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Intensive Care Management of Subarachnoid Haemorrhage

Article  in  Journal of the Intensive Care Society · January 2013

DOI: 10.1177/175114371301400108

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Review articles © The Intensive Care Society 2013

Intensive care management of

subarachnoid haemorrhage 2C04, 3C00
D Highton, M Smith

Aneurysmal subarachnoid haemorrhage (SAH) is a devastating disease associated with high mortality and poor outcome
in many survivors. Aggressive treatment by a comprehensive multidisciplinary team is associated with improved
outcome, but the intensive care management of SAH presents significant challenges. Multimodal neuromonitoring may
detect secondary insults before irreversible neuronal damage has occurred, and is increasingly being used to guide
treatment. This article reviews current trends in the intensive care management of SAH from aspects of initial
resuscitation to recent developments in the prevention and management of complications, including delayed cerebral
ischaemia. Evidence from clinical trials and recent consensus guidance is reviewed.

Keywords: subarachnoid haemorrhage; delayed cerebral ischaemia; cerebral vasospasm; multimodal monitoring

Introduction leading to a temporary arrest of the cerebral circulation and

Aneurysmal subarachnoid haemorrhage (SAH) is a devastating
disease with an incidence of 2 to 22.5 per 100,000 population.1
Although it accounts for only 3-5% of strokes overall, it is
responsible for a large loss of productive life years because it
commonly occurs in younger people, peaking between 40 and
60 years. One-month case fatality is as high as 35% even in
high income countries, and around one third of those who
survive need life-long care, with a further third having residual
cognitive impairment that affects their functional status and
quality of life.2 Mortality is higher and good functional
outcome less likely in patients with poor grade SAH, those
over 65 years of age and those who develop complications.3,4
Early aggressive resuscitation and multidisciplinary intensive
care management is associated with improved outcomes5 and
consensus guidelines for the intensive care management of
SAH have recently been published.6
Pathophysiology
Approximately 85% of cases of SAH are related to spontaneous
rupture of an intracranial aneurysm in the basal cerebral
arteries, leading to escape of blood at high pressure into the
subarachnoid space. Non-aneurysmal peri-mesencephalic
bleeds, with haemorrhage centred anterior to the midbrain or
pons, account for 10% of cases. A further 5% are divided
between multiple, rarer pathologies, including traumatic
causes. Several SAH grading scales have been described but the
World Federation of Neurological Surgeons (WFNS) scale,
based on the Glasgow Coma Scale (GCS) and presence of
motor deficits, is most commonly used because of its simplicity
and objectivity.7 Such scales guide management that is
influenced by the severity of the SAH, and also offer an early
estimation of prognosis.
In severe SAH, intracranial pressure (ICP) may rise to levels
approaching or above mean arterial blood pressure (ABP),
unconsciousness.8 Global cerebral oedema causing widespread
ischaemic neuronal injury may ensue and this is associated
with poor outcome.9 There are multiple cerebral metabolic
repercussions of SAH and these are also recognised as
independent factors influencing outcome.10,11
Clinical presentation and diagnosis
The classic history of SAH is one of sudden onset headache,
often described as the ‘worst imaginable.’ However, this is non-
discriminatory and only around 1% of patients presenting to
emergency departments with headache will subsequently be
diagnosed with SAH.12 Other clinical features range from neck
stiffness, vomiting and altered consciousness, to seizures, loss
of consciousness and sudden death.
Standard non-contrast CT is the investigation of choice and
is diagnostic in up to 95% of cases. A normal scan, particularly
early after the ictus, does not exclude SAH and in the presence
of a good history and normal scan, lumbar puncture should be
performed.12 Confirmation of the presence of red blood cells or
their metabolites in the cerebrospinal fluid identifies an
additional 3% of patients who subsequently have an aneurysm
detected by cerebral angiography.13 The diagnostic sensitivity of
lumbar puncture is increased when performed at least six to 12
hours after the initial ictus, although this results in a delay in
initiating treatment.
Acute treatment
Acute treatment is similar to that for any critically ill patient
and focuses on maintenance of adequate ventilation and
haemodynamic stabilisation. In addition, attention must be
given to maintenance of cerebral perfusion, minimising the risk
of re-bleeding and achieving a rapid diagnosis. This presents
many challenges in the emergency department as multiple
goals must be achieved simultaneously, often remote from

28 Volume 14, Number 1, January 2013 JICS

 Review articles

neuroscience input. Unconscious patients, or those with a

falling GCS, should be intubated and ventilated to maintain
PaO2 >13.0 kPa and PaCO2 4.5-5.0 kPa. Short-term moderate
hyperventilation (PaCO2 4.0-4.5 kPa) may be indicated if
intracranial hypertension is suspected, eg in the presence of
hydrocephalus, an expanding intraparenchymal haematoma or
cerebral oedema. Hypertension is a normal response to SAH,
although high blood pressure increases the risk of re-bleeding,
whereas excessive reductions in blood pressure risk the
development of cerebral ischaemia. Extreme hypertension
should be treated cautiously with short-acting agents but
modest elevations in blood pressure (mean ABP <110 mm Hg)
do not require treatment.6 Prior to securing the aneurysm, pre-
morbid blood pressure should be used to refine pressure
targets, although mean ABP is usually maintained between
90-110 mm Hg. Hypotension should be meticulously avoided.
Once the poor grade patient is stabilised, immediate transfer
to a neurosciences centre should be undertaken. Stable patients
with good grade SAH should be transferred urgently so that
definitive treatment can be undertaken within 24 hours of the
ictus. Recent guidance recommends that patients with SAH
should be treated at high-volume centres with timely access
to multidisciplinary teams since this is associated with
improved outcomes.6
Figure 1 Non-contrast CT scans showing (A) subarachnoid
Diagnostic imaging haemorrhage; (B) subarachnoid haemorrhage with extensive
intraventricular blood and associated hydrocephalus; (C)
A repeat CT scan may be necessary to confirm the diagnosis, subarachnoid haemorrhage with intraventricular drain in situ; (D)
identify acute hydrocephalus and allow treatment planning of subarachnoid haemorrhage and cerebral oedema with loss of
the causative aneurysm (Figure 1). CT angiography (CTA) is appearance of the brain sulci and gyri, and effaced ventricles
an appropriate first step to identify the anatomical territory (with ventricular drain in situ)
of the aneurysm and interpretation by an experienced
neuroradiologist reliably identifies aneurysms >4 mm.14 Formal assessment that their aneurysm was not suitable for coiling.
four-vessel digital subtraction angiography (DSA) remains the There was a rarity of posterior circulation and middle cerebral
investigation of choice in many centres and is required if CTA artery aneurysms in ISAT and, because posterior circulation
is equivocal. and middle cerebral artery aneurysms are preferentially treated
Additional imaging can inform treatment planning, by coiling and clipping respectively, this also raises the
particularly in poor grade patients. Perfusion CT quantifies possibility of sample bias. However, the proportion of cases
regional and global hypoperfusion15 and various magnetic that are unsuitable for endovascular treatment is likely to be
resonance imaging (MRI) sequences identify ischaemia and much lower today because of advances in technology and
provide a wealth of information on metabolic and perfusion expertise since 2002. The majority of aneurysms are now
variables.16 primarily treated by endovascular options, but coiling is still
not a replacement for surgical treatment. Aneurysms in
Securing the aneurysm selected locations, those >25 mm, those with a wide neck or
Early aneurysm control reduces the risk of re-bleeding and with branches arising from the aneurysm, may not be
allows higher ABP to prevent or treat cerebral hypoperfusion. amenable to coiling, and some may have a worse outcome with
The widespread use of endovascular coiling of intracranial coiling compared to clipping.18 Each patient and aneurysm is
aneurysms represents a major advance in the treatment of SAH different and a treatment decision must be made for each
because minimally invasive and effective treatment is possible patient individually by a multidisciplinary team.
even in the sickest patients. The International Subarachnoid
Aneurysm Trial (ISAT) compared endovascular and surgical Re-bleeding
techniques and confirmed an improvement in early survival in Re-bleeding was previously the primary cause of death
selected patients receiving endovascular therapy, with a small following poor grade SAH but rates have dramatically reduced
excess of late bleeds.17 since the shift towards early securing of the ruptured
ISAT has been criticised for many reasons.18 In brief, 69% of aneurysm. The greatest risk of re-bleeding occurs within the
the 9,559 patients eligible for recruitment into the study were first 24 hours and is highest in those with the poorest grade.
excluded because of lack of equipoise. Since almost all The overall re-bleeding rate is 4-7%, with a 1.5% risk per day
intracranial aneurysms can be treated by surgery, it follows that for up to two weeks after the ictus.
a large proportion of patients was excluded because of an Acute antifibrinolytic therapy may reduce the risk of

JICS Volume 14, Number 1, January 2013 29

Review articles
Method Diagnostic indices
Neurological examination Conscious level and motor deficit
Cerebral angiography Vascular anatomy
CT angiography and perfusion CT Vascular anatomy and perfusion deficits
Transcranial Doppler FV>120-140 cm/sec or increase in
ultrasonography FV>50 cm/sec per 24 hours
Cerebral microdialysis Increases in lactate:pyruvate ratio,
glycerol and glutamate
Brain tissue PO2 PbrO2 <15 mm Hg
Table 1 Diagnosis and monitoring of delayed cerebral ischaemia. DCI=delayed cerebral ischaemia; FV=blood flow velocity.
re-bleeding by as much as 40% but is not associated with
improved outcome, possibly because of micro-thrombosis-
related cerebral ischaemia.19 The short-term use of anti-
fibrinolytics should currently be considered only in those at
high risk of re-bleeding in whom definitive treatment of the
aneurysm is delayed.20
Intensive care management
Following securing of the aneurysm, the intensive care
management of SAH involves treatment of acute complications
such as hydrocephalus requiring external ventricular drainage
(Figure 1), optimisation of systemic physiology and the
prevention or treatment of delayed cerebral ischaemia (DCI)
and non-neurological complications. Aggressive treatment is
now recommended for all but the most hopeless cases since
substantial numbers of even poor grade patients may do well
following comprehensive multidisciplinary therapy.5,21
Nevertheless, some patients will have a poor outcome despite
maximal therapy and it is essential that early aggressive
treatment is linked to compassionate end-of-life care if a
satisfactory degree of clinical recovery does not occur within
an appropriate time scale.
Monitoring
Multimodal cerebral monitoring, including ICP, brain tissue
oxygen tension, transcranial Doppler ultrasonography (TCD),
cerebral microdialysis and electrophysiological monitoring,
allows integration of multiple aspects of cerebral physiology
with systemic physiological variables.23,24 In this way
individualised patient care can be delivered with the aim of
preventing or minimising secondary ischaemic injury. After
SAH, this is particularly relevant in terms of balancing cerebral
oxygen supply and demand in the setting of acute injury,
and in the subsequent detection and treatment of DCI.25
Intracranial pressure is increasingly being monitored,
particularly in poor grade patients, as the need for aggressive
management of intracranial hypertension is undisputed.22,26
This can be achieved via a ventricular catheter placed to
relieve hydrocephalus or via a standard transducer-
tipped intraparenchymal monitor. Changes in brain tissue
30
Comments
Gold standard in non-sedated patients
No assessment of cerebral hemodynamic
and metabolic consequences of DCI
Quantifies perfusion deficits
Widely used bedside technique
Considerable inter-individual variation
Restricted to specialist centres
Focal measure
Cellular metabolic changes may predict DCI
before its clinical appearance
Restricted to specialist centres
Focal measure
biochemistry and oxygenation may identify impending or
actual cerebral hypoxia/ischaemia before changes in other
monitoring modalities or the patient’s clinical status are
apparent.27 Although this extends the potential treatment
window, it remains to be determined whether interventions
directed towards normalisation of these biomarkers will result
in improved clinical outcome. Impaired vascular reactivity has
been linked with poor outcome after SAH and integration of
cerebral monitoring signals can be used to derive indices of
cerebrovascular reactivity.28
There is recent interest in electrophysiological monitoring
after SAH. Nonconvulsive seizures and status epilepticus occur
more frequently than previously recognised and continuous
electroencephalography has a key role in their detection and
therefore management.29 Cortical spreading depolarisations
(SDs) are pathological events characterised by near-complete
sustained depolarisation of neurons and astrocytes that result
in secondary injury related to mitochondrial damage,
accumulation of intracellular calcium and excitotoxicity. SDs
may occur in up to 70% of patients after SAH30 but their
detection currently requires placement of an electrode strip
directly onto the brain surface, thus limiting routine
monitoring on the ICU.
There is currently no consensus regarding multimodal
monitoring in patients with SAH and the majority of modalities
have not been thoroughly validated nor their influence on
outcome determined.23
Delayed cerebral ischaemia
DCI is a term applied to any neurological deterioration,
including focal neurological deficits and altered consciousness,
which persists for more than one hour and cannot be
explained by other abnormalities identified by radiographic,
laboratory or electrophysiological investigations. It may be
unrecognised clinically in some patients because of their poor
clinical grade or the concurrent administration of sedatives.
DCI occurs in around 30% of patients, peaks between four and
10 days after the ictus and persists for several days. It is second
only to the initial haemorrhage as a cause of morbidity and
mortality after SAH.
Volume 14, Number 1, January 2013 JICS

Treatment Proven outcome benefits
Nimodipine Yes
Magnesium No
Statins Possible
Anti-fibrinolytics No
Anti-platelet agents No
Triple-H therapy None for prevention
Possible benefit of hypertension in DCI
Endovascular treatment Likely
Table 2 Treatment of delayed cerebral ischaemia. DCI=delayed cerebral ischaemia.
Pathophysiology
Although DCI has been attributed to cerebral vasospasm, the
exact relationship between the two is unclear. DCI can occur in
the absence of vasospasm and vice versa, and ischaemia often
involves more than one vascular territory.31 Other mechanisms
contributing to DCI include vascular dysautoregulation, micro-
thrombi, direct neurotoxic effects and cortical SDs.5
Diagnosis
DCI is detected clinically by a reduction in level of
consciousness with or without a focal neurologic deficit. In
unconscious or sedated patients, several methods can be used
to identify DCI but DSA remains the diagnostic gold standard
(Table 1). The risks and time requirements of this invasive
intervention mean that alternative and complementary
diagnostic tools such as CT angiography and CT perfusion,
which together allow characterisation of vascular anatomy and
associated cerebral perfusion abnormalities, are increasingly
being used.32
Transcranial Doppler measures blood flow velocity (FV) in
basal cerebral arteries, and consecutive TCD examinations
should be carried out after SAH; blood flow velocity (FV)
>120-140 cm/s, or FV increases >50 cm/s/day from baseline,
are generally accepted to be indicative of developing or
established DCI. However, there is considerable inter-
individual variation and a recent study analysing 1,877 TCD
examinations found that almost 40% of patients with clinical
evidence of DCI never had FVs that exceeded 120 cm/s.33
Treatment decisions should not therefore be based on TCD
findings alone. As changes in the cerebral blood flow (CBF)
affect FV, the Lindegaard ratio, which compares FV in the
ipsilateral middle and internal carotid arteries and is unaffected
by changes in cerebral blood flow (CBF), is often used.
A ratio >3.0 is indicative of vasospasm and values >6 suggest
severe spasm.
Multimodal monitoring, particularly brain tissue PO2 and
cerebral microdialysis, might also identify vasospasm and
JICS Volume 14, Number 1, January 2013
Review articles
Comments
Treat all patients immediately after diagnosis
Avoid hypomagnesaemia
Do not induce hypermagnesaemia
Continue statins in patients on chronic therapy
Consider statins in patients at high risk of DCI
Reduce risk of re-bleeding
Increased risk of DCI
Trend towards improved outcome
Increased risk of haemorrhage
Target euvolaemia not hypervolaemia
Haemodilution contraindicated except in polycythaemia
Graded hypertension in DCI if aneurysm secured
Consider after failure of medical therapy
Angioplasty and/or intra-arterial vasodilators
identify treatment targets, although these are focal techniques
and the monitoring probe must be accurately located in the
region of interest.27,34
Treatment
Since DCI is delayed and may be reversible, it is an obvious
target for preventative and treatment strategies (Table 2).
Nimodipine
All patients should receive enteral nimodipine, a specific
antagonist of L-type voltage-gated calcium channels, 60 mg
four-hourly immediately after diagnosis. This reduces the
incidence of DCI and improves outcome.35 The mechanisms by
which nimodipine reduces DCI are uncertain because it does
not reverse angiographic vasospasm in humans. Although
intravenous nimodipine is sometimes used in critically ill
patients, this route of administration is unproven and care
must be taken to avoid hypotension.
Triple H therapy
Triple H therapy, hypervolaemia, haemodilution and
hypertension, has been widely used to prevent and treat DCI
but the combination has never been tested in a randomised
controlled trial. While fluid therapy is a key component of the
management of SAH, prophylactic hypervolaemic therapy is
not effective in raising CBF or improving neurological
outcome, and there is some evidence of harm from overly
aggressive filling.36 Recent consensus guidance recommends
that euvolaemia rather than hypervolaemia should be the target
for both prophylaxis and treatment of DCI, and that
haemodilution should not be used.37 Isotonic crystalloids are
the fluids of choice, although hypertonic saline solutions have
a place in patients who are hyponatraemic. In the presence of a
secured aneurysm, maintenance of ABP at supra-normal levels
is the mainstay of treatment of DCI.38 Pressure should be
increased in a stepwise fashion, guided by assessment of
neurological function, neuromonitoring or radiological
evidence of improved perfusion.6 In the presence of adequate
31
Review articles
volume status, noradrenaline is widely used to augment ABP.
Central venous pressure is an unreliable indicator of volume
status after SAH and although invasive ABP and cardiac output
monitoring are often used to guide goal-directed volume and
vasopressor therapy, no technology has been demonstrated to
be superior to another.39
Endovascular therapies
Endovascular treatment options for cerebral vasospasm are
effective in some cases which are resistant to medical therapy.6
Balloon angioplasty has been widely used to reverse vasospasm
in major basal arteries, but it may also be effective for
more distal spasm.40 Angioplasty is often combined with the
selective intra-arterial administration of vasodilators, including
verapamil, nimodipine, nicardipine, milrinone and fasudil,
although comparisons with conventional (non-interventional)
therapy have been made.41
Novel treatments
Since DCI is unlikely to be related only to vasospasm, several
pharmacological agents have been tested in this context.42,43
Statins have multiple beneficial effects on vascular function
and have been used to prevent and treat DCI. However, a
recent meta-analysis found that statins have no significant
effect on the incidence of DCI, poor neurological outcome or
mortality.44 Current guidance recommends that patients already
on statins should have these drugs continued but that the
introduction of acute statin therapy should only be considered
in carefully selected patients at high risk of DCI.45 The on-
going STASH trial is designed to determine the outcome
effects of statins after SAH (http://clinicaltrials.gov/ct2/show/
NCT00731627).
Magnesium reverses cerebral arterial spasm in animal
models of SAH, but the only randomised clinical trial
demonstrated no beneficial effect on the incidence of DCI
and cerebral infarction or on clinical outcome.46 A subsequent
post hoc analysis showed that high plasma magnesium
levels are associated with worse clinical outcomes47 and
although hypomagnesaemia should be avoided, induced
hypermagnesaemia is therefore not recommended.46
Endothelin has a key role in maintaining vascular tone and
endothelin-A antagonists such as clazosentan have been
studied but have not been shown to reduce mortality or
improve neurological outcome after SAH.48 Since activation of
the coagulation cascade and microthrombosis might play a role
in DCI, attention has also focussed on agents affecting these
variables. A Cochrane review suggested a non-significant trend
towards improved outcome in patients treated with anti-
platelet agents but this was accompanied by an increased risk
of haemorrhagic complications.49 Two large randomised
controlled trials provided contradictory results about the effect
of enoxaparin on outcome after SAH50,51 and, although anti-
fibrinolytic agents reduce the rates of rebleeding-related
mortality, this is offset by a higher rate of DCI.19
Seizure control
Seizures occur in approximately 20% of patients after SAH but
treatment remains controversial. Actual seizures must be
treated aggressively but universal prophylaxis is not
32
Complication Incidence
Fever 54%
Anaemia 36%
Hyperglycaemia 30%
Hypertension 27%
Hypernatraemia 22%
Pneumonia 20%
Hypotension 18%
Pulmonary oedema 14%
Hyponatraemia 14%
Life-threatening arrhythmia 8%
Myocardial ischaemia 6%
Modified from Wartenberg et al, Crit Care Med 2006;34:617-23.4
Table 3 Non-neurological complications of subarachnoid
haemorrhage.
recommended. Three days of treatment offers similar seizure
prevention and better outcome than longer-term therapy.52
Phenytoin should be avoided because of associated cognitive
effects and poor outcome and a short course of levetiracetam
is recommended.53
Non-neurological complications
Non-neurological complications are common after SAH and
independently associated with poor outcome (Table 3).54 In a
study from a single centre, 79% of patients developed at least
one medical complication4 and, in the Cooperative Aneurysm
Study, the proportion of deaths related to non-neurological
complications was 23% (similar to that of vasospasm at 22%).55
As they are independently associated with poor outcome after
SAH, non-neurological complications represent potentially
modifiable risk factors and early recognition and prompt
intervention might therefore improve outcome.56 However, the
intensive care management of non-neurological organ
dysfunction and failure presents significant challenges because
optimum treatment for the failing systemic organ system may
have potentially adverse effects on the injured brain.21
Cardiopulmonary complications
Cardiac complications are common and associated with DCI
and poor outcome.57 These are manifest as an abnormal ECG,
elevated cardiac troponin (cTnI), and a spectrum of ventricular
dysfunction collectively referred to as the neurogenic stunned
myocardium (NSM) syndrome.58 ECG abnormalities are
extremely common after SAH (Table 4), elevation of cardiac
cTnI occurs in 20-40% of patients and left ventricular (LV)
dysfunction in around 18%.
NSM is caused by excessive noradrenaline release from
myocardial sympathetic nerve terminals resulting in a
physiological myocardial denervation in the presence of
normal coronary perfusion.59 This results in a characteristic
pattern of LV regional wall motion abnormalities involving the
Volume 14, Number 1, January 2013 JICS

ECG abnormality Reported incidence
ST-segment changes 15-51%
Inverted or isoelectric T waves 12-92%
QTc prolongation 11-66%
Prominent U waves 4-47%
Sinus bradycardia 16%
Sinus tachycardia 8.5%
Table 4 ECG changes after subarachnoid haemorrhage.
basal and middle portions of the anteroseptal and anterior
ventricular walls with relative apical sparing, reflecting the
distribution of sympathetic nerves rather than specific vascular
territories.60 The degree of myocardial dysfunction and damage
is related to the severity of the SAH61 and, although LV
dysfunction is usually temporary, it is associated with higher
mortality after SAH. Takotsubo cardiomyopathy, also referred
to as left apical ballooning, is a transient, virtually global LV
dysfunction characterised by apical and mid-ventricular
akinesia with relative sparing of the basal segment.62 It may
occur as a response to sudden physical or emotional stress,
when it generally has a benign prognosis, but it is also a rare
cause of ventricular dysfunction after SAH, when it is
associated with increased mortality.
NSM may be associated with minimal clinical effects but, in
severe cases, can lead to cardiogenic shock and pulmonary
oedema.59 Cardiovascular dysfunction often resolves
spontaneously after a variable period, emphasising the
importance of general supportive intensive care during periods
of instability.
Modification of the sympathetic response might limit cardiac
dysfunction after SAH and patients on chronic antihypertensive
therapy have a lower incidence of SAH-associated cardiac
injury.63 However, there is no strong evidence to recommend
this line of therapy and, in any case, the risk of hypotension is a
cause for concern. Inotropic support with dobutamine and, less
so, milrinone is beneficial in the setting of low cardiac output,
despite a mechanism of action similar to the cause of cardiac
injury.64 Pure vasopressors are often necessary to maintain
cerebral perfusion but their adverse effects on cardiac work
risks potentiating myocardial injury. Characterising cardiac
performance using echocardiography and continuous cardiac
output monitoring may be useful in guiding therapy in patients
with symptomatic NSM.
Neurogenic pulmonary oedema (NPO) and pneumonia are
common after SAH and associated with adverse outcome.65,66
The mechanism of NPO is controversial but likely to be related
to neurogenic-mediated catecholamine release that leads to
both hydrostatic and permeability oedema. Many patients with
SAH and acute lung injury can be managed safely using lung
protective ventilation strategies, but in others there can be a
conflict between treating the lungs and the injured brain.67 A
ventilation strategy that maximises oxygenation while
balancing risks to the lungs and injured brain should be
identified individually for each patient.66,68
JICS Volume 14, Number 1, January 2013
Review articles
Dysnatraemia
Hyponatraemia after SAH is often related to the syndrome of
inappropriate antidiuretic hormone secretion (SIADH),
although the cerebral salt wasting (CSW) syndrome and
iatrogenic haemodilution can be implicated.69 As plasma
tonicity reduces, fluid shifts may precipitate cerebral oedema
and neurological sequelae. SIADH occurs because of excess
antidiuretic hormone secretion, causing water retention, volume
overload and dilutional hyponatraemia. CSW on the other hand
is associated with raised atrial and brain natiuretic peptide and
excessive renal sodium and water loss, leading to circulating
volume contraction. It is important to distinguish between
SIADH and CSW syndrome, since the treatment of the two is
diametrically opposed.70 Electrolyte-free water restriction,
initially to 1,000-1,500 mL/day, forms the usual mainstay of
treatment of SIADH but this may worsen cardiovascular
instability and increase the risk of cerebral hypoperfusion after
SAH. Consideration should be given to the use of hypertonic
saline (1.8%) in hyponatraemic patients with a high risk of
DCI. Pharmacological therapies such as demeclocycline and
ADH-receptor antagonists may have a place in some patients.
The primary treatment of CSW syndrome is volume and
sodium resuscitation. Fludrocortisone or hydrocortisone may
also be used to limit the natiuresis but care must be taken to
monitor for hypokalaemia and hyperglycaemia.6
Hypernatraemia independently increases the risk of
adverse cardiac outcome and death after SAH and patients
with hypernatraemia should be monitored for evidence of
cardiac dysfunction.71
Fever
Fever occurs in up to 70% of patients, is more common in
poor grade SAH and associated with worse outcome.72 While
an infective cause should be excluded (pneumonia is
particularly common), the fever can be related to the
hypothalamic effects of subarachnoid blood. Paracetamol is
first line therapy for fever control and although active cooling
to normothermia has been associated with improved outcome,
the adverse effects of shivering73 might offset its benefits.
Glycaemic control
Hyperglycaemia is common after SAH, occurring in around
30% of patients, and is associated with adverse outcome.74
Tight glycaemic control is not recommended since it can be
associated with increased cerebral metabolic crises.75 Current
practice has adopted more relaxed glycaemic targets (typically
6-11 mmol/L) limiting overly-aggressive insulin administration
and minimising the risk of hypoglycaemia and its known
adverse effects on the injured brain.76
Anaemia
Anaemia is very common and associated with poor outcome
after SAH, although transfusion is itself similarly associated
with adverse outcome effects.77 Current guidance recommends
that packed red cells be administered to maintain haemoglobin
concentration between 8-10 g/dL, although higher thresholds
might be appropriate in patients at high risk of DCI.6
33
Review articles
Disclosures
MS is part funded by the Department of Health’s National
Institute for Health Research Centres funding scheme via the
UCLH/UCL Biomedical Research Centre.
MS is a member of the JICS Editorial Board.
DH – no conflict of interest declared.
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David Highton Academic Clinical Fellow in Anaesthesia and
Critical Care
Martin Smith Consultant and Honorary Professor in
Neurocritical Care, The National Hospital for Neurology and
Neurosurgery
martin.smith@uclh.nhs.uk
University College London Hospitals
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