1. ICP and management
July 2014

2. Outline Intracranial contents Monroe-Kellie Doctrine
ICP monitors and waveforms
Calculate cerebral perfusion pressure
Types of edema and Herniation Syndromes
Management of ICP

3. Vault Contents

4. Monroe-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 increase
V (vault)= V (CSF) + V (brain) + V (blood) + V (other)
First described over 200 years ago.

5. Intrinsic Compensatory Mechanisms
Brain- none
CSF- redistributed into compliant paraspinal CSF space
Blood- venous blood forced into internal jugular veins
When compensatory mechanisms are exhausted, ICP rises more rapidly
Eventually, 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.

6. CBF via auto-regulation
Maintains CBF via auto-regulation over wide range of MAP by altering resistance of cerebral blood vessels
This insures supply of oxygen and metabolic substrates to neurons are unaltered
ICP > 20 has been shown in both adult and pediatric studies to be associated with increased morbidity and mortality
Ischemia, disrupted BBB, inc ICP
Maximally Dilated
Ischemia

7. Loss of auto-regulation
CPP = MAP – ICP
Minimal CPP is age variant
Infants 50 mmHg
Children 60 mmHg
Adults 70 mmHg
A 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.

8. Maintaining Adequate Brain Oxygenation
Hypoxia results in vasodilation therefore increasing CBF and potentially worsening ICP
Another way of maintaining good oxygenation is to attack it from the consumptive end
Decrease cerebral metabolism
Keep patient adequately sedated
In extreme cases, use a pentobarbital induced coma

9. Etiologies of elevated ICP
Increased ICP can occur with any CNS pathology that results in a space
occupying mass lesion, edema (osmotic, vasogenic, cytotoxic), or obstruction to
CSF flow. Some common etiologies include:
• Trauma: epidural, subdural bleeds, contusion, hematomas, diffuse axonal
injury, 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

10. Icp monitors and waveforms
Intraventricular monitoring
advantage of accuracy, simplicity of measurement, and the unique characteristic of drainage of CSF.
disadvantage is infection, up to 20 percent of patients, hemorrhage
Intraparenchymal (thin electronic or fiberoptic transducer)
Advantages include ease of placement, and a lower risk of infection and hemorrhage (<1 percent) than with intraventricular devices
Disadvantages 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 placement
Drift- . One group found only a small (1 mmHg) drift in a group of 163 patients [37]; however, a second report found that readings varied by >3 mmHg in more than half of the 50 patients studied [38].

11. Interpreting 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.

12. Ways to decrease icp Size of the box
May increase size of vault with decompressive crainectomy
Decrease the volume of the contents
Remove “others”- tumors, crowbars, hematomas, bullets, etc.
Must decrease volume of one of the components of the intracranial vault
Brain
CSF
Blood

13. Types 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 injury
Edema 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 [5].

14. Brain 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 [6]:
●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].

15. 5 Ways to Decrease Intracranial Pressure Using the Monro-Kellie Doctrine
Enhance venous drainage
Elevate head 30°
If in a cervical collar, check fit
Hyperosmolar therapy
Hyperventilation
CSF Drainage
Decompression
So 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.”

16. Decompressive Craniectomy
Done infrequently
Usually done at an OSH prior to transfer OR in conjunction with hematoma evacuation
Remember to save the bone flap for reimplantation later
The 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.

17. CSF Drainage Neurosurgical Procedure
Always push for an EVD, not just an ICP monitor
Therapeutic AND diagnostic
Can stay in long-term (no drift)
Requires INR < 1.5 and PLTS > 100K
taining adequate CPP is an important factor in survival for patients with
elevated ICP. Several forms of ICP monitors exist.
• Intraventricular monitor is the gold standard. It is accurate and can be
re-zeroed. Most importantly, it can withdraw CSF for ICP management.
Risks include infection, hemorrhage at time of insertion or removal, and
obstruction of the catheter. Insertion of the catheter becomes difficult if
the ventricles are small or displaced from shift or mass effect. It is usually
positioned at 15cm H2O above the ear. Excessive drainage should be
avoided to prevent ventricular collapse.
• Intraparenchymal monitors are generally fiber optic, and are placed
directly into brain parenchyma. They can be easily inserted. Although
they are fairly accurate initially, they cannot be re-zeroed and will develop
CSF 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.

18. Hyperosmolar therapy
Increase serum osmolality to draw water out of brain parenchyma
Mannitol
Decreases bld viscosity
g/kg
Maximal effect in 10 min, duration 75 min
3% Saline (500 mEq/L)
Osmotic, hemodynamic, vasoregulatory, and immunodmodulatory
Every 1.5 cc/kg will increase Na by ≈ 1 mEq/L
Known to have a longer lasting effect
In general, check Na+ and osmolality q6h
Target Na
Target osmolality > 300
Other effects may include decreased vascular resistance with improved cerebral blood flow by decreasing
vascular endothelial edema.
Inhibition of posttraumatic activation of
leukocytes also decreases the degree of inflammation.
3% NS has the added advantage over mannitol of maintaining hemodynamic stability
by 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

19. Hyperventilation Causes a Decrease in Cerebral Blood Flow
Pic of blood flow with hypervent
Skippen. Crit Care Med Aug;25(8):1402-9
Hyperventilation, 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.

20. Use of Hyperventilation
Worse long-term outcome
Target normocapnea
Works for acute spikes in ICP
Target pCO2 of about 35
Avoid hypercapnea
Hyperventilation, 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 of
Avoid hypercapnea which would result in increased cerebral blood flow.

21. Avoid the Bad “H”s Hypotension Hypoxia Hyponatremia Hypervolemia
Hyperglycemia
Hyperthermia
Hypermetabolism (seizures, agitation)
In addition to ways of reducing ICP, these are things that can exacerbate it, increase metabolic demand or decrease CPP.

22. Summary of Key Points
Many of the goals of increased ICP management are based using the Monro-Kellie Doctrine to our advantage
Goal ICP < 20 mmHg
Hyperventilation is not a long-term strategy
CPP = MAP – ICP; Maintain CPP > 40 mmHg
Goal Na
Avoid the bad “H’s”