• Knowledge of neuroanatomy and physiology is needed.

• Understanding is needed regarding the assembly and maintenance of the intraventricular catheter with an external transducer and drainage system, care of the insertion site, and drainage techniques.

• Principles of aseptic technique should be understood. Of all the intracranial pressure monitoring devices, external ventricular drains (EVDs) have the greatest risk of infection.^3,6

• The normal range for intracranial pressure (ICP) is 0 to 15 mm Hg.^3,25,28 This measurement reflects the pressure exerted by the intracranial contents within the skull, including brain, blood, and cerebrospinal fluid.²⁵

• Cerebral perfusion pressure (CPP) is a derived mathematic calculation that indirectly reflects the adequacy of cerebral blood flow. The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP); thus, CPP = MAP – ICP. ^3,27 The normal CPP range for adults is approximately 60 to 100 mm Hg²¹ or a mean of 80 mm Hg.^19,28 The optimal CPP for a given patient and clinical condition is not entirely known. ICP and CPP should be managed concomitantly. According to the Brain Trauma Foundation Guidelines, an acceptable CPP for an adult with a severe traumatic brain injury (Glasgow Coma Scale [GCS] score of equal to or less than 8) lies between 50 and 70 mm Hg.⁶ Patients with aneurysmal subarachnoid hemorrhage vasospasm may need higher CPPs to maintain adequate perfusion through vasospastic cerebral blood vessels.² Patients with other neurologic injuries require individualized CPP parameters reflective of the neuropathology and brain perfusion needs.

• Elevations in ICP result when one or more intracranial components—blood, cerebrospinal fluid (CSF), or brain tissue—increase without an accompanying decrease in one or two of the other intracranial components. This is known as the Monro-Kellie doctrine or hypothesis.^3,19

• Clinical conditions that frequently result in increased intracranial pressure include traumatic brain injury, subarachnoid hemorrhage,² intraparenchymal hemorrhage,⁸ brain tumor, meningitis, and hydrocephalus.^3,26 An EVD may be indicated in the management of intracranial pressure in each of these conditions.²¹

• Fiberoptic catheters and the microsensors that are placed during surgery in the surgical site or through a bolt in the skull are also used to monitor the ICP. They may be placed in the epidural, subdural, subarachnoid, ventricular, and intraparenchymal spaces.^27,28 These catheters are sentinels for increased ICP but are not designed for treatment of increased ICP with CSF drainage.^27,28 In contrast, when the ventricular catheter is inserted and transduced at the level of the foramen of Monro, approximately at the level of the external auditory canal, it produces a value and a waveform that reflects the ICP. The EVD is considered the most accurate ICP monitor.^3,6

• CSF is formed within the lateral ventricles of the cerebral hemispheres by the choroid plexus. From the lateral ventricles, fluid drains into the foramen of Monro, the intraventricular foramina, into the third ventricle adjacent to the thalamus. Although most of the CSF is made in the choroid plexus of the lateral ventricles, the third ventricle contributes some CSF, which then passes through the aqueduct of Sylvius into the fourth ventricle at the pons and medulla. The choroid plexus in the roof of the fourth ventricle contributes an additional small amount of CSF. The fluid then enters into the subarachnoid space, with the major portion of the fluid moving through the foramen of Magendie, where it is dispersed around the spinal cord and through the foramen of Luschka, where it flows around the brain. CSF is absorbed by the arachnoid villi, also known as arachnoid granulations, where it drains into the venous system to be returned to the heart.^5,7

• CSF is a clear colorless liquid of low specific gravity with no red blood cells and only 0 to 5 white blood cells (WBCs). Approximately 150 mL of CSF circulates within the CSF pathways in the brain and spinal subarachnoid space. CSF is secreted at the rate of 0.35 mL/min or approximately 20 mL/hr.⁵

• ICP waveform morphology reflects transmission of arterial and venous pressure through the CSF and brain parenchyma. The normal ICP waveform has three or four peaks, with P₁ being of greater amplitude than P₂, and P₂ of greater amplitude than P₃. P₁ is thought to reflect arterial pressure; P₂, P₃, and P₄ (when present) have been described as choroid plexus or venous in origin (see Fig. 88-2).^3,27 The amplitude of P₂ may exceed P₁ with increased ICP or decreased intracranial compliance (see Fig. 88-3).

• ICP waveform trends include a, b, and c waves. The a waves, also referred to as plateau waves, are associated with ICP values of 50 to 100 mm Hg and last 5 to 20 minutes. The a waves are associated with abrupt neurologic deterioration and herniation (Fig. 88-4). The b waves (Fig. 88-5), with ICP values of 20 to 50 mm Hg, last 30 seconds to 2 minutes and may become a waves. The c waves (Fig. 88-6) may coincide with ICPs as high as 20 mm Hg but are short lasting and without clinical significance (see Fig. 88-6).³

• Some external ventricular drainage systems may also provide simultaneous drainage and trending of the intracranial pressure.

• Management of acute brain injury is aimed at decreasing secondary brain injury from increased intracranial pressure, decreased cerebral perfusion pressure, impaired autoregulation, hypotension, hypoxemia, cerebral ischemia, hypercarbia, hyperthermia, hypoglycemia, hyperglycemia, or abnormalities in cerebral blood flow. Interventions should include a decrease in environmental stimuli, elevation of the head of the bed, alignment of the head and neck in a straight position to promote venous drainage, the avoidance of constrictive devices about the neck that might impede arterial flow to the brain and venous drainage from the brain, and attaining and maintaining normothermia without shivering.^3,25

• In addition to CSF drainage, management of increased ICP frequently requires the use of certain pharmacologic agents to lessen intracranial pressure, including sedation and analgesia, osmotic diuretics, hypertonic saline, neuromuscular blockade, and barbiturates. In the case of barbiturate coma, continuous electroencephalographic (EEG) monitoring for burst suppression is necessary to achieve the desired decrease in cerebral oxygen consumption and electrical stimuli.¹³ Additional strategies include decompressive craniectomy and hemispherectomy.^3,12,27,32

• Underdrainage of CSF may result in sustained increased intracranial pressure and herniation.^21,24,27,28