations in thoracic pressure.
12Ways to decrease icp Size of the box May increase size of vault with decompressive crainectomyDecrease the volume of the contentsRemove “others”- tumors, crowbars, hematomas, bullets, etc.Must decrease volume of one of the components of the intracranial vaultBrainCSFBlood
13Types of edema Vasogenic Interstitial Cytotoxic Increased permeability of brain capillary endothelium leads to edema and is usually seen around tumors, abscesses, intracerebral hematomas, encephalitis & meningitis.Neurons are not primarily injured.Reduction of this type of edema can minimize secondary injuryEdema results from increased CSF hydrostatic pressure and is usually seen in hydrocephalus or decreased CSF absorption by arachnoid villi, e.g. intraventricular hemorrhage.Neuronal swelling occurs secondary to cell injury caused by failure of the ATPase – dependent pump as occurs in diffuse axonal injury.This type of injury is often irreversible.Cytotoxic edema is common in patients who have severe cerebral injuries such as traumatic brain injury, diffuse axonal injury, or hypoxic-ischemic injury.●Vasogenic edema- Steroid therapy may be beneficial for vasogenic edema that occurs in the setting of mass lesions.●Interstitial edema is characterized by increased fluid in the periventricular white matter. Increased CSF hydrostatic pressure, as occurs with hydrocephalus, is the most common cause. Interstitial edema responds to therapy to reduce CSF pressure .
14Brain herniation syndromes — Herniation of brain tissue can cause injury by compression or traction on neural and vascular structures [6,8]. Herniation results when there is a pressure differential between the intracranial compartments and can occur in four areas of the cranial cavity :●Transtentorial herniation is the most common type (figure 4). It results from downward displacement of supratentorial brain tissue into the infratentorial compartment, and can be caused by supratentorial mass lesions, diffuse brain swelling, focal edema, or acute hydrocephalus. Transtentorial herniation can cause compression of the third cranial nerve, the upper brainstem, and the cerebral peduncles, as well as distortion or traction of the superior portion of the basilar artery.●Subfalcine herniation occurs when increased pressure in one hemisphere displaces brain tissue under the falx cerebri. Subfalcine herniation can cause compression of the anterior cerebral artery and extensive infarction of the frontal and parietal lobes.●Foramen magnum herniation occurs when downward pressure forces the cerebellar tonsils into the foramen magnum, where they compress the medulla oblongata and upper cervical spinal cord.●Retro-alar herniation occurs when increased pressure in the frontal lobes causes posterior displacement over the lesser wing of the sphenoid bone. Retro-alar herniation can cause carotid artery compression with anterior and middle cerebral artery infarction [4,6,8].
155 Ways to Decrease Intracranial Pressure Using the Monro-Kellie Doctrine Enhance venous drainageElevate head 30°If in a cervical collar, check fitHyperosmolar therapyHyperventilationCSF DrainageDecompressionSo we were manipulating CPP via the MAP or brain metabolism. The other half of the equation, ICP, can be manipulated using the Monro-Kellie Doctrine.Here are 5 ways that we can decrease ICP. To review, the skull has a fixed volume with usually just three contents, brain, blood and CSF. In the setting of increased ICP, reduction in the volume of one of these should result decreased pressure.Enhance venous drainage – and thus reduce the volume of blood. You can do this by head elevation. Also bear in mind that if a patient has a cervical collar, it could be impeding venous drainage.Hyperosmolar therapy – with the idea being to decrease the volume of the brain.Hyperventilation – not to be used regularly, but in the acute setting it can reduce cerebral blood flow, and thus blood volume.CSF Drainage – decreasing ICP through reducing the CSF volume.Decompression – works by expanding the volume and making the skull no longer a “locked box.”
16Decompressive Craniectomy Done infrequentlyUsually done at an OSH prior to transfer OR in conjunction with hematoma evacuationRemember to save the bone flap for reimplantation laterThe last way of reducing ICP actually “changes the rules” of the Monro-Kellie Doctrine. By removing part of the cranium you’re actually changing volume of the skull, “unlocking the locked box”, thus allowing more room for the three components previously discussed.
17CSF Drainage Neurosurgical Procedure Always push for an EVD, not just an ICP monitorTherapeutic AND diagnosticCan stay in long-term (no drift)Requires INR < 1.5 and PLTS > 100Ktaining adequate CPP is an important factor in survival for patients withelevated ICP. Several forms of ICP monitors exist.• Intraventricular monitor is the gold standard. It is accurate and can bere-zeroed. Most importantly, it can withdraw CSF for ICP management.Risks include infection, hemorrhage at time of insertion or removal, andobstruction of the catheter. Insertion of the catheter becomes difficult ifthe ventricles are small or displaced from shift or mass effect. It is usuallypositioned at 15cm H2O above the ear. Excessive drainage should beavoided to prevent ventricular collapse.• Intraparenchymal monitors are generally fiber optic, and are placeddirectly into brain parenchyma. They can be easily inserted. Althoughthey are fairly accurate initially, they cannot be re-zeroed and will developCSF drainage can, obviously, reduce the volume of CSF.Ideally an external ventricular drain would be placed instead of an ICP monitor. A drain is both therapeutic and diagnostic in that it can measure the ICP as well as give a means of reducing it. It can also stay in place long term. An ICP monitor, which is more easily placed, can move over time and can be inaccurate in it’s measurements.If you’re even considering an EVD or ICP monitor, begin correcting a coaugulopathy to reduce the delay.
18Hyperosmolar therapyIncrease serum osmolality to draw water out of brain parenchymaMannitolDecreases bld viscosityg/kgMaximal effect in 10 min, duration 75 min3% Saline (500 mEq/L)Osmotic, hemodynamic, vasoregulatory, and immunodmodulatoryEvery 1.5 cc/kg will increase Na by ≈ 1 mEq/LKnown to have a longer lasting effectIn general, check Na+ and osmolality q6hTarget NaTarget osmolality > 300Other effects may include decreased vascular resistance with improved cerebral blood flow by decreasingvascular endothelial edema.Inhibition of posttraumatic activation ofleukocytes also decreases the degree of inflammation.3% NS has the added advantage over mannitol of maintaining hemodynamic stabilityby maintaining intra-vascular volume status.A minimum serum sodium of 145 meq/L should be maintained.A hypothetical risk of central pontine myelinolysis by rapid increase of serum sodium levels
19Hyperventilation Causes a Decrease in Cerebral Blood Flow Pic of blood flow with hyperventSkippen. Crit Care Med Aug;25(8):1402-9Hyperventilation, as you may know, causes a decrease in cerebral blood flow. Here’s a perfusion scan done with a normal pCO2 and then a lower one. You’ll note how the brain is less perfused in conjunction with the decreased pCO2.
20Use of Hyperventilation Worse long-term outcomeTarget normocapneaWorks for acute spikes in ICPTarget pCO2 of about 35Avoid hypercapneaHyperventilation, however, is associated with worse long-term outcomes. Furthermore, the brain “resets” and cerebral blood flow will creep back to normal after hours at a lower pCO2.Thus, ideally aim for normocapnea unless in an emergent situation where you can use hypercapnea as a temporizing maneuver while waiting for other things, such as mannitol.When hyperventilating target a pCO2 ofAvoid hypercapnea which would result in increased cerebral blood flow.
21Avoid the Bad “H”s Hypotension Hypoxia Hyponatremia Hypervolemia HyperglycemiaHyperthermiaHypermetabolism (seizures, agitation)In addition to ways of reducing ICP, these are things that can exacerbate it, increase metabolic demand or decrease CPP.
22Summary of Key PointsMany of the goals of increased ICP management are based using the Monro-Kellie Doctrine to our advantageGoal ICP < 20 mmHgHyperventilation is not a long-term strategyCPP = MAP – ICP; Maintain CPP > 40 mmHgGoal NaAvoid the bad “H’s”