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Information ⬇

Author: Michael Canty

Consider subarachnoid haemorrhage (SAH) (Box 67.1) in any patient with:

Most patients with SAH will complain of nausea and vomiting, photophobia, and eventually neck stiffness. Some will present in an acute confusional state and a collateral history is essential.

In the conscious patient, examination is often normal. In others, there may be objective neck stiffness, mild disorientation, or subtle deficits such as dysphasia or pronator drift. Uncommonly, the presence of subhyaloid or vitreous haemorrhage is detected on fundoscopy; in the context of a suggestive history these findings are usually pathognomonic.

Priorities ⬆ ⬇

  1. If you suspect SAH
    • Assess the airway, breathing and circulation, and correct abnormal physiology.
    • Assess the conscious level: seek an urgent anaesthetic/intensive care opinion for patients flexing to painful stimuli or worse.
    • Nurse the patient 30o head-up to optimize cerebral venous drainage; provide oxygen if arterial oxygen saturation is <94%; establish IV access; make nil by mouth; start IV 0.9% saline, usually at 125 mL/h.
    • Check full blood count, coagulation screen, blood glucose, urea, creatinine and electrolytes.
    • Record an ECG to assess for myocardial ischaemia or ‘stunning’ secondary to SAH.
    • Provide analgesia – opioid if required. Stop antiplatelet therapy and reverse anticoagulation (Chapter 103).
  2. Arrange brain CT
    • The primary investigation in suspected SAH is non-contrast CT scanning of the brain, from vertex to foramen magnum. As a general rule, this should be performed as an emergency including when out of hours. Many UK units will defer imaging to daylight hours in fully conscious patients without neurological deficit; this decision should be made by a senior clinician in the context of each individual case.
    • It is helpful to think of CT as a screening investigation to decide whether or not a lumbar puncture (LP) is necessary. In the presence of a ‘positive’ CT scan demonstrating SAH, a lumbar puncture is not required and a referral should be made immediately to neurosurgery. If, however the CT does not demonstrate SAH or an alternative diagnosis, LP should be considered mandatory to confirm or exclude SAH.
    • In a conscious patient with a severe headache, the presence of a unilaterally dilated pupil, often accompanied by a significant ptosis of the same eye, usually indicates an expanding aneurysm of the ipsilateral posterior communicating artery. Refer urgently to neurosurgery, even if the CT scan is normal: a so-called ‘painful third nerve palsy’ often heralds an imminent aneurysm rupture.
  3. If CT is normal, perform lumbar puncture (LP)
    • LP should be performed >12h after the onset of symptoms; earlier LP may be falsely negative. See Chapter 123 for the technique of LP.
    • Ideally performed by an experienced clinician to reduce the risk of a ‘traumatic tap’, which often makes a definite diagnosis impossible.
    • Measure opening pressure; send CSF for microscopy, cell count and culture, and spectrophotometry to assess for the presence of CSF bilirubin. Samples should be analysed immediately on receipt; if analysis is delayed, false positives may occur.
    • All positive or equivocal results should be referred to neurosurgery. A negative result excludes SAH (but see Box 67.2).

Further Management ⬆ ⬇

  1. If SAH is confirmed by CT/LP, refer immediately to neurosurgery
    • CT or MR angiography is occasionally requested following advice from the regional neurosurgical unit in specific cases. This should only be requested with the agreement of local radiology. Regional neuroradiology consultation may be required to offer a specialist opinion on such imaging.
    • Consider starting nimodipine 60 mg orally/NG 4-hourly (to reduce the incidence of delayed ischaemic neurological deficit) after discussion with neurosurgery. In severe hypertension, active pharmacological blood pressure control (Chapter 55) may be required: discuss with neurosurgery.
    • Most patients with SAH will be transferred to the regional neurosurgical unit for further assessment and management. Specialist management usually involves further investigation with CT angiography, which identifies causative aneurysms or arteriovenous malformations with high sensitivity. If CT angiography is normal, most patients will proceed to digital-subtraction catheter angiography.
    • If systolic BP is >160 mmHg, start antihypertensive therapy aiming for a target <160 mmHg. We would not normally expect referring clinicans to institute vasoactive blood pressure management of SAH; doing so and inadvertently dropping BP precipitously is potentially dangerous.
    • Consider giving labetalol or nicardipine by infusion (as for acute ischaemic stroke): see Chapter 55. However be cautious about excessive lowering of blood pressure.
  2. Management of culprit intracranial aneurysm
    • Definitive treatment of responsible aneurysms has markedly changed since the publication of the International Subarachnoid Aneurysm Trial (ISAT) in 2005. This trial demonstrated the superiority of endovascular ‘coiling’ of aneurysms versus the traditional method of surgical ‘clipping’ via craniotomy.
    • Clipping is now carried out almost exclusively by subspecialist vascular neurosurgeons, usually for complex aneurysms not easily treated by coiling, or in the presence of an intracerebral haematoma requiring evacuation.
  3. Management of other complications of SAH

Delayed Ischaemic Neurological Deficit (Dind)

  • Incidence peaks at 4–14 days post-ictus.
  • Presents with new focal neurological deficit, severe headache, or reduced conscious level.
  • Managed with aggressive fluid administration, induced hypertension (assuming a secured aneurysm), and occasionally endovascular intervention such as balloon angioplasty and intra-arterial administration of nimodipine or nicardipine.

Hydrocephalus

  • Often occurs very early in SAH, but may also present weeks or months post-ictus.
  • Typically presents with features of raised intracranial pressure, with headache, vomiting, lethargy, confusion, incontinence or deterioration in mobility. CT imaging of the brain usually confirms the diagnosis.
  • Acute presentation with hydrocephalus requires an urgent neurosurgical opinion. Most of these patients will require surgical CSF diversion (e.g. insertion of an external ventricular drain). Hydrocephalus presenting in a delayed fashion is often picked up once the patient is in the rehabilitation phase, and may simply present with a plateau or regression in rehab progress. Most of these patients will benefit from permanent CSF diversion, usually a ventriculoperitoneal shunt, and this should be discussed with neurosurgery.

Hyponatraemia

  • Common post-SAH and may by itself cause neurological deterioration.
  • The usual differential diagnosis is syndrome of inappropriate ADH secretion (SIADH) and cerebral salt wasting (CSW). Differentiating between the two is difficult, but crucial as treatment varies markedly (although perhaps less so in SAH – see below).
  • Cerebral salt wasting manifests as salt loss in a dehydrated patient. The patient may be clinically dry; have biochemical features such as a high haemoglobin/haematocrit, high urea, or high serum urate. Urine output is relatively high; urinary sodium levels are elevated; plasma osmolality is low (due to salt loss).
  • SIADH manifests as inappropriate free water retention in a euvolaemic patient. Similarly to CSW, urinary sodium levels are high, while plasma osmolality is low; however, urine output is relatively low, and the patient is not dehydrated.
  • CSW is treated by increasing intravascular volume with fluids; depending on the degree of hyponatraemia they may also require salt, usually in the form of hypertonic saline. SIADH is classically treated with fluid restriction; however, in acute subarachnoid haemorrhage this is usually contraindicated as it may contribute towards the development of DIND. Most SIADH is mild and resolves spontaneously; if sodium drops precipitously then hypertonic saline may be required.

Further Reading ⬆

Macdonald RL, Schweizer TA. (2016) Spontaneous subarachnoid haemorrhage. Lancet 389, 655–666.