Aneurysmal Subarachnoid Haemorrhage - Guidelines for the Management of

Publication: 19/11/2013  
Next review: 10/10/2022  
Clinical Guideline
ID: 3577 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2019  


This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Please check the patients allergy status, as they may be allergic to Chlorhexidine, and alternative ( Providine iodine) solution will be required.
Be aware: Chlorhexidine is considered an environmental allergen.
Refer to the asepsis guidance.

Guidelines for the Management of aneurysmal Subarachnoid Hemorrhage (referring hospital and LTHT management)

Guideline Detail

These guidelines establish a standard of care for patients admitted with aneurysmal Subarachnoid Haemorrhage (aSAH). They provide a framework of best practice to manage the presenting condition and prevent complications.
Recommendations are made for management of patient presenting at non-LTH hospitals as well as management within LTHT.

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Aneurysmal (spontaneous) subarachnoid haemorrhage occurs with an incidence of approximately 10 cases per 100, 000 person years. It most commonly affects people aged 40-60 years old. It is twice as common in women as men and is associated with a high mortality and morbidity with over a third of patients dying by the end of the first week from ictus. Risk factors include cigarette smoking, hypertension, moderate to heavy alcohol consumption use of sympathomimetic drugs (e.g. cocaine) ,  a history of familial aneurysms and (rarely) genetic disorders such as autosomal dominant polycystic kidney disease, and type IV  Ehlers-Danlos syndrome. Early diagnosis and treatment is critical to improve the survival from this devastating medical condition. All cases should be discussed with the Regional Neuroscience Centre.

Risk factors for and prevention of aSAH

  1. Treatment of hypertension is recommended to prevent ischaemic stroke, ICH and cardiac, renal and other end-organ injury (Level 1/A evidence)
  2. Hypertension should be treatment and such treatment may reduce the risk of aSAH (Level 1/B evidence)
  3. Tobacco use and alcohol misuse should be avoided to reduce the risk of aSAH (Level 1/B evidence)

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If aneurysmal (spontaneous) subarachnoid haemorrhage (aSAH) is suspected, establish the diagnosis as soon as possible following initial resuscitation when the patient is in a stable clinical condition.

Typical presentations include ‘thunderclap’ headache, collapse with or without loss of consciousness, seizures and associated nausea, vomiting and photophobia. Examination may reveal focal neurology including neck stiffness.

Complications of aSAH, for example acute hydrocephalus, may require emergency neurosurgical intervention.

The World Federation of Neurological Surgeons grading scale should be recorded in the clinical notes

The Fisher CT score (see appendix 1) should be recorded in the clinical notes. Fisher score of 3-4 is predictive for the presence of vasospasm and poor clinical outcome.

The presence of an intra-cerebral haematoma causing mass effect is a contraindication to lumbar puncture (LP) as is the presence of obstructive  hydrocephalus.  A lumbar puncture should not be performed in the absence of a prior CT scan in these patients.  A positive CT scan result precludes the need for a lumbar puncture.

Level of evidence B

  • Patients not displaying visible blood on CT scan should have a diagnostic lumbar puncture; this particularly applies to patients with a delayed presentation and those whose clinical condition suggests that a small haemorrhage may have occurred. 
  • It is recommended to discard the first mL of cerebrospinal fluid (CSF) (i.e. collect a mid-stream sample for analysis), reducing the chance of sample contamination by epidural blood which can give a false positive result.
  • Analyse the sample for red blood cell count and xanthochromia.  A red blood cell count in excess of 10,000 per mL uniformly seen in three successive samples secures the diagnosis. However, patients who have suffered a small subarachnoid haemorrhage, or those who present in a delayed fashion may have fewer red blood cells in the CSF.  In the latter group of patients the presence of xanthochromia (either by naked eye or spectrophotometry) is diagnostic. The CSF result can only be properly interpreted in the light of the clinical history.  Patients who have a convincing history despite a negative CT scan and equivocal CSF analysis should be discussed with the neurosurgical team.

Level of evidence B

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Management at primary receiving hospital

If the patient initially presents at Leeds General Infirmary, follow the assessment and initial management plan as per primary hospital management.

Although definitive treatment is undertaken in specialist centres, the stabilization, diagnosis, initial management and transfer is often undertaken in non-specialist hospitals and is of the utmost importance. 

1.1 Initial Management

1.1.1 Assessment, oxygen therapy and fluid status

  • Assess cardiovascular, respiratory and neurological function.
  • Perform a focused neurological examination to determine the level of consciousness (using the fifteen point Glasgow Coma Score - GCS) and degree of neurological deficit including higher brain functions associated with language and comprehension, cranial nerves II, III, IV, VI, VII and XII and the peripheral motor system if possible.
  • Give supplementary oxygen via facemask and obtain at least one (preferably two) large bore peripheral venous access. 
  • Commence fluid resuscitation with 0.9% sodium chloride. For patients with clinical signs of hypovolaemia a bolus of 0.9% sodium chloride (e.g. 200 - 500 mL) can be given.
  • Continue hydration with a continuous infusion of 0.9% sodium chloride or Hartmann’s solution given between 125 mL - 166 mL per hour (3 - 4 L in 24 hours).
  • The patient should have a urinary catheter inserted.

1.1.2  Level of care

  • Patients with SAH should be cared for in a level 2 or level 3 environment (HOBS, HDU or ICU) as soon as practicable, depending on GCS and presence of early complications. See appendix 1 for clinical and radiological grading of SAH.
  • Select patients who are considered low risk (those who are WFNS grade 1 and felt likely to be perimesencephalic SAH) may be managed in a level 1 (ward) bed if agreed with the on-call neurosurgical consultant.
  • Start continuous monitoring of pulse, blood pressure (via invasive (arterial line) monitoring if indicated), ECG, respiratory rate and pulse oximetry

1.1.3  Nursing care and observations

  • Establish baseline observations - observations should include pulse, blood pressure and oxygen saturation as well as GCS evaluation and assessment of peripheral limb power.
    Glasgow Coma Scale and Pupil Responses in Adults
  • Deterioration in level of consciousness or the development of a new neurological deficit should trigger a review by medical staff and a CT scan. 
  • Repeat observations at 15 minute intervals until transfer agreed to the Neurosurgical Unit.
  • If patient is deemed unsuitable for transfer care returns to a supportive manner delivered within the initial hospital.

1.1.4  Referral and Transfer

  • Once the diagnosis of aSAH (see above) has been established the patient should be referred to the neurosurgical registrar on call via the online referrals software, accessed via, the patient should also be discussed with the on-call neurosurgical team at Leeds General Infirmary. Telephone:  079799289120
  • All patients should be discussed regardless of age and clinical condition. 
  • The referral should be made by an experienced clinician who has been involved in the care of the patient.  All patients should be discussed with the referring consultant responsible for the patient.    
  • For patients with a depressed level of consciousness an anaesthetic opinion should be requested.
  • Be prepared to give a full history
  • The neurosurgical on-call team will request the following information.

Name, grade, speciality and contact number of the referring doctor
Name and age of the patient.
Consultant responsible for the patient.
Ward name or number and a contact telephone number.
Brief details of the history of the subarachnoid haemorrhage, specifically the date and time of the ictus, and whether a seizure was observed.
Significant co-morbidity, drug and allergy history.
The general and neurological condition of the patient including pulse, blood pressure, oxygen saturation, level of consciousness and the degree of neurological deficit (motor deficit, pupillary reaction to light and the presence or absence of dysphasia).
The level of consciousness as assessed by the Glasgow Coma Score is of particular importance and should be given verbally for each subsection (e.g. “The patient is eye-opening spontaneously, obeys verbal commands and is fully orientated” rather than “The patient is Glasgow Coma Score 15”).
CT findings (and where appropriate lumbar puncture result).

There is an online neurosurgical referral system in place but for patients with SAH a telephone discussion is required in addition to sending the online referral.  Based on the information received, the neurosurgical team may elect not to transfer some patients to the neurosurgical unit, but this decision should be made on a case-by-case basis. 

Level of evidence B

  • Once accepted by the on-call neurosurgical registrar, transfer to a level three (ICU) or level two (HDU) unit is arranged through the nursing staff. Some  patients may be suitable to be looked after in High Observation ward beds (HOBS). The nurse in charge of the receiving ward will contact the primary hospital to arrange transfer.
  • Patients in a stable neurological condition may be transferred with a nurse escort.  If any doubt exists about the patient’s neurological or general state then a medical escort with appropriate airway skills, usually an anaesthetist is mandatory.
  • Patients with (or at high risk of) a deteriorating level of consciousness may require intubation and ventilation prior to transfer. For example following a seizure or with accompanying significant hydrocephalus.  This decision is at the discretion of the primary hospital anaesthetist and the referring team.  If intubation is considered necessary for a safe transfer the change in patient condition should be discussed with the neurosurgical team who will then be able to liaise with the neurointensive unit.
  • Appropriate levels of monitoring should be continued for transfer. As a minimum (if not intubated) - non-invasive or invasive blood pressure (at least 5 minute intervals), continuous 3-lead ECG monitoring and peripheral oxygen saturations.
  • If intubated (in addition) - end tidal carbon dioxide monitoring and invasive arterial blood pressure monitoring are essential.
  • ICS guidelines for transfer of critically ill adult available from
  • It is not necessary to send the hospital notes but a detailed transfer letter should accompany the patient as should photocopies of any relevant notes.
  • CT images should be imaged-linked to the LGI from the radiology department of the referring hospital. If this is not possible hard copy images must accompany the patient.

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Continued care at Regional Neuroscience Centre

2.1 Additional assessment - Following transfer to the specialist neurosurgical service reassess the following systems:

2.2 Resuscitation 

  • Continue administration of supplementary oxygen regardless of oxygen saturation readings. 
  • Ensure patient has secure IV access and continue infusion of 0.9% sodium chloride.   The majority of patients have clinical evidence of intravascular fluid depletion either resulting from delayed presentation, inadequate fluid replacement or fluid shifts associated with acute SAH.  This must be considered when prescribing a fluid replacement regimen and fluid resuscitation may include the use of a rapid bolus - between 200-500 mL of 0.9% sodium chloride or a colloid suspension. 
  • Hypotonic solutions such as 4% glucose-0.18% sodium chloride and 5% glucose should not be used for fluid resuscitation in SAH as they may worsen brain oedema.
  • Confusion or restlessness may indicate hypoxia, intravascular fluid depletion, pain or developing hydrocephalus and must not be attributed to the cerebral consequences of SAH without excluding these reversible causes.

2.3  Level of care

  • As these patients demonstrate the potential for rapid, dramatic changes, there is often a need for invasive monitoring to facilitate appropriate fluid therapy and direct their management in a level two (HDU) or level three (ICU) units.  
  • Decision to transfer to a ward environment is taken by a senior neurosurgeon in conjunction with the intensive care consultant and senior nurse.

2.4  Nursing care

  • Constant monitoring and vigilance is essential in this group of patients.
  • Rapid deterioration in the clinical condition may result in loss of consciousness and a compromised airway. 
  • Significant changes in the patient’s condition must be reported immediately to the appropriate medical staff to facilitate early intervention and prevent secondary neurological damage.

2.4.1.  Positioning of patients
Traditionally, patients with SAH have been nursed in a horizontal supine position. There is little evidence that this position reduces the incidence of re-haemorrhage and it may even be detrimental by compromising respiratory function.  Patients are nursed in a position that they find comfortable to reduce anxiety and pain; this may mean raising the bed to a semi-recumbent or sitting position.

2.4.2  Environment
Staff should aim to reduce anxiety and physiological stress by maintaining as calm and relaxed an environment as possible. Consideration should be given to the levels of noise and lighting to which the patient may be acutely sensitive.

2.4.3  Symptom control
Pain - See analgesia Section 9.0
Nausea and vomiting.  Vomiting can cause a transient rise in blood pressure and places the patient at risk of aspiration and subsequent pneumonitis. Anti-emetics should be prescribed regularly where patients are nauseated.
Pyrexia may be an indication of infection but in the initial phase is more likely to be centrally mediated as a result of SAH. Pyrexia should trigger appropriate investigations to identify its cause. Pyrexia places an additional metabolic burden on the injured brain and may adversely affect outcome. Symptom control may be achieved by regular paracetamol and/or ibuprofen and the use of a cooling fan.  In severe cases (for example temperatures of 40°C and above) refractory to the above methods, a cooling blanket or the use of cooled intravenous fluids may be indicated. 

2.4.4  Nutrition
Whenever possible patients should be encouraged to eat and drink normally.  Oral fluids should be supplemented with intravenous fluids. Nauseated patients or those with impaired level of consciousness may not be able to take nutrition orally.  In these cases nasogastric feeding should be instituted.  Nasogastric feeding should be delivered in consultation with the Dietetics Department. In a minority of patients with bulbar problems a SALT referral maybe necessary.

  • Bowel Care

    Constipation may become a problem in patients with restricted mobility and those receiving opiate analgesia.  Straining at stool is to be avoided in these patients thus aperients and stool softeners should be administered regularly starting on the day of admission.  Whenever possible, patients should be allowed to use the bedside commode rather than a bedpan.

2.4.6   Psychological Support and Information
Deal with patients in a calm and sensitive manner.  Patients may suffer from confusion and disorientation following SAH. Coupled with pain and psychological stress, this may result in seemingly inappropriate behaviour in some patients. Explain in advance all interventions and confirm that the patient understands the procedure to be performed. Provide information in clear and simple terms and, where possible, support with written information.  Give information in the presence of a third party (for example a close relative) whenever possible as patient comprehension and memory may be affected.
The onset of confusion, disorientation or inappropriate behaviour in a patient in whom these symptoms have not been previously observed may herald a physical cause such as hypoxia, hydrocephalus or infection.  These possible causes must be investigated.

          2.4.7    Care of Relatives
Keep relatives informed about the patient’s condition and management.  Good communication with relatives helps the patient during the acute phase of care and with rehabilitation.  Give information in private, free from distraction and in clear, non-technical language.  If possible, a close relative or trusted friend should be identified as the key contact for nursing and medical staff.  Changes in the patient’s condition or management priorities should be communicated in a timely manner and opportunity for deliberation and questioning should be provided.

   2.5 Monitoring

  • Use continuous ECG recording to identify dysrhythmias or cardiac ischemia commonly associated with SAH.
  • Use invasive monitoring of arterial blood pressure to enable accurate blood pressure assessment and regular arterial blood gas, haematological and biochemical analysis. 
  • Central venous pressure monitoring should be instituted in patients deemed to be at significant risk of; delayed neurological deficit, cardiovascular instability, neurogenic pulmonary oedema, significant electrolyte and fluid disturbance. Seek senior medical advice if uncertain.
  • Monitor hourly urine output and start a 24-hour urine collection for electrolyte and osmolality analysis.
  • Use pulse oximetry and arterial blood gas analysis to assess respiratory function. 
  • Assess the patient’s neurological condition by use of Glasgow Coma Score, pupillary light reaction and motor neurological deficit evaluation. 
  • Compressed spectral array (CSA) analysis is recommended for patients who are sedated and ventilated to aid early recognition and treatment of seizures and ischaemia.
  • Initially observations should be made at fifteen minute intervals until the neurological condition has stabilised for one hour of observation. Thereafter, formal observations should be made on an hourly basis, although interaction with the patient during normal nursing care should alert the nurse to changing neurological condition. 
  • Report deterioration in the patient’s neurological condition to medical staff for further investigation / intervention and trigger an increase in the frequency of formal neurological assessment to every fifteen minutes until stability is once again achieved. 
  • Continue appropriate invasive monitoring until the patient is deemed fit for discharge from the specialist unit or until removal is deemed medically appropriate.

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Interventional management

3.1 Choice of treatment
The Consultant Vascular Neurosurgeon and the Consultant Interventional Neuroradiologist should determine the most appropriate choice of definitive aneurysm treatment based upon the clinical condition of the patient and the configuration of the aneurysm. 
Endovascular coiling is the preferred treatment for the majority of anterior and posterior circulation aneurysms.
Where endovascular coiling is unlikely to produce a satisfactory result or, in cases where endovascular treatment has failed to occlude the aneurysm or the aneurysm is subsequently found to be unsuitable for coiling, surgical clipping should be performed. 
Once the optimum treatment has been decided, the management options should be discussed with the patient and relatives.  A clear recommendation for treatment should be made to help the patient come to a decision.

Level of evidence B

   3.2 Timing of treatment

  • Aneurysms should ideally be secured within 24-48 hours of ictus in patients deemed fit for the procedure and anaesthesia.

   3.3  Anaesthetic considerations

  • A full anaesthetic assessment should be performed and necessary pre-optimisation undertaken.
  • The majority of the patients are smokers and known to be hypertensive. Consideration should be given to continuing their anti-hypertensive medication as an unsecured aneurysm has a high chance of rebleeding (40% in 4 weeks), which can be reduced by avoiding extreme surges in blood pressure. See Table 1 for suggested blood pressure targets.

This in part can be achieved by:

  • adequate oxygenation
  • careful fluid management
  • maintaining normocapnia (PaCO2 4.0- 4.5 kPa)
  • appropriate sedation
  • avoidance of straining/coughing
  • effective analgesia

General anaesthesia should be induced using a familiar selection of drugs to the anaesthetist. The technique should make allowances for avid blood pressure control, avoidance of coughing and straining. It should also allow a smooth emergence and extubation with rapid neurological assessment if appropriate - remifentanil is an ideal agent in this respect.

Level of evidence B

   3.4  Interventional neuroradiology considerations

  • After ‘coiling’ procedures patients should be managed on either level two (HDU) or level three units (ICU), as appropriate for their underlying condition.
  • Patients normally have a 6F ‘Angioseal’ device inserted in the common femoral artery to secure haemostasis. 
  • Patients are allowed to sit up almost immediately.
  • Patients are returned with an ‘Angioseal’ information card, which should be attached to the outside of the notes.

   3.5  Anticoagulation

  • Most patients are administered heparin during the coiling/stenting procedure, and the ACT (Activated Clotting Time) is monitored using the point of care ACT machine in the angiography suite. Heparin can usually be allowed to wear off post-procedure without the need for formal reversal with protamine
  • Occasionally where there has been a thrombotic or thromboembolic complication, or this is high risk post procedure (coil encroachment on parent artery) IV heparinisation will be required for a minimum of 24 hours.
  • Additional aspirin (either intravenously or loaded post-procedure PO or by NGT) will be required. This may be continued for a variable period post-procedure.
  • In a small proportion of cases   Eptifibatide (Integrelin®) is administered during the procedure. This is to lyse stubborn acute platelet-rich (white) thrombus which may accumulate during the procedure and threaten patency of major intracranial arteries.  .


  • Eptifibatide: 180 micrograms /Kg bolus (IV) and continued as a IV infusion at a rate of 0.5 micrograms / Kg / minute – 1 microgram / Kg / minute up to 24 hours
  • Continued up to 24 hours, from theatre onto ICU/HDU
  • Eptifibatide has a short half-life; platelet function returns to 50% within 4 hours of cessation
    • Any bridging plan on ICU/HDU   with oral anti-platelets and IV infusion MUST be clearly documented and relayed to critical care/ neurosurgical team by the INR team
  • Elective patients only:
    • GP’s will be advised to initiate anti-platelets on the instruction of the Consultant Interventionalist Radiologist for  Aspirin and Clopidogrel
    • If Prasugrel is opted for instead of clopidogrel, this will be loaded on the day of the operation, 2 -3 hours prior to stent insertion
      • Prasugrel loading dose is 30mg (stock on neurosurgical wards/contact pharmacy)
      • Any delay in administration must be communicated to the Consultant
        • Prasugrel dose is off-label and not weight or age dependent
  • Oral anti-platelets (treatment POST- OP stent deployment)
    • Options of treatments include:
      • Aspirin 75mg OD  (lifelong) + Clopidogrel 75mg OD
    • Aspirin 75mg OD  (lifelong) + Prasugrel 5mg OD
      • Prasugrel dose is off-label and not weight or age dependent
    • Co-prescribe Lansoprazole (or alternative gastro-protection) for the duration of the second anti-platelet (6 months)
  • Details for dosing will be documented in post-operative notes by the INR’s. Liaise with them for any queries/concerns
  • Indication and start/stop dates with anti-platelets must be documented within the prescription and on eDANS

3.6  Patient Follow-up
Imaging follow-up is required for coiled aneurysms in most patients below 70 years of age. This will be way of either MRI or catheter angiography. This is performed at 6 months and 2 years post-procedure. Occasionally follow up of up to 5 years is required for some lesions.

Clinical follow-up will normally be at 6 weeks where appropriate. This is ideally at the combined neurovascular clinic, particularly if there are concerns regarding the initial procedure durability, or where there are additional aneurysms that may need to be considered for treatment.

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Anti-platelet treatment

Pharmacological management

4.1 Nimodipine

  • Dose: 60mg every 4 hours (fractionate the dose to 30mg every 2 hours if hypotension observed post dose)
  • Tablets can be crushed for NGT administration 
    • C/I: within one month of a MI /unstable angina /hypersensitivity to active/excipients (in both cases liaise with the consultant neurosurgeon)

Level of evidence A

In circumstances where enteral (PO/NG) nimodipine cannot be given/absorbed the use of intravenous nimodipine should not occur without a discussion, between a senior neurosurgeon and the relevant ICU consultant, of the relevant risks and benefits.

Intravenous nimodipine can precipitate profound hypotension and worsen existing cerebral ischaemia. It must be administered via a central vein and from the instruction of the Consultant Anaesthetists/Neurosurgeon.  For further information refer to the SmPC and appendix 5

4.2 Fluid therapy

  • Following initial resuscitation manoeuvres and restoration of an adequate circulating volume, the fluid therapy regimen should target a neutral fluid balance. 
  • Allow for insensible fluid losses, which may be higher in the SAH patient as a result of pyrexia, increased respiratory rate and supplementary oxygen therapy. 
  • Avoid hypovolaemia.
  • Fluid therapy should maintain an adequate circulating volume as determined by clinical assessment, pulse rate, central venous pressure, arterial blood pressure and urine output.  A baseline input of at least 3 L 0.9% sodium chloride per 24 hours is recommended. This volume should be adjusted to individual patient requirements, as clinical need dictates, and should be reviewed on an 8-hour cycle for uncomplicated cases. 
  • Fluid therapy should be guided by hourly input-output measurements and by 8-12 hourly blood sampling for urea and electrolytes.
  • Patients who are able may take oral nutrition and fluids although the recommended intravenous fluid regimen outlined above should be maintained in the acute period.

Table 1 .  Suggested target parameters for blood pressure, central venous pressure and urine output


No pre-existing hypertension

Known pre-existing hypertension

Systolic BP (mmHg)


Within 20% of normal systolic BP

CVP (mmHg)



Urine Output (mL/Kg/hr)



Level of evidence B

These target parameters are for patients without signs of delayed neurological deficit.  Patients with evidence of delayed neurological deficit are considered in later sections of this document.

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Blood pressure management

The optimal blood pressure for patients with aneurysmal SAH is not established. 

A threshold systolic blood pressure of less than 100 mmHg in previously normotensive patients or a reduction below 20% of the normal value in those with pre-existing hypertension should trigger intervention. 

Patients who present with suspected long-standing, but untreated hypertension should not have antihypertensive therapy instituted in the acute phase of their care unless clinical judgement suggests that there is an increased risk of aneurysm rupture. 
These patients may require ‘supra-normal’ blood pressures to maintain cerebral perfusion and antihypertensive therapy may compromise this.

Patients without known or suspected pre-existing hypertension who have sustained systolic blood pressures of greater than 180 mm Hg should be considered for acute reduction in blood pressure. 
In these patients treatment should only be considered if the blood pressure is being monitored invasively and technical causes of falsely elevated readings have been excluded. 
Transient surges in systolic blood pressure do not require treatment.
Other causes of elevated blood pressure should be excluded, for example pain and pyrexia. 

If treatment is considered necessary the patient should be discussed with NICU medical staff. 
Labetolol (up to 20 mg intravenous bolus followed by 20 – 160 mg / hour intravenous infusion) is the treatment of choice. 
Esmolol (50 – 200 microgram / kg / min intravenous infusion) may be used as an alternative.

Level of evidence B

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Management of seizures and prophylactic use

Seizures are a relatively common problem following SAH, occurring in up to 25% of aneurysmal bleeds. Seizures can be related to the initial ictus of aneurysm rupture, mass effect from large aneurysms, metabolic consequences of aneurysm rupture (electrolyte derangements), or delayed ischaemic neurologic deficit. Following SAH, and particularly in un-secured aneurysms, rebleeding must be considered as a cause for seizure activity.

Bedside assessment of blood glucose should be undertaken and any abnormality treated early in the process.  Management of seizures following SAH is multimodal and uses an escalating series of pharmacological strategies depending upon the severity of the seizures and the response to treatment. In the initial stages there is little difference between the management of seizures following SAH and seizures from other origins.

There is no RCT to guide routine antiepileptic treatment in aSAH however short term prophylactic antiepileptic therapy is commonly used and influenced on intervention and other risk factors i.e. aneurysm at the MCA, associated intracerebal haematoma, rebleeding, poor neurological grade, prior seizure etc.

If initiated levetiracetam is the preferential AED (unless C/I)

  • Endorse “prophylactic” and ensure stop date actioned on prescription
  • Dose: 500mg BD PO/IV/NG

(if seizure activity occurs whilst on prophylactic management, follow management as per below and liaise with the consultant neurosurgeon)

6.1 Pharmacological Management-suspected /established seizures
If the above measures fail to control seizure activity then an expert opinion should be sought.

Levetiracetam (Keppra ®) is increasingly used at LTHT for seizure prophylaxis as it does not require plasma level monitoring and has good oral bioavailability. Other agents to consider are phenobarbitone (ICU supervision required)

  • Investigation

Pharmacological management of seizures should run parallel with attempts to delineate a cause. CT scan of the brain should be considered as it may reveal a surgically remediable cause of fitting that could limit the effectiveness of any pharmacological manoeuvre. If there is any concern regarding the conscious level of the patient relating either to a post-ictal state, drug therapy or underlying disease process, then anaesthetic staff should accompany the patient to scan.

Electrolyte abnormalities should be sought and corrected (hypomagnesaemia is a particular problem, especially if the patient has had a large diuresis).

CSF sampling may be appropriate, especially if drainage devices have been used, for example, an external ventricular drain or lumbar drain. This should be discussed with the neurosurgical team.

6.3  Post Seizure Care
The level of care that the patient requires after termination of the seizure largely depends on his/her clinical state. If the patient has fully recovered to their pre-fit conscious level with no focal deficit, then it may be appropriate to keep them on a level two unit (HDU).  If there is any concern about conscious level, their ability to maintain a safe airway or other changes in neurology then escalation to a level three unit (ICU) may be appropriate.
The patient should be closely monitored for further seizures and the development of complications of fitting or the drugs used to control any fits.

Level of evidence B

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Management of specific complications

7.1 Delayed neurological deficit (DND)

Delayed neurological deficit is a term that encompasses clinically detectable neurological deterioration in a patient with SAH following initial stabilisation that excludes further SAH due to rebleeding from the ruptured aneurysm.  There are a number of causes all of which are potentially reversible therefore early diagnosis and intervention may significantly alter the clinical course of this complication.  Causes include delayed cerebral ischaemia (DCI), hydrocephalus, cerebral oedema, fevers, seizures and electrolyte abnormalities.  The onset of symptoms is typically seen between 3 and 14 days post-SAH, but not usually earlier.  DND is seen in 20 – 30% of patients with aneurysmal SAH and leads to a completed stroke in 30% of these and death in a further 30%. 

Cerebral vasospasm is a term applied to arterial narrowing after SAH demonstrated radiologically or sonographically.  This leads to a reduction in cerebral blood flow and oxygen delivery which may precipitate cerebral ischaemia or infarction.  The term is often used interchangeably with that of DCI however it should only be used to describe radiographic findings.

Delayed cerebral ischaemia (DCI) is a term applied to any neurological deterioration (e.g. hemiparesis, aphasia, altered conscious level) that is attributed to ischaemia, lasts longer than one hour and cannot be explained by other physiological abnormalities noted on standard radiological, electrophysiological or laboratory investigation. The occurrence of DCI may be masked by the poor clinical condition of the patient or the administration of sedatives

  • Investigation of DND
  • An urgent CT scan should be organised to exclude surgically treatable causes of clinical deterioration, specifically hydrocephalus, intracranial haematoma and intracranial sepsis (for patients who have had surgical treatment of their aneurysm) and to identify areas suggestive of ischaemia.
  • A full general clinical examination should be performed to identify other causes of deterioration or other conditions that may compound DND.  Problems typically seen in SAH patients include respiratory tract infection, pulmonary oedema, and pulmonary embolism, sepsis from invasive monitoring lines, surgical wounds or urinary tract infection. 
  • Perform a full neurological examination to identify further changes, deterioration or response to treatment. The possibility of meningitis must be considered and a low threshold for lumbar puncture maintained. 
  • Laboratory investigations should be performed urgently and the results telephoned back to the ward.   Mandatory investigations are full blood count, urea and electrolytes and arterial blood gas analysis.  Full blood count analysis will identify anaemia and may give an indication of the patient’s degree of hydration. 
  • Sodium abnormalities are a common finding in SAH.  Low serum sodium levels may indicate the possibility of Cerebral Salt Wasting Syndrome (CSWS) - see section below on fluid / electrolyte imbalance.  Whether CSWS is a separate clinical entity or another manifestation of DND is unknown, however the volume depletion seen with CSWS exacerbates DND and must be addressed.
  • Urea and creatinine levels may aid the assessment of volume status.  Urea and electrolyte analysis should be performed at eight-hourly intervals during the period of DND until the patient’s condition has reversed or an established deficit has occurred.  Thereafter daily urea and electrolytes should be performed or more often if clinical need dictates. 
  • Perform arterial blood gas analysis to monitor for hypoxaemia and hypercapnia.
  • Occasionally, when the diagnosis is in doubt and/or to better direct specific interventional therapy (intra-arterial nimodipine infusion and/or intracranial angioplasty), CT angiography may be used. CT Perfusion has a limited role generally, but may be useful in selected individual cases. The use and interpretation of these additional investigations should involve the Consultant Interventional Neuroradiologist.
  • Management of DND

The principal aim is to ensure an adequate supply of well-oxygenated blood to the brain.  The traditional approach of Triple-H therapy (Hypertension, Hypervolaemia and Haemodilution) is now largely historical with the latest evidence tipping in favour of induced hypertension, in the context of adequate intravascular volume alone.  Hypervolaemia has not been shown to incur any additional benefit over euvolaemia but has been associated with a higher rate of complications, both pulmonary and as a result of haemodilution reducing the oxygen-carrying capacity of blood.
All patients with suspected DND should have:

  • Invasive arterial blood pressure monitoring.
  • A central venous catheter.
  • A urinary catheter.
  • Continuous pulse oximetry to monitor arterial oxygen saturation and respiratory rate.

Persistence of a neurological deficit for 24 hours or more despite maximum inotropic/vasopressor or vasopressors may indicate a permanent deficit and continued administration of agents is unlikely to result in clinical improvement.

Vigilance for ECG changes is needed. If cardiac ischaemia is suggested, serial 12 lead ECGs and troponins are required and a cardiology assessment is warranted.
Patients with pre-existing cardiac disease, pulmonary oedema or impaired cardiac function secondary to aSAH should be considered for pulmonary arterial catheter placement to enable accurate cardiac function monitoring.  These patients require admission to a level three unit (ICU).

All patients should be receiving nimodipine (60 mg / 4 hourly, PO/NGT.) routinely for 21 days. If this results in significant hypotension, consider altering the dose to 30mg / 2 hourly. 

Management of Anaemia

The optimal haemoglobin level for patients with aSAH has not been precisely determined. A haemoglobin level above 8 g/dL (80 g/L) is recommended to ensure adequate oxygen-carrying capacity, although a higher target (>10 g/dL) may be appropriate in patients with associated co-morbidities and those at highest risk of DCI.  Haemodilution in an attempt to improve blood rheology should not be undertaken except in the case of polycythaemia.  Reduction in the oxygen-carrying capacity of blood can have deleterious effects.

Management of groin Haematoma

For patients undergoing endovascular procedure via femoral artery puncture, the puncture site should be inspected for any underlying haematoma. Unexplained drop in Hb, groin/leg or back pain should prompt a review to rule out haematoma at puncture site. An urgent ultrasound examination should be requested for further investigations. Early involvement of endovascular and vascular surgery teams is recommended.

Risk factors for groin haematoma include multiple punctures, difficult access, use of large bore sheaths and catheters and patient factors predisposing them to formation of haematoma, antiplatelet and anticoagulation medication. Consideration for a pelvic CT scan is indicated in patients at increased risk of haematoma with severe back pain and/or unexplained hypotension/anaemia (an ultrasound may have difficulty in detecting a retroperitoneal haematoma and there may be NO outward sign of bleeding at the puncture site).

Management of Sodium Balance

Aim for plasma sodium ≥140mmol/l and <150mmol/l.  Hypertonic sodium chloride solutions can be used e.g. 1.8% sodium chloride along with oral sodium supplementation. Frequent monitoring of plasma Na levels is mandatory especially if hypertonic sodium chloride solutions are used to avoid too rapid a correction and also over correction of sodium levels.
See appendix 2 for guidance regarding sodium level correction.


  • Sodium chloride modified release tablet (Slow Sodium®) 600mg/10mmol

Dose: Two Tablets BD (prophylactic)
            Dose can be increased with appropriate fluid intake-refer to the BNF

A liquid is available for NG administration

Hypertonic saline (HDU/ICU only)

1.8% sodium chloride
Rate: 50-150mL/hour

Low sodium-containing solutions such as 4% glucose-0.18% sodium chloride or 5% glucose may aggravate brain oedema and may compound the hyponatraemia. They should NOT be used in the context of DCI, unless the patient requires glucose to prevent hypoglycaemia (eg IDDM).

Urine collection should be instituted for 24-hour urine volume, electrolyte and osmolality analysis.

  • Lumbar Drains

There is emerging evidence for the use of early lumbar drain insertion in order to reduce the occurrence of DND. Refer to Appendix 3.

Level of evidence B

  • Fluid and electrolyte abnormalities including hyponatraemia

Sodium disorders

Sodium disorders are relatively common after subarachnoid haemorrhage often in the conjunction with DND. Their diagnosis and treatment can prove challenging.


Important causes to consider are (cranial) diabetes insipidus (DI) and iatrogenic. In DI a relative or complete absence of anti-diuretic hormone results in large volume loss of dilute urine with subsequent hypernatreamia and hypovoleamia. Diagnosis is made by measuring high plasma osmolality together with low urine osmolality. Treatment is with fluid repletion (0.45% sodium chloride) plus enteral water and desmopressin (0.5-1.0 microgram bolus). Discussion with the endocrinology team may be helpful for patient specific treatment.
Iatrogenic causes can arise from inappropriate diuretic administration and fluid restriction. Mild hypernatreamia (145-150 mmol/l) may have a protective effect against the development of vasogenic oedema.

Hyponatraemia is common following SAH. The causes of hyponatraemia can be categorised depending on the volume status of the patient - hypovolaemic, normovolaemic or hypervolaemia
In the context of SAH - Syndrome of Inappropriate Anti-Diuretic Secretion (SIADH) and Cerebral Salt Wasting Syndrome (CSWS) are important to recognise and treat.

SIADH results in elevated circulatory volume     - hypervolaemia
CSWS results in a reduced circulatory volume    - hypovolaemia.

It must be emphasised that the clinical syndromes can be complicated by fluid therapy.  Furthermore, a combination of syndromes (SIADH and CSWS occurring in the same patient) may further cloud the clinical picture.

CSWS is seen more commonly than SIADH following SAH.  The presence of progressive symptomatic hyponatraemia, not easily corrected by extra sodium supplementation, requires admission to HDU for CVP and intra-arterial blood pressure monitoring.  Consideration of hypertonic sodium chloride mandates HDU admission.

Volume status determined by clinical examination and CVP measurement will suggest one or other diagnosis and plasma and urine electrolyte levels will confirm the diagnosis.


SIADH is usually self-limiting after SAH. Conventional treatment includes fluid restriction; however, following subarachnoid haemorrhage this is potentially hazardous as it is associated with a higher risk of cerebral infarction.
If the hyponatraemia is severe (< 125 mmol/l) and symptomatic then hypertonic sodium chloride can be used with extreme caution.

Drug-related causes of SIADH



Anti-epileptic medication

 Carbamazepine, sodium valproate


ACEi, ARB, amlodopine

Anti-psychotic medication

Phenothiazines, Butyrophenones


Omeprazole, Lansoprazole

Close attention must be paid to the neurological condition of the patient when treating DI, CSW and SIADH as rapid sodium shifts may result in impaired conscious levels, neurological deficit or seizures.


CSWS is treated by volume and sodium replacement. 
The fluid volume and sodium requirements to normalise intravascular volume and plasma sodium should be determined and an appropriate fluid regimen prescribed (using 0.9% or 1.8% sodium chloride solution).
Aim to keep sodium greater than 140mmol/L, and less than 150mmol/L. (see Appendix 2)

Further fluid therapy should be prescribed by estimating the volume and sodium replacement needs for each 24-hour period.
Adjustments to the fluid regimen should be made based upon 8 hourly plasma and urine electrolyte levels.

The mineralocorticoid fludrocortisone can be used to aid sodium and fluid retention, typical starting dose 50 micrograms TDS. Sodium loss can also be offset with oral supplementation with ‘slow sodium’ tablets or sodium chloride liquid 1mmol/ml (unlicensed medicine) ) (level of evidence Class IIA /B)

Level of evidence  B

Close attention must be paid to the neurological condition of the patient when treating DI, CSW and SIADH as rapid sodium shifts may result in impaired conscious levels, neurological deficit or seizures.





Plasma Sodium




Urine Sodium excretion




Plasma osmolality


Normal / increased


Urine osmolality

Inappropriately reduced

Normal/ high


Volume status
(Clinical exam/ CVP)



Normal/ Increased

Table 2: Summary of physiological derangements in Diabetes Insipidus (DI), Cerebral Salt Wasting Syndrome (CSWS) and Syndrome of Inappropriate Anti-Diuretic Hormone secretion (SIADH)

      7.2.1 Sodium monitoring on neurosurgical wards.
It is advisable to remain vigilant for sodium imbalances after discharge from critical care. All patients should have accurate cumulative fluid balance, including twice weekly weights, and daily plasma sodium levels (U and Es) monitored for at least one week following critical care discharge and longer if concerns remain.  If plasma sodium levels falls by ≥5 mmol/L/day or an absolute value less than 130 mmol/L then this should trigger immediate assessment as to the underlying cause (CSWS, SIADH or DI) and treatment directed towards the suspected cause. Measurement of plasma and urinary electrolytes and commencement of a 24 hour urine collection should be initiated to confirm the suspected diagnosis and prompt clinical assessment by senior members of the neurosurgical and neurocritical care team is warranted to decide appropriate treatment and level of care. A urinary catheter should be placed if not already in situ.

7.3  Hydrocephalus
Hydrocephalus may present acutely as a rapid deterioration in the level of consciousness post subarachnoid haemorrhage or insidiously over several days or weeks.

It is characterised by:
Decreasing level of consciousness
With or without signs of raised intracranial pressure. 

Two main causes of hydrocephalus following SAH. 

  • acute intraventricular haemorrhage may cause obstruction to the ventricular outflow, typically at the aqueduct of Sylvius. 
  • impaired absorption of CSF at the arachnoid villi resulting in communicating hydrocephalus. 

      7.3.1 Treatment of hydrocephalus
Acute hydrocephalus should be treated with external ventricular drainage (EVD) of CSF emergently. Remove the EVD as soon as possible when the patient is judged to have restored normal CSF flow and absorption. A lumbar drain may be chosen over an EVD for CSF drainage in hydrocephalus - refer to Appendix 3.

A period of 24-hour observation with the drain in-situ, but closed, should precede removal. 
CSF sampling from the drainage system is not recommended unless there is clinical suspicion of CSF infection. 
A subset of patients will remain drain dependent and will require insertion of a ventriculoperitoneal (VP) shunt.

Patients presenting with insidious hydrocephalus should be treated by lumbar drainage of CSF in the first instance. 
In many cases this may avoid the need for a permanent VP shunt. 
Repeat procedures are possible, but VP shunting is unavoidable in some patients. 

Level of evidence  B

7.4  Respiratory Complications

7.4.1 Neurogenic Pulmonary Oedema (NPO)
Poor clinical grade at the time of admission is associated with a higher frequency of respiratory complications.
Optimal treatment of NPO differs from the standard treatment of hydrostatic pulmonary oedema and may involve cautious fluid loading combined with ventilatory support with adequate/high PEEP, vasopressor infusion, vasodilators and inodilators (dobutamine, adrenaline and phosphodiesterase inhibitors).
Pulmonary artery catheterisation can be very helpful in this patient group.
Treatment decisions should be made on a case by case basis with senior medical staff.

7.4.2  Infection and Atelectasis
The risk of aspiration and subsequent pneumonia is greater with poorer grades of SAH (GCS<8).
Prolonged ventilation places the patient at risk for ventilator associated pneumonia (VAP). Refer to below hyperlink for investigation and treatment of VAP.

Ventilator-associated pneumonia management

Severe vasospasm requiring long periods of vasopressor infusion and immobility also increases the likelihood of developing atelectasis and pneumonia; particularly if a fluctuant GCS is an issue.
Regular physiotherapy can help to control atelectasis.
Early consideration of a tracheostomy in this group aids reduction in sedation (with easier attainment of target levels for blood pressure), weaning, mobilization and physiotherapy +/- mucolytics

7.5  Cardiac Complications

7.5.1 Cardiac Ischaemia and Myocardial Infarction
The ‘sympathetic storm’ associated with SAH results in significant cardiovascular changes and may even mimic an acute myocardial infarct.
The ECG may show:
Non-specific ST and T wave changes in particular symmetrical T wave inversion
Prolonged QT interval (>500ms)
Repolarization abnormalities with a concurrent rise in cardiac troponins and CK-MB.
The myocardial dysfunction seems to correlate more with the degree of neurological deficit than with the severity of the ECG abnormalities.
ECG changes should never be ignored in these patients and discussion with senior colleagues and/or cardiology is advised.

7.5.2  Takotsubo Cardiomyopathy (Apical LV ballooning syndrome)
A well described cardiomyopathy associated with intracerebral haemorrhage and aneurysmal SAH characterised by dilatation and ballooning of the LV apex with associated systolic dysfunction with preserved (and even hyperkinetic) basal contraction. It represents the extreme form of catecholamine induced myocardial dysfunction. Treatment is supportive with inotropes and vasopressors guided by echocardiography or pulmonary artery catheter placement.

7.5.3 Cardiac Dysrrhythmia
ECG abnormalities have been reported in 25-100% of cases. These are mainly prolonged QT, widened QRS complexes and tachyarrhythmias. There is no evidence that these arrhythmias require any different treatment than if they were to occur in the non-SAH population.

  • Hyperglycaemia/Glycaemic Control

Hyperglycaemia is a common occurrence after SAH, associated with increased mortality and morbidity. Hyperglycaemia is a cause of secondary injury after SAH, causing cerebral ischaemia and neuronal death by increasing cerebral lactic acid production.
Glycaemic control – maintain between 5-10 mmol/L- prevents secondary insult. This must be balanced against the adverse effects of episodes of hypoglycaemia. . (Level of evidence IIb/B)

Guidelines on the management of hyperglycaemia are adapted from the intensive care unit care pathway:

Critical care glycaemic control guideline (under review)

It should be remembered that both hyper/hypo- glycaemia and -natraemia have detrimental effects to the injured brain via osmotic shifts and increased lactic acid production. Both sodium and glucose levels must be regularly monitored to prevent the above abnormalities.

  • Rebleeding

Rebleeding is common and its incidence highest immediately following the initial haemorrhage (5-10% over the first 72 hours). Early rebleeding, within hours of the initial haemorrhage, occurs in at least 15% of patients. Risk factors include poor grade of SAH, larger aneurysms and sentinel bleeds. At present it is virtually impossible to prevent this from happening, but medical or surgical intervention can prevent recurrent haemorrhages occurring later. Rebleeds in the first days are thought to be related to the unstable nature of the aneurysmal thrombus, as opposed to lysis of the clot sitting over the rupture site.  Clinical factors that increase the likelihood of rebleeding include extreme hypertension, anxiety, agitation, and seizures so monitoring and prompt treatment of these factors can reduce the rebleeding rate.
Some authorities recommend the use of antifibrinolytic agents such as tranexamic acid from admission until securing of the aneurysm to reduce rebleeding. This is not universally accepted and exposes the patient to a higher risk of thromboembolic complications.

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Thromboprophylaxis of DVT/PE

Patients with aneurysmal SAH are classified as having a moderate risk (10-40%) of developing DVT. SAH itself induces a prothrombotic state. In addition, patients are often elderly, immobile and initially dehydrated.

All patients should be assessed for their risk of DVT following local approved tools.

VTE Prophylaxis for Neurological Surgery patients

  • Thromboprophylaxis should be routinely used in patients undergoing major neurosurgery.
  • Adequate hydration and early mobilisation are important preventative factors
  • Intermittent pneumatic calf compression with or without elasticated stockings is recommended from admission and should be continued for up to two weeks post-haemorrhage.
  • Pharmacological prophylaxis should be considered 24-hours post-procedure (surgery or interventional radiology) unless contraindicated for other reasons.
  • Prophylaxis with low molecular weight heparin is the preferred pharmacological method.
  • A combination of mechanical and pharmacological prophylaxis is recommended in high-risk neurosurgery patients.

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SAH can lead to a significant degree of pain that can be difficult to treat. Remember that photophobia is best treated by subdued lighting and a quiet environment.
Many commonly used analgesics have side effects, which make them relatively contra-indicated following SAH.

Assess the character of that pain and to ensure that it is not in excess of that expected from the underlying disease state, which may indicate a worsening of the underlying pathology.

9.1 Pharmacological management

Unless contraindicated start with paracetamol 1g (if over 50 kg) administered orally, rectally or parenterally. If pain persists paracetamol should be administered regularly (qds) and more potent agents should be added. [Step-up to the next ‘rung’ of the analgesic ladder]. Patients <50kg -  IV dose is 15mg/kg

Second line analgesic agents include opiates. Codeine or dihydrocodeine is usually administered in doses of 30-60 mg qds. If codeine appears to be of limited efficacy alternative agents to codeine exist for oral administration (morphine sulphate). Seek advice from anaesthetic and pharmacy staff. The use of morphine PCAS is controversial but may have a role in the analgesic ladder for subarachnoid haemorrhage. As above, seek specialist advice.

Tramadol is equi-potent to dihydrocodeine; all opioids have the potential to lower the seizure threshold. It has been more observed with Tramadol so optimise alternative analgesia prior to commencing this.

Acute pain guidelines

The use of NSAIDS is controversial and recent studies have shown they add little to post op craniotomy analgesia. Their use must be considered on an individual risk-benefit assessment.

NSAIDS are not recommended if patients have had stents deployed and are on dual anti-platelet therapy to prevent thrombosis. (NSAIDS increase risk of bleeding, in particular with Prasugrel (shows approx 70% platelet inhibition)

If NSAID are opted for consider the broader class vs. cox-2 selective inhibitors and for short term only.

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Infection Prevention and Control

Refer to High Impact Intervention 1 and Standard Infection Control Precautions Policy and LTHT Hand Hygiene Policy.

Hand hygeine policy
Standard precaution guidelines

At present all level 3 critical care patients should undergo decolonisation. With regard to level 2 patients, if it is likely the patient will undergo surgical clipping or interventional radiological ‘coiling’ then decolonisation should be commenced from admission. All patients should still be risk assessed for MRSA.

Treatment includes (after checking allergy status in particular to nuts);

  • Bactroban® (Mupirocin 2%), nasal ointment three times a day for 5 days.
  • Chlorhexidine wash once a day for 5 days, with two hair washes within those 5 days.

The first hair wash should be administered prior to a surgical procedure.
MRSA policy

Peripheral venous cannulae guidelines

Urinary catheter guidelines


New measures to reduce the risk of hospital acquired infections for patients with a central venous access device were introduced in September 2012. This comprises of daily antiseptic washes with 4% chlorhexidine and twice weekly hairwashes with 4% chlorhexidine. Octenisan should be used if the patient is allergic to chlorhexidine.

Arterial line management
Central Venous Catheter management

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Record: 3577

To provide evidence-based recommendations for appropriate diagnosis, investigation and management of aneurysmal Subarachnoid Haemorrhage 

Clinical condition:

aneurysmal Subarachnoid Haemorrhage

Target patient group: aSAH patients
Target professional group(s): Secondary Care Doctors
Secondary Care Nurses
Registered Nurses Working in Critical Care
Adapted from:

Evidence base

Evidence Base: References

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Evidence levels:
A. Meta-analyses, randomised controlled trials/systematic reviews of RCTs
B. Robust experimental or observational studies
C. Expert consensus.
D. Leeds consensus. (where no national guidance exists or there is wide disagreement with a level C recommendation or where national guidance documents contradict each other)

Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.1

Related information

Appendix 1: Clinical and radiological scoring systems in aneurysmal subarachnoid haemorrhage

WFNS (World Federation of Neurosurgeons Scale)



Motor deficit

















Hunt and Hess scale


Signs and symptoms



Asymptomatic or minimal headache and slight neck stiffness



Moderate to severe headache; neck stiffness; no neurologic deficit except cranial nerve palsy



Drowsy; minimal neurologic deficit



Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances



Deep coma; decerebrate rigidity; moribund


Fisher score

Fisher Score/Grade

CT Brain

Vasospasm Risk


No Subarachnoid Blood detected



Diffuse or vertical layers < 1mm thick



Localised clot and/or vertical clot >1mm thick



Intracerebral or intraventricular clot with diffuse or absent subarachnoid blood


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Appendix 2: Management of sodium disorders in aneurysmal subarachnoid haemorrhage

CSWS is clinically more likely than SIADH following aSAH.
Aim for increase in [Na] level of no more than 0.5 mmol/hr to a maximum rise of 10 mmol per day.
Avoid hypovolaemia.
To confidently diagnose SIADH exclude renal, thyroid, pituitary, hepatic and cardiac causes.
Monitor [Na] levels 6-8 hourly until ‘normalised’ and stable.


Total Body Water (litres)          = 0.6 x body weight (men)
                                                = 0.5 x body weight (women)
                                                = 0.5 x body weight (men >65years)
                                                = 0.45 x body weight (women>65years)

Example A

Estimates effect of 1 litre of 1.8% sodium chloride (308 mmol/L).
Dividing the desired change in serum Na by the formula result determines the volume of infusate required and the rate of administration.

60 year old man, 100 kg. serum Na 114. Desired Na 130 mmol/L.
1 litre of 1.8% sodium chloride (308 mmol/L) would change serum Na by
(308-114) / [(100 x 0.6) + 1] = 3.2 mmol

If desired correction is 130-114 = 16 mmol
Then volume of fluid is 16 / 3.2 = 5 litres of 1.8 litres of 1.8% sodium chloride (5000ml)
Correction over 32 hours (0.5 mmol/hr) then rate of correction is 5000 / 32 = 156 ml/hr

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Appendix 3: Guidelines for the use of lumbar drains in patients with aneurysmal subarachnoid haemorrhage

Without hydrocephalus
Class II evidence for the use of early lumbar drain insertion in order to reduce the prevalence of delayed ischaemic neurological deficit (DIND) and improve early clinical outcome in World Federation of Neurological Surgeons (WFNS) grade I-III patients with aneurysmal subarachnoid haemorrhage (aSAH).

Insertion should be aimed for as early as possible following aneurysmal diagnosis and treatment (or placed during general anaesthetic for aneurysmal treatment).  Insertion should not be performed later than four days post haemorrhagic ictus.  There is no evidence to suggest that insertion of a lumbar drain will reverse established DIND unless there is an element of hydrocephalus thought to be contributing to the neurological deficit (in which case DIND should not be diagnosed until hydrocephalus has been excluded). 


Insertion should be performed in an aseptic manner with gown and gloves and a complete sterile field created in the appropriate lumbar interspace (L3-5).  Local anaesthetic should be applied to the skin and subcutaneous tissue and allowed to work (3 minutes) prior to attempted insertion of the drain.

Once inserted, the drain should be secured with suture and dressed.  This dressing should not be removed unless there are concerns over the function of the drain or the integrity of the exit site.  The Becker collecting system should be placed on level with the drain exit site and adjusted hourly in order to aim for 5-10 ml of CSF drainage per hour.

The drain is to remain in situ until the cerebrospinal fluid (CSF) is visibly clear or xanthochromic or until the drain has been in situ for eight days.  CSF sampling is not routinely required if the drain is less than 4 days old and should be performed every 48 hours thereafter (using aseptic technique).  When the drain is to be removed, it should be removed immediately without prior clamping and a non-silk suture placed over the exit site.

With hydrocephalus
Any patient with aSAH and an altered consciousness (GCS <13-14) may have symptomatic hydrocephalus.  If this is thought to require treatment, a lumbar drain may be chosen to treat this over an external ventricular drain (EVD).  In any patient not obeying commands, insertion of an EVD should be preferred instead of a lumbar drain.  If following treatment of hydrocephalus the patient has improved to a GCS of 13 or greater, the above protocol for lumbar drain management can be applied.  The only difference to above is that on removal of the drain, it should be clamped for 24 hours prior to removal in order to assess whether the patient is dependent on the drain for CSF drainage.  If so, a VP shunt may be required (or if still heavy blood load), a replacement lumbar drain if the original is greater than 10 days old.

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Appendix 4: Phenytoin (monitoring and formula)

Top up dose : Patients who are currently taking Phenytoin

Use a recent phenytoin level (last 24-48 hours) and correct this using the formula above for patients with hypoalbuminaemia prior to calculating the top-up dose.

Top-up phenytoin sodium dose (mg) = [20 – (phenytoin level (mg/L)] x 0.7 x  weight(kg)

Loading dose: Patients who are NOT on phenytoin prior to admission

20mg/Kg IV Infusion

Weight (KG)

Loading dose of Phenytoin (250mg/5mL)

45 – 54

1000mg (20mL)

55 – 64

1200mg (24mL)

65 – 74

1400mg (28mL)

75 - 84

1600mg (32mL)

85 – 94

1800mg (36mL)


2000mg (40mL) max dose

Take a level 6-24 hours after loading dose

Therapeutic drug monitoring:

PPM reported level does NOT correct the phenytoin level if patients albumin is <35g/L. In critically ill patients this calculation acts as a guide in the context of the patients clinical condition due to rapidly changing albumin levels.

For full information refer to:

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Appendix 5: Nimodipine (IV and oral)- under the instruction of the Consultant (ICU only)

  • IV infusion
    • 10mg /50mL, draw contents of vial in a 50mL syringe and prime non-PVC extension tubing (for administration via syringe driver)
    • Do not dilute
    • Should be administered via a dedicated lumen of a CVAD with a co-infusion
    • Can be administered via a peripheral line whilst waiting placement of a triple or quad-lumen central line
    • IV infusions must have a 3-way tap attached with concomitant infusion of diluents. Infuse a compatible fluid at a rate of 4 times the nimodipine infusion rate:





Nimodipine infusion rate




Fluid co-infusion rate




  • Compatible fluids: 0.9% sodium chloride, albumin 4%, Hartmann’s, mannitol 10%
  • For central administration ONLY, the co-infusion can be omitted
  • Infusions are stable for 10 hours in overhead electric light/artificial light

Infusion rate:

  • Commence at 15 micrograms/ Kg/ hour (5mL/hour i.e. 1mg/hour) for the first 1-2 hours, if BP stable; proceed to recommended dose
  • May need to commence slowly (2.5mL/hour) if patient has significant hypotension
  • Recommended dose: 30 micrograms / Kg/ hour @ 10mL/ hour i.e. 2mg/hour
  • Patient weighing less than 70kg or with unstable blood pressure should be started on 0.5mg/hour and titrated  
  • Correct fluid imbalance, commence CVP monitoring for trend, volume load as clinically indicated
  • Maintain MAP and CPP according to pre and post-operative needs
  • All infusion tubing must be changed every 24 hours

Weaning from IV therapy → oral therapy (Weaning commences when the first dose of oral therapy is administered)

  • Half-life for nimodipine is between 1.1 -1.7 hours (the terminal ½ life of 5-10 hours is not relevant for establishing the dosing interval)
  • Administer 1st dose of oral 60mg nimodipine (prescribed at 4 hourly intervals)
  • Infusion weaning: 1mL every hour for 5 hours, then cease infusion
  • Observe for neurological deterioration (decrease in GCS or development of focal deficit), notify Neurosurgeons urgently
  • If the patient does deteriorate neurologically, cease weaning IV nimodipine and return to full IV therapy

Additional information:

  • IV solution contains 23.7% ethanol (alcohol)
    • This can be potentially harmful for those suffering from ETOH excess and additional monitoring will be needed for high-risk groups such as patients with hepatic impairment or epilepsy.
  • Metabolised by hepatic CYP450 3A4 iso-enzymes
  • Caution / avoid combination with strong CYP3A4 inducers /inhibitors

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