Intracranial pressure

From Free net encyclopedia

Intracranial pressure, or ICP, is the pressure of the brain, Cerebrospinal fluid (CSF), and the brain's blood supply within the intracranial space. Intracranial pressure can be measured in centimetres of water (cmH₂O) or millimeters of mercury (mmHg). ICP is normally 0 to 15 mmHg in adults, up to 10 mmHg in children, and up to 5 mmHg in infants (Shepherd, 2004, Tolias and Sgouros, 2003). Since the skull is a rigid compartment of a fixed size, swelling of the brain can lead to increases in ICP, with potentially deadly results.

Contents 1 Increased ICP 1.1 Results of increased ICP 1.2 Monro-Kellie model of ICP 1.3 Causes of increased ICP 1.4 Signs and symptoms of increased ICP 1.5 Treatment of increased ICP 2 Low ICP 3 References

Increased ICP

One of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure (Orlando Regional Healthcare, 2004). ICP cannot go past 40 mmHg in an adult without causing severe harm (Dawodu, 2004). Even intracranial pressures between 25 and 30 mm Hg are usually fatal if prolonged, except in children, who can tolerate higher pressures for longer times (Tolias and Sgouros, 2003). Most commonly due in head injury to intracranial hematoma or cerebral edema, an increase in pressure can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause the brain to herniate, and restrict blood supply to the brain, leading to an ischemic cascade (Graham and Gennareli, 2000).

Results of increased ICP

One of the main dangers of increased ICP is that it can cause ischemia by decreasing cerebral perfusion pressure (CPP), the amount of blood able to reach the brain. As pressure in the brain increases, it becomes more and more difficult to squeeze blood into the intracranial space. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.

Highly increased ICP, if caused by a one-sided space-occupying process (eg. an haematoma) can result in midline shift, a dangerous condition in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to buildup of CSF (Downie, 2001). Prognosis is much worse in patients with midline shift than in those without it (National Guideline Clearinghouse, 2005). Another dire consequence of increased ICP combined with a space-occupying process can be brain herniation, in which the brain is squeezed past structures within the skull, severely compressing it.

Monro-Kellie model of ICP

According to the Monro-Kellie model of intracranial pressure, the brain, CSF, and cerebral blood make up three compartments within the skull, which remains a fixed size (Gruen, 2002). The extent to which each compartment takes up space within the skull is the amount of pressure it exerts; if a compartment increases in size, the intracranial pressure increases accordingly (Gruen, 2002). Thus if the brain swells, intracranial pressure goes up, unless the volume of CSF or blood can be reduced by the same amount (Gruen, 2002). Thus in head injury, CSF is commonly displaced and blood flow is reduced to reduce the intracranial volume. Unfortunately, reduction in cerebral perfusion pressure can lead to ischemia and damage to or death of brain cells, which in turn can cause the brain to swell more. The need to reduce blood volume and pressure and the need for adequate blood supply are opposing factors that make management of increased intracranial pressure especially difficult.

Causes of increased ICP

Causes of increased intracranial pressure include:

• Traumatic brain injury
• Pseudotumor cerebri (Idiopathic intracranial hypertension)
• Arnold-Chiari malformation
• A brain tumor or other mass lesion
• Severe hypertension
• Lyme disease
• Hydrocephalus

One major reason for increased ICP in brain injury is dilatation of cerebral blood vessels due to a loss of autoregulation (Su and Huh, 2005). Another is cerebral edema. Another contributor to increased ICP is the reduced ability of veins to remove blood from the intracranial space, leading to its buildup. This can occur when the head is turned to the side or when medical instruments such as spinal stabilization collars are too tight, restricting flow from the jugular veins (Tolias and Sgouros, 2003). It can also occur in a condition called venous sinus thrombosis, in which a clot becomes lodged in a cerebral vein and prevents blood from exiting the skull (Shepherd, 2004). The treatment is thrombolysis to dissolve the clot, but this procedure is risky in head injury patients because it could cause other intracranial bleeds (Shepherd, 2004).

Signs and symptoms of increased ICP

The body's compensatory response to an increase in ICP leads to a set of symptoms by which the condition can be recognized in a patient. In addition to other symptoms that suggest a rise in ICP including headache, visual disturbances, nausea, vomiting, and altered level of consciousness, a cluster of symptoms called Cushing's triad indicate the body’s response to a rise in ICP. Cushing's triad involves an increased systolic blood pressure, an increasing difference between systolic and diastolic blood pressures, a decrease in pulse rate, and an abnormal respiratory pattern (Sanders et al). Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Cheyne-Stokes respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon (Stock and Singer, 2004). Hyperventilation occurs when the brain stem or tegmentum is damaged (Stock and Singer, 2004). In children, a slow heart rate is especially suggestive of high ICP. In infants, the fontanels, or soft spots on the head where the skull bones have not yet fused, bulge when ICP gets too high. Papilledema, while being a classic sign of elevated intracranial pressure, takes several hours to develop and is often not present in an acute setting. However, these symptoms may be vague or absent. The most reliable sign of increased intracranial pressure is decreased level of consciousness.

Treatment of increased ICP

One of the most important treatments for high ICP is to ensure adequate airway, breathing, and oxygenation, since inadequate oxygen levels or excess carbon dioxide cause cerebral blood vessels to dilate and ICP to rise (Su and Huh, 2005). Inadequate oxygen also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, which dilates blood vessels (Orlando Regional Healthcare, 2004). On the other hand, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a patient with a ventilator or bag valve mask can temporarily reduce ICP but limits blood flow to the brain in a time when the brain may already be ischemic. Artificially ventilating a patient at a fast rate used to be a standard part of head trauma treatment because of its ability to rapidly lower ICP, but the chance of developing ischemia was recognized as too much of a risk (Shepherd, 2004). Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon dioxide levels were returned to normal too quickly (Shepherd, 2004). Now hyperventilation is used when signs of brain herniation are apparent because the damage herniation can cause may make it worthwhile to constrict blood vessels. Another way to lower ICP is to raise the head of the bed, allowing for venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in inadequate blood supply to the brain.

In the hospital, blood pressure can be artificially raised in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes and thereby lessen swelling (Shepherd, 2004). Since hypertension is the body's way of forcing blood into the brain, medical professionals do not normally interfere with it when it is found in a head injured patient (Stock and Singer, 2004). When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers (Orlando Regional Healthcare, 2004).

Struggling can increase metabolic demands and oxygen consumption, as well as increasing blood pressure (Bechtel, 2004; Su and Huh, 2005). Thus children may be paralyzed with drugs if other methods for reducing ICP fail. Paralysis allows the cerebral veins to drain more easily, but can mask signs of seizures, and the drugs can have other harmful effects (Su and Huh, 2005).

Pain is also treated to reduce agitation and metabolic needs of the brain, but some pain medications may cause low blood pressure and other side effects (Orlando Regional Healthcare, 2004).

Intracranial pressure can be measured by means of a lumbar puncture or continuously with intracranial transducers (only used in neurosurgical intensive care). A catheter can be surgically inserted into one of the brain's lateral ventricles. The same catheter can also be used to drain CSF to reduce pressure (Orlando Regional Healthcare, 2004).

Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain (Orlando Regional Healthcare, 2004).

A drastic treatment for increased ICP is decompressive craniectomy, in which a part of the skull is removed and the dura mater is expanded to allow the brain to swell without crushing it or causing herniation (Shepherd, 2004).

Low ICP

It is also possible for the intracranial pressure to drop below normal levels, though increased intracranial pressure is a far more common (and far more serious) sign. The symptoms for both conditions are often the same, leading many medical experts to believe that it is the change in pressure rather than the pressure itself causing the above symptoms.

References

1. Bechtel K. 2004. "Pediatric Controversies: Diagnosis and Management of Traumatic Brain Injuries." Trauma Report. Supplement to Emergency Medicine Reports, Pediatric Emergency Medicine Reports, ED Management, and Emergency Medicine Alert. Volume 5, Number 3. Thomsom American Health Consultants.
2. Dawodu S. 2004. "Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology" Emedicine.com.
3. Downie A. 2001. "Tutorial: CT in Head Trauma"
4. Gruen P. 2002. "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery.
5. National Guideline Clearinghouse. 2005. Firstgov.
6. Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries."
7. Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
8. Shepherd S. 2004. "Head Trauma." Emedicine.com.
9. Stock A and Singer L. 2004. "Head Trauma." Emedicine.com.
10. Su F and Huh J. 2006. "Neurointensive Care for Traumatic Brain Injury in Children." Emedicine.com
11. Tolias C and Sgouros S. 2003. "Initial Evaluation and Management of CNS Injury." Emedicine.com.he:לחץ תוך גולגולתי