Intracranial hypertension and traumatic brain injury

1

Define intracranial hypertension.

Intracranial pressure (ICP) in humans is normally between 5 and 15 mm Hg. Intracranial hypertension is defined as a sustained ICP greater than 20 mm Hg.

2

What are the determinants of ICP?

The brain parenchyma, cerebrospinal fluid (CSF), and the blood perfusing the brain are all contained within the fixed volume of the cranial vault. The Monro-Kellie doctrine defines the relationship between these components where any increase in a single component must be matched by a decrease in another to maintain a stable ICP. Once compensatory mechanisms are exhausted, including translocation of CSF into the spinal cord and compression of the cerebral vascular bed, any increase in volume will increase ICP.

3

Summarize the conditions that commonly cause intracranial hypertension.

See Table 44.1 .

4

What are the symptoms of intracranial hypertension?

Early symptoms associated with increased ICP include headache, nausea and vomiting, and lethargy. Signs of elevated ICP include papilledema, focal neurological deficits, cranial nerve palsies, progressive decerebrate/decorticate posturing, abnormal brainstem reflexes, abnormal respiratory patterns, and eventually hemodynamic instability/collapse. The constellation of signs and symptoms are related to the severity of the intracranial hypertension and the regional/global compression of brain structures.

5

How can you monitor ICP?

ICP can be monitored either noninvasively or invasively. Common noninvasive methods include imaging studies and physical examination. Imaging studies may show effacement or obliteration of cistern, sulcal, or ventricle CSF spaces, midline shift, and brain herniation, depending upon etiology and severity of ICP. Physical examination with fundoscopy may reveal papilledema, as the CSF is in continuity with the optic nerve.

Invasive methods directly measure ICP and are divided into fluid-based catheter systems (e.g., external ventricular drain) and implantable microtransducers (e.g., fiberoptic sensor). Invasive techniques require access to the intracranial compartment and carry the risk of brain tissue damage, hematoma, and infection. The external ventricular drain (EVD) is a common fluid-based catheter system, which involves placement of a small catheter into the lateral ventricle. The EVD is considered the gold standard because it is cheap, reliable, and allows therapeutic drainage of CSF to treat elevated ICP. The major risks of EVDs include overdrainage of CSF, infection, and hemorrhage. Implantable microtransducers are often placed intraparenchymal but can also be placed in the epidural, subdural, or subarachnoid space. These devices are less traumatic to brain tissue and have less infection and bleeding complications compared with an EVD. However, these devices are prone to measurement “drift,” where the integrity of pressure monitoring decreases over time and cannot be corrected by recalibrating the transducer. This is because the pressure transducer is implanted invasively and cannot be “rezeroed” to atmospheric pressure in contrast to fluid-filled transducer systems (i.e., EVD), where the transducer is external to the patient, often at the level of the tragus or inner ear.

6

Discuss the possible consequences of intracranial hypertension.

Intracranial hypertension can result in a decrease in cerebral perfusion pressure and cerebral blood flow, leading to ischemia. Critical elevations of ICP may precipitate herniation of brain tissue across pressure gradients between dura and bony boundaries. Unilateral brain edema can cause a pressure gradient, leading to uncal herniation, compression of the midbrain, coma, and ipsilateral pupil dilation/hemiparesis. Globally, elevated ICP may cause downward compression and herniation of the brainstem and cerebellum through the foramen magnum. Medullary compression and subsequent ischemia will cause a profound sympathetic activation known as the Cushing reflex : systemic hypertension, reflex bradycardia, and irregular breathing. Brain herniation may damage the cardiorespiratory centers in the medulla, causing respiratory arrest, cardiac arrest, and brain death.

7

What are the determinants of cerebral perfusion pressure?

Cerebral perfusion pressure (CPP) is calculated by the following equation:

CPP, cerebral perfusion pressure ; MAP, mean arterial pressure ; ICP, intracranial pressure ; CVP, central venous pressure

CPP is the difference between MAP and ICP (or CVP, whichever is higher). In an intact autoregulatory system, CBF is maintained at a constant level, despite changes in CPP, where arterial constriction occurs with increases in CPP and arterial dilation occurs with decreases in CPP. Chronic hypertension, strokes, traumatic brain injury (TBI), and brain tumors can shift or blunt cerebral autoregulation of CBF.

8

What is intracranial elastance? Why is it clinically significant?

Intracranial elastance describes the variation in ICP in response to changes in intracranial volume (Elastance = ΔPressure/ΔVolume). Although intracranial elastance is the reciprocal of compliance (Compliance = 1/Elastance = ΔVolume/ ΔPressure), the term elastance better defines this relationship because the ICP change is the result of a change in volume within a closed space. Initially, ICP remains somewhat constant over a limited range of intracranial volumes because of the ability to translocate intracranial CSF and venous blood to the spinal compartments and extracranial vascular beds, respectively. However, when these compensatory mechanisms are exhausted, the intracranial elastance increases (i.e., decreased compliance) and ICP rises exponentially with the slightest increase in volume ( Fig. 44.1 ).

9

How is CBF regulated?

CBF is influenced by several factors, including cerebral metabolic rate, arterial O ₂ and CO ₂ tension, CPP, and intracranial pathology. In general, an increase in the cerebral metabolic rate for oxygen (CMRO ₂ ) leads to an increase in CBF. An increase in the partial pressure of carbon dioxide in arterial blood (PaCO ₂ ) is an extremely powerful cerebral vasodilator, with CBF increasing 1 to 2 mL/100 g/min for every 1 mm Hg change in PaCO ₂ . A decrease in the partial pressure of oxygen (PaO ₂ ) in arterial blood increases CBF, when the PaO ₂ falls below 50 mm Hg. Variations in MAP also may result in changes in CBF. However, with an intact autoregulation system, between a CPP of 50 to 150 mm Hg, flow is nearly constant. Chronic hypertension shifts the autoregulation curve to the right, necessitating a higher baseline MAP to adequately perfuse the brain. In addition, following a brain injury, such as stroke or trauma, autoregulation is impaired, and CBF becomes pressure dependent ( Fig. 44.2 ).

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