Chapter 100 Intracranial Hypertension
The collective volume of intracranial contents is the major determinant of intracranial pressure (ICP). The cranial space may be divided into four distinct physiologic compartments, each with separately regulated water content: blood, cerebrospinal fluid (CSF), intracellular fluid (ICF), and extracellular fluid (ECF).
Most CSF is formed by ultrafiltration of fluid from the blood vessels of the choroid plexus lining the ventricles and drains into the subarachnoid space, from where it is absorbed. When ventricular pressure is elevated the flow of fluid may be reversed, back into the brain parenchyma.2 As compensation for intracranial hypertension (ICH), CSF production falls, absorption increases, and a greater volume of CSF is displaced into the spinal subarachnoid space.1,3
The blood-brain barrier (BBB) tightly regulates the entry of solutes into the brain but is permeable to water. Changes in effective osmolality across the BBB are accompanied by water movement to equalize osmolality, but at the expense of changes in cell volume. With increases in the osmolality of intravascular fluid or ECF, ICF may shift to the extracellular environment. With persistence of hyperosmolar conditions in the extracellular fluid for many hours, brain cells, having lost volume, will compensate by generating intracellular osmolytes (idiogenic osmoles) to raise the osmotic pull intracellularly and restore cell volume. Breakdown of these idiogenic osmoles occurs over several days. Rapid decreases in ECF osmolality should be prevented, because the intracellular osmolytes may draw water into the cell, causing cell swelling, membrane disruption, and exacerbation of ICH.4
The high metabolic demands of the brain require maintaining cerebral blood flow (CBF) in the normal range at all times. CBF is dependent on cerebral perfusion pressure (CPP), which is calculated as mean arterial pressure (MAP) minus ICP4-6:
The volume of blood in the brain (cerebral blood volume [CBV]) is affected by factors that change CBF, such as altered vascular tone, and those that impair venous outflow, such as head-down posture, jugular vein compression, or increased intrathoracic pressure.1,4,5 Cerebrovascular vasodilation serves to increase CBF and thereby CBV, leading to increased ICP; cerebral vasoconstriction decreases CBF, CBV, and therefore ICP, but may result in hypoxia and neuronal ischemia.1,4,5
Intracranial pressure ICP is the pressure inside the cranial vault exerted by the tissues and fluids against the encasing bone. Normal ICP in the dog is 5 to 12 mm Hg, similar to that of humans for whom 20 mm Hg is an arbitrary upper limit beyond which treatment for ICH may be instituted1,3 (see Chapter 209, Intracranial Pressure Monitoring). The upper limit of ICP above which treatment is indicated for ICH has not been defined in dogs and cats. It seems reasonable to utilize the human guidelines for ICH until species-specific information is available.
The brain is relatively noncompressible and is encased in bone, causing the volume of the intracranial contents to be fixed. Increase in the volume of one component requires a compensatory decrease in one or more of the others if ICP is to remain unchanged (Monroe-Kellie doctrine). Sources of added volume include hemorrhage, CSF accumulation, vascular congestion, cerebral edema, and decreases in venous outflow (Figure 100-1). Immediate volume buffering responses, specifically displacement of blood and CSF extracranially, are reflected by the pressure-volume curve that relates the temporal change in ICP to expanding intracranial volume.
Figure 100-1 Pressure-volume curve. An idealized elastance curve that illustrates changes in intracranial pressure (ICP) accompanying the progressive addition of intracranial volume. First segment: Compliance is high, compensatory mechanisms are functioning well, primarily a result of expansion of the dura mater in the cranial and cervical spinal space, allowing for added volume with no or little increase in ICP. Second segment: As volume is added to the system, displacement of cerebrospinal fluid and blood allow for further volume additions with progressive changes in ICP. Third segment: The vertical portion of the elastance curve shows the high-pressure, low-compliance situation that occurs when the volume buffering capacity is exhausted. Further displacement of intracranial fluids is not possible and addition of more volume causes an exponential rise in ICP. Decompensation is occurring and any volume buffering at this point is due to distention, compression, and eventual herniation of neural tissues.
Autoregulation of CBF results from a vascular (myogenic) reflex that changes resistance of cerebral arterioles in response to changes in transmural pressure. The purpose is to prevent underperfusion or overperfusion of the brain. Normally this mechanism operates at perfusion pressures between 50 and 150 mm Hg. Outside this range, CBF becomes linear with MAP (Figure 100-2).1,4,5
Figure 100-2 Classic cerebral pressure autoregulation curve. Cerebral autoregulation maintains a relatively constant rate of cerebral blood flow across a wide of range of cerebral perfusion pressures as shown (50 to 150 mm Hg). With intact autoregulation, cerebrovascular tone appears to respond to transmural pressure, which is approximately the same as cerebral perfusion pressure. Note the marked rise and fall in cerebral blood flow as cerebral perfusion pressure changes above and below, respectively, the normal limits of autoregulation. With impairment of autoregulation in the injured brain, cerebral blood flow will passively follow systemic arterial blood pressure.
Chemical regulation of cerebral vascular resistance is influenced by three factors: partial pressure of arterial carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2), and cerebral metabolic rate of oxygen consumption.1,4,5
Cerebral vascular resistance is directly responsive to changes in PaCO2 concentrations, because carbon dioxide combines with water to form hydrogen ions, which when increased in concentration stimulate cerebral vasodilation and when decreased may cause vasoconstriction. Therefore, in the normal brain, hyperventilation decreases PaCO2 causing vasoconstriction, reduced cerebral blood volume, and lowering of ICP.
CBF is coupled to local cerebral metabolism. In regions of high cerebral metabolic activity, pH alterations in the perivascular environment will have a direct influence on cerebral vascular tone. Increased hydrogen ion concentration, as seen with lactic acidosis or accumulation of other acids formed during the course of cerebral metabolism, will cause an increase in CBF. When cerebral metabolic rate of oxygen consumption is decreased, low levels of hydrogen ion concentration will result in decreased CBF locally as a result of arteriolar constriction.
Autoregulation often is impaired in animals with intracranial disease where pressure autoregulation generally is affected first and chemically mediated regulation is affected more as brain injury progresses. When volume buffering and autoregulatory adjustments are exhausted, ICH will lead to decreased CBF, cerebral ischemia, and accumulation of carbon dioxide. Decreased CBF and elevated carbon dioxide levels can stimulate the release of catecholamines which may cause systemic vasoconstriction and increased cardiac output. Baroreceptors sense this hypertensive state and cause a vagally mediated bradycardia. Hypertension and bradycardia secondary to ICH is known as the Cushing response. The catecholamine release also may result in cardiac arrhythmias due to myocardial ischemia, the so-called brain-heart syndrome.
In general terms, causes of ICH can be classified as vascular or nonvascular. Vascular mechanisms of ICH include cerebral vasodilation caused by increased PaCO2, distention of cerebral vessels due to loss of vascular tone, or venous outflow obstruction. Nonvascular mechanisms are increased brain water (interstitial edema or intracellular swelling), masses, or obstruction of CSF outflow.
Pressure gradients associated with ICH may result in movement of neural tissues within and between anatomic compartments (brain herniation) that may perpetuate injury and ischemia by distorting or fracturing brain tissue, and by compression and shearing of cerebral vasculature.1,7
A complete history and physical examination are essential in the assessment of patients suspected to have ICH. A careful neurologic examination is required for accurate clinical diagnosis, institution of therapy, and determination of a baseline to which results of future examinations may be compared. Aspects of the neurologic examination that are of particular importance include level of consciousness, brain stem reflexes, respiratory pattern, motor responses, abnormal postures, and breathing patterns. Papilledema identified on fundic examination is a reliable sign of ICH.