Intracranial Pressure Monitoring 

Updated: Apr 01, 2018
Author: Gaurav Gupta, MD, FAANS, FACS; Chief Editor: Jonathan P Miller, MD 

Overview

Background

Elevated intracranial pressure (ICP) is seen in head trauma,[1] hydrocephalus,[2] intracranial hemorrhage, sub-arachnoid hemorrhage from ruptured brain aneurysm, intracranial tumors,[3] hepatic encephalopathy,[4] and cerebral edema.[5] Intractable elevated ICP can lead to death or devastating neurological damage either by reducing cerebral perfusion pressure (CPP)[6] and causing cerebral ischemia or by compressing and causing herniation of the brainstem or other vital structures. Prompt recognition is crucial in order to intervene appropriately.

Intractable high ICP is the most common "terminal event" leading to death in neurosurgical patients.[7] The association between the severity of intracranial hypertension and poor outcome after severe head injury is well recognized.[6] Outcomes tend to be good in patients with normal ICP, whereas those with elevated ICP are much more likely to have an unfavorable outcome.[8] Elevated ICP carries a mortality rate of around 20%.[9]

The rapid recognition of elevated ICP is therefore of obvious and paramount importance so that it can be monitored and so that therapies directed at lowering ICP can be initiated. A raised ICP is measurable both clinically and quantitatively. Continuous ICP monitoring is important both for assessing the efficacy of therapeutic measures and for evaluating the evolution of brain injury.[10]

Although some investigators have questioned invasive ICP monitoring in improving patient outcomes,[11, 12] numerous retrospective series and data bank studies have favored the technique.[13, 14, 15, 16]

The goal of ICP monitoring is to ensure maintenance of optimal CPP. The ICP also forms a basis for medical or surgical intervention in cases of increased ICP with agents such as 3% sodium chloride (NaCl), mannitol, or diuretics (Lasix), ventriculostomy, cerebrospinal fluid (CSF) diversion, and pentobarbital coma or surgical decompression in cases of intractable ICP elevation that do not respond to conservative management.

ICP monitoring may be discontinued when the ICP remains in the normal range within 48-72 hours of withdrawal of ICP therapy or if the patient’s neurological condition improves to the point where he or she is following commands.

History

The concept of ICP (normal or abnormal) being a function of the volume and compliance of each component of the intracranial compartment was proposed by the Scottish anatomist and surgeon Alexander Monro (1733-1817) and his student George Kellie (1758-1829) during the late 18th century.[17, 18] The interrelationship came to be known as the Monro-Kellie hypothesis. This doctrine states that the cranial compartment is encased in a nonexpandable case of bone, and, thus, the volume inside the cranium is fixed.

The doctrine further states that, in an incompressible cranium, the blood, CSF, and brain tissue exist in a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. For example, the arterial blood entering the brain requires a continuous outflow of venous blood to make room. If something does not exit the cranial compartment to make room, the ICP increases, resulting in pathology.

The confirmatory exsanguination experiments of Abercrombie, also a student of Monro, demonstrated graphically the extent to which the body placed physiological priority on maintaining the perfusion of the brain.[19] He drained dogs of their blood and was able to observe that the brain remained comparatively well perfused until shortly before death regardless of the dog’s position in space (hanging upside down or right side up, to control for the effects of gravity), unless the blood was drained from an intracranial vessel directly, in which case death resulted almost immediately.

The reciprocal relationship between venous and arterial blood was considered the main variable in ICP and perfusion until 1848, when George Burrows, an English physician, repeated many of the exsanguination and gravitational experiments of Abercrombie and Kellie and found a reciprocal relationship between the volume of CSF and the volume of blood in the intracranial compartment.[20]

Leyden, working in Germany in 1866, demonstrated that elevated ICP leads to a slowed pulse and difficulty breathing, with eventual arrest of breathing entirely.[21] This work was built on in 1890 by Spencer and Horsley[22] , who found that, in the case of intracerebral tumors, death was brought about by the arrest of breathing due to increased ICP. Increased ICP was thus taken to represent a common endpoint for several insults to the brain.

In 1891, Quinke published the first studies on the technique of lumbar puncture (LP) and insisted that a glass pipette be affixed to the needle so that the CSF pressure could be measured.[23] This technique for repeated measurement of CSF fluid pressure as an assessment of ICP became widely used and was the earliest clinical method of ICP measurement.

In 1903, Cushing described what is now widely known as the "Cushing Triad" as a clinical tool for recognizing the presence of elevated ICP. The triad consists of a widening pulse pressure (rising systolic, declining diastolic), irregular respirations, and bradycardia.[24] In 1922, Jackson noted that the pulse, respiration, and blood pressure are affected only once the medulla is compressed, and some patients with clinical signs of brain compression had normal lumbar CSF pressures.[25] Cushing quantified the Monro-Kelly doctrine, writing that the sum of the volume of the brain plus the CSF volume plus the intracranial blood volume is constant. Therefore, an increase in one should reduce one or both of the others.[26]

In 1964, Langfitt demonstrated that LP could induce brainstem compression through transtentorial herniation or herniation of the tonsils through the foramen magnum and that, further, when the ventricular system does not communicate, spinal pressure is not an accurate reflection of ICP.[27] LP fell into disuse for ICP monitoring, and researchers began to directly cannulate the ventricular system.[28]

In 1965, Nils Lundberg revolutionized ICP monitoring with his work using bedside strain gauge manometers to record ICP continuously via ventriculostomy.[29] In his technique, a ventricular catheter was connected to an external strain gauge. This method has proven to be accurate and reliable and also permits therapeutic CSF drainage. Catheter-based ventricular monitoring systems were not applied systematically until the mid-1970s, when monitoring via a strain gauge became widespread after Becker and Miller reported good results in 160 patients with traumatic brain injury. They demonstrated clear evidence of good outcomes among patients in whom elevated ICP could be quickly recognized and subsequently lowered.[13]

Physiology

The most important role of the circulatory system, aside from transporting blood into all parts of the body, is to maintain optimal CPP.[30] The formula for calculating CPP is below.

CPP = mean arterial blood pressure (MAP) - mean intracranial pressure (MIC)

CPP is the pressure gradient acting across the cerebrovascular bed and, therefore, a major factor in determining cerebral blood flow (CBF).[31] CBF is kept constant in spite of wide variation in CPP and MAP by autoregulation.

Autoregulation is a process of adjustment on the part of the brain’s arterioles that keeps cerebrovascular resistance constant over a range of CPP. Increased CPP causes stretching of the walls of the arterioles, which compensate by dilating and relieving this pressure. Likewise, in the setting of decreased pressure, the arterioles constrict to maintain CPP. This autoregulation prevents transient pressure increases from being transmitted to smaller distal vessels. When the MAP is less than 65 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate, and blood flow becomes entirely dependent on the blood pressure, a situation defined as "pressure-passive flow." The CBF is no longer constant but is dependent on and proportional to the CPP.

Thus, when the MAP falls below 65 mm Hg, the cerebral arterioles are maximally dilated and the brain is at risk for ischemia because of insufficient blood flow to meet its needs. Likewise, at a MAP greater than 150 mm Hg, the cerebral arterioles are maximally constricted and any further increases in pressure cause excess CBF that may result in increased ICP.

Note that, while autoregulation works well in the normal brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain. Ideally, the goal is to maintain the CPP more than 60 mm Hg, and this can be done by either decreasing the ICP or increasing the systolic blood pressure using vasopressors. Caution should be used to use only vasopressors that do not increase ICP.

The volume of the skull contains approximately 85% brain tissue and extracellular fluid, 10% blood, and 5% CSF. If brain volume increases, for example in the setting of cancer, there is a compensatory displacement of CSF into the thecal sac of the spine followed by a reduction in intracranial blood volume by vasoconstriction and extracranial drainage. If these mechanisms are successful, ICP remains unchanged. Once these mechanisms are exhausted, further changes in intracranial volume can lead to dramatic increases in ICP.

The time course of a change in the brain has significance for how ICP responds. A slow-growing tumor, for example, is often present with normal or minimally elevated ICP, as the brain has had time to accommodate. On the other hand, a sudden small intracranial bleed can produce a dramatic rise in ICP. Eventually, whether acute or insidious in progression, compensatory mechanisms are exhausted, and elevated ICP follows.

The relationship between ICP and intracranial volume is described by a sigmoidal pressure-volume curve. Volume expansion of up to 30 cm3 usually results in insignificant changes in ICP because it can be compensated by extrusion of CSF from the intracranial cavity into the thecal sac of the spine and, to a lesser extent, by extrusion of venous blood from the cranium. When these compensatory mechanisms have been exhausted, ICP rises rapidly with further increases in volume until it reaches the level comparable with the pressure inside of cerebral arterioles (which depends on MAP and cerebrovascular resistance but normally measures between 50 and 60 mm Hg). At this point, the rise of ICP is halted as cerebral arterioles begin to collapse and the blood flow completely ceases.

The relationship between ICP and CBF and functional effects was described thoroughly by Symon and colleagues, as follows:[32]

  • CBF of 50 mL/100 g/min: Normal

  • CBF of 25 mL/100 g/min: Electroencephalogram slowing

  • CBF of 15 mL/100 g/min: Isoelectric electroencephalogram

  • CBF of 6 to 15 mL/100 g/min: Ischemic penumbra

  • CBF of less than 6 mL/100 g/min: Neuronal death

Normal intracranial pressure

ICP is generally measured in mm Hg to allow for comparison with MAP and to enable quick calculation of CPP. It is normally 7-15 mm Hg in adults who are supine, with pressures over 20 mm Hg considered pathological and pressures over 15 mm Hg considered abnormal.[33]

Note that ICP is positional, with elevation of the head resulting in lower values. A standing adult generally has an ICP of -10 mm Hg but never less than -15 mm Hg.[34] In supine children, ICP is normally lower, in the range of 15 mm Hg, with infants having ICP from 5-10 mm Hg and newborns have subatmospheric pressures regardless of position.[35]

In adults, the choroid plexus and other locations in the CNS produce CSF at a rate of 20 mL/hour, for a total of 500 mL/day. It is reabsorbed by the arachnoid granulations into the venous circulation. CSF volume is most commonly increased by a blockage of absorption due to ventricular obstruction, occlusion of venous sinuses, or clogging of the arachnoid granulations.

Causes of increased intracranial pressure

Increased ICP may result from the following:

  • Space-occupying lesions: Tumor, abscess, intracranial hemorrhage (epidural hematoma, subdural hematoma, intraparenchymal hematoma)

  • CSF flow obstruction (hydrocephalus): Space-occupying lesion that obstructs normal CSF flow, aqueductal stenosis, Chiari malformation

  • Cerebral edema: Due to head injury, ischemic stroke with vasogenic edema, hypoxic or ischemic encephalopathy, postoperative edema

  • Increase in venous pressure: Due to cerebral venous sinus thrombosis, heart failure, superior vena cava or jugular vein thrombosis/obstruction

  • Metabolic disorders: Hypo-osmolality, hyponatremia, uremic encephalopathy, hepatic encephalopathy

  • Increased CSF flow production: Choroid plexus tumors (papilloma or carcinoma)

  • Idiopathic intracranial hypertension

  • Pseudo tumor cerebri

Indications

The most common indication for invasive ICP monitoring is closed head injury.[33] Per the Guidelines for the Management of Severe Traumatic Brain Injury,[36] an ICP monitor should be placed in patients with a Glasgow coma score less than 8T (after resuscitation) and after reversal of paralytics or sedatives that may have been used during intubation. (See the Glasgow Coma Scale calculator.)

Other candidates for ICP monitoring are as follows:

  • A patient who is awake yet at risk for increased ICP under general anesthesia for a necessary nonneurosurgical procedure (eg, orthopedic limb-saving procedure), rendering clinical observation impossible

  • Patients who have nonsurgical intracranial hemorrhage but are intubated for nonneurosurgical reasons, preventing clinical examination

  • Patients with moderate head injury who have contusions to the brain parenchyma that are at risk of evolving (Extreme caution and clinical judgment must be exercised for lesions in the temporal fossa, since their proximity to the brainstem can lead to catastrophic herniation and brainstem compression with little change in the global ICP.)

Perioperative ICP monitoring is indicated in patients who have just undergone tumor or arteriovenous malformation resection and are at risk for cerebral edema with an inability to follow a clinical neurological examination.

Contraindications

Placement of an ICP monitor has no absolute contraindications, because it is a relatively low-risk procedure. However, clinical judgment should be exercised, especially in patients with a known bleeding disorder. Patients with thrombocytopenia (platelets count of < 10,000/µL), known platelet dysfunction (inhibition due to antiplatelet agents such as aspirin/clopidogrel or uremic encephalopathy), prothrombin time greater than 13 seconds, or an international normalized ratio (INR) greater than 1.3 are at elevated risk for hemorrhage secondary to placement of an ICP monitor.

Complications

EVD placement

Potential complications include intraparenchymal, intraventricular, or subdural hemorrhage. Recent studies have shown that catheter-related hemorrhages occur in 1%-33% of patients.[37]

Infection occurs in 1%-12% of patients. Symptoms suggestive of infection should prompt CSF analysis for cell count and culture along with antibiotic therapy, as appropriate. Staphylococci are the most common pathogens. Higher rates of bacterial ventriculitis/meningitis occur with longer duration of EVD placement.[38] Risks may be minimized with careful placement of the catheter and maintenance of the system under strict sterile conditions, use of antibiotic prophylaxis (eg, cefuroxime 750 mg every 8 hours from the time of catheter insertion until 24-48 hours after removal).[39] Exchange of the catheter every 5 days, although a common practice, does not appear to decrease the risk of infection; in fact, repeated catheter insertions have been found to be associated with higher risk of ventriculitis.[40]

Catheter occlusion due to clotted blood at the EVD orifice may be relieved by irrigation with sterile saline or catheter replacement.

System malfunction is possible. For example, damping of the waveform may be caused by apposition of the catheter tip against the ventricular wall or obstruction of the catheter by a blood clot or an air bubble.

Intraparenchymal fiberoptic catheter placement

Potential complications of intraparenchymal fiberoptic catheter placement include intraparenchymal, cortical, or subdural hemorrhage. Infection can occur, although it is rare.

The catheter can be kinked or bent, leading to errors in measurement. If the monitor is damaged, the fiberoptic probe should be replaced. Usually, the bolt itself (which secures the probe to the skull) does not need to be replaced.

 

Periprocedural Care

Patient Education & Consent

Explain the procedure to the patient and family. Consent should be obtained from the patient or a responsible family member. Obtain written consent from the patient or family per institution protocol.

Equipment

Several prepackaged EVD kits are commercially available. Equipment includes the following:

  • Preoperative gram-positive antibiotic prophylaxis (cefuroxime 1.5 g IV before the procedure)

  • Hair clipper

  • Sterile gloves/drapes/mask

  • Chlorhexidine solution

  • Sterile fenestrated drape

  • Sterile marker for drawing standard landmarks on head for placing EVD

  • Syringe (3 mL) for local anesthetic

  • Needle (18 gauge, 3/4 in) for injecting local anesthetic

  • Local anesthetic (usually 1% lidocaine with epinephrine)

  • Skin knife/scalpel #15

  • Twist drill

  • Sterile spinal needle (18 or 20 gauge) to puncture dura

  • Ventriculostomy drain (antibiotic or nonantibiotic impregnated)

  • External drainage set/Buretrol (including drainage tubing and sterile collection bag)

  • Sterile CSF collection tubes for sending CSF as specimen

  • Suture material

  • Dressings (4X4)

  • IV pole and standard ICP transducer setup (similar to arterial-line setup that is used for measuring blood pressure)

Equipment for intraparenchymal fiberoptic catheter placement includes the following:

  • Sterile gloves/mask/gown

  • Local anesthetic (usually 1% lidocaine with epinephrine)

  • Chlorhexidine or Betadine solution

  • Sterile fenestrated drapes or towels

  • Syringe (3 mL) for local anesthetic

  • Needle (25 gauge 3/4 inch) for injecting anesthetic

  • Sterile spinal needle (18 gauge) for puncturing dura

  • Small skin retractor

  • ICP monitor "bolt" to secure the ICP fiberoptic probe

  • No. 36 drill bit (2.71-mm diameter) with safety stop

  • Spacer/guard to adjust seating depth of bolt

  • Strain relief protective sheath

  • Stylet (1.3-mm diameter) to ensure no debris in the bolt prior to inserting the fiberoptic probe

  • Hex wrench to secure the drill bit into the drill

  • Zero adjustment tool for zeroing the fiberoptic probe to the atmospheric pressure

  • Fiberoptic catheter

  • Two small plastic dressings (Tegaderm) to place on the zero-adjustment screw so it is not moved during manipulation later

Patient Preparation

EVD placement

The procedure should be performed in an ICU only under strict sterile precautions.

A “time out” is done for correct site identification, per nursing protocol.

Perform a baseline neurological assessment.

Intraparenchymal fiberoptic catheter placement/intraparenchymal pressure monitor kit

Open the intracranial pressure monitor kit with a sterile technique and inspect expiration dates.

Perform a baseline neurological assessment.

Wash hands.

Illuminate the area.

Anesthesia

Intraparenchymal fiberoptic catheter placement

Adequate anesthesia should be ensured for the procedure.

Positioning

The patient should be placed in a supine position.

During placement of the monitor, the physician should be comfortable, so the height of the bed should be adjusted accordingly.

Elevate the head of the bed 15-30° while keeping it in the midline position with pillows or sandbags to enhance cerebral venous outflow. Even slight movement of the head to a few degrees off midline may double the ICP.

After the procedure, an elevation of 30° is optimal for allowing brain perfusion while minimizing ICP.

 

Technique

Approach Considerations

Noninvasive intracranial pressure monitoring

Clinical examination

The most important tool for diagnosing potential elevation of ICP and monitoring its progression is the clinical neurological examination.[41] In the modern era, noninvasive imaging studies have made clinical observation less important for initial diagnosis of elevated ICP; however, clinical observation has not lost its importance for ongoing monitoring of a patient’s condition. Therefore, the examination should occur frequently.

The patient should be evaluated for the following:

  • Headache, nausea, and vomiting

  • Degree of alertness or consciousness (Glasgow coma score should be assessed in the unconscious patient. See the Glasgow Coma Scale calculator as well as a description of the scale in the Medscape Reference article Head Trauma.[42] )

  • Language comprehension, repetition, fluency, articulation

  • Pupillary reactivity (Pupillary asymmetry or anisocoria of more than 2 mm should be noted.)

  • Extraocular movements and visual fields in all quadrants (If the patient is unable to follow commands, check visual pursuit, blink to visual threat, or dolls eye maneuver. Pay particular attention for a VI nerve palsy.)

  • Funduscopic examination (This also remains the criterion standard in the evaluation of increased ICP.)

  • Vital signs (Note particularly the absence or presence of Cushing triad: respiratory depression, hypertension, bradycardia.)

  • Gag or cough reflex and response to noxious stimuli (This must be performed with caution, as these can provoke increases in ICP that may persist for some time.)

Funduscopic examination

In funduscopic examinations, careful attention to the optic nerve can prove useful for evaluating the ICP.[43] The optic nerve is surrounded by subarachnoid space and experiences pressure changes in the same way that the intracranial compartment does. Pressure on the optic nerve as it exits the cranial vault blocks retrograde intraaxonal transport, resulting in axoplasmic stasis at the nerve head. This leads to secondary vascular changes and edema that manifest as a swelling of the optic disk, referred to as papilledema.[44]

Papilledema is almost always bilateral and generally develops 1-5 days after an increase in ICP. In the setting of subarachnoid hemorrhage, it develops far more rapidly, in a range of 2-8 hours. It can be recognized on funduscopic examination as accentuation of the nerve fiber striations of the disk margins, hyperemia of the disk, and dilation of the capillaries of the optic disk.[43] The disk is elevated, with partial or complete obscuring of the “cup” of the optic disk.[45] This can be evaluated by bringing the “top” of the disk into focus and measuring, in diopters, the distance to the base. Three diopters is the equivalent of approximately 1 mm elevation.

Hemorrhage on or near the disk may occur, manifesting as a flame-shaped, or splinter appearance. Concentric retinal stress lines around the base of the swollen disk may be present. Spontaneous venous pulsations, present in most normal eyes, are absent. If venous pulsations are present, papilledema may be ruled out.

Imaging

Noncontrast CT scanning of the head is a fast, cost-effective method to evaluate for elevated ICP and associated pathology. Findings suggestive of elevated ICP are as follows:

  • Intracranial blood/bony fractures

  • Mass lesions

  • Obstructive hydrocephalus

  • Cerebral edema (both focal or diffuse)

  • Midline shift

  • Effacement of normal CSF spaces, basilar cisterns, loss of gray white differentiation and loss of normal gyri and sulci pattern[46]

MRI can be costly and time consuming and is not indicated as a first line of diagnostic modality in the acute care setting. Many patients who undergo MRI for other reasons (ie, stroke, liver failure, meningitis, meningoencephalitis, and postresuscitation syndrome) are later found to have elevated ICP. Fat-suppressed T2-weighted MRI can facilitate measurement of the optic nerve and its surrounding sheath.[47] MRI is also useful in the setting of idiopathic intracranial hypertension.[48, 49]

Invasive intracranial pressure monitoring

The most common surgically placed monitors for ICP measurement are intraventricular catheters (external ventricular drain [EVD] or a ventriculostomy drain) and fiberoptic ICP monitors implanted into the parenchyma of the brain.

External ventricular drain placement

An EVD is a highly accurate tool for monitoring ICP. It requires placement of a catheter into the lateral ventricle at the level of the foramen of Monro. In addition to monitoring, an EVD allows for therapeutic relief of elevated ICP via CSF drainage.

An EVD requires skill and training for optimal placement. Potential risks of EVD placement include parenchymal hematoma and infection/ventriculitis. Obstruction of the drain requires replacement. Continuous monitoring requires nursing staff to be educated on management of the EVD.

Intraparenchymal fiberoptic catheter placement

And intraparenchymal fiberoptic catheter is used to measure the ICP without CSF diversion. It has a lower complication rate, lower infection rate, and no chance of catheter occlusion or leakage. Neurological injury is minimized because of the small diameter of the probe. In addition, malpositioning of the transducer has less impact on errors of measurement. Drawbacks include the high expense of the procedure and the inability to calibrate it once it has been placed.

External Ventricular Drain Placement

Adequate sedation of the patient should be ensured.

Clip the appropriate area of the head.

Prepare by washing with chlorhexidine and drape in a sterile fashion.

In the absence of contraindications, the right side of the brain in generally chosen.

Lidocaine (1%) is injected in a radial fashion with a 3-mL syringe and the 25-gauge needle around the planned incision site until a wheal is raised in the skin.

See Local Anesthetic Agents, infiltrative technique.

Draw a line on the scalp along the midline from nasion backward to the vertex of the skull.

Draw a perpendicular line 13 cm from the nasion.

At 13 cm behind the nasion, mark the Kocher point, a point 3 cm from the midline laterally just anterior to the coronal suture roughly in the midpupillary line. This point is chosen because it minimizes the involvement of eloquent brain through which the catheter must pass and facilitates nursing care while the patient is supine.

Mark the proposed trajectory of the catheter. Draw a line from the Kocher point to the ipsilateral medical canthus. Draw a second line from the Kocher point to a point 1 cm in front of the ipsilateral tragus.

The incision should be made at the Kocher point with a scalpel, approximately 2 cm long, and carried down to the skull.

The skull should be cleared of periosteum as best as possible and a small retractor placed.

A manual twist drill aimed perpendicular to the skull should be carefully used to penetrate both the outer and the inner tables of the skull. The stop guard should be used for the drill so as not to accidently plunge into the brain parenchyma when the inner table of the skull is breached.

A probe/18-gauge needle should be introduced through the hole to ensure that the drill completely penetrated the bone.

An 18-gauge needle or dural needle should then be used to score and puncture the dural surface.

The ventricular catheter is taken with the stylet or the metal wire in place.

The catheter should be directed in a plane toward the medial canthus of the ipsilateral side in the sagittal plane and toward a point 1 cm anterior to the tragus in the coronal plane, essentially aiming toward the foramen of Monro.

The catheter should be advanced to 5 cm below the dura, which is 6-7 cm below the skull surface. This will place the tip of the catheter just above the ipsilateral foramen of Monro.

Usually, a "pop" or a "give in" is felt at about 3-4 cm, indicating entry into the ventricle. Advance the catheter so it remains 6 cm at skull. This ensures all the holes in the ventricular catheter to be in the ventricle.

Immediate egress of clear or bloody (depending on the pathology) CSF is seen. Care must be taken not to lose too much CSF at this point, as the brain may not tolerate sudden decompression of the ventricles.

The probes should be secured externally by tunneling under the scalp 5-7 cm posteriorly and laterally to prevent infection. The drain is then looped around itself to secure it with 2-0 nylon suture and stitched into place using 3 suture points.

A sterile dressing is then placed and the EVD connected to the external collection system/Buretrol and ICP-measuring transducer.

Other approaches include Keens point, 2.5 cm posterior and superior to the top of the ear, and the occipital parietal, 6 cm above the inion, 4 cm from the midline.

Confirmation of catheter placement should be attained via head CT scanning.

The CT should also be inspected for hyperdensity along the ventricular catheter and the corresponding subdural space, which would indicate catheter tract, subdural, or intraparenchymal hemorrhage.

The EVD is calibrated at the level of the tragus. Depending on the indication for CSF drainage, the height of the EVD can be kept at 10-20 cm above tragus. The drain should be kept open at the desired height so as to allow the CSF to escape if the ICP rises above that level. The EVD should be transduced hourly to measure the ICP.

Weaning the external ventricular drain

Once the patient neurologically improves with CSF diversion and has normal ICP, it is essential to determine whether external CSF diversion is necessary and whether the patient’s own intrinsic CSF absorption pathways are functional enough to maintain equilibrium between CSF production and absorption. In this case, the EVD weaning protocol is instituted.

The height of the EVD is gradually increased from 10 cm above tragus to 15 cm and then to 20 cm above tragus. If the patient’s neurological status and ICP remain stable, the EVD is then clamped to allow the patients intrinsic CSF pathways to assume full control of the CSF equilibrium.

If, after 24 hours of clamping the EVD, the patient remains neurologically stable with normal ICP and head CT scanning demonstrates stable ventricular size, the EVD is removed and a single stitch placed at the skin entry site.

However, if the patient does not tolerate EVD weaning (manifested by increased headaches, neurological deterioration, or increased ICP or increased ventricular size head CT scanning) permanent CSF diversion is necessary in the form of a permanent ventriculoperitoneal shunt. Other options include ventriculopleural shunt and ventriculoatrial shunt. CSF shunting procedures are discussed elsewhere.

Intraparenchymal Fiberoptic Catheter Placement

The monitor is placed in the right or left prefrontal area, allowing the patient’s head to be rotated without interfering with the monitor’s function. Select the most injured side in a focal injury; in diffuse injury, the right hemisphere is generally used.

The incision site should be chosen behind the hairline, in a cosmetically acceptable fashion.

Xylocaine (1%) is injected in a radial fashion with a 3-mL syringe and the 25-gauge needle around the planned incision site until a wheal is raised in the skin.

See Local Anesthetic Agents, infiltrative technique.

The incision site should be 2-3 cm anterior to the coronal suture in a plane with the midpupillary line behind the hairline and performed usually on the right (nondominant) side of the brain, unless contraindicated.

Clip the hair and prepare the area by washing with chlorhexidine or Betadine and drape in sterile fashion.

Measure and mark the incision site with a sterile skin marker.

A 0.5-cm linear incision should be made and carried down to the bone.

Use a small skin retractor to expose the bone and achieve hemostasis of the skin edges.

Drill a twist drill hole though the outer and inner tables of the skull. Take care not to penetrate the dura or cause trauma to the brain by ensuring the drill guard is in place.

Remove the drill and irrigate the whole with sterile saline.

Puncture the dura with a spinal needle available in the kit.

Screw the bolt into the skull manually.

Insert the stylet through the bolt to remove any bone or soft tissue debris

Remove the fiberoptic catheter from the package and attach it to the monitor. If the system does not display zero initially, adjust the monitor per manufacturer instructions to calibrate the fiberoptic cable to "zero."

Insert the fiberoptic catheter through the strain-relief protective sheath and then into the bolt so that it extends 0.5 cm beyond the end of the bolt into the brain parenchyma. Any significant resistance usually results from nonpenetration of both tables of skull or nonpenetration of dura.

After placing the fiberoptic cable intraparenchymally, pull back on the catheter a millimeter or two so that it is not under tension against a blood vessel or brain parenchyma. Then, turn the compression cap clockwise to secure the monitor in place. Place Tegaderm to secure the strain-relief protective sheath to the fiberoptic cable.

Check for a pressure waveform and record initial ICP.

Interpretation of Waveforms

Interpretation of Waveforms

Four major waveforms are of clinical importance: normal, A, B, and C.

Normal

Normal ICP waves have a steep upward systolic slope followed by a downward diastolic slope with a dicrotic notch. In most cases, this waveform occurs continuously and indicates that the ICP is between 0 and 15 mm Hg.

A wave

Also known as plateau waves, these are the most clinically concerning waveforms. They have a duration of 5-20 minutes and an amplitude of 50 mm Hg over the baseline ICP, up to 100 mm Hg. After an episode of A waves dissipates, the ICP drops sharply and is reset to a baseline level that is higher than when the waves began.

A waves are a sign of severely compromised intracranial compliance. The rapid increase in ICP caused by these waves can result in a significant decrease in CPP and may lead to herniation.

B wave

These appear sharp and rhythmic with a sawtooth pattern. They have duration of less than 2 minutes and have an amplitude of 10-20 mm Hg above the baseline ICP. The waves appear to correlate with respiratory changes and increase in frequency as compensation decreases. They often precede A waves; however, because of their smaller amplitude and shorter duration, B waves are not as deleterious as A waves.

C wave

Also known as Hering-Traube waves, C waves are rapid and rhythmic low-amplitude waves that may be superimposed on other waves. They may be related to increased ICP; however, C waves can also occur in the setting of normal ICP and compliance and appear to fluctuate with respirations or systemic blood pressure changes.