Subarachnoid Haemorrhage (SAH)

This document provides an overview of SAH, many aspects of SAH are covered in detail elsewhere (See References and Links)

OVERVIEW

Subarachnoid Haemorrhage (SAH) potentially fatal bleeding into the subarachnoid space, usually due to a ruptured cerebral aneurysm

PATHOPHYSIOLOGY

Aneurysmal SAH (aSAH)

  • rupture of saccular aneurysm (60%)
  • rarely mycotic aneurysm

Non-aneurysmal SAH

  • perimesencephalic SAH (never associated with intraventricular extension)
  • AVM
  • angioma
  • neoplasm
  • cortical thrombosis
  • traumatic SAH

Aneurysm sites – usually saccular or berry aneurysms

  • PCOM (40%)
  • ACOM (35%)
  • MCA (20%)
  • Vertebrobasillar (4%)

CLINICAL FEATURES

  • sudden onset severe occipital is classic
  • suspect in any headache that is unusual for the patient
  • sentinel headache (40%)
  • transient or persistent loss of consciousness
  • vomiting
  • seizure or posturing
  • meningism
  • ophthalmoscopy: subhyaloid retinal haemorrhage, papilloedema
  • neurological signs in keeping with area near aneurysm
  • risk factors

RISK FACTORS

  • female(esp post-menopausal)
  • age >50y
  • smoking
  • OCP
  • alcohol abuse
  • Hypertension
  • Connective tissue disorders – Marfan syndrome, Ehlers-Danlos syndromes
  • Polycystic kidney disease
  • previous aneurysm or SAH
  • family history
  • coarctation of the aorta
  • fibromuscular dysplasia

INVESTIGATIONS

Bedside

  • ECG: tall peaked T waves, ST depression, prolonged QT, arrhythmia
  • Echo: neurogenic cardiomyopathy

Laboratory

  • hyponatraemia + hypovolaemia from SIADH or cerebral salt wasting -> worsens vasospasm
  • LP: most sensitive at 12 hours for xanthochromia
  • troponin rise due to cardiomyopathy

Imaging

  • CXR: neurogenic pulmonary oedema
  • CTH: 90% sensitive within 24 hrs, 50% @ 72 hrs, detects hydrocephalus
  • CTA: assesses vascular anatomy
  • DSA: gold standard for diagnosis, allows intervention
  • MRI: mostly used for detection of AVM

GRADING

Clinical – Hunt and Hess/WFNS (the latter is more objective)

I – asymptomatic or mild headache/GCS 15, no motor deficit
II – moderate-severe headache, meningism and no weakness/GCS 13-14, no motor deficit
III – mild alteration in mental status, GCS 13-14, motor deficit
IV – depressed LOC and/or hemiparesis/GCS 7-12 +/- motor deficit
V – posturing or comatose/GCS 3-6, motor deficit present or absent

CT – Fisher

I – no blood
II – diffuse deposition of SAH without clots or layers of blood >1mm
III – localized clots and/or vertical layers of blood 1mm or > thickness
IV – diffuse or no subarachnoid blood but intracerebral or intraventricular clots

MANAGEMENT

Resuscitation

  • if airway not patent or requires protection -> elective intubation
  • routine monitoring
  • consider arterial line placement
  • if has a seizure -> anticonvulsants (no indicated prophylactically)
  • dexamethasone used by some to decrease meningeal irritation + oedema -> no convincing evidence
  • maintain intravascular volume with isotonic fluids (watch for hyponatraemia)
  • hypertension -> manage with analgesia + nimodipine +/- other antihypertensives

Specific treatment

  • clipping vs coiling (see CCC entry)
  • coil if possible -> better outcomes in terms of disability @ 1 year (controversial ISAT trial)
  • clip if uncoilable -> perform within 72 hours

Poor Grade SAH

  • German retrospective audit (Eleftherios, Vascular and Health Risk Management, 2007)
  • some data that early aneurysm securing, decompressive craniectomy and aggressive ICP management and CPP optimization can reduce mortality and disability
  • H&H grades IV and V with a motor response

COMPLICATIONS

Re-bleeding

  • avoid hypertension
  • avoid decreases in ICP
  • sedation in the agitated
  • no coughing or Valsalva
  • antifibrinolytic agents decrease rebleeding -> but increase vasospasm and hydrocephalus (not used now)

Hydrocephalus

  • indicated in: deteriorating LOC and enlarging ventricles on CT
  • EVD

Vasospasm

  • prevention: removal of SAH at surgery, nimodipine, maintenance of euvolaemia, avoiding hypotension
  • monitoring: clinical, transcranial Doppler, 4 vessel angio, CTA/MRI, EEG, SPECT/PET, microdialysis catheters
  • treatment: haemodynamic augmentation to reverse neurological deficits, endovascular treatment (balloon angioplasty, papaverine, nicardipine), investigational therapies
  • because of the disparity between vasospasm on trans-cranial Doppler, angio and what happens clinically there is disagreement about how aggressively vasospasm should be treated.

MONITORING

This is discussed in more detail in Monitoring in Subarachnoid Haemorrhage

  • Clinical assessment
  • Transcranial Doppler
  • 4-vessel angiography
  • CTA/ MRA
  • EEG
  • SPECT/ PET
  • Microdialysis catheter

PROGNOSIS

  • 25% die prior to reaching hospital.
  • worsens with increasing grade (I – 70% survival, V – 10% survival).
  • predictors of poor prognosis:
    -> high grade
    -> old age
    -> co-morbidities
    -> blood > 1mm thick on CT
    -> seizures
    -> cerebral oedema
    -> basilar artery aneurysm
    -> symptomatic vasospasm
    -> complications

References and Links

LITFL

Journal articles

  • Connolly ES Jr ,et al. 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. PMID: 22556195.
  • Diringer MN, et al; Neurocritical Care Society. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011 Sep;15(2):211-40. PMID: 21773873.
  • Edlow JA, Samuels O, Smith WS, Weingart SD. Emergency neurological life support: subarachnoid hemorrhage. Neurocrit Care. 2012 Sep;17 Suppl 1:S47-53. PMID: 22932990.

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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