Page 495 - ACCCN's Critical Care Nursing

472 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

glucose levels are independently associated with enlar- which might precipitate ischaemia in the region sur-
gement of the haematoma. About half of spontaneous rounding the haematoma.
ICH cases originate in the basal ganglia, a third in the The Australian Stroke Foundation’s current guidelines
cerebral hemispheres, and a sixth in the brainstem or recommend a target systolic BP below 180 mmHg or a
cerebellum. 130
mean arterial blood pressure of 130 mmHg. 133 Mana-
There is growing evidence that more than a simple mass gement of BP is particularly important in ICH and
effect compromises the region surrounding the haema- is currently the subject of a large Australian RCT
toma. The haematoma induces an inflammatory response (Interact-2). 134
from plasma that is rich in thrombin and other coagula-
tion end-products released by the clotted haematoma.
Activation and expression of cytotoxic and inflammatory Prevention of cerebral ischaemia
mediators, induction of matrix metalloproteases, leuco- and secondary brain injury
cyte recruitment and disruption of the blood–brain Intravenous therapy should be aimed at maintaining
barrier are all implicated in the inflammation response. euvolaemia with an isotonic fluid, such as normal
Both vasogenic and cytotoxic oedema contribute to saline. Potassium supplementation is often necessary,
ischaemia. although glucose should be avoided, except in rare
cases of hypoglycaemia. Emergency measures for ICP
Clinical manifestations control are appropriate for stuporous or comatose
patients, or those who present acutely with clinical
In 40% of cases, ICH is accompanied by intraventricular signs of brainstem herniation (see the section on
haemorrhage, which can cause acute hydrocephalus and Management of intracranial hypertension and ischaemia).
high ICP, and lessens the chance of a good outcome. The head should be elevated to 30 degrees for optimal
Rapid onset of a focal neurological deficit with clinical balance between perfusion and intracranial pressure
signs of high ICP – such as an abrupt change in level of and to prevent aspiration. Warfarin increases the risk
consciousness, headache, and vomiting – suggest a diag- of ICH 5–10 times, and presenting patients should have
nosis of ICH. However, these symptoms can also take this reversed with fresh frozen plasma, prothrombin-
place after acute ischaemic stroke. For this reason, CT or complex concentrates and vitamin K. Early in the
MRI is essential for confirming dziagnosis. Rapid progres- course of patients with ICH, even with exclusion of
sion to coma with motor posturing suggests massive coagulopathy, injection of activated factor VII results
supratentorial haemorrhage, bleeding into the brainstem in significant reduction in the rate of haematoma
or diencephalon, or acute obstructive hydrocephalus due expansion. 90
to intraventricular haemorrhage. Over 90% of patients
have acute hypertension exceeding 160/100 mmHg,
whether or not there is a history of pre-existing hyper- SUMMARY
tension. Dysautonomia in the form of central fever,
hyperventilation, hyp er glycaemia, and tachycardia or bra- Support of neurological function commences with an
dycardia is also common. 131 overview of specific pathophysiological alterations of
consciousness, seizures, motor and sensory function,
cerebral perfusion, ischaemia, cerebral oedema and
Nursing Practice intracranial hypertension. Therapeutic management of

The following nursing practice should be undertaken. intracranial hypertension and vasospasm are applied to
brain injury in general. Central nervous system dis orders
include traumatic brain and spinal injury, their aetio-
Intubation logy, clinical pathophysiology and management. Cere-
Patients with ICH, especially those with infratentorial brovascular disorders focus on intracerebral ha emorrhage
bleeding, may require intubation for protection of the and subarachnoid haemorrhage. Ischaemic stroke is dis-
airway as well as sometimes to acutely lower ICP. The cussed briefly.
decision to intubate should be based on the individual’s Meningitis and encephalitis are presented in infection
level of consciousness, ability to protect the airway and inflammation with Guillain–Barré syndrome, myas-
and arterial blood gas levels, rather than on an arbitr- thenic crisis in neuromuscular alterations. The selected
ary GCS score. neurological cases include caring for a potential organ
donor patient, status epilepticus and intracerebral haem-
Specific blood pressure management orrhage. A traumatic brain injury case is presented with
clinical questions.
There is a high risk of deterioration, death or dep-
endency with raised blood pressure after ICH; thus it The research vignette is an Australian and NZ TBI epi-
and should be corrected immediately to minimise the demiological study that defines the burden of TBI
potential for haematoma expansion and to maintain and compares clinical practice with the published TBI
adequate cerebral perfusion pressure. 132 Extreme hyper- Guidelines. ICP monitoring practice was deficient in
tension within the first six hours is common and comparison to the guidelines at the time of the study,
should be aggressively but carefully treated to avoid but a later study reported an improvement in this
excessive reduction of the cerebral perfusion pressure, practice.