Subarachnoid haemorrhage

Aneurysms

Intracranial aneurysms are not congenital. Rather, they develop during the course of life. An estimate of the frequency for an adult without risk factors is 2.3%, with the proportion increasing with age. Most aneurysms will never rupture, but the risk increases with size. Paradoxically, because the vast majority of aneurysms are small, most aneurysms that rupture are small. An aneurysm of the posterior circulation is more likely to rupture than one of comparable size in the anterior circulation.

Risk factors can be divided into those that are modifiable and those that are not. Modifiable risk factors include cigarette smoking, hypertension, the use of sympathomimetic drugs (e.g. cocaine) and excessive alcohol intake. Non-modifiable factors include history of previous aneurysmal SAH, a family history of first-degree relatives with SAH, inherited connective tissue disorders (particularly polycystic kidney disease, Marfan syndrome, Ehlers-Dahnlos syndrome and neurofibromatosis), coarctation of the aorta, sickle cell disease and α ₁ -antitrypsin deficiency.

Non-aneurysmal peri-mesencephalic haemorrhage

This type of SAH is defined by the characteristic distribution of blood in the cisterns around the midbrain in combination with normal angiographic studies. It usually carries a relatively benign prognosis. A small proportion of patients with this distribution of blood may have a ruptured aneurysm of a vertebral or basilar artery.

History

The history is critical to the diagnosis of SAH.

• Headache is the principal presenting symptom, being present in up to 95% of patients with SAH and being the solitary symptom in up to 40% of patients. It is typically occipital, severe (‘worst’), of sudden onset, almost instantaneously reaching peak intensity and often being the worst headache ever experienced. Approximately 25% of patients presenting with sudden severe headache will have SAH. The pain differs from any other headache the patient might have had (‘first’).

• One-third of patients experience a warning leak (sentinel haemorrhage) in the hours to weeks before the major bleed. This headache may be mild, generalized or localized and of variable duration; it may resolve spontaneously within minutes to hours or last several days and usually responds to analgesic therapy. It does, however, tend to develop abruptly and to differ in quality from other headaches that the patient may previously have experienced. Hence a patient’s worst or first headache is suggestive of SAH.

• Upper neck pain or stiffness (and then meningism) is common.

• About half of patients will develop SAH during strenuous exercise (e.g. bending or lifting).

• Nausea and vomiting are present in 75% of patients.

• Brief or continuing loss of consciousness may occur, the headache typically occurring just prior to loss of consciousness.

• Seizures occur in circa 10%. When associated with headache, they are a strong indicator of SAH, even if the patient is neurologically normal when assessed.

• Prodromal symptoms—particularly involving the third cranial nerve with pupillary dilatation and sixth cranial nerve palsies—are uncommon but may suggest the presence and location of a progressively enlarging unruptured aneurysm.

• No clinical feature can reliably identify SAH.

Examination

There is a wide spectrum of clinical presentations, the level of consciousness and clinical signs being dependent on the site and extent of the haemorrhage, as follows:

• On ED presentation, two-thirds of patients have an impaired level of consciousness, 50% with coma. Consciousness may improve or deteriorate. An acute confusional state can occur, which may be mistaken for a psychological problem.

• Signs of meningism, photophobia and neck stiffness are present in 75% of patients but may take several hours to develop and may be absent (particularly with more severe bleeds). Absence of neck stiffness does not exclude SAH. Photophobia is neither sensitive nor specific for SAH. Fever may be present.

• Focal neurological signs are present in up to 25% of patients and are secondary to associated intracranial haemorrhage, cerebral vasospasm, local compression of a cranial nerve by the aneurysm (e.g. oculomotor nerve palsy by posterior communicating aneurysm or bilateral lower limb weakness due to anterior communicating aneurysm) or raised intracranial pressure (sixth-nerve palsy).

• Ophthalmological examination may reveal papilloedema (40%), retinal haemorrhages (25%) or, rarely, subhyaloid haemorrhages (see Entezari et al., 2009 ).

• Systemic features associated with SAH include hypertension, hypoxia and acute electrocardiographic (ECG) changes that may mimic acute myocardial infarction.

• Neurogenic pulmonary oedema is more common in obtunded SAH patients.

• A small proportion of patients present in cardiac arrest. Resuscitation attempts are vital, as half of the survivors regain independent function.

Patients are categorized into clinical grades from I to V, according to their conscious state and neurological deficit. Two grading schemes, that of Hunt and Hess and that of the World Federation of Neurosurgeons, which is preferred, are depicted in Table 8.3.1 . The higher the score, the worse the prognosis.