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Intracranial Pressure Monitoring


Elevated intracranial pressure (ICP) is seen in head trauma,
intracranial hemorrhage, sub-arachnoid hemorrhage from ruptured brain aneurysm, intracranial tumors,
hepatic encephalopathy,
and cerebral edema.
Intractable elevated ICP can lead to death or devastating neurological damage either by reducing cerebral perfusion pressure (CPP)
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.
The association between the severity of intracranial hypertension and poor outcome after severe head injury is well recognized.
Outcomes tend to be good in patients with normal ICP, whereas those with elevated ICP are much more likely to have an unfavorable outcome.
Elevated ICP carries a mortality rate of around 20%.

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.

Although some investigators have questioned invasive ICP monitoring in improving patient outcomes,
numerous retrospective series and data bank studies have favored the technique.

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.


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.
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.
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.

Leyden, working in Germany in 1866, demonstrated that elevated ICP leads to a slowed pulse and difficulty breathing, with eventual arrest of breathing entirely.
This work was built on in 1890 by Spencer and Horsley
, 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.
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.
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.
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.

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.
LP fell into disuse for ICP monitoring, and researchers began to directly cannulate the ventricular system.

In 1965, Nils Lundberg revolutionized ICP monitoring with his work using bedside strain gauge manometers to record ICP continuously via ventriculostomy.
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.


The most important role of the circulatory system, aside from transporting blood into all parts of the body, is to maintain optimal CPP.
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).
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:

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.

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.
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.

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

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