Keeping the balance: Understanding intracranial pressure 
Andrew H. Wyatt RN 
Melissa V. Moreda RN, BSN-C 
DaiWai M. Olson RN, CCRN, PhD 

Nursing2009 Critical Care
September 2009 
Volume 4 Number 5
Pages 18 - 23

You arrive to work only to find that it's your turn to float. You report to the neurologic ICU where you're assigned to care for Kendra McClure, 34, who suffered a severe closed traumatic brain injury after being thrown from her horse. During shift report you're told that Ms. McClure is at risk for increased intracranial pressure (ICP). Before you panic, relax, because you may be surprised at how much you already know about ICP. In this article, we'll help you reinforce that knowledge and understand the dynamics of ICP. In an upcoming article, we'll discuss ICP monitoring and how you'd care for a patient like Ms. McClure.

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Understanding ICP

ICP is literally the pressure inside the cranium as a result of blood, tissue, and the cerebrospinal fluid (CSF) that circulates in the ventricles and subarachnoid space. The normal range of this pressure is between zero and 10 mm Hg; 15 mm Hg is considered the upper limit of normal.1 Cerebral perfusion pressure (CPP), another key value, is an expression of the driving force for supplying blood to the brain cells. The value is the difference between mean arterial pressure (MAP) and ICP, and should be maintained between 50 and 70 mm Hg.

The brain and interstitial fluid occupy 80% of the space inside the skull, with the remaining space equally divided between CSF and blood in circulation. As with any pressure, ICP is an expression of the relationship between size and volume. The Monro-Kellie hypothesis (also called the Monro-Kellie doctrine) states that the adult skull is a rigid compartment filled to capacity with three essentially noncompressible contents: brain tissue, CSF, and blood. These contents can change in volume but strive to remain in equilibrium—if the volume of one increases, the others must reciprocally decrease. If this doesn't occur, for example, in cerebral edema, cerebral perfusion is at risk, and the patient can suffer secondary brain injuries.2

In any patient, ICP is a dynamic value, can vary significantly over a short period, and is different within the different compartments in the brain. For example, the patient's intraventricular pressure may be normal at the same time that pressure can be elevated in tissue adjacent to a tumor.1

Many normal body processes, such as pressure changes that occur throughout each cardiac cycle and each respiratory cycle, alter ICP.3 Short bursts of elevated ICP are common, even in healthy people. For example, when you sneeze, ICP rises suddenly and transiently, but the uninjured brain can quickly adjust. However, Ms. McClure's injured brain may have lost compliance, posing the risk that her ICP may stay elevated above 15 mm Hg, a condition also known as intracranial hypertension. Compliance is a measure of the brain's ability to maintain intracranial equilibrium in response to physiologic or external challenges.

Sustained increased ICP can cause secondary brain injury, so monitor changes in ICP over time and be ready to respond. You can evaluate the patient's ICP by performing serial neurologic assessments, or by using radiographic imaging (computed tomography [CT] or magnetic resonance imaging), pupillometry, ICP monitoring devices such as an intraventricular catheter, and lumbar puncture.

What can raise ICP?

Anything that increases the volume of brain, blood, or CSF can raise ICP. Let's look at some examples.

* Brain. We don't normally think of the brain as changing in size, but it does. Brain tissue, like any tissue, can swell, and cerebral edema (an abnormal fluid accumulation in the intracellular space, extracellular space, or both, associated with an increased brain volume) is one of the most dangerous causes of increased ICP. For example, damaged brain cells are more permeable to sodium and water, resulting in intracellular edema. The patient's serum sodium and albumin levels also come into play, as they determine serum osmolality (the affinity for water). As serum osmolality decreases, for example, secondary to hyponatremia or hypoalbuminemia, capillary colloidal osmotic pressure decreases and water flows more freely into the cell, leading to cerebral edema and increased ICP. Brain-occupying lesions such as cerebral tumors are another cause of increased brain volume.

* Blood. The amount of blood inside the skull can increase or decrease dramatically in short periods. The classic example of an increase in intracranial blood is hemorrhage. The location of the bleeding determines how fast the blood accumulates and the amount of devastation that occurs. For example, bleeding in the subdural space is venous, and therefore slower than the arterial bleeding that can occur in the subarachnoid space. Accumulating blood displaces brain tissue, often into the ventricles.

Chemical changes also can increase or decrease blood volumes. Carbon dioxide (CO2) is a potent cerebral vasodilator, so excess CO2, such as in an oversedated patient experiencing bradypnea, increases cerebral blood flow, potentially increasing ICP. Hypercapnia (defined as a PaCO2 of 45 mm Hg or more) is dangerous because as the brain tissue continues to swell, it compresses the vessels supplying the brain with oxygen-rich blood. This compression also prevents the removal of CO2, which causes a decrease in brain tissue pH and an acidic environment. The body attempts to compensate for the acidosis by sending more oxygen-rich blood to the brain, further causing ICP to rise.

* CSF. The average adult produces CSF at a rate of about 20 mL/hour or about 500 mL/day. This clear, odorless solution fills the ventricles in the brain, the subarachnoid space, and the spinal cord, acting as a shock absorber and providing nutrients to the neural structures. The CSF flows through the brain, spinal cord, and four ventricles and exits the cisterns (reservoirs) at the base of the brain. The arachnoid villi act as one-way valves, letting CSF flow into the bloodstream when its pressure is greater than the venous pressure. Obstruction of this system can cause a buildup of CSF or noncommunicating hydrocephalus. Other conditions that increase CSF volume include increased CSF production (as in choroid plexus papilloma) and decreased CSF absorption (as in subarachnoid hemorrhage and communicating hydrocephalus).

Secondary brain injury

Brain damage after traumatic brain injury falls into two categories: primary injury from direct contact to the head or brain can be focal (a contusion or laceration) or diffuse (a concussion). Secondary injury, which develops later from physiologic processes triggered by the injury, includes increased ICP, intracranial hemorrhage, cerebral edema, ischemic brain damage, and infection.1

Ms. McClure suffered her primary brain injury at the time she was thrown from her horse. From the moment the paramedics arrived at the scene, medical interventions have been aimed at preventing secondary brain injury, in which cerebral autoregulation is impaired or lost. Autoregulation is the organ's ability to maintain constant blood flow despite significant changes in arterial perfusion pressure. In healthy adults, cerebral blood flow automatically decreases if MAP falls below 60 mm Hg (the lower end of normal), and cerebral blood flow increases if MAP exceeds 150 mm Hg, the upper end of normal.1 Disruptions in autoregulation mean that areas of the brain can be over- or underperfused, and cerebral tissues begin to die.

Brain cells can die through necrosis or apoptosis (programmed cell death). In the first phase of apoptosis, which lasts for 12 to 24 hours after the injury, cerebral blood flow drops, reducing tissue perfusion. The second phase (24 hours to 5 days after the injury) is marked by cellular edema; during this phase, you'll commonly see ICP start to rise. The third phase (starting on the sixth day after injury) may last for several weeks and is characterized by slow blood flow, which further decreases cerebral perfusion and sets the stage for final cell death.

Signs and symptoms of increased ICP

Halfway through your shift, you recognize that Ms. McClure had been alert and cooperative, but is now restless and agitated. She's still oriented, but slower to respond than she was at the start of your shift. Suspecting that these assessment findings may be signs of elevated ICP, you perform a full neurologic assessment, looking for the following signs and symptoms of increased ICP:

* Decreased level of consciousness. In most cases, this is an early sign of increasing ICP. Expect that she'll have subtle changes in her assessment with small changes in her ICP and drastic changes in her exam with drastic elevations in her ICP. This is why your baseline exam is crucial—by detecting signs and symptoms of increased ICP early, you have the best chance of intervening before it's too late for medical treatments to be effective.

* Pupillary dysfunction. Pupillary reaction to light is an essential component of the neurologic assessment. When assessing pupils, note the size, shape, and reaction to light of each pupil.

One of Ms. McClure's pupils (ipsilateral to the lesion) is now larger and reacts more slowly than the other, an early indication of uncal herniation. Early on, edema tends to be compartmentalized, so the pupillary dysfunction occurs ipsilateral to the lesion. Later, both pupils dilate to the midpoint and become nonreactive to light. Bilaterally dilated and fixed pupils indicate brainstem herniation.

* Abnormalities in vision and extraocular movements. These changes occur in the early stages of increased ICP. Ms. McClure must be conscious and cooperative to perform a full assessment of her visual acuity, extraocular muscle movements, and visual fields. Look for decreased visual acuity, field cuts, and patient complaints of blurred vision and diplopia.

* Deteriorating motor function. Early signs include monoparesis or hemiparesis on the same side as the cerebral lesion. Later, as pressure increases on the brainstem, you'll see hemiplegia and unilateral or bilateral decortication or decerebration. Assess your patient's motor system, including grading of muscle strength.

* Headache. If cerebral perfusion decreases to compensate for the edema, the cerebrovascular system will dilate in a response to restore homeostasis by increasing cerebral blood flow. This vasodilation pulls on the bridging veins and arteries in the brain and can cause headache.

* Vomiting. In a patient with increasing ICP, vomiting is a result of infratentorial lesions or direct pressure on the vagal motor centers in the floor of the fourth ventricle in the medulla. These motor centers control vomiting.

* Changes in vital signs. Changes in BP are a late sign, reflecting pressure on the brainstem. In the compensatory phase of increasing ICP, you'll see increasing systemic BP with a widening pulse pressure. As the patient's clinical condition deteriorates and decompensation occurs, BP decreases. Changes in pulse rate are associated with brainstem involvement. Pressure on the vagal control mechanism in the medulla may cause bradycardia. During decompensation, the pulse becomes irregular, rapid, and thready before stopping. Changes in the patient's respiratory pattern are caused by direct pressure on the respiratory centers of the pons and medulla; respiratory patterns depend on the anatomic level affected. (For example, central neurogenic hyperventilation is associated with midbrain and upper pons lesions.) An acute increase in ICP can trigger acute neurogenic pulmonary edema in a patient without cardiac dysfunction.

Temperature variations usually are the result of hypothalamic dysfunction. The patient's body temperature typically remains within normal limits during the compensatory phase of increasing ICP, but may become elevated during decompensation.

* Papilledema. Optic disc swelling doesn't develop in all patients, and because it doesn't occur until ICP is markedly elevated, it may be a late sign in some patients or the first finding if the patient's ICP increased slowly. The subdural and subarachnoid spaces continue along the optic nerve, so increased ICP is transmitted along this nerve. Using an ophthalmoscope, you'll see optic disc swelling.

* Signs and symptoms of impending herniation. These include impaired brainstem reflexes (corneal, gag, and swallowing), and Cushing's triad (bradycardia, hypertension, and respiratory irregularity).

Turning to treatment

Based on your exam of Ms. McClure and the changes in her clinical status, you suspect that her ICP is increasing and must be treated immediately. Follow your facility's policy to notify the appropriate healthcare personnel (typically the physician and your nurse manager) of this potentially life-threatening condition. Although you should expect to receive a set of emergency medical orders, not all of the interventions to reduce ICP require an order.

For example, proper positioning can promote venous return from the brain. Obstruction of venous return increases cerebral blood volume, which in turn increases ICP.1 Unless contraindicated, raise the head of the bed to 30 degrees to improve jugular venous drainage and to lower ICP and help prevent aspiration pneumonia.4 If the patient is hypovolemic, elevating the head of the bed could threaten CPP even more. Maintain adequate intravascular volume.1 Avoid the prone position, extreme hip flexion, and neck flexion. The venous cerebrovascular system lacks valves, so an increase in intra-abdominal, intrathoracic, or neck pressure impedes venous return and increases ICP. Avoid Trendelenburg's position, which is contraindicated in patients with neurologic dysfunction. Also avoid tight tracheostomy securement devices, soft collars, or any other device that would place pressure on the neck and impede venous drainage from the brain.1

Emesis, frequent suctioning, and Valsalva's maneuver may increase intrathoracic or intra-abdominal pressure and may increase ICP, so intervene as necessary and limit interventions that could raise ICP.

Temperature control is emerging as a key physiologic parameter in controlling ICP. The uninjured brain is typically 0.5° C to 1° C (0.9° F to 1.8° F) warmer than core body temperature. As temperature rises, so do cerebral blood flow and cerebral metabolic rate, which in turn increase ICP and produce more CO2 and lactic acid. Hyperthermia also acts as a catalyst for neuronal apoptosis (programmed cell death).5

Although therapeutic hypothermia is being investigated as a way to reduce ICP, the standard of care is to maintain your patient's core body temperature as close to normal as possible.5 Monitor the core body temperature hourly, adjust the room temperature as needed, and administer antipyretics and fluid resuscitation as indicated, or in specific cases, by using noninvasive or invasive cooling devices, like temperature-regulating blankets or intravascular cooling devices. Cool the patient slowly and try to prevent shivering, which will increase ICP.

Nursing and medical interventions to reduce ICP will most likely occur simultaneously and may include:

* Ensuring adequate oxygenation. Brain cells can't store oxygen, so interventions to promote adequate oxygen saturation levels are vital.

* Seizure control, including prophylaxis for patients at high risk. Seizures increase metabolic rate and ICP.

* Osmotic diuretics to reduce cerebral edema. Mannitol, the most commonly used osmotic diuretic, pulls fluid from edematous cerebral tissue into the plasma and promotes systemic diuresis. Because mannitol crystallizes easily, use an I.V. inline filter when administering it.

* Analgesics, sedatives, neuromuscular blockade, or a high-dose barbiturate coma. Because pain and agitation can exacerbate increased ICP, analgesics and sedatives may help. Sedation goals should be based on patient needs and reassessed regularly. Neuromuscular blockade also may be used to control agitation (which can increase cerebral metabolism, BP, and ICP). For more on monitoring a sedated patient, see Bispectral index monitoring in critical care: What's the science? in the July issue of Nursing2009 Critical Care.

A high-dose barbiturate coma is a second-line intervention for hemodynamically stable patients whose increased ICP is refractory to medical and surgical interventions. Barbiturates cause vasoconstriction and decrease cerebral blood flow, reducing cerebral blood volume and ICP.1

Frequently monitor your patient's ICP, CPP, and serum osmolality, keeping the latter value between 310 and 315 mOsm.1

* Hyperventilation. Historically, reducing CO2 has been used to decrease ICP, but research now supports CO2 reduction only as a temporary measure, unless your facility is capable of monitoring for adequate cerebral oxygenation.5–7

* Fluid management and euvolemia. Hypertonic sodium chloride solution in varying concentrations, such as 1.8%, 3%, or 7.2%, may be ordered for varying durations to reduce cellular edema and ICP. Intermittent bolus doses of 23.4% sodium chloride solution also may be ordered to further control refractory elevated ICP.

Helping Ms. McClure

The results of a stat brain CT scan confirm that Ms. McClure has significant cerebral edema. She's prescribed osmotic diuretics and you're asked to prepare for an emergent bedside ventriculostomy, to establish ICP monitoring, the subject of our next article.

REFERENCES

1. Hickey JV. The Clinical Practice of Neurological & Neurosurgical Nursing, 6th ed. Lippincott Williams & Wilkins; 2008. [Context Link]

2. Arbour RB. Intracranial hypertension: monitoring and nursing assessment. Crit Care Nurse. 2004;24(5):19–33. [Context Link]

3. Hickey JV, Olson D, Turner D. Intracranial pressure waveform analysis during rest and suctioning. Biol Res Nurs. April 26, 2009 [epub ahead of print]. [Context Link]

4. Grap MJ, Munro CL. Preventing ventilator-associated pneumonia: evidence-based care. Crit Care Nurs Clin North Am. 2004;16(3): 349–358. [Context Link]

5. Brain Trauma Foundation; American Association of Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care, AANS/CNS, Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2007;24(suppl 1):S1–S106. [Context Link]

6. Littlejohns LR, Bader MK. Prevention of secondary brain injury: targeting technology. AACN Clin Issues. 2005;16(4):501–514. [Context Link]

7. Andrews PJ, Citerio G, Longhi L, Polderman K, Sahuquillo J, Vajkoczy P. NICEM consensus on neurological monitoring in acute neurological disease. Intensive Care Med. 2008;34(8):1362–1370. [Context Link]


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