Page 475 - ACCCN's Critical Care Nursing

452 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

Management of Cerebral Oxygenation potential to become established as a key component of
and Perfusion multi-modality monitoring during management of acute
Cerebral monitoring in brain-injured patients has focused brain injury during neurointensive care.
on the prevention of secondary injury to the brain owing Management of Intracranial Hypertension
to impaired perfusion. However, ICP monitoring and ICP
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manipulation does not equal cerebral oxygenation. Raised ICP is treated by removing mass lesions and/or
There are currently four techniques that can be used to increasing the volume available for expansion of injured
assess cerebral oxygenation: jugular venous oxygen satu- tissue. This may be achieved by reducing one of the other
ration, positron emission tomography, near-infrared available intracranial fluid volumes:
spectroscopy, and brain tissue oxygenation monitoring 1. CSF by ventricular drainage (as discussed
(PbtO 2 ). Their strengths and weaknesses are the subject previously)
of several recent reviews. 30,31 The selection among these 2. cerebral blood volume by hyperventilation,
forms of oxygenation monitoring is focused on the osmotic diuretic therapy or hypothermia
appropriateness of focal or global monitoring, the loca- 3. brain tissue water content by osmotic diuretic
tion of the monitor in relation to the injury, and the therapy
intermittent or continuous nature of the monitoring. The 4. removing swollen and irreversibly injured brain
use of PbtO 2 , as assessed by the intraparenchymal polaro- 5. increasing cranial volume by craniotomy
graphic oxygen probe, has the advantage of directly moni- decompression.
toring the zone of injury and thus earlier detection of
perfusion abnormalities that may impact global cerebral Each modality will be discussed in terms of its physiologi-
oxygenation later. This may also allow the rescue of cal effect, efficacy and potential use for prevention of
watershed areas of perfusion. However, there is contro- secondary brain injury.
versy regarding the appropriate placement of such moni-
tors. Insertion of the probe into non injured areas yields Hyperventilation
data equivalent to global assessments of cerebral oxygen- Hyperventilation reduces PaCO 2 and will reduce ICP by
ation. Consequently, close attention should be paid to vasoconstriction induced by alkalosis but it also decreases
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the location of the catheter in relation to the injury in cerebral blood flow. The fall in ICP parallels the fall in
interpretation and use of PbtO 2 results. Jugular venous CBV. Hyperventilation decreases regional blood flow to
oxygen saturation (SjO 2 ) is representative of global cere- hypoperfused areas of the brain. Thus, generally PaCO 2
bral oxygen metabolism, but technically it is difficult to should be maintained in the low normal range of about
obtain reproducible results. Cerebral tissue oxygenation 35 mmHg. Hyperventilation should be utilised only
values of <20 mmHg are targeted for intervention based when ICP elevations are refractory to other methods and
on Brain Trauma Foundation (BTF) guidelines but only when brain tissue oxygenation is in the normal range.
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at level III evidence. PbtO 2 can be increased by increas- The BTF Guidelines recommend hyperventilation therapy
ing the FiO 2 /PaO 2 ratio and by reducing cerebral meta- only for brief periods when there is no neurological dete-
bolic requirements for oxygen (CMRO 2 ) using brain rioration or for longer periods when ICP is refractory to
temperature control with active cooling and metabolic other therapies. 32
rate control with sedation and adequate feeding. Addi-
tional interventions such as volume infusion, transfu- Osmotherapy
sion, and inotropic support directed at improving cardiac
output can also be used to increase oxygen delivery. 33 Acute administration of an osmotic such as mannitol or
hypertonic saline produces a potent antioedema action,
Brain inflammation after injury contributes to impaired primarily on undamaged brain regions with an intact
oxygenation and perfusion, but currently its management BBB. This treatment causes the movement of water from
has not translated to successful clinical management. the interstitial and extracellular space into the intravascu-
However, the use of cerebral microdialysis (MD) and the lar compartment, thereby improving intracranial compli-
measurement of biochemical markers (lactate, glutamate, ance or elastance. In addition to causing ‘dehydration’ of
pyruvate, glycerol and glucose) of cerebral inflammation the brain, osmotic agents have been shown to exert ben-
and metabolism do contribute towards early warnings of eficial non-osmotic cerebral effects, such as augmentation
impending hypoxia/ischaemia and neurological deterio- of cerebral blood flow (by reducing blood viscosity,
ration, and this may allow timely implementation of resulting in enhanced oxygen delivery), free radical scav-
neuroprotective strategies. Elevation of the lactate/ enging, and diminishing CSF formation and enhancing
pyruvate ratio is typically seen in cerebral ischaemia and CSF reabsorption. 37
mitochondrial dysfunction, and has been used to tailor
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therapy. However, MD reflects only local tissue bio- The BTF recommends mannitol in intracranial hyperten-
chemistry and the accurate placement of the catheter is sion in bolus administration, keeping the serum osmolari-
+
crucial. Furthermore, because there are wide variations in ties greater than 320 mOsm/L, plasma Na <160 mmol/L
measured variables, trend data are more important than and avoiding hypovolaemia. Urine output after mannitol
absolute values. Although MD is used routinely in a few administration needs to be replaced, generally with
centres it has not yet been introduced into widespread normal saline. Brain free water is increased with 5% dex-
clinical practice and, at present, should be considered a trose and hyperglycaemia; hence these need to be avoided.
research tool for use in specialist centres. MD has the The use of frusemide in conjunction with mannitol