Subarachnoid haemorrhage.

Background

Any patient with abrupt onset severe headache, with or without neurological signs, and with or without neck stiffness should be considered to possibly have a subarachnoid haemorrhage. CT scan is the investigation of choice.

Prognosis: Missing the diagnosis is most important in patients who are relatively well, and prompt early diagnosis can have a significant effect on mortality. Common mistaken alternative diagnoses in such patients are migraine, tension headache, or ‘meningitis with a bloody tap’.

Perspective – effect of early diagnosis on prognosis in SAH.

A study from Columbia University in New York¹ found that among patients with normal mental status at first medical contact, mortality was 5% at one year amongst those diagnosed correctly at that stage, as opposed to 19% amongst those initially misdiagnosed. (Absolute difference 14.6%, 95% CI 3.9% – 30.4%. This gives a ‘NND’ – number needed to diagnose – of 7. In other words, for every seven patients diagnosed promptly and correctly, you will save one life!) The same study found an overall mortality at one year, regardless of mental state at presentation, of 26%; the proportion at one year who were dead or disabled in any way was 59% (despite optimum treatment), so this is not a trivial illness. Overall 12% of patients were initially misdiagnosed.

History

(In casualty or outpatients be very wary of labeling a new headache as migraine.) If the patient answers ‘yes’ to the question ‘is this the worst headache of your life?’ and there are no neurological signs, then the chance that this is a subarachnoid haemorrhage is 12%. If there are neurological signs, then the probability increases to 25%². Although the presentation with an exertion-related thunderclap headache and a stiff neck is straightforward, the headache can be mild (relieved by paracetamol), unilateral, may come on at rest or during sleep, and may resolve spontaneously. Nearly half of all patients have had minor episodes of bleeding previously³.

If available, the investigation of choice in a suspected SAH is CT scanning (sensitivity nearly 100% if done within 24 hours.)⁴ In patients presenting beyond three days, a negative CT should be followed by an LP to rule out SAH.

Lumbar puncture is appropriate if the CT is equivocal or if there is little chance of getting the patient scanned in < 2 days. If there are focal signs, the chance of deterioration after LP may be as high as 15%. If in doubt, treat as bacterial meningitis initially. Up to 20% of all LPs may be ‘traumatic’ – clinical ‘impression’ and clearing with sequential tubes are not entirely reliable ways to diagnose a traumatic tap. However, clearly visualization of a little stream of blood swirling within the drop of CSF is very strong evidence in favour of a traumatic tap. Xanthochromia is reliable, but this should only be excluded after spectrophotometric examination in the laboratory. It only occurs 12 hours after the bleed, but will then persist for about 2 weeks. (70% still at 3 weeks, 40% at 4 weeks.)⁵

Management of SAH

• Consult a neurosurgeon!
• Intubate if the patient can’t protect his or her airway – lignocaine 1 mg/kg I.V. ‘premedication’ to reduce intubation related intracranial pressure elevation may help.
• Cautious blood pressure control – avoid precipitous drops.
• Seizure prophylaxis – phenytoin load and maintenance is recommended on general principles in the face of little evidence of efficacy.
• Hydration – avoid dehydration by giving normal saline in excess of maintenance requirements. It is theorised that dehydration may worsen vasospasm.
• Control pain with adequate 4 hourly doses of morphine (10-15 mg).
• Vasospasm prophylaxis with (if available) nimodipine 60 mg 4 hourly P.O.⁶

Perspective – nimodipine in SAH.

There was a flurry of studies looking at the use of nimodipine in both SAH and traumatic brain haemorrhage; it doesn’t seem to help for the latter, but two systematic reviews ⁷,⁸reached the same conclusion about benefit in SAH, largely based on the results of a single large RCT, but to some extent confirmed by the smaller trials. The Cochrane review showed:

Outcome measure	Relative risk reduction	Confidence interval	ARR	NNT
‘Overall poor outcome’	0.81	0.72 – 0.92	0.051	19
Mortality	0.94	0.8 – 1.10	NS
Stroke	0.67	0.59 – 0.76	NS

A more recent meta-analysis took basically the same old information and reached more positive conclusions, claiming a clear mortality benefit⁹ The data remains weak.

There is adequate evidence of improved outcome but no statistically significant mortality advantage. As with many composite outcomes, however, the clinical significance of reduction in ‘overall poor outcome’ is not entirely clear.

Hypopituitarism after subarachnoid haemorrhage

It may be convenient to think that all abnormal findings after either a SAH or a severe head injury or just due to diffuse neuronal injury, but it is worth bearing in mind that specific hormonal changes may be relatively common, even in the chronic phase. One systematic review ¹⁰ provided a pooled prevalence for hypopituitarism of 27.5% (95% CI 22.8 – 28.9%), so if there is genuine clinical suspicion, at least do a TSH, FSH/LH, and a random morning cortisol. Formal testing requires varies provocation tests (e.g. GHRH, insulin tolerance, and an ACTH level), but these should ideally only be performed in consultation with an endocrinologist.

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1. Kowalski RG, Claasen J, Kreiter KT, et al. Initial misdiagnosis and outcome after subarachnoid haemorrhage. JAMA. 2004;291:866-9 ↩

2. Linn FH, Wijdicks EF, van der Graaff Y, et al.  Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage. Lancet. 1994;344:590-3 ↩

3. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid haemorrhage. N Engl J Med. 2000;342:29-35 ↩

4. Cortum S, Sorensen P, Jorgensen J. Determining the sensitivity of computed tomography scanning in early detection of subarachnoid haemorrhage. Neurosurgery 2010;66:900-3 ↩

5. Schievink WI. Intracranial aneurysms. N Engl J Med. 1997;336:28-39. ↩

6. Miller J, Diringer M. Management of aneurysmal subarachnoid haemorrhage. Neurological Clinics. 1995;13:451-77 ↩

7. Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage.  (Cochrane review). In: The Cochrane Library, Issue 3, 2000. Oxford: Update Software ↩

8. Barker FG, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischaemic deficit after subarachnoid haemorrhage: a meta-analysis. J Neurosurgery. 1996;84:405-14 ↩

9. Hao, Guangzhi & Chu, Guangxin & Pan, Pengyu & Han, Yuwei & Ai, Yunzheng & Shi, Zuolin & Liang, Guobiao. (2022). Clinical effectiveness of nimodipine for the prevention of poor outcome after aneurysmal subarachnoid hemorrhage: A systematic review and meta-analysis. Frontiers in Neurology. 13. 982498. 10.3389/fneur.2022.982498. ↩

10. Schneider HJ, Ilonka KA, Ghigo E, et al. Hypothalamopituitary dysfunction following traumatic barin injury and aneurysmal subarachnoid haemorrhage.JAMA. 2007;298:1429-38 ↩

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