Oxygenation and ventilation are initially the top priority.
Assess this first and consider intubation if:

• Insufficient airway protection , often if GCS < 8
• Hypoventilation – a high or rising PaCO2
• Hypoxemia 
• Unable to safely manage without e.g for CT scan
• Borderline situation and about to have an anaesthetic for procedure e.g. angiogram, EVD insertion, clipping of aneurysm

Intubation / anaesthesia must take these factors into account:

• Avoid hypertension (SBP > 140 mmHg) to reduce chance of re-bleed
• Avoid hypotension (SBP < 100 mmHg) to maintain cerebral perfusion to damaged brain
• Minimise stimulation of oropharynx to avoid hypertensive event
• Maintain oxygenation and normocapnoea throughout

Here’s a simulated example of how to intubate a patient with an unsecured ruptured cerebral aneurysm:

More resources on the Neurocritical Care Intubation
MORE ON NEUROCRIT CARE INTUBATION

Control Blood Pressure

• Target non-invasive systolic blood pressure 100-140 mmHg for unsecured aneurysm
• Insert an arterial line
• A CVC is often required to titrate IV antihypertensives or vasopressors if required
• There can be a significant variation between invasive and non-invasive BPs REF.
• IABP gives better moment to moment BP visualisation but is at risk of under and over dampening.
• Medications used include IV hydralazine, IV metoprolol, clevidipine infusion depending on local policies

Normalise Coagulation

• Send coagulation studies as priority
• Consider ROTEM or TEG if available
• If good history of taking anticoagulant, reverse immediately

Specifically

WARFARIN

> Vitamin K IV 10 mg

> Weight based dose prothrombin complex concentrate first choice

> FFP is the alternative.

ASPIRIN OR CLOPIDOGREL

> Anti-platelet agents can potentially increase the risk and severity of aneurysm re-rupture, as well as neurosurgical complications.

> Platelet transfusion is recommended for patients with aspirin- or adenosine diphosphate (ADP) inhibitor-associated SAH who will undergo a neurosurgical procedure.

> Platelet transfusion is not recommended if no neurosurgical procedure is planned.

> The risk–benefit ratio of anti-platelet therapy reversal using other hemostatic agents such as desmopressin (DDAVP) should be considered for individual patients.

DABIGATRAN (PRADAXA)

> Idarucizumab (Praxbind) 5 g IV

RIVAROXABAN (XARELTO) and APIXABAN (ELIQUIS)

> Andexanet alfa (AndexXa) 200 mg IV

Acute

If there are active seizures, treat as per usual practice with parenteral benzodiazepine followed by second line agent e.g.

• Lorazepam 0.1 mg /kg (or diazepam 10 mg IV)
• Levetiracetam 60 mg/kg

Seizure prophylaxis will be discussed in more depth elsewhere in the module

Acute hydrocephalus (HCP) is cuased by blood interfering with CSF flow through the Sylvian aqueduct, fourth ventricle outlet and subarachnoid space, as well as impaired CSF re-absorption via arachnoid granulations.

15–20% of SAH patients get HCP

30–60% of these show no impairment of consciousness

Only 3% of those without HCP on initial CT develop HCP within 1 week

About half the patients with acute HCP and impaired consciousness improved spontaneously

Patients with altered consciousness with large ventricles may be symptomatic from the HCP and consideration should be given to ventriculostomy /external ventricular drain insertion, which causes improvement in ≈ 80%

Image ReferenceCase courtesy of Assoc Prof Craig Hacking, Radiopaedia.org. From the case rID: 37854

Some Ventricle Anatomy

• Looking for evidence of ischaemia (especially ST depression), heart failure, tall peaked T waves, QT prolongation and arrhythmia’s

• FBC (anaemia may contribute to brain injury; thrombocytopenia exacerbates bleeding)
• EUC, LFT, CMP (electrolytes should be normalised; important to know baseline renal and liver function)
• Coags (must be normalised, see below)
• Troponin (Look for evidence of Takotsubo’s cardiomyopathy)

• Non-contrast CT imaging of the brain is the gold-standard for identifying SAH

  CT imaging is more sensitive in the first few hours (<6h) following a SAH and becomes progressively less sensitive with time; by 3 days, it is approximately 85% sensitive.

  Besides time, other reasons for a false negative CT include anemia, low volume SAH and a technically poor scan.

  Some clinicians advocate for a CT angiogram (CTA) at the time of the CT scan to look for an intracranial aneurysm. Although this is helpful if an aneurysm is seen, the negative predictive value is less clear. One should not use a negative CTA alone to rule out SAH.

  MRI is useful in patients who are imaged a few days following the SAH; specific sequences can be used to image subarachnoid blood even several days later.

  To revise interpretion and grading of the CTB go back to GRADING SYSTEMS

• If CT negative but history suggestive, perform an LP to look for xanthochromia.

  • Xanthochromia is the staining of CSF by heme breakdown products (chiefly bilirubin).
  • It takes several hours for blood in the subarachnoid space to break down, so the presence or absence of xanthochromia is time dependent.
  • If CSF shows xanthochromia, the diagnosis of SAH is confirmed (note, if the CSF protein exceeds 100 mg/dl as this can cause a false positive).
  • If the CSF is clear of RBCs and xanthochromia is absent, it is highly unlikely that the patient had a subarachnoid hemorrhage. However, a rapidly expanding aneurysm without subarachnoid rupture can present with a classic thunderclap headache, so if you still suspect an aneurysm on clinical grounds, emergent neurosurgical consultation is recommended.
  • Typical findings of SAH on cerebrospinal fluid analysis are:
  • • Some RBCs
    • < 5 WBCs
    • WBC:RBC ratio 1:700
    • Xanthochromia is present
    • Minimal clearing of RBCs between tubes 1 and 4.

  N.B.

  • RBCs in the spinal fluid is also more likely to be seen early and will clear with time.
  • Xanthochromia is absent early and nearly always present by 12 hours after the bleed.
  • Spectrophotometry is more sensitive but much less specific for xanthochromia than visual inspection

Once aSAH diagnosed, early referral to Neurosurgery and Intensive Care is important
Make sure you cover:

• Direct and collateral history of presentation
• Airway + respiratory status
• Haemodynamic status and blood pressure control, including what medications given.
• Neurological exam giving WFNS score; specifically mention best motor score and pupillary exam, as well as specific cranial nerve abnormalities
• Imaging
  • Ideally Modified Fisher grade
  • Presence or absence of hydrocephalus
• LP results if done
• Coagulation studies results
• Medications given (dose and time administered), including: sedatives, analgesics, seizure prophylaxis, anti-hypertensives, and nimodipine.
• Coordination of other vascular imaging

Lines – An arterial and central line are usually needed to closely control blood pressure even though we go off non-invasive systolic blood pressure

Further imaging after consulting Neurosurgery
This may be a CT angiogram or Digital Subtraction Angiogram (DSA) depending on the circumstances & setting

Commence nimodipine
More on this in the next section!