North Wales Critical Care Network
SUBARACHNOID HAEMORRHAGE
PATHWAY
&
CARE BUNDLE
(for Adult patients requiring Critical Care)
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
1
North Wales Critical Care Network
Adult Subarachnoid Haemorrhage
Pathway and Care Bundle
Introduction
Early aggressive treatment of patients with a poor grade Subarachnoid
Haemorrhage has resulted in favourable outcomes1.
The aim of this paper therefore is to provide consistency across the North
Wales Network region for Critical Care patients with a spontaneous
Subarachnoid Haemorrhage (SAH).
Because there are some differences in the management of spontaneous
SAH patients from those with a Severe Brain Injury it was considered
‘safer’ to document their care separately. As with the Severe Brain Injury
pathway however this document includes a referral pathway, ICU
maintenance care and repatriation process for all SAH patients from the
three hospitals, much of it being very similar.
The first section provides a pathway and checklist for referral of the
Subarachnoid Haemorrhage patient to the Walton Neurological Centre.
This pathway has been agreed by Intensivists in North Wales with
colleagues at the Walton Centre.
The second section includes the guidelines that underpin the Subarachnoid
Haemorrhage Care Bundle. This should be utilised for all Subarachnoid
Haemorrhage patients who remain in the local ICUs. A quick guide of
these more detailed guidelines is also included.
The final section is a pathway for repatriating patients back to the local
ICUs from Walton.
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
2
N
Noorrtthh W
Waalleess C
Crriittiiccaall C
Caarree N
Neettw
woorrkk
Pathway for Referral of Adult Critical Care Patients with
Subarachnoid Haemorrhage to Walton Neurological Centre
Patient identified for referral to
Walton Neurological Centre
(CT/LP positive for blood)
Immediate transfer
not required
Checklist complete
(PTO)
Referral to Neurosurgical
SpR (0151 525 3611)
Patient
accepted (by
neurosurgeons
& intensivists)
Handover to
Critical Care
staff (0151 529
5772)
Image link CT Scan &
inform Neuro SpR when
CT sent
Patient fully
monitored
Immediate transfer
required
(Ref Designed for Life: Welsh Guidelines for the transfer of the
critically ill adult 2009)
(Ref: All Wales Transfer
Guidelines)
Optimise
patient for
transfer
Write discharge
letter/plan &
send with
patient
Contact Walton
ICU
(0151 529 5772)
with ETA
Call ambulance control
(01248 689089) stating
IMMEDIATE Transfer
(Ref: Welsh Transfer
Guidelines)
Patient
declined
Admit locally to
Critical Care
Avoid secondary
brain injury
Initial resuscitation and
stabilisation complete
Walton to return call
within agreed timescale
(Ref: NICE CG56)
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
Call ambulance control
(01248 689089) stating
URGENT Transfer
Monitoring (during transfer) MUST include:
ECG
Invasive BP and NIBP
SaO2
EtCO2
Temperature
U/O by urinary catheter
Pupillary size and reaction
CVP where indicated
Follow
SAH Care
Bundle
Liaise with Walton
Neurosurgical SpR re
ongoing clinical
management (Ref: NICE CG56)
NB: Where transfer is necessary but
Walton cannot accommodate the
WCNN is responsible for finding a
bed (SBNS). For Neuro ICU beds in
the North West telephone ICBIS:
0161 720 2554
3
1
2
3
4
Referral Checklist - For Adult Subarachnoid Haemorrhage Patients to Walton
Admitting DGH Consultant:
Referring DGH Doctor:
Referring DGH Consultant:
Referring Hospital:
Time of Call:
Time of first contact Neuro SpR:
Patient Details
Name:
Age:
DOB:
Sex:
Brief description of SAH onset:
5
6
Time of onset:
GCS, pupils and time of arrival on
scene:
7
GCS, pupils and time of arrival at
ED:
8
GCS, pupils at time of call:
9
Current observations at time of
call:
Any treatment given e.g. intubated /
10
Glasgow Coma Score
Motor
6 Obeys Commands
5 Localises Pain
4 Flexes (withdraws) to Pain
3 Abnormal Flexion
2 Extension to Pain
1 No Movements
Verbal
5 Orientated
4 Confused
3 Words Not Sentences
2 Noises Not Words
1 No Sounds
Eyes
4 Open Spontaneously
3 Open to Voice
2 Open to Pain
1 Closed
Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
HR:
BP:
SaO2
ventilated
11
Past medical history:
12
Is patient on Warfarin, Aspirin, or
Clopidogrel?
Reversal medication given e.g. Vitamin K,
13
Yes
No
Don’t know
Yes
No
Don’t know
Prothrombin Complex Concentrate (PCC)
14
15
16
17
18
19
Referral Clinician Tel No. & Ext No.
Name of Neuro SpR spoken to:
Name of Neurosurgical Consultant:
Time of first contact with Neuro SpR:
CT Scan report received and discussed with
Neuro SpR:
Outcome of call – comments:
Yes
PATIENT
DECLINED
No
PATIENT
ACCEPTED
WHERE IS PATIENT TO
GO TO?
Walton Theatres
Walton ICU
Other:
PLEASE TICK AS APPROPRIATE
USEFUL TELEPHONE NUMBERS:
Walton Switchboard:
Walton ICU Phone:
0151 525 3611
0151 529 5772
Neurosurgical SpR:
Walton ICU SpR:
Ask switch to bleep
Bleep 2018
PRIOR TO TRANSFER FAX THIS FORM TO WALTON ICU ON 0151 529 5510
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
4
Subarachnoid Haemorrhage (SAH) Care Bundle
(for adult patients requiring Critical Care)
Background Information
Nontraumatic spontaneous SAH usually is the result of a ruptured cerebral
aneurysm or arteriovenous malformation (AVM). Blood extravasation into the
subarachnoid space has a detrimental effect on both local and global brain function
and leads to significant morbidity and mortality.
Although mortality rates of SAH have decreased, it remains a devastating
neurological problem. An estimated 15% of patients die before reaching hospital.
Approximately 25% of patients die within 24 hours, with or without medical
attention. The mortality rate at the end of one week approaches 40%. Half of all
patients die in the first 6 months.
Recent developments in neurocritical care including enhanced monitoring
techniques, normalisation of pathophysiological states and better recognition and
management of complications following subarachnoid haemorrhage have improved
the level of care for SAH patients1. As a result mortality has decreased2,3. Advanced
age, worse clinical grade, rebleeding, larger aneurysm size, global cerebral
oedema, delayed cerebral ischaemia and medical complications all have a
detrimental impact on outcome after SAH4-6. Reports of early and aggressive
treatment of poor grade patients demonstrated unexpected improvements of long
term functional outcome7-9.
SAH is classified according to 5 grades:
Glasgow Coma Score

Grade I: Mild headache with or without meningeal irritation
15



Grade II: Severe headache and a no focal deficit
Grade III: Severe headache with focal neurological deficit
Grade IV: Depressed level of consciousness with or without
focal deficit
Grade V: Unconscious patient
13 or 14
13 or 14
7 to 12

3 to 6
World Federation of Neurological Surgeons.
The ICUs in North Wales are familiar with the concept of care bundles; therefore a
care bundle is described below to assist in the management of the subarachnoid
haemorrhage patients who remain in the local ICUs.
Subarachnoid Haemorrhage Care Bundle
Early neurological and cardiopulmonary resuscitation of poor grade patients
followed by high quality and comprehensive critical care should be the standard and
based on a team approach1. This Subarachnoid Haemorrhage care bundle therefore
aims to optimise care for the individual patient by addressing possible secondary
cerebral insults and limiting ongoing brain damage.
The three elements are:
1. Control of Intracranial Pressure (ICP) (caused by hydrocephalus and
global cerebral oedema).
2. Optimisation of cerebral perfusion and oxygenation.
3. Prevention of aneurysm rebleeding; control of blood pressure, seizure
prophylaxis.
It should be noted that in order to be compliant with the elements in this bundle
some elements of the Ventilator bundle may need to be excluded e.g. transfusion
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
5
guidelines and low tidal volume.
Bundle Element 1
Control of Intracranial Pressure (ICP)
In acute SAH the sudden rise in ICP up to the levels of MAP leads to an arrest of
cerebral circulation which is clinically seen as loss of consciousness and to the
development of global cerebral oedema. Cerebral oedema and the resultant
cerebral hypermetabolism are linked to increased risk of death, disability and
cognitive dysfunction4. Altered level of consciousness may also be related to
haematoma formation, hydrocephalus, vasospasm, or reduced cerebral blood flow.
Early detection of deterioration in the patient's neurological condition is essential for
the prompt treatment of complications such as vasospasm, rebleeding and/or
hydrocephalus.
Patients with a SAH therefore require frequent neurological observations. Pupil size
and reaction are paramount in the sedated ICU patient where sedation will prevent
motor responses. If ‘deep’ painful stimuli are required this should be performed
with supra-orbital pressure or trapezius squeeze10.
Additional measures to prevent increases in ICP are also indicated;
a. Perform Neurological Observations
 ½ hourly for 12 hours, hourly for 24 hours, then 2 hourly thereafter10
 Clinician discretion will be needed after the acute phase.
b. Avoid venous congestion
 head tilt 20-300 (preferably 300 but be mindful of compromising MAP and
thus cerebral perfusion pressure)
 avoid external compression; use adhesive ETT tapes or loose tapes)
 avoid high thoracic pressures (adhere to bowel protocol).
c. Control agitation / maintain adequate analgesia and sedation if
intubated
 analgesia and sedation (local protocol)
 (if required) muscle relaxant with neuromuscular monitoring
Bundle Element 2
Optimisation of cerebral perfusion and oxygenation
There is often an imbalance in cerebral oxygen delivery and cerebral oxygen
consumption resulting in tissue hypoxia11. A labile BP is common in high-grade
subarachnoid hemorrhage. Hypotension must be avoided at all costs as it will cause
a reduction in cerebral blow flow and will result in cerebral ischaemia12. Both
hypoxia and ischaemia will increase ICP.
Myocardial injury in patients with SAH occurs as a result of excessive sympathetic
drive and catecholamine release. ECG abnormalities occur in approximately 35% of
patients and a similar percentage of patients will also have an elevation of
Troponin. Echocardiographic wall motion abnormalities occur in about 25% of
patients.
Significant pulmonary complications occur in approximately 20% of patients and
this spectrum ranges from acute lung injury to pulmonary oedema. This may
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
6
complicate clinical management when trying to ensure adequate intravascular
volume on one hand and trying to avoid pulmonary oedema on the other13.
Cerebral vasospasm is a devastating medical complication of aneurysmal SAH that
is associated with high morbidity and mortality rates. It is most likely to develop 312 days post SAH, lasting approximately two weeks and occurs in about two thirds
of SAH patients, of which half will develop symptomatic cerebral ischaemia causing
neurological deficit of varying severity. Cerebral vasospasm may also lead to
increased ICP, secondary to infarction.
Fever (>380C) is a frequent event in SAH patients and is associated with
symptomatic vasospasm14 and an increased ICU and hospital length of stay15.
Administration of oral Nimodipine improves outcome after SAH16. The oral (or NG)
route has been shown to be just as effective as intravenous administration, but is
associated with less hypotension.
d. Nimodipine administration
 Administer Nimodipine to all SAH patients; 60mg orally every 4 hours,
continued for 21days. If enteral route is not possible, consider IV infusion
via CVP as per the British National Formulary; 0.02% (neat from vial into
50ml syringe) at 5-10mls/hr. NB use giving set supplied with the vial.
Adequate cerebral oxygen delivery depends primarily on satisfactory cardiorespiratory performance, but can further be categorised by those aspects which
need to be in place before transfer of oxygen from haemoglobin to the tissues
occurs, namely;
e. an adequate circulating volume
Aim for:
 capillary refill <2 seconds
 CVP minimum 8mmHg1 using isotonic crystalloids 0.9% NaCl at 1.0-1.5
mls/kg/hr.
 consider hypertonic saline where hyponatraemia present (consider
cerebral salt wasting)
 if u/o >4mls/kg consider treatment for Diabetes Insipidus
NB: If problems with fluid or sodium balance advice from neuro-critical care Intensivist at ICU
(Walton) can be sought 24hrs/day.
f. adequate perfusion pressure
Aim for:
 Systolic <160mmHg1, diastolic <110mmHg1
 MAP >80mmHg
o adequate filling (as above)
 Vasopressors as necessary12
 Antihypertensives as necessary1
g. adequate oxygenation
Aim for:
 SaO2 >93%
 pO2 >13kPa10,17
h. avoid hyperaemia
Aim for:
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
7

CO2 4.5-5.0kPa10,17,18
i. control pyrexia
 maintain normothermia <370C1

(NB: Every 10C increase in core temperature causes a 6-10% increase in cerebral
blood flow. The increase in cerebral blood flow causes an increase in cerebral
blood volume therefore contributing to an increase in ICP).
j. control hyperglycaemia
 maintain blood glucose 6-10mmol-1

(NB: Avoid hypoglycaemia at all costs)
Bundle Element 3
Prevention of rebleeding; control of blood pressure, seizure prophylaxis.
Rebleeding, a major complication, carries a mortality rate of 51-80%. It is hard to
predict which patients will suffer a rebleed, yet it may happen at any time. After the
first 24 hours have passed, rebleeding risk remains around 40% over the
subsequent four weeks, suggesting that interventions should be aimed at reducing
this risk as soon as possible.
The main aim of treatment for SAH is prevention of rebleeding while preventing
secondary ischaemia.
Prolonged seizures may result in hypoxaemia and cerebral infarction due to cerebral
hypoxia
k. control of blood pressure (see also f – adequate perfusion pressure)
 Systolic <160mmHg1, diastolic <110mmHg1
o adequate filling (as above) see above note
 Vasopressors as necessary12
 Antihypertensives as necessary1
l. control fitting
 Consider the context and requirement for induction of anaesthesia /
intubation and ventilation
 If clinically indicated – Phenytoin 20mg/kg IV bolus followed by 5mg/kg
daily1 (adjust dose according to plasma levels corrected for serum
albumin); not exceeding 1.5 grams in 24hrs.
m. Pharmacological thromboprophylaxis is generally contraindicated until the
aneurysm is secured.
 Use
Summary
As well as optimising care of the SAH patient this care bundle should facilitate audit
of process. Although compliance is expected, especially where deviations from this
agreed practice cannot be justified, the bundle is not designed to replace clinician
judgment.
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
8
Quick Guide for Subarachnoid Haemorrhage (SAH) Care Bundle
Bundle Element
Element 1:
Control of
Intracranial
Pressure (ICP)
Aims
Pupillary reflexes performed minimum ½ hourly for
12 hours. Hourly for 24 hours, then 2 hourly
thereafter.
Avoid venous congestion




Head tilt 20-300, preferably 300
Neutral head position
Avoid external compression (consider use adhesive
or loose ETT tapes)
Avoid high thoracic pressures (adhere to bowel
protocol).
Control agitation/maintain adequate analgesia and
sedation


Element 2:
Optimisation of
cerebral perfusion
and oxygenation
Analgesia and sedation.
(If required) muscle relaxant with neuromuscular
monitoring.
Administer Nimodipine to all SAH patients

60mg orally/NG every 4 hours, continued for 21
days. If enteral route is not possible, consider IV
infusion via CVP as per BNF; 0.02mg/ml at 510mls/hr.
Adequate circulating volume




Capillary refill <2 seconds
CVP minimum 8mmHg (zero at mid-axilla) using
isotonic crystalloids 0.9% NaCl at 1.0-1.5 mls/kg/hr.
Consider hypertonic saline where hyponatraemia
present
If u/o >4mls/kg consider Rx for D.I.
Adequate perfusion pressure
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
Rationale
Pupillary reactions will provide prognostic information.
Prompt detection of changes in size, shape and/or reaction
of pupils any indicate swelling/an expanding lesion and
increasing ICP.
Head elevation will reduce oedema (and thus ICP) but >300
may reduce MAP and therefore CPP.
Head rotation and neck flexion can increase ICP by impeding
cerebral venous drainage.
Tight ETT tapes will impede venous return.
Straining will increase abdominal and thoracic pressures.
Avoid ‘clustering’ care – stagger interventions giving time for
ICP to settle in between.
Sedation will help dampen the effect of any stimuli that might
increase ICP.
NB Beware of hypotensive effects of sedation, especially boluses.
Exclusion
Terminal care.
EOL Care
Pathway.
Are all patients nursed
 Head elevated
 In a neutral position
Patient does
not require
neuromuscular
blockade
Neuromuscular blockade may need to be considered if
patient movement or ventilation remains problematic despite
full sedation. It will also help to avoid rises in ICP due to
coughing, straining etc.
Administration of oral Nimodipine improves outcome after
SAH. The oral (or NG) route has been shown to be just as Terminal care.
effective as intravenous administration, but is associated with EOL Care
less hypotension.
Pathway.
Maintenance of cerebral perfusion pressure (the variable
which defines the pressure gradient driving cerebral blood
flow) can be achieved with fluid replacement and inotropes
(see below).
Hyponatraemia occurs in 20-40% SAH patients as result of
the syndrome of inappropriate excretion of anti-diuretic
hormone (SIADH).
Hypotension will result in a reduction in cerebral blood flow
Compliance Audit Point
Are there attempts to
control ICP?
Do all patients with a GCS
less than 15 have
Neurological observations
performed as described?
Are all patients adequately
sedated and analgesed?
Are there attempts to
optimise cerebral
perfusion and
oxygenation?
Do all patients have
 Nimodipine
 CVP minimum 8mmHg
 pO2 >13kPa
 MAP >80mmHg
 pCO2 4.5-5.0kPa
9





Systolic <160mmHg, diastolic <110mmHg
MAP >80mmHg
o adequate filling (as above)
Vasopressors as necessary
Antihypertensives as necessary
Adequately filled (as above)
Adequately oxygenated


Hypoxia is the second most influential cause of secondary
brain injury after hypotension and worsens outcome.
Hypoxia causes vasodilation which will increase ICP.
SaO2 >93%
PaO2 >13kPa
Avoid hyperaemia

thus causing tissue hypoxia.
Hypotension has been uniformly identified as the
predominant factor in secondary brain injury and has highest
correlation with morbidity and mortality.
Hypertension
Hypercapnia causes vasodilation which increases cerebral
blood flow and volume and therefore ICP.
pCO2 4.5-5.0kPa
NB Beware low VT (e.g. Ventilator bundle causing an increase in PaCO2)
Hypocarbia causes vasoconstriction which may exacerbate
the risk of ischaemia.
Control pyrexia

Maintain normothermia <
37.00C
Control hyperglycaemia


Element 3:
Prevention of
rebleeding; control
of blood pressure,
seizure
prophylaxis.
Maintain blood glucose or 6-10mmol-1
(Avoid hypoglycaemia at all costs)
Control of blood pressure (see also f – adequate
perfusion pressure)



Systolic <160mmHg, diastolic <110mmHg
 adequate filling (as above)
Vasopressors as necessary
Antihypertensives as necessary
Control fitting


Consider the context and requirement for induction
of anaesthesia/intubation and ventilation
If indicated; load with Phenytoin 20mg/kg IV bolus
followed by 300mg/day* (adjust dose according to
plasma levels corrected for serum albumin); not
exceeding 1.5grams/24hrs.
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
For every 10C increase in temperature there is a 10-13%
increase in metabolic rate. Therefore pyrexia will exacerbate
ischaemia. Shivering markedly increases ICP
Hyperglycaemia may worsen cerebral ischaemia by
decreasing cerebral blood flow.
NB Beware of hypoglycaemia – the injured brain cannot tolerate it
A labile BP is common in high-grade SAH. Hypertension
increases the risk of re-bleeding however hypotension must
be avoided at all costs as it causes a reduction in cerebral
blow flow resulting in cerebral ischaemia.
Patient does
not require
antiepileptics.
Terminal care
Seizure activity may cause rebleeding. It may also cause
secondary brain injury as a result of increased metabolic
demands, raised ICP and excess neurotransmitter release.
Steps taken to reduce the
risk of re-bleeding?
Are all patients with SAH
 Normotensive
 Adequate control of
fitting (where
necessary)
Or is there an attempt to
achieve these parameters?
10
References:
1 Wartenberg K.E. (2011) Critical Care of poor grade subarachnoid hemorrhage. Current Opinion in
Critical Care 17: 85-93.
2 Feigin V.L., Lawes C.M., Bennett D.A., Barker-Collo S.L. and Parag V. (2009) Worldwide stroke incidence
and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurology
8:355-369
3 Taylor C.J., Robertson F., Brealey D., O'Shea F., Stephen T., Brew S., Grieve J.P., Smith M. and Appleby
I. (2011) Outcome in poor grade subarachnoid hemorrhage patients treated with acute endovascular coiling
of aneurysms and aggressive intensive care. Neurocritical Care. 14(3):341-7.
4 Claassen J., Carhuapoma J.R., Kreiter K.T., Du E.Y., Connolly E.S. and Mayer S.A. (2002) Global cerebral
edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome. Stroke. 33(5):122532.
5 Frontera J.A., Fernandez A., Schmidt J.M., Claassen J., Wartenberg K.E., Badjatia N., Parra A., Connolly
E.S. and Mayer S.A. (2008) Impact of nosocomial infectious complications after subarachnoid hemorrhage.
Neurosurgery 62:80-87.
6 Wartenberg K.E., Schmidt J.M., Claassen J., Temes R.E., Frontera J.A., Ostapkovich N., Parra A.,
Connolly E.S. and Mayer S.A. (2006) Impact of medical complications on outcome after subarachnoid
hemorrhage. Critical Care Medicine. 34(3):617-23
7 Le Roux P.D., Elliott J.P., Newell D.W., Grady M.S. and Winn H.R. (1996) Predicting outcome in poorgrade patients with subarachnoid hemorrhage: a retrospective review of 159 aggressively managed cases.
Journal of Neurosurgery. 85(1):39-49.
8 Huang A.P., Arora S., Wintermark M., Ko N., Tu Y.K. and Lawton M.T. (2010) Perfusion computed
tomographic imaging and surgical selection with patients after poor-grade aneurysmal subarachnoid
hemorrhage. Neurosurgery. 67(4):964-74
9 Haug T., Sorteberg A., Finset A., Lindegaard K.F., Lundar T. and Sorteberg W. (2010) Cognitive
functioning and health-related quality of life 1 year after aneurysmal subarachnoid hemorrhage in
preoperative comatose patients (Hunt and Hess Grade V patients). Neurosurgery. 66(3):475-84;
10 UK National Institute for Health and Clinical Excellence. Head injury: Triage, assessment, investigation
and early management of infants, children and adults. (2007)
http://www.nice.org.uk/nicemedia.pdf/CG56NICEGuideline.pdf Accessed 4th October 2007.
11 Werner, C. and Engelhard, K. (2007) Pathophysiology of traumatic brain injury. British Journal of
Anaesthesia. 99(1):4-9.
12 Helmy, A., Vizcaychipi, M. and Gupta, A.K. (2007) Traumatic Brain Injury: intensive care management.
British Journal of Anaesthesia. 99(1):32-42.
13 Diringer M N et al. (2011) Critical Care Management of Patients following Aneurysmal Subarachnoid
Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus
Conference. Neurocritical Care. 15:211-240
14 Naidech A.M., Bendok B.R., Bernstein R.A., Alberts M.J., Batjer H.H., Watts C.M. and Bleck T.P. (2008)
Fever burden and functional recovery after subarachnoid hemorrhage. Neurosurgery. 63(2):212-7
15 Naidech A.M., Bendok B.R., Tamul P., Bassin S.L., Watts C.M., Batjer H.H. and Bleck T.P. (2009)
Medical complications drive length of stay after brain hemorrhage: a cohort study. Neurocritical Care. 10(1):
11-9.
16 Pickard J., Murray G., Illingworth R., Shaw M.D., Teasdale G.M., Foy P.M., Humphrey P.R, Lang D.A.,
Nelson R. and Richards P. (1989) Effect of oral nimodipine on cerebral infarction and outcome after SAH:
British aneurysm nimodipine trial. British Medical Journal. 298(6674): 636–642.
17 The Association of Anaesthetists of Great Britain and Ireland. (2006) Recommendations for the Safe
Transfer of Patients with Brain Injury. London: The Association of Anaesthetists of Great Britain and
Ireland.
18 Oertel, M., Kelly, D.F., Lee J.H. et al. (2002) Efficacy of hyperventilation, blood pressure elevation, and
metabolic suppression therapy in controlling intracranial pressure after head injury. Journal of
Neurosurgery. 97(5):1045-53.
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
11
N
Noorrtthh W
Waalleess C
Crriittiiccaall C
Caarree N
Neettw
woorrkk
Pathway for Repatriating Patients Subarachnoid Haemorrhage to
North Wales Hospitals from Walton Neurological Centre
Intensive Care Unit Telephone numbers:
Wrexham Maelor
01978 725447 or 01978 725608
Glan Clwyd
01745 534806 or 01745 534547
Bangor
01248 384244 or 01248 384436
Patient identified for
repatriation to North Wales
from Walton
Neurological Centre
Walton to contact
referring hospital’s ICU
(see ICU telephone no's red
box opposite)
Consider evidence of
infection
(where possible this should
NOT delay patient’s
repatriation)
Yes
Repatriate patient
ASAP
(to maintain ‘flow’
through Walton ICU)
Bed available?
No
North Wales
Critical Care Network [APPROVED]
Amended March 2012.
Discuss patient
repat on daily
teleconference –
repatriate ASAP
If no bed available
liaise with Walton in
24hrs
12