Subarachnoid Hemorrhage


Subarachnoid haemorrhage


Findings on Investigations:

Diagnosis is established by neuroimaging (CT or MRI) or by lumbar puncture
Non-contrast CT:

  • Demonstrates subarachnoid hemorrhage in the acute phase.
  • May be negative, but is positive in the majority of cases. If CT is negative LP is indicated.
  • Blood in CSF spaces: sulci & cisterns. May also be associated with blood in ventricles (intraventricular hemorrhage IVH) especially the occipital horns of the lateral ventricles
  • Obscured sulci & sylvian fissures
  • Mild hydrocephalus especially temporal horns of the lateral ventricles
  • Diffuse cerebral oedema
  • Hypodensities: secondary ischemia in; perisylvian, pericallosal interfrontal, inferior frontal areas
  • Contrast CT shows up most medium to large AVMs

Lumbar puncture after 12hr from onset if CT is negative:

  • Negative LP combined with negative CT rules out SAH. [prospective large].  This is provided the LP is not delayed for weeks. Best timing is 6-12 hours from symptom onset.
  • Markedly elevated opening pressure
  • RBC/mm3:
    • Usually 100,000- over 1 million:
    • Occurs early in SAH
    • Clearing if RBCs from tube 1 to 3 (or 4) is occurs in traumatic taps. In traumatic taps it should approach zero. 25% reduction in RBCs is not enough.
  • Supernatant of centrifuged CSF: xanthochromia due to Bilirubin and oxyhemoglobin
  • Xanthochromia by Visual inspection may occur before 12 hrs and may miss SAH.
  • Xanthochromia analysis by spectrophotometry (spectroscopy) timed from 12 hrs to 2 weeks post onset helps exclude ruptured aneurysm.
  • WCC: raised or in chemical meningitis markedly raised with reduced glucose


  • If > 4 days consider MRI especially gradient echo GRE (hypointense).
  • If >3 weeks, MRI (especially FLAIR: hyperintense CSF spaces) & MRA: shows hemosiderin deposition.
  • T1: isointense CSF, T2/FLAIR: hyperintense CSF, GRE: hypointense CSF
  • DWI: foci of restriction (vasospasm, ischemia)
Cerebro-Vascular imaging:


  • After diagnosis is confirmed, to diagnosed the cause. Aneurysm, AVM, intracranial dissection
  • CTA helps more so later in the hospital course to detect vasospasm
  • Detects aneurysms =or> 2mm. Catheter angiogram is more sensative and specific.

Cerebral Angiography:

  • After diagnosis, to diagnose underlying cause
  • Both carotids & vertebral arteries
  • Best sensitivity and specificity. This is further improved if catheter rotational angiography is also performed
  • Repeat if negative, false negatives with vasospasm or thrombosis or very small causative lesion. Occurs in 5% of patients.
  • Repeat once if negative, especially if CT shows hemorrhage & more so if it is outside perimesencephalic region

Cerebral Vasospasm:

This can occur as a complication of subarachnoid hemorrhage. It may occur  from other conditions as well. It may be clinical vasospasm if this occurs with symptoms  or infarction. It also may be radiological vasospasm where there is evidence of vasospasm on imaging without clinical deficits or infarction.
Clinical features of cerebral vasospasm:

  • Confusion, motor deficit, aphasia or seizure

Radiological vasospasm, determined by:

  • Cerebral angiography
  • CT angiography (CTA)
  • Transcranial ultrasound (trancranial doppler ultrasound, TCD): shows increased mean flow velocity (MFV) if proximal vasospasm is present, increased pulsatility index if distal vasospasm is  present
  • MR Angiography (MRA)

Scales & Grading:

Hunt-Hess scale:

Grade 1: Asymptomatic, mild headache, slight nuchal rigidity
Grade 2: Moderate to severe headache, nuchal rigidity , no neurologic deficit other than cranial nerve palsy
Grade 3: Drowsiness / confusion, mild focal neurologic deficit
Grade 4: Stupor, moderate-severe hemiparesis
Grade 5: Coma, decerebrate posturing

World federation of neurosurgeons WFNS grading:

Grading is done after the patient is stable
Grade 1, GCS 15, no focal signs
Grade 2, GCS 13-14, no focal signs
Grade 3, GCS 13-14, with focal signs
Grade 4, GCS 7-12
Grade 5, GCS 3-6

Fischer grading:

Grade 1: no SAH on CT
Grade 2: diffuse SAH or vertical layers <1mm thick
Grade 3: diffuse clot or vertical layer >1mm thick
Grade 4: intracerebral/intraparenchymal or intraventricular clot with diffuse SAH or no blood

Modified Fisher grade

0 None evident, no IVH either
1 Thin without IVH
2 Thin with IVH
3 Thick without IVH
4 Thick with IVH

Findings on other investigations:

  • Chemistry panel: hyponatremia often occurs
  • Urine drug screen: for cocaine in some cases
  • Non-contrast CT: see above
  • LP: see above
  • MRI: see above
  • CTA, catheter angiogram: see above
  • Transcranial doppler ultrasound: see above
  • ECG, continuous monitoring
  • ECG Changes with SAH: ST depression, peaked T waves, flat T waves or T wave inversion, tall U waves, long QT interval (VT, VFib, Torsades), PSVT. Most go away within 48-72 hours. T wave inversion may persist.
  • ECG Changes with nemodipine: bradycardia, AV block
  • Consider Troponin if ECG changes
  • Echocardiogram: stress induced cardiomyopathy may occur


For aneurysmal subarachnoid hemorrhage (aSAH). There are two periods to consider depending on whether the aneurysm is secured:

  • Initial period: ruptured aSAH or re-ruptured aSAH
  • Second period, secured aSAH, vasospasm & medical complications

Goals & targets:

  • Optimise Cerebral perfusion pressure CPP, MAP and ICP
  • Ruptured aSAH, unsecured: avoid high systolic mmHg (<140), keep EVD open at 20cm (to avoid reducing ICP too much, theoretical temponade effect of higher ICP)
  • Ruptured aSAH, secured: use MAP as primary BP target rather than Systolic BP, drop EVD to 10cm, allow patient to ambulate

Treatment of underlying lesion:

  • Aneurysmal SAH: Endovascular treatment (coiling or assisted techniques) is the standard of care. However some aneurysm are not suitable for endovascular treatment. Surgery should be considered for those cases.
  • AVM: definitive treatment is usually performed at a later stage unless there is venous outflow obstruction. Treatment may involve a combination of endovascular therapy, surgery or radiosurgery.

Consider hematoma evacuation if large

  • Avoid antiplatelets until aneurysm is secured

Prevent raise in intracranial pressure:

  • Absolute bed rest, until aneurysm is secured. Then early ambulation
  • Tilt the bed head 15-20 degrees
  • Analgesia for headache
  • Antiemetic

Consider Antifibrinolytic therapy:

  • Avoid after treatment of aneurysm or delayed administration. [Metanalysis]
  • Avoid antifibrinolytic therapy after 48 hours or for >3 days
  • Consider Tranexamic acid 1g I.V. STAT & 1g q6h until aneurysm treatment or 72hrs. [RCT]


  • Nimodipine 60 mg P.O. every 4 hours, after BP is corrected, X 21 days +monitor BP & heart rate [RCT]


Prophylaxis of complications:

Delayed cerebral ischemia DCI, Avoid:

  • Hypovolemia, hypotension, and hyponatremia (see below)
  • Hyperthermia: paracetamol & cooling blankets. Hyperglycemia: insulin therapy


  • Only use prophylaxis prior to aneurysm being secured
  • Avoid phenytoin as it is associated with poor cognitive outcomes in observational studies
Mx. Of complications:

Raised intracranial pressure ICP:

  • Ventriculostomy= External ventricular drain EVD

If vasospasm occurs:

  • Increase MAP by 30%, EVD 0 and open, CPP goal >60
  • Induce hypertension with phenylephrine or dopamine
  • Euvolemia: NaCl 0.9% 200ml/hr, consider albumin infusion if electrolyte abnormalities develop
  • Consider optimizing cardiac output: i.e. Cardiac index CI.
  • Consider endovascular therapy (balloon angiopasty if proximal, intraarterial verapamil if distal)

If hyponatremic:

  • Treat the cause: usually syndrom of inappropriate anti-diuretic hormone (SIADH) or cerebral salt wasting
  • Sodium replacement with NaCl P.O. or 3% normal saline I.V.
  • D not use fluid restriction as hypovolemia can be harmful

Neurogenic pulmonary oedema:

  • Supportive care

Stress-induced cardiomyopathy:

  • Supportive care

Related articles:


  1. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Council on Cardiovascular Surgery and Anesthesia; Council on Clinical Cardiology. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012 Jun;43(6):1711-37. doi: 10.1161/STR.0b013e3182587839. Epub 2012 May 3.
  2. van Gijn, J. and G.J. Rinkel, Subarachnoid hemorrhage: diagnosis, causes and management. Brain, 2001. 124(Pt 2): p. 249-78.
  3. van Gijn, J. and G.J. Rinkel, Subarachnoid hemorrhage: diagnosis, causes and management. Brain, 2001. 124(Pt 2): p. 249-78.
  4. Brouwers, P.J., et al., Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage. Stroke, 1989. 20(9): p. 1162-7.
  5. Report of World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. J Neurosurg, 1988. 68(6): p. 985-6.
  6. Roos, Y.B., et al., Antifibrinolytic therapy for aneurysmal subarachnoid hemorrhage. Cochrane Database Syst Rev, 2003(2): p. CD001245.
  7. Heasley, D.C., M.A. Mohamed, and D.M. Yousem, Clearing of red blood cells in lumbar puncture does not rule out ruptured aneurysm in patients with suspected subarachnoid hemorrhage but negative head CT findings. AJNR Am J Neuroradiol, 2005. 26(4): p. 820-4.
  8. Perry, J.J., et al., Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med, 2008. 51(6): p. 707-13.
  9. MacDonald, A. and A.D. Mendelow, Xanthochromia revisited: a re-evaluation of lumbar puncture and CT scanning in the diagnosis of subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry, 1988. 51(3): p. 342-4.
  10. Vermeulen, M., et al., Xanthochromia after subarachnoid hemorrhage needs no revisitation. J Neurol Neurosurg Psychiatry, 1989. 52(7): p. 826-8.
  11. Mitchell, P., et al., Detection of subarachnoid hemorrhage with magnetic resonance imaging. J Neurol Neurosurg Psychiatry, 2001. 70(2): p. 205-11.
  12. Imaizumi, T., et al., Detection of hemosiderin deposition by T2*-weighted MRI after subarachnoid hemorrhage. Stroke, 2003. 34(7): p. 1693-8.
  13. Fisher, C.M., J.P. Kistler, and J.M. Davis, Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery, 1980. 6(1): p. 1-9.
  14. Jung, J.Y., et al., Spontaneous subarachnoid hemorrhage with negative initial angiography: a review of 143 cases. J Clin Neurosci, 2006. 13(10): p. 1011-7