Intracranial Pressure Monitoring Technique

Updated: Sep 17, 2015
  • Author: Gaurav Gupta, MD; Chief Editor: Jonathan P Miller, MD  more...
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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.


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 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.