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448 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
immune system. There are two phases. In the relatively passages connecting the ventricles become blocked, pre-
early phase, activated spleen cells and lymph nodes and venting movement of CSF to its drainage sites in the
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blood mononuclear cells secrete significantly enhanced subarachnoid space just inside the skull. This type of
levels of TNF-α, IL-6 and IL-2. This then results in global hydrocephalus is called ‘non-communicating’. Reduction
immunosuppression affecting the spleen, lymph nodes, in absorption rate, called ‘communicating hydrocepha-
thymus and a significant decrease in the number of lus’ can be caused by damage to the absorptive tissue.
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immune cells in the circulation. When cerebral blood Both types lead to an elevation of the CSF pressure within
flow (CBF) falls to about 40% of normal, EEG slowing the brain. A third type of hydrocephalus, ‘normal pres-
occurs. When CBF falls below 10 mL/100 g/min (20%), sure hydrocephalus’, is marked by ventricle enlargement
the function of ionic pumps fails, which leads to mem- without an apparent rise in CSF pressure, which mainly
brane depolarisation. Cerebral ischaemia and reperfusion affects the elderly.
injury contri bute to the cascade of physiological events,
termed secondary brain injury. Recent studies have shown Hydrocephalus may be caused by: congenital brain
that low-dose paracetamol reduces inflammatory protein defects; haemorrhage, in either the ventricles or the sub-
release from brain endothelial cells exposed to oxidant arachnoid space; CNS infection (syphilis, herpes, menin-
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stress and that propofol protects against neuronal gitis, encephalitis or mumps); and tumours. Irritability is
apotosis. 17 the commonest sign of hydrocephalus in infants and, if
untreated, may lead to lethargy. Bulging of the fontanelle,
Cerebral Oedema the soft spot between the skull bones, may also be an
early sign. Hydrocephalus in infants prevents fusion of
Cerebral oedema is defined as increased brain water the skull bones, and causes expansion of the skull. Symp-
content. The brain is particularly susceptible to injury toms of normal pressure hydrocephalus include demen-
from oedema, because it is located within a confined tia, gait abnormalities and incontinence. Tre atment
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space and cannot expand, and because there are no lym- includes ventriculostomy drainage of CSF in the short
phatic pathways within the CNS to carry away the fluid term, or a surgical shunt for those with chronic condi-
that accumulates. The white matter is usually much more tions. Either is predisposed to blockage and infection.
involved, as myelinated fibres have a loose extracellular
space, while the grey matter has a much higher cell
density with many connections and much less loose Intracranial Hypertension
extracellular space. The two main subdivisions of cere- Intracranial pressure is the pressure exerted by the con-
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bral oedema are extracellular and intracellular. tents of the brain within the confines of the skull and
the BBB. The Munro–Kelly hypothesis states that the
Intracellular (cytotoxic) oedema contents of the cranium (60% water, 40% solid) are
Cellular swelling, usually of astrocytes in the grey matter, not compressible and thus an increase in volume causes
a rapid rise in pressure and changes to the compen-
is generally seen after cerebral ischaemia caused by cardiac satory reserve and pulse amplitude, as illustrated in Figure
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arrest or minor head injury. The blood–brain barrier 17.2. Normal ICP is 0–10 mmHg, and a sustained
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(BBB) is intact and capillary permeability is not impaired. pressure of >15 mmHg is termed intracranial hyperten-
The cause of intracellular oedema is anoxia and isch- sion, with implications for CBF. Areas of focal ischaemia
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aemia; it is usually not clinically significant, and is revers- appear when ICP is >20 mmHg and global ischaemia
ible in its early phases.
occurs at >50 mmHg. ICP waveform contains valuable
information about the nature of cerebrospinal patho-
Extracellular (vasogenic) oedema physiology. ICP increased to the level of systemic arterial
Extracellular oedema involves increased capillary perme- pressure extinguishes cerebral circulation, which will
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ability, and had been termed ‘BBB breakdown’. Rises restart only if arterial pressure rises sufficiently beyond
in brain water content with extracellular oedema are the ICP to restore cerebral blood flow. Autoregulation
often quite dramatic, because the fluid that results from of cerebral blood flow and compliance of the cerebro-
increased capillary permeability is usually rich in pro- spinal system are both expressed in ICP. Methods of
teins, resulting in the spread of oedema and brain isch- waveform analysis are useful, both to derive this infor-
aemia. This can lead to cytotoxic oedema, and to the mation and to guide the management of patients. 25
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progressive breakdown of both astrocytes and neurons.
While the classification of oedema is useful to define Initially, intracranial compliance allows compensation
specific treatments, it is somewhat arbitrary, as cytotoxic for rises in intracranial volume due to autoregulation.
and vasogenic oedema often occur concurrently. In fact, During a slow rise in volume in a continuous mode, the
each of these processes may cause the other. Ultimately, ICP rises to a plateau level at which the increased level
these changes can lead to raised intracranial pressure and of CSF absorption keeps pace with the rise in volume
herniation. with ample compensatory reserve. This is expressed as
an index, as shown in Figure 17.3. Intermittent expan-
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sion causes only a transient rise in ICP at first. When
Hydrocephalus sufficient CSF has been absorbed to accommodate the
Hydrocephalus is the result of an imbalance between the volume, the ICP returns to normal. The ICP finally rises
formation and drainage of cerebrospinal fluid (CSF). to the level of arterial pressure which itself begins to rise,
Reduced absorption most often occurs when one or more accompanied by bradycardia or other disturbances of

