What are the signs of increased intracranial pressure?

General Physiology of Intracranial Pressure

The upper limit of normal ICP in adults and older children is given as 15 to 20 mm Hg, although the usual range is 5 to 10 mm Hg. Transient physiologic changes resulting from coughing or sneezing often produce pressures exceeding 30 to 50 mm Hg, but ICP returns rapidly to baseline levels.

ICP can be measured with the use of low-volume displacement transducers to interface with CSF pathways in the intraventricular, intraparenchymal, subdural, or epidural space. The ICP waveform is normally pulsatile and can be divided into three major components (Fig. 52-1). The baseline, or average, level is commonly referred to as the ICP, whereas rhythmic components superimposed on this level are associated with cardiac and respiratory activity. In order to completely describe ICP, one should specify the magnitude of the baseline, or “steady state” level and the amplitude and periodicity of the pulsatile components. Changes in these pulsatile components can be one of the earliest signs that the ICP is beginning to rise, as a reflection of the increased conductance of pressure waves through a “tightening” brain.

Cardiac and respiratory activity creates pulsatile components via cyclical changes in cerebral blood volume. Left ventricular contraction contributes the cardiac component, which has a frequency similar to that of the peripheral arterial pulse. The exact vessels that transmit the peripheral pulse remain to be established. Early studies suggested that the choroid plexus and pial arteries were responsible,6 although later analysis has implicated the high-compliance venous blood vessels.7

The respiratory contribution to the ICP waveform arises as a result of fluctuations in arterial blood pressure and cerebral venous outflow during the respiratory cycle, generated by pressure changes in the thoracic and abdominal cavities. During inspiration there is a fall in arterial blood pressure and an increase in pressure gradient from cerebral veins to central venous capacitance vessels. This gradient drives cerebral venous return, which is therefore increased on inspiration, with a concomitant drop in cerebral blood volume. Mechanical ventilation and intrathoracic disease may considerably alter the respiratory contribution to the ICP waveform. This concept has resulted in experimental and clinical trials of devices that can alter intrathoracic pressure during the respiratory cycle of resuscitation. The impedance threshold device limits inflow of respiratory gas and therefore creates greater and longer negative intrathoracic pressure.8 The device has been shown to improve cerebral perfusion and coronary perfusion and to reduce ICP in cardiac arrest and hypotension.9,10 Its application to or effect on elevated ICP in primary CNS disease such as traumatic brain injury is yet to be determined.

If the ICP waveform is examined in more detail and at a higher chart speed, then the waveform of highest frequency can be seen to consist of as many as five smaller peaks. Three of these are relatively constant (Fig. 52-2)—the percussion wave (W1), the tidal wave (W2), and the dicrotic wave (W3).7,11 The percussion wave, the most constant in amplitude, derives from pulsations in large intracranial arteries.12 The tidal wave has a more variable shape and is thought to arise from brain elastance. The tidal wave and the dicrotic wave are separated by the dicrotic notch, which corresponds to the dicrotic notch in the arterial pulse waveform.

Raised intracranial pressure

Raised intracranial pressure is a medical emergency. It causes headache, ataxia, confusion, drowsiness and coma. Papilloedema is usually present if the raised pressure has been longstanding, but because it takes time to develop, may be absent. Sixth nerve palsy is a common false localizing sign due to compression of the 6th nerve as it passes over the petrous ridge. Other signs include 3rd nerve palsy in temporal lobe herniation, failure of upgaze, due to midbrain compression, a rise in systolic blood pressure and a fall in pulse due to medullary involvement.

Intermittent obstruction of CSF flow can cause sudden headache with loss of consciousness. For example, intraventricular tumours may block CSF flow on sudden manoeuvres such as coughing or straining.

In children who develop raised intracranial pressure, usually a result of hydrocephalus, before closure of the skull sutures, presentation may be with a rapidly enlarging head size and minimal neurological compromise.

Control of Intracranial Pressure and Brain Relaxation

The necessity of preventing increases in intracranial pressure (ICP) or reducing ICP that is already increased is recurrent in neuroanesthesia. When the cranium is closed, the objectives are to maintain adequate cerebral perfusion pressure (CPP) (CPP = mean arterial pressure [MAP] − ICP) and prevent the herniation of brain tissue between intracranial compartments or through the foramen magnum (Fig. 57.1).1 When the cranium is open, the issue may be to provide relaxation of the intracranial contents to facilitate surgical access or, in extreme circumstances, reverse ongoing brain herniation through the craniotomy site. The principles that apply are similar whether the cranium is open or closed.

The various clinical indicators of increased ICP include headache (particularly headache that awakens the patient at night), nausea and vomiting, blurred vision, somnolence, and papilledema. Computed tomography (CT) findings suggestive of either increased ICP or reduced intracranial compliance reserve include midline shift, obliteration of the basal cisterns, loss of sulci, ventricular effacement (or enlarged ventricles in the event of hydrocephalus or ventricular trapping), and edema. Edema appears on a CT scan as a region of hypodensity. The basal cisterns appear on CT as a dark (hypodense fluid) halo around the upper end of the brainstem (Fig. 57.2). They include the interpeduncular cistern, which lies between the two cerebral peduncles, the quadrigeminal cistern, which overlies the four colliculi, and the ambient cisterns, which lie lateral to the cerebral peduncles.

Fig. 57.3 presents the volume-pressure relationship of the intracranial space. The plateau phase occurring at low volumes reveals that the intracranial space is not completely closed, which confers some compensatory latitude. Compensation is accomplished principally by the translocation of cerebrospinal fluid (CSF) and venous blood to the spinal CSF space and the extracranial veins, respectively. Ultimately, when the compensatory potential is exhausted, even tiny incremental increases in volume can substantially increase ICP. These increases have the potential to result in either herniation of brain tissue from one compartment to another (or into the surgical field) (seeFig. 57.1), with resultant mechanical injury to brain tissue, or in reduction of perfusion pressure, leading to ischemic injury.

Several variables can interact to cause or aggravate intracranial hypertension (Fig. 57.4). For clinicians faced with the problem of managing increased ICP, the objective is, broadly speaking, to reduce the volume of the intracranial contents. For mnemonic purposes, the clinician can divide the intracranial space into four subcompartments (Table 57.1): cells (including neurons, glia, tumors, and extravasated collections of blood), fluid (intracellular and interstitial), CSF, and blood.

The cellular compartment. This compartment is largely the province of the surgeon. However, it may be the anesthesiologist’s responsibility to pose a well-placed diagnostic question. When the brain is bulging into the surgical field at the conclusion of evacuation of an extra-axial hematoma, the clinician should ask whether a subdural or extradural hematoma is present on the contralateral side that warrants either immediate burr holes or immediate postprocedure radiologic evaluation.

The CSF compartment. There is no pharmacologic manipulation of the CSF space with a time course and magnitude that is relevant to the neurosurgical operating room. The only practical means of manipulating the size of this compartment is by drainage. A tight surgical field can sometimes be improved by passage of a brain needle by the surgeon into a lateral ventricle to drain CSF. Lumbar CSF drainage can be used to improve surgical exposure in situations with no substantial hazard of uncal or transforamenal magnum herniation.

The fluid compartment. This compartment can be addressed with steroids and osmotic/diuretic agents. The use of these agents is discussed later.

The blood compartment. This compartment receives the anesthesiologist’s greatest attention because it is the most amenable to rapid alteration. The blood compartment should be viewed as having two separate components: venous and arterial.

Measurement of ICP

ICP is referenced at the level of the foramen of Monro, and in a supine adult is between 7 and 15 mmHg. Intracranial hypertension is defined as ICP > 20 mmHg sustained for > 5 min (Brain Trauma Foundation et al., 2007). An acute increase in ICP to this level may begin to manifest clinical symptoms (Table 5.1) requiring intervention. While isolated intracranial hypertension does not decrease the level of consciousness until ICP > 40 mmHg, the concurrent shift of brain structures may result in a coma even at lower ICP levels (Ropper, 1986). Aside from an ICP value, visualization of the ICP waveform itself is crucial in determining intracranial compliance, which will guide ICP therapies (Fig. 5.2 and the following section). In the intensive care unit, there are several methods for directly monitoring ICP.

Table 5.1. Signs and symptoms of increased intracranial pressure

The transduction of ICP via an external ventricular drain is the gold standard for measurement. Less invasive options, including intraparenchymal, subdural, and epidural pressure monitors, although these devices do not allow for drainage of CSF, may have drifting accuracy over time and may not reflect global ICP but rather the local pressure in their corresponding cranial compartments (Fig. 5.3). Noninvasive ICP measurement is likewise an area of heavy research focus. Ultrasound methods are well described, including optic nerve ultrasound for measurement of optic nerve sheath diameter to quantify papilledema, and a transcranial doppler ultrasound to measure parameters affected by ICP, such as pulsatility index. While efforts have been made to correlate these measurements with quantitative values for ICP, they remain largely binary measures (elevated or not), with an insufficient resolution to replace invasive methods, and reliability and repeatability highly dependent on the operator (Zhang et al., 2017).

Reduction of Intracranial Pressure

For patients with bacterial meningitis who have signs of increased intracranial pressure (e.g., altered level of consciousness; dilated, poorly reactive, or nonreactive pupils; ocular movement disorders) and who are stuporous or comatose, it has been suggested that intracranial pressure–guided treatment could be beneficial.513 However, it is unclear which patients may benefit from such an approach, and interventions to decrease the intracranial pressure may be harmful as well. A study in 1412 episodes of bacterial meningitis showed that half of the patients had a very CSF high openings pressure at the lumbar puncture (>40 cm H2O/>29 mm Hg), of whom the majority had a favorable outcome.60 Studies advocating reduction in intracranial pressure have advised to reduce the pressure below 20 mm Hg. In one study of 15 patients with bacterial meningitis in whom intracranial pressure was measured,514 intracranial pressure was successfully lowered in most patients by a broad range of measures and using unconventional volume-targeted (“Lund concept”) intracranial pressure management, which consisted of sedation, corticosteroids, normal fluid and electrolyte homeostasis, blood transfusion, albumin infusion, decrease of mean arterial pressure, treatment with a prostacyclin analogue, and eventually thiopental, ventriculostomy, and dihydroergotamine. In nonsurvivors, mean intracranial pressure was significantly higher and cerebral perfusion pressure was markedly lower than in survivors despite treatment; however, this was not a comparative study and the results should be interpreted with caution.

Several methods are available to reduce intracranial pressure,290,513 including elevation of the head of the bed to 30 degrees to maximize venous drainage with minimal compromise of cerebral perfusion; hyperventilation to maintain the Paco2 between 27 and 30 mm Hg, which causes cerebral vasoconstriction and a reduction in cerebral blood volume; use of hyperosmolar agents (e.g., mannitol) to make the intravascular space hyperosmolar to the brain and permit movement of water from brain tissue into the intravascular compartment; and corticosteroids. However, some experts have questioned the routine use of hyperventilation to reduce intracranial pressure in patients with bacterial meningitis. In infants and children with bacterial meningitis who have initially normal CT scans of the head, hyperventilation can safely reduce elevated intracranial pressure because it is unlikely that cerebral blood flow would be reduced to ischemic thresholds. However, in children with cerebral edema evident on head CT, cerebral blood flow is more likely to be normal or reduced. Although hyperventilation might decrease intracranial pressure, it would do so at the cost of a significant reduction in cerebral blood flow, possibly approaching ischemic thresholds. These patients may benefit more from the early use of diuretics, osmotically dehydrating agents (provided that intravascular volume is protected), and corticosteroids; however, controlled trials exploring these issues have yet to be performed.

Intracranial Pressure and Cerebral Perfusion Pressure

Elevated ICP may occur in patients with intracranial pathology such as severe traumatic brain injury, subarachnoid hemorrhage, intracranial tumors, and cerebral edema. Obviously, prompt recognition and treatment of elevated ICP is important. The ICP can be measured using an intraventricular catheter (external ventricular drain), fiberoptic monitor implanted into the parenchyma of the brain, or subdural/epidural bolt. The intraventricular catheter provides the most accurate monitoring of ICP; it also allows for therapeutic CSF drainage to treat raised ICP. The management of ICP has the potential to influence outcome, particularly when care is targeted, individualized, and supplemented with data from other monitors.

KEY POINTS

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ICP reflects the ability of the craniospinal axis to accommodate extra volume.

Within a rigid skull any increase in one volume compartment needs to be matched by an equal decrease in another or ICP will rise (Monro-Kellie doctrine).

The CSF and CBF compartments provide some buffering of increasing volume.

Once compensatory capacity is exhausted, further small increases in volume lead to a large rise in ICP.

The most common causes of raised ICP are mass lesions, brain edema, and increased cerebral blood or CSF volume.

In patients with headache, altered consciousness, or papilledema, elevated ICP needs to be suspected.

There are no pathognomonic radiologic signs of high ICP, although some features may suggest intracranial hypertension.

Introduction

Raised intracranial pressure (RICP) may be caused by space-occupying lesions including intracranial tumors, obstructed circulation and readsorption of cerebrospinal fluid (CSF) resulting in hydrocephalus, or pseudotumor cerebri syndromes. These conditions generate frequent clinical questions in the eye clinic. For example, patients in primary eye care may have physical signs which point toward RICP and which require urgent neurologic evaluation; other specialists frequently request ophthalmic assessment when there is known or suspected RICP and patients with treated RICP need to be followed carefully to be sure that vision remains stable.

Delivery considerations

Intracranial pressure can increase to as high as 70 cm H2O (normal, 20 cm H2O) during the first and second stages of labor. Patients with intracranial neoplasms can have baseline increases in intracranial pressures, placing them at risk of cerebral herniation during valsalva or placement of neuraxial anesthesia (Stevenson and Thompson, 2005). An assisted second stage of labor with vacuum or forceps may be indicated in instances when valsalva is contraindicated. Vaginal delivery is often still preferred over cesarean delivery to minimize fluid shifts associated with the perioperative period and increases in intracranial pressure associated with intubation.

Abstract

Elevated intracranial pressure (ICP) represents one of the most serious complications of acute brain injury, contributing a significant degree of morbidity and mortality in this patient population. Etiologies of elevated ICP can range from mass lesions and cerebral edema to accumulation of fluid in the ventricular and vascular intracranial compartments. Owing to its deleterious effects on outcome, elevated ICP is considered to be a medical and surgical emergency, requiring prompt recognition and appropriate management. Management strategies for elevated ICP include maintenance of adequate perfusion/ventilation/temperature control, neurosurgical intervention, sedation, osmotic therapy, and hyperventilation.