Aneurysmal SAH S n Guideline Liverpool

7/28/2019 Aneurysmal SAH S n Guideline Liverpool

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Liverpool Health Service CORPORATE MANUAL Neurological CarePolicy Issued: July 2002 PATIENT CARE

Reviewed: October 2004 Neurological Care Aneurysmal Subarachnoid HaemorrhageReview Date: October 2006 Page 1 of 1

MANAGEMENT OF THE PATIENT WITH CEREBRALANEURYSM / ANEURYSMAL SUBARACHNOID

HAEMORRHAGE (SAH)

Expected OutcomeStaff utilising the following protocol will have the necessary information to appropriatelymonitor, assess and intervene in the care of patients who have been diagnosed with acerebral aneurysm and/or have had a subarachnoid haemorrhage requiring medicalmanagement, surgical clipping or endovascular coiling of the aneurysm.

Patients admitted to Liverpool Health Service with a diagnosis of cerebralaneurysm/aneurysmal subarachnoid haemorrhage will be managed in a holistic mannerincorporating all members of the health care team whose goals are to: prevent cerebral bleeding, infection and the consequences of vasospasm and

hydrocephalus. reduce intracranial pressure and neurological deficits related to the primary mechanism

of injury. avoid hypoxia and secondary brain damage. commence rehabilitation and foster neurological and total body functioning to pre-

admission state or better.

Policy Statement

Haemodynamic or neurological deterioration (as per the patients level ofconsciousness, Glasgow Coma Score assessment or evidence of focal deficit)

will be

assessed, documented and reported - intervention strategies will be implemented andassessed for their effectiveness.

Protocol Contents:3.1.1. Pre-operative management of the patient with suspected subarachnoid haemorrhage

[SAH] in the Emergency Department or ICU.

3.1.2 Pre-operative management of the patient with confirmed subarachnoid haemorrhageand vasospasm in the Intensive Care Unit.

3.1.3. Pre-operative management of the patient with suspected subarachnoid haemorrhage[SAH] in the Neurosurgical Ward.

3.1.4. Post-operative management of the patient with elective clipping/coiling of a cerebralaneurysm.

3.1.5. Post-operative management of the patient with aneurysmal subarachnoidhaemorrhage in the Recovery Room and ICU.

3.1.6. Post-operative management of the patient with aneurysmal subarachnoidhaemorrhage in the Neurosurgical Ward.

3.1.7. Background Information for these Policies: Vasospasm Cranial Nerve Deficit Testing Focal Deficits Hunt and Hess Classification of SAH Grades References


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PRE-OPERATIVE MANAGEMENT OF THE PATIENTWITH SUSPECTED SAH IN THE EMERGENCYDEPARTMENT OR ICU

Expected Outcome Patients presenting to the Emergency Department and transferred to the Intensive Care

Unit with a diagnosis of subarachnoid haemorrhage will have haemodynamic monitoringand neurological assessment performed frequently to assess current condition and allowinterventions to occur.

Policy Statement

The Neurosurgical Registrar must be informed when a patient with a suspected orconfirmed subarachnoid haemorrhage arrives in the Emergency Department - prior to aproposed transfer to the Ward or ICU.

The patient will have continuous haemodynamic monitoring with attention toelectrocardiograph (ECG) irregularities and prompt intervention.

Blood pressure (BP) will be normalised to the patients pre-morbid level and peaks andtroughs in the BP will be avoided or managed.

Frequent neurological assessment using the Glasgow Coma Scale (GCS) will beattended as the patient is at risk of re-bleeding (estimated incidence of 35-40%).

History should be assessed for incidence of a previous cerebral bleed (sentinel bleed),as vasospasm may already be insitu, thus delaying surgery.

The presence of vasospasm, raised intracranial pressure and/or neurologicaldeterioration necessitates transfer to the Intensive Care Unit.

There is to be no avoidable delay in the commencement of the prescribed drug therapynimodipine.

A Medical Emergency Team (MET) call is to be initiated when the GCS falls by 2points, and as per MET calling criteria.

Documentation of neurological assessment is to occur even where protocols exist fordocumentation by exception.

Emergency and ICU Observations Hourly or more frequent neurological and haemodynamic observations. Maintain systolic BP


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Environment: non-stimulating, quiet, comfortable. Maintain patient on bed-rest with toilet privileges or as required.

Visitors are limited.

Assist with activities of daily living.

Antiembolic stockings are worn to reduce the incidence of deep venous thrombosis orcalf-compression device is insitu.

Hair wash (gentle) on day of surgery where possible, nil head shave unless specificallyrequested.

ICU Procedures Insert a triple lumen central venous access using a subclavian or internal jugular

approach.

Attach a transducer and monitor central venous pressure.

Intubate and ventilate as indicated.

Utilise a volume-controlled ventilatory mode e.g. Synchronised intermittent mandatoryventilation with pressure support (SIMV + PS), it is inappropriate to wean ventilation

prior to surgery.

ICU Tests ECG.

Chest X-Ray.

Bloods: as per Medical Officer.

Neurological status Report any deterioration in the level of consciousness and neurological functioning. Maintain hourly assessment of GCS, observe for focal neurological deficits (see

Background Information Policies at the end of this document).

If a change is noted, record and report to the Intensive Care Registrar and NeurosurgicalRegistrar.

Maintain patient position at 15-300

head up.

Hydration/Nutrition Nil by Mouth (NBM) if for surgery maintain euvolaemia using IV sterile 0.9% normal

saline at 1.5mL/kg/hr.

Enteral nutrition/oral diet as tolerated if not for same-day surgery.

May require indwelling urinary catheter if using excess energy to move or urinate.

Avoid straining or valsalva manoeuvres, consider laxative and stool softener.

Nil digital examination or medication rectally.

Drug Therapy Nimodipine 30mg x 2 orally every 4 hours or nimodipine 10mg/50mL vial IV, via central

access, dedicated lumen at a rate as specified in the drug protocol.

Interruption to the IV infusion or delay in administering oral/nasogastric dose must beavoided. Oral dosage must be administered at

4/24 intervals neither late nor early.

When NBM prior to surgery, ensure patient receives oral medications or have theprescription altered to an appropriate route.

Histamine antagonist if NBM for > 48 hours or on steroidal therapy.

Surgeons preference for both steroid and anti-convulsant therapy.

Analgesia is vital: oral paracetamol/codeine or subcutaneous/IV morphine. IV morphinein association with midazolam when patient is ventilated.

Regardless of choice of analgesia, obtain regular prescription for stool softener andlaxative to prevent straining.


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PRE-OPERATIVE MANAGEMENT OF THE PATIENT WITHSUSPECTED SAH AND VASOSPASM (VSP) IN THEINTENSIVE CARE UNIT.

Expected Outcome Patients diagnosed with vasospasm preoperatively will be managed supportively to

reduce the effects of VSP (decreased blood flow with ischaemia and infarction) untilsurgery is possible.

Policy Statement

Patients presenting to the hospital with a diagnosis of ruptured cerebral aneurysm will beassessed for a history of previous headache suggestive of aneurysmal haemorrhage.

Patients with suspected previous aneurysmal headache will be assessed for evidence ofclinical VSP or VSP evidenced on angiography or with the use of transcranial Doppler(tcD) ultrasonography.

Patients admitted to the hospital for clipping of a cerebral aneurysm with a diagnosis ofsubarachnoid haemorrhage and vasospasm, will be transferred to the Intensive Care Unitfor on-going management.

The Neurosurgical Registrar must be informed when a patient with a suspected orconfirmed subarachnoid haemorrhage arrives in the Emergency Department - prior to aproposed transfer to the Ward or ICU.

The Intensive Care Registrar and the Neurosurgeon/Neurosurgical Registrar will beinformed when a patient has neurological deterioration/increased intracranial pressures.

The patient will have continuous haemodynamic monitoring with attention to ECGirregularities and prompt intervention.

Blood pressure (BP) management will occur to ensure adequate cerebral perfusion in thepresence of vasospasm without incidence of peaks and troughs in the systolic BP.

Frequent neurological assessment using the Glasgow Coma Scale (GCS) will beattended as the patient is at risk for re-bleeding (estimated incidence of 35-40%) orinfarction due to VSP.

There is to be no avoidable delay in the commencement or progression of the prescribeddrug therapy nimodipine.

A MET call is to be initiated when the GCS falls by 2 points, and as per calling criteria.

Documentation of the neurological assessment, ICP and Cerebral Perfusion Pressure(CPP) is to occur even where protocols exist for documentation by exception.

Emergency and ICU Observations: Hourly or more frequent neurological and haemodynamic observations. Maintain systolic BP at 140-160mmHg to create a systolic push, aid cerebral perfusion

and avoid re-rupture of the aneurysm. Maintain mean arterial pressure (MAP) at 90 110 mmHg; inotrope of choice may be

adrenaline (as opposed to first-line choice of noradrenaline) to maintain an increasedMAP without undue increase in the systolic pressure, thus avoiding peaks and troughs inblood pressure.

Maintain SpO2 95% with nil respiratory distress. If GCS < 9, protect the airway andprepare for intubation.

Obtain 12 lead ECG, commence continuous ECG monitoring; observe and treat cardiacdysrhythmias.

If monitoring Intracranial Pressure (ICP), Cerebral Perfusion Pressures [CPP] ismaintained at 70mmHg.

ICP is tolerated at 20mmHg if higher, drain cerebrospinal fluid (CSF), then utilise drugtherapies as prescribed by Intensive Care or Senior Neurosurgical Registrar.

Maintain normothermia if temperature increases above 370C, use paracetamol andcooling (as per the Temperature Regulation protocol); avoid shivering.

Maintain normal electrolyte and blood sugar levels.


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Ensure accurate fluid balance documentation, urinary output at minimum of 0.5mls/kg/hr. Ensure family/carers informed, contact Social Worker as required; document all

teaching/information given. Report any deterioration in the Glasgow Coma Score or evidence of focal deficit

immediately.

Environment: non-stimulating, quiet, comfortable Maintain patient on bed-rest with toilet privileges or as required.



Antiembolic stockings are worn to reduce the incidence of deep venous thrombosis orcalf-compression device is insitu.


ICU Procedures Insert a triple lumen central venous access using a subclavian or internal jugular

approach.


Intubate and ventilate as indicated.

Utilise a volume-controlled ventilatory mode e.g. SIMV + PS, it is inappropriate to weanventilation prior to surgery.

ICU Tests ECG, Chest X-Ray, Bloods: as per Medical Officer.

Repeat tcD, angiogram, CT as per Intensive Care Registrar/Neurosurgical Registrar.

Neurological status Report any deterioration in the level of consciousness and neurological functioning. Maintain hourly assessment of GCS, observe for focal neurological deficits (see

Background Information for Protocol at the end of this document).

If change is noted, record and report to the Intensive Care/Neurosurgical Registrar.


head up.

Hydration/Nutrition NBM if for surgery maintain euvolaemia using IV Normal Saline at 1.5ml/kg/hr.

Enteral nutrition/oral diet as tolerated if not for same day surgery.




Drug Therapy Nimodipine 30mg x 2 orally every 4 hours or nimodipine 10mg/50mL vial IV, via central


Interruption to the IV infusion or delay in administering oral/NG dose must be avoided.Oral dosage must be administered at fourth hourly intervals neither late nor early.



Surgeons preference for both steroid and anti-convulsant therapy.

Analgesia is vital: oral paracetamol/codeine or subcutaneous/IV morphine. IV morphine

in association with midazolam when patient is ventilated. Regardless of choice of analgesia, obtain regular prescription for stool softener and

laxative to prevent straining.


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PRE-OPERATIVE MANAGEMENT OF THE PATIENT WITHSUSPECTED SAH IN THE NEUROLOGICAL WARD.

Expected Outcome Patients presenting to the Emergency Department and then transferred to the Ward with

a diagnosis of subarachnoid haemorrhage will have haemodynamic monitoring andneurological assessment performed frequently to assess current condition and allowinterventions.

Policy Statement

The Neurosurgical Registrar must be informed when a patient with a suspected orconfirmed subarachnoid haemorrhage arrives in the Emergency Department - prior to aproposed transfer to the Ward.

Patients who are stable (haemodynamically and neurologically) with no focal deficits anda Glasgow Coma Score (GCS) > 12 may be transferred to a neurosurgical ward that has

adequate registered nurse staffing levels.

Patients who deteriorate neurologically or who are haemodynamically unstable or whohave labile blood pressure must be transferred to the ICU.

The patient will have frequent haemodynamic monitoring including heart rate, bloodpressure, respiratory rate, temperature and SpO2 monitoring.

Blood pressure (BP) will be normalised to the patients pre-morbid level and peaks andtroughs in the BP will be avoided or managed.

Frequent neurological assessment using the Glasgow Coma Scale (GCS) will beattended as the patient is at risk for re-bleeding (estimated incidence of 35-40%).

There is to be no avoidable delay in the commencement of the prescribed drug therapynimodipine.

A MET call is to be initiated when the GCS falls by 2 points.

Nursing Care of the Patient in the Ward Environment:

Environment: non-stimulating, quiet, comfortable. Maintain patient on bed-rest with toilet privileges.



Antiembolic stockings are worn to reduce the incidence of deep venous thrombosis.


Haemodynamic and Neurological Assessment: If the patient has a Glasgow Coma Score less than 13 or evidence of focal deficits the

Neurosurgical Registrar is informed and liases with the ICU Senior Registrar for patienttransfer to the ICU.

Observations are performed 2 - 4th

hourly or more frequently if the patient deteriorates Maintain systolic BP


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Ward Procedures Insert an intravenous line for medications.

Ward Tests

ECG if not attended in Emergency Department or if heart rate becomes irregular. Bloods: as per Medical Officer.

Neurological status Report any deterioration in the level of consciousness and neurological functioning. Maintain 2

nd- 4

thhourly assessment of GCS, observe for focal neurological deficits (see

Background Information for Protocols at the end of this document).

If a change is noted, record and report to the Medical Officer/Neurosurgical Registrarimmediately.


head up.

Hydration/Nutrition Patient kept NBM if for surgery. Maintain hydration using IV Normal Saline at 1.5ml/kg/hr.

Encourage fluid intake if surgery not scheduled report incidences of nausea andvomiting as this may indicate neurological deterioration.

Enteral nutrition/oral diet as tolerated if not for same day surgery.




Drug Therapy Administer nimodipine 30mg x 2 orally every 4 hours as prescribed (longer intervals or a

decreased dose is inappropriate).

Delay in administering oral/NG dose must be avoided. Oral dosage must be administeredat




Surgeons preference for steroid, anti-convulsant therapy.

Analgesia is vital: oral paracetamol/codeine or SC morphine for headache is essential.

Regardless of the choice of analgesia, obtain regular prescription for stool softener andlaxative to prevent straining.


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POST OPERATIVE MANAGEMENT OF THE PATIENTWITH ELECTIVE CLIPPING/COILING OF A CEREBRALANEURYSM

Expected Outcome Patients presenting to the hospital with a diagnosis of unruptured cerebral aneurysm will

be managed for elective neurosurgery and will be nursed in the appropriate environmentto ensure their recovery.

Policy Statement

Patients who are stable (haemodynamically and neurologically) with no focal deficits anda Glasgow Coma Score [GCS] > 12 may be transferred to a neurosurgical ward after

elective clipping of a cerebral aneurysm. Patients who deteriorate neurologically or who are haemodynamically unstable or who

have labile blood pressure will be transferred to the ICU.

The patient will have frequent haemodynamic monitoring including heart rate, bloodpressure, respiratory rate, temperature and SpO2 monitoring.

Blood pressure (BP) will be normalised to the patients pre-morbid level or to a systolic

BP than 140-160mmHg.

Frequent neurological assessment using the Glasgow Coma Scale (GCS) andassessment for focal deficit will be attended.

A MET call is to be initiated if the GCS falls by 2 points.

Patient Care Maintain blood pressure and fluid status within normal parameters.

Administer analgesia and antiemetics.

Administer bowel medications to prevent constipation.

If managed within the Intensive Care Unit, discharge on Day 1 from ICU whenneurological assessment, electrolytes and vital signs are stable.

Nimodipine is not indicated unless intra-operative bleeding has occurred: see SAH -Post-Operative Management.

Patients are managed as per protocols for cranial neurosurgery.


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POST-OPERATIVE MANAGEMENT OF THE PATIENTWITH ANEURYSMAL SAH IN THE RECOVERY ROOMAND ICU.

Expected Outcome Patients progressing through the Recovery Room to ICU or from the Operating Theatre

direct to ICU will be managed in a safe environment with medical, nursing and alliedhealth care to assist in their recovery and the prevention of further brain injury.

Policy Statement

Patients who have not had clipping or coiling of their aneurysm but who have hadinsertion of an Intracranial Pressure (ICP) monitoring device/External Ventricular Drain(EVD) will be cared for as per Protocol 3.1.1 preoperative management of SAH in theICU.

The Intensive Care Registrar and Neurosurgeon/Neurosurgical Registrar will be informedwhen a patient has neurological deterioration, increased intracranial pressure ordecreased cerebral perfusion pressure.

The patient will have frequent (usually hourly) continuous haemodynamic monitoring andneurological assessment.

With infratentorial (posterior fossa) approach, haemodynamic and neurologicalassessment will occur half-hourly, for 6-12 hours or until the patient is stable.



Documentation of the neurological assessment, ICP and Cerebral Perfusion Pressure(CPP) is to occur even where protocols exist for documentation by exception.

SAH - Post-Operative Management in Recovery On arrival: q15 minutely vital signs for the first 4 hours, then hourly until transfer

(temperature, pulse, BP, RR, SpO2). On arrival GCS, limb strength, pupillary and focal deficit assessment, then every 30

minutes until transfer. Monitor input and output

1/24, maintain urinary output at 0.5mL/kg/hr.

Keep within vital sign parameters as per ICU care; seek immediate senior medicalintervention if unable to maintain.

Any sign of neurological deterioration or new focal deficit - seek immediate neurosurgicalregistrar intervention.

Patients that are nursed within the Recovery Room for extended periods of time will bemanaged as per the following:

SAH - Post-Operative Management in the ICU Observe neurological status and immediately intervene to address changes in the level of

consciousness, movement, sensation, vitals or blood values using a multidisciplinaryapproach.

Ensure adequate hydration and haemodynamic state, obtain and maintain set bloodpressure parameters.


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Vital Signs: SpO2 95%, unless pre-existing history of pulmonary disease.

PETCO2 monitored if ventilated, maintain at a PaCO2 of 35mmHg.

MAP via arterial line at minimum of 90mmHg.

ICP < 20-25mmHg; record sudden spontaneous spikes, report sustained increase andobtain immediate assessment/intervention.

CPP (if monitoring ICP) at 70mHg; consult with Intensivists and Neurosurgeon if unableto maintain.

Administer maintenance fluid at 1.5mL/kg/hr sterile 0.9% normal saline and colloid tomaintain set BP parameters

MonitorCVP and maintain adequate hydration.

Administer noradrenaline 4mg/50ml in glucose (in consultation with the Intensivist) tomaintain MAP if fluid loading does not achieve goal. Note that pre-existing cardiacdisease requires cautious use of fluid and inotropic therapy.

HR: observe for cardiac dysrhythmias and treat where indicated; aSAH is associated withcardiac damage signified by inverted T-wave, ST depression, AF and other dysrhythmias.

Daily ECG required if unstable ECG rhythm and/or use of inotropic therapy.

Temperature kept 370C [brain temp is 1

0 body temp], initially use passive cooling

without shivering, tepid sponging and paracetamol; (see Temperature Regulationprotocol No_).

Initiate active cooling when patient is ventilated and sedated in the presence of increasedICP and Vasospasm (VSP).

Neurological Assessment Assess neurological status by performing a GCS and assessment of limb strength and

pupillary response. Assess for focal deficit. These may indicate clinical VSP(referred toas delayed ischaemic neurological deficit: DIND), rebleeding or oedema.

Observe results of transcranial Doppler (tcD) studies as a possible predictor ofdeterioration/evidence of VSP.

VSP is most likely to present Day 4 Day 10, peak incidence at Day 7 after initial bleed,(admission may not relate to the primary bleed). Observe for cranial nerve dysfunction Observe for focal deficits

Report any deterioration in the GCS/focal deficit to the medical officer immediately.

ICU Procedures Ensure triple lumen central venous access is insitu using a subclavian or internal

jugular approach.


Intubate and ventilate as indicated, using a volume-controlled ventilatory mode e.g.synchronised intermittent mandatory ventilation with pressure support (SIMV + PS).

ICU Tests upon admission ECG.

Chest X-Ray.

Bloods: as per Medical Officer.

Drug Therapy Nimodipine 30mg x 2 orally every 4 hours or nimodipine 10mg/50mL IV, via central


Interruption to the IV infusion or delay in administering oral/NG dose must be avoided.Oral dosage must be administered at


When NBM prior to procedure, ensure patient receives oral medications or have theprescription altered to an appropriate route.



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Surgeons preference for steroid, anti-convulsant therapy.

Analgesia is vital: oral paracetamol/codeine or SC/IV morphine. IV morphine in

ription for stool softener and

parin at twenty four hours post surgery; or as per

nalgesiato relieve pain of residual SAH, effects of surgery, ICU based care, bed

in from injury. Also, if

s.

Ventilation:rapy as required. If the patient has raised ICP; avoid percussion and use

tioning. If patient is analgesed,

V portion of ventilatory support if patient has raised ICP and there are no

ventilatory (and breath rate) support when in the presence

Therapy, Hydration, Electrolytes d for unstable patients or patients with 0.9% normal saline at 1.5ml/kg/hr.

).

d 5.0,r low

IT/Feeding/Eliminationequate urinary output at 0.5mL/kg/hr. ium levels, pre-

if there is suspicion/evidence of a fractured base of skull;

d intervention if bowels not opened > 2 days: there is a risk of

revent aspiration. If

ndwelling catheter once patient is stable and hydration issues are

xamination or medication rectally secondary to the risk of a valsalva response

association with midazolam when patient is ventilated

Regardless of choice of analgesia, obtain regular presclaxative to prevent straining.

Commence subcutaneous heNeurosurgeons preference.

A Administered

rest, headache, raised ICP and stress associated with ventilation.

In the presence of deep coma it is logical to suspect a degree of paICP rises with nursing/medical/ environmental input administer further prescribedmedication without unduly affecting neurological assessment and/or haemodynamic

Utilise analgesia as an adjunctive therapy for raised ICP, in combination with sedation,propofol and thiopentone therapy.

Chest physiothevibes, suction for < 15 seconds, observe ICP response.

Allow adequate rest in between episodes of required sucsedated and nil cough reflex, suction as per respiratory assessment and ventilatorypressures.

Maintain SIMplans to wean to extubate.

Do not wean the patient fromof raised ICP that is being actively managed.

IV Triple lumen access with transduced CVP require

SAH - Hunt and Hess Grade 3.

Maintain euvolaemia using sterile

Ensure intake at 2-3 litres/day when on nimodipine therapy (IV or oral

Maintain magnesium at 1.5 mmols and 2 mmols, potassium 4.0 annormalise phosphate and glucose levels, monitor sodium levels and report high o

levels, keep Hb 100.

G

Monitor fluid balance, maintain ad Place nasogastric tube, establish if special feeds are required as per sod

existing conditions, and trauma.

Do not place a nasogastric tubeplace an orogastric tube.

Abdominal assessment anpseudo-obstruction (Ogilvies syndrome) associated with nimodipine.

If patient progresses to oral intake, assess adequate cough reflex to psuspected (voice changes to raspy, gurgling or hoarse speech post oral intake, continuedcoughing or drooling) keep patient NBM and seek swallow assessment consult fromSpeech Pathologist.

Consider removal of iresolved.

Nil digital eand subsequent rise in ICP.


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Patient Positioning and Care Maintain neutral alignment, avoid hip flexion, nil compression or kinking of venous

te ICP

umber when patient unstable or

drainage vessels, maintain patient position at 15-300

head up. Normalise when acuissues stabilised.

Visitors limited in n ensure quiet environment.

tween

p venous thrombosis and use of calf

ied health support, notify Social Worker of unstable SAH patient as

ferred to the allied

aged to sit out of bed and mobilise with assistance when intracranial

post clipping of aneurysm to visualise accurate placement as per the

giogram if sudden deterioration/focal deficit such as leg weakness

g. verapamil) may be

andage is to remain insitu until Day 1 post surgery. Observe surgical site

moved at 5-7 days unless union has not occurred (report) or is otherwise

erapist

athologist(Referral)

Reduce noise wherever possible and allow the patient to have rest periods benursing, allied health and medical interventions.

Antiembolic stockings to reduce incidence of deecompression device.

Involve appropriate alltheir involvement is usually necessitated for patient and family care.

Patients with impaired physical mobility/signs of contracture will be rehealth care team.

Patients are encourpressure and haemodynamic state has stabilised and there is minimal headache.

Document communications between medical and nursing staff with family.

Document all teaching/explanations conducted at the bedside.

Imaging Angiogram

Neurosurgeon.

CT scan and Andevelops that was not present prior to clipping of the aneurysm.

Papaverine [an arterial smooth muscle relaxant] or other drugs (einjected during cerebral angiography to relax arteries affected by vasospasm.

Wound Care A turban-style b

for bleeding, CSF ooze or infection, cover wound with non-adherent dressing and secure.Wound may remain exposed 48 hours post surgery and showering/hair wash allowedafter this time.

Clips/sutures represcribed and documented.

Allied Health Involvement Social Worker

Physiotherapist

Occupational Th

Dietitian

Speech P Rehabilitation Team


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POST-OPERATIVE MANAGEMENT OF THE PATIENTWITH ANEURYSMAL SUBARACHNOIDHAEMORRHAGE [ASAH] IN THE WARD

Expected Outcome Patients progressing through the Recovery Room to the Ward will be managed in a safe

environment with medical, nursing and allied health care to assist in their recovery andthe prevention of further brain injury.

Policy Statement

The Neurosurgeon/Neurosurgical Registrar will be informed when a patient deterioratesneurologically.

The patient will have frequent haemodynamic monitoring and neurological assessment.

With infratentorial (posterior fossa) approach, haemodynamic and neurologicalassessment will occur half-hourly for 6 hours or until the patient is stable.



Ward management of patient post SAH Observe neurological status and immediately intervene to address changes in level of

consciousness, vital signs, blood values using a multidisciplinary approach.

Ensure adequate hydration and haemodynamic status, maintain set blood pressureparameters.

Ensure rehabilitation commences in the ward, continue/initiate process of discharge

planning.

Vital signs and neurological assessment upon arrival to theWard from RecoveryFrequency is:

Hourly for 6 hours, then if stable, second hourly for 6 hours, then fourth hourly.

If deterioration occurs, frequency is increased until the patient has received definitivetreatment.

If the patient has been transferred from ICU; observations are as per frequency last usedwithin the ICU usually second to fourth hourly.

SpO2 95%, unless pre-existing history of pulmonary disease.

BP maintained at a normal pre-SAH level or as per pre-existing antihypertensive therapy

(SBP at 140-160mmHg). Administer maintenance fluid at 1.5mL/kg/hr sterile o.9% normal saline or as per

Medical Officers prescription. Maintain adequate hydration at all times if IV tissues, ensure timely replacement. Hypotension must be avoided, inform Neurosurgical Registrar promptly and ensure

therapy implemented to address hypotension. Changes to these guidelines are to be documented by the Neurosurgical

Registrar/VMO in patient case notes.

HR: observe for irregular rhythm; obtain 12-lead ECG to identify dysrhythmia, repeat BD.

External Ventricular Drain (EVD): as per protocol.

Temperature: maintain less than 370-37.5

0C, use passive cooling (tepid sponging and

paracetamol) without shivering.


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Neurological Assessment Any decrease in the level of consciousness (LOC) must be reported and acted upon. This

may indicate clinical vasospasm[VSP], rebleeding or oedema.

Call MET if GCS falls by 2 points, and as per calling criteria.

Observe results of transcranial Doppler [tcD] sonography as a possible predictor ofdeterioration/evidence of VSP.

VSP is most likely to present Day 4 Day 10, peak incidence at Day 7 after initial bleed.The patient admission may not relate to the primary bleed.

Observe for cranial nerve dysfunction, (see appendix Background): any deteriorationmust be reported and acted upon.

Observe for focal deficits (Background): any deterioration must be reported and actedupon.

Respiratory Status: Chest physiotherapy as required, allow adequate rest in between episodes of required

suctioning.

Tracheostomy care as per hospital protocol.

IV Therapy, Hydration Ensure intake at 2-3 litres/day when on nimodipine therapy (IV or oral).

Strict fluid balance documentation until nimodipine therapy ceases: inclusive of both inputand output.

GIT/Feeding Monitor fluid balance.

Commence nutrition as soon as possible.

Establish if special feeds are required as per sodium levels, pre-existing conditions, andtrauma.

Do not place a nasogastric tube if there is suspicion/evidence of a fractured base of skull;place an orogastric tube.

Bowel medications are required due to use of opioids, immobilization, altered nutrition,stress, and use of nimodipine.

Abdominal assessment and intervention if bowels not opened > 2 days. There is a risk ofpseudo-obstruction (Ogilvies syndrome) associated with Nimodipine.

Vomiting must be controlled. Use anti-emetics, ensure medications absorbed andadequate hydration is maintained. Vomiting may be a sign of raised ICP.

Oral diet may recommence as soon as the patients level of consciousness is adequate,with nil contraindications.

If patient progresses to oral intake, assess for adequate cough reflex to preventaspiration. If suspect, a swallow assessment is required; consult with Speech Pathologist.

Patients who have had posterior fossa approach remain NBM (with enteral feeding) untilswallow assessment can be formally obtained.

If patient has voice changes [raspy, gurgling, hoarse speech] post oral intake orcontinued coughing or drooling cease oral intake and obtain Speech Pathology consult.

Analgesia/Agitation Administered to relieve pain of residual SAH, effects of surgery, bed rest, headache.

Obtain prescription to relieve patients perceived level of discomfort; paracetamol withcodeine combinations used as a baseline.

Agitation may be cerebrally related or be a sinister representation of oxygen/glucosedepletion/neurological deterioration. Avoid sedatives until other causes of agitation havebeen ruled out.


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Patient Positioning and Care When in bed/sitting in chair - maintain neutral alignment, avoid hip flexion, nil

compression of venous drainage vessels, head of bed raised 15-300.

Visitors encouraged to assist with rehabilitation and arousal therapy, ensure episodes ofquiet during each shift.

Reduce noise wherever possible and allow the patient to have rest periods betweennursing, allied health and medical interventions.

Antiembolic stockings to reduce incidence of deep venous thrombosis.

Commence subcutaneous heparin at twenty four hours post surgery; or as perNeurosurgeons preference.

Involve appropriate allied health support, notify Social Worker of unstable SAH patient.

Document communication between medical and nursing staff with families.

Document teaching and explanations conducted at the bedside.

Mobilisation Patient is encouraged to sit out of bed and mobilise with assistance as soon as tolerating

an upright position without undue headache.

Patients with impaired physical mobility/signs of contracture will be referred to the alliedhealth care team upon transfer or admission to the ward.

Wound Care A turban-style bandage is to remain insitu until Day 1 post surgery. Observe surgical site

for bleeding/CSF ooze/infection, cover with non-adherent dressing and secure.

Wound may remain exposed 48 hours post surgery and showering/hair wash allowedafter this time.

Clips/sutures removed at 5-7 days unless there is poor union (document and report) or isotherwise prescribed and documented.

Discharge Advice: dependent upon the individual Neurosurgeon.

Follow-Up appointment:to be booked for 2 weekspost clipping/coiling of aneurysmand discharge.

Swimming:allowed post clipping/coiling of aneurysm - when wound has fully healed. Return to work: as per medical advice at two-week post-discharge from hospital

appointment, consult with Neuropsychologist. Flying:as per medical advice at six-week post-discharge from hospital appointment. Driving:allowed at 6 monthspost clipping/coiling of aneurysm when visual fields

cleared; requires neurosurgical and ophthalmology review, also dependent upon beingseizure-free.

Sexual Activity:according to patient comfort, advise patient to go slowly and gently anddetermine their response based upon perception of well-being.


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Background Information for Policies 3.1.1 to 3.1.4 Aneurysmal Subarachnoid Haemorrhage Management

1.Vasospasm: Spasticity and narrowing of cerebral arteries (vasospasm) affects blood flow to braintissue, resulting in ischaemia, altered neurological functioning and possible infarction.

Signs of vasospasm may include deterioration in the Glasgow Coma Scale or may beseen solely as a focal deficit; both instances indicate direct brain ischaemia/infarct andare as much of an emergency as impending myocardial infarction.

Treatment includes administration of nimodipine and ifaneurysm is clipped: elevated BPabove the normal level. Usually at MAP of 90-110mmHg and SBP at 160180mmHg.Administration of IV fluids and inotropes is used to accomplish this increase.

Rarely, vasospasm that is present prior to clipping of the aneurysm may delay surgery.There is concomitant risk of infarction secondary to the vasospasm. The neurosurgicalteam may, in consultation with the Intensivists, decide to increase MAP with fluid andinotropes to provide perfusion, ensuring that the SBP remains less than @140mmHg.

Maintaining BP parameters at all times is imperative swings in BP with an unclippedaneurysm can cause ischaemia/infarction or catastrophic re-bleeding. Alternately,hypotension in the clipped aneurysm patient can lead to brain cell death, widespreadinfarction, gross neurological disability or death.

2. Fisher Grade for VasospasmGreenberg, M (1994). Handbook of Neurosurgery.Greenberg Graphics, Lakeland, Florida, page 720.

Group Blood on CT

1234

No blood detectedDiffuse or vertical layers < 1mm thickLocalized clot and/or vertical layer > 1mm thickIntracerebral or intraventricular clot with diffuse or no SAH

Thus, vasospasm is most likely to occur in Grades 2 and 3 and not likely to occur inGrades 1 and 4.

3. Cranial Nerve Assessment(simplistic outline) CN I- Olfactory: sense of smell, not tested in acute setting. CN II Optic: vision, test for ability to read, discern number of fingers held in front of

patients face. CN III Oculomotor: pupillary constriction and eyelid elevation, shine torch in eye

pupil should constrict. CN IV Trochlear: eye muscle control, check gaze by asking patient to look down and

out.

CN V Trigeminal: sensation to forehead, cheek, jaw; clench jaw, ask patient to grittheir teeth observe for symmetry. CN VI Abducens: eye muscle control, ask patient to look to the left and right without

moving their head. CN VII Facial: facial muscle control, ask patient to frown and smile observe for

symmetry. CN VIII Acoustic [Vestibulocochlear]: hearing/balance, ask patient to repeat whispered

statement, test ears separately. CN IX Glossopharyngeal: taste, gag and cough reflex, check with CN X. CN X- Vagus: gag, stimulus results in gagging or bradycardia and increased gut

peristalsis to stimulus, check patients cough/ gag reflex. CN XI Spinal Accessory: neck and shoulder muscle innervation,patient shrugs

shoulders while assessor presses down, assess equality and strength.

CN XII Hypoglossal: tongue movement, ask patient to poke tongue out, assess fordeviation to left/right or long term deficit seen as muscle wasting.


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4. Focal DeficitsA focal (neurologic) deficit is a loss of movement, sensation, or function of a nerve in aspecific location. The loss is related to dysfunction in the brain or peripheral nervous system.There may be no decrease in the level of consciousness. Focal neurologic deficits may affect the left or right side of the face, arms or legs or be

related to a specific region within the brain e.g. speech may be affected but not the abilityto write.

Sensation changes include paraesthesia (abnormal sensations), decrease in sensation ornumbness.

Movement changes include paralysis, weakness, loss ofmuscle control, increased ordecreased muscle tone. The terms paresis and plegia are used to describe severeweakness and lack of movement.

5. Other types of focal deficit: Speech orlanguage changes such as aphasia ordysarthria (impaired speech and

language skills), poor enunciation, poor understanding of speech, impaired writing,impaired ability to read or to understand writing, inability to name objects (anomia).

Vision changes such as reduced vision, decreased visual fields, sudden vision loss,double vision (diplopia) or homonymous hemianopia (loss of a visual sector in one eye).

Neglect or inattention to the surroundings on one side of the body - see Pronator Drift. Loss of coordination, fine motor control, or ability to perform complex movements. Horner's syndrome: one-sided eyelid drooping (ptosis), absent sweating on one side of

the face, and retraction of one eye into the socket, poor gag reflex, swallowing difficulty,and frequent choking.

6. Hunt and Hess Classification of SAH (Greenberg, 1994, page 858)

Grade Classification

011a2345

Unruptured aneurysmAsymptomatic, or mild headache and slight nuchal rigidityNo acute meningeal/brain reaction, but with fixed neurological deficitCranial nerve palsy (e.g. III, IV), moderate to severe headache, nuchal rigidityMild focal deficit, lethargy or confusionStupor, moderate to severe hemiparesis, early decerebrate rigidityDeep coma, decerebrate rigidity, moribund appearance

Add one grade for serious systemic disease (e.g. Hypertension, Diabetes) or severe VSP onangiography

7. World Federation of Neurological Surgeons Scale(Liebeskind, 2002)

Grade Glasgow Coma Scale score Clinical findings

I 15 No headache or focal signs

II 15 Headache, nuchal rigidity, no focal signs

III 13 - 14 Headache, nuchal rigidity, no focal signs

IV 7 - 12 Headache, rigidity, focal signs

V 3 - 6 Headache, rigidity, focal signs
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Reviewed: October 2004 Neurological Care Aneurysmal Subarachnoid Haemorrhage

References

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Fukuda T., Hasue M. and Ito H. 1998 Does traumatic subarachnoid haemorrhage caused by diffuse brain injurycause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by rupturedintracranial aneurysms. Neurosurgery. 43 (5): 1040-1049.

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Neurosurgery. 87: 436-439. Weaver J.P. and Fisher M. 1994 Subarachnoid hemorrhage: an update of pathogenesis, diagnosis and

management. Journal of the Neurological Sciences. 125:119-131.

Hunt W.E. and Hess R.M. 1968 Surgical risk as related to time of intervention in the repair of intracranialaneurysms. Journal of Neurosurgery. 28 (1): 14-20.

Lasner T., Weil R., Riina H., King J., Zager E., Raps E. and Flamm E. 1997 Cigarette smoking-induced increasein the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. Journal of Neurosurgery.87:381-384.

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Morgan M., Day M., Little N., Grinnell V. and Sorby W. 1995 The use of intrarterial papaverine in themanagement of vasospasm complicating arteriovenous malformation resection. Journal of Neurosurgery. 82:296-299.

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Focal Deficits: http://thriveonline.com/medical/library/article/003191.html

Greenberg M. 1994 Handbook of Neurosurgery. Greenberg Graphics Florida: Lakeland.

Liebeskind DE. 2002 Cerebral aneurysms. eMedicine Journal, May 23, 3 (5).http://www.emedicine.com/NEURO/topic503.htm

Policy Author: M. Edgtton - Winn, CNC ICU for working party: K. Wright, CNC Neurosciences and M. Perry,CNE Recovery.

Policy Reviewer/s: CNC ICU, CNC Neurosciences and Consultant for Intensive Care and Neurosurgery.
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Aneurysmal SAH S n Guideline Liverpool

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