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 aspontaneous 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 pathwayand checklist for referral of the Subarachnoid Haemorrhagepatient 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 CareBundle. This should be utilised for all Subarachnoid Haemorrhagepatients 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.

1

North Wales

Critical Care Network[APPROVED]

Amended March 2012.

1

North Wales

Critical Care Network[APPROVED]

Amended March 2012.

Referral Checklist - For AdultSubarachnoid HaemorrhagePatients to Walton

1 / Admitting DGH Consultant:
Referring DGH Doctor:
Referring DGH Consultant:
Referring Hospital:
Time of Call:
2 / Time of first contact Neuro SpR:
3 / Patient Details / Name: DOB:
Sex:
Age:
4 / Brief description of SAH onset:
5 / Time of onset: /
6 / GCS, pupils and time of arrival on scene: / Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
7 / GCS, pupils and time of arrival at ED: / Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
8 / GCS, pupils at time of call: / Time:
Pupils:
Eye Opening
Motor Response
Verbal Response
9 / Current observations at time of call: / HR: / BP: / SaO2
10 / Any treatment given e.g. intubated/ventilated
11 / Past medical history:
12 / Is patient on Warfarin, Aspirin, or Clopidogrel? / Yes / No / Don’t know
13 / Reversal medication given e.g. Vitamin K, Prothrombin Complex Concentrate (PCC) / Yes / No / Don’t know
14 / Referral Clinician Tel No. & Ext No.
15 / Name of Neuro SpR spoken to:
16 / Name of Neurosurgical Consultant:
17 / Time of first contact with Neuro SpR:
18 / CT Scan report received and discussed with Neuro SpR: / Yes / No
19 / Outcome of call – comments: / Patient Declined / Patient Accepted / Where is patient to go to?
Walton Theatres
Walton ICU
Other:
Please tick as appropriate
USEFUL TELEPHONE NUMBERS:
Walton Switchboard: Neurosurgical SpR: / 0151 525 3611
Ask switch to bleep / Walton ICU Phone:
Walton ICU SpR: / 0151 529 5772
Bleep 2018

Prior to transfer fax this form to Walton ICU ON 0151 529 5510

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 nofocal deficit
/ 13 or 14
  • Grade III: Severe headache with focal neurological deficit
/ 13 or 14
  • Grade IV: Depressed level of consciousness with or without focal deficit
/ 7 to 12
  • Grade V: Unconscious patient
/ 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. ThisSubarachnoid 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 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 cerebralblood flow.

Early detection of deterioration in the patient's neurological condition is essential for the prompt treatment of complications such asvasospasm, rebleeding and/or hydrocephalus.

Patients with a SAH thereforerequire 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. Alabile 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 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 3-12 days post SAH, lasting approximately two weeks and occurs in about two thirds of SAH patients, of which half will develop symptomaticcerebral 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 vasospasm14and 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 effectiveas intravenous administration, but is associated with less hypotension.

d.Nimodipine administration

  • Administer Nimodipine to allSAH patients; 60mg orallyevery 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 cardio-respiratory 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 1.0-1.5mls/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
  • 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:

  • 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 24hours have passed, rebleeding risk remains around 40% over the subsequent fourweeks, 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
  • 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.

1

North Wales

Critical Care Network[APPROVED]

Amended March 2012.

Quick Guide for Subarachnoid Haemorrhage (SAH)Care Bundle

Bundle Element / Aims / Rationale / Exclusion / Compliance Audit Point
Element 1:
Control of Intracranial Pressure (ICP) / Pupillary reflexes performed minimum ½ hourly for 12 hours. Hourly for 24 hours, then 2 hourly thereafter. / 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. / Terminal care.
EOL Care Pathway.
Patient does not require neuromuscular blockade / Are there attempts to control ICP?
Do all patients with a GCS less than 15 have Neurological observations performed as described?
Are all patients nursed
  • Head elevated
  • In a neutral position
Are all patients adequately sedated and analgesed?
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).
/ 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.
Control agitation/maintain adequate analgesia and sedation
  • Analgesia and sedation.
  • (If required) muscle relaxant with neuromuscular monitoring.
/ Sedation will help dampen the effect of any stimuli that might increase ICP.
NB Beware of hypotensive effects of sedation, especially boluses.
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.
Element 2:
Optimisation of cerebral perfusion and oxygenation / 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 5-10mls/hr.
/ Administration of oral Nimodipine improves outcome after SAH. The oral (or NG) route has been shown to be just as effective as intravenous administration, but is associated with less hypotension. / Terminal care.
EOL Care Pathway. / 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

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.
/ 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).
Adequate perfusion pressure
  • Systolic <160mmHg, diastolic <110mmHg
  • MAP >80mmHg
  • adequate filling (as above)
  • Vasopressors as necessary
  • Antihypertensives as necessary
  • Adequately filled (as above)
/ Hypotension will result in a reduction in cerebral blood flow 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
Adequately oxygenated
  • SaO2 >93%
  • PaO2 >13kPa
/ Hypoxia is the second most influential cause of secondary brain injury after hypotension and worsens outcome.
Hypoxia causes vasodilation which will increase ICP.
Avoid hyperaemia
  • pCO2 4.5-5.0kPa
/ Hypercapnia causes vasodilation which increases cerebral blood flow and volume and therefore ICP.
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
/ For every 10C increase in temperature there is a 10-13% increase in metabolic rate. Therefore pyrexia will exacerbate ischaemia. Shivering markedly increases ICP
Control hyperglycaemia
  • Maintain blood glucose or 6-10mmol-1
  • (Avoid hypoglycaemia at all costs)
/ Hyperglycaemia may worsen cerebral ischaemia by decreasing cerebral blood flow.
NB Beware of hypoglycaemia – the injured brain cannot tolerate it
Element 3:
Prevention of rebleeding; control of blood pressure, seizure prophylaxis. / Control of blood pressure (see also f – adequate perfusion pressure)
  • Systolic <160mmHg, diastolic <110mmHg
  • adequate filling (as above)
  • Vasopressors as necessary
  • Antihypertensives as necessary
/ A labile BP is common in high-grade SAH. Hypertension increases the risk of re-bleeding howeverhypotension 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 / 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?
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.
/ 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.

1

North Wales

Critical Care Network[APPROVED]

Amended March 2012.

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., BennettD.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):1225-32.

5 Frontera J.A., Fernandez A., Schmidt J.M., Claassen J., Wartenberg K.E., Badjatia N., Parra A., Connolly E.S. andMayer S.A. (2008) Impact of nosocomial infectious complications after subarachnoid hemorrhage. Neurosurgery 62:80-87.

6Wartenberg K.E., Schmidt J.M., Claassen J., Temes R.E., Frontera J.A., Ostapkovich N., Parra A., Connolly E.S. andMayer S.A. (2006) Impact of medical complications on outcome after subarachnoid hemorrhage.Critical Care Medicine.34(3):617-23

7Le Roux P.D., Elliott J.P., Newell D.W., Grady M.S. andWinn H.R. (1996) Predicting outcome in poor-grade patients with subarachnoid hemorrhage: a retrospective review of 159 aggressively managed cases. Journal of Neurosurgery. 85(1):39-49.

8Huang 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;