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ICP and management July 2014.

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Presentation on theme: "ICP and management July 2014."— Presentation transcript:

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”

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