Background

Subarachnoid haemorrhage (SAH) is a diagnosis that carries significant morbidity and mortality but is an infrequent presentation to the emergency department (ED). The classical presentation is of ‘thunderclap’ headache but may present in a variety of ways, including loss of consciousness, which may be transient. Transient loss of consciousness (TLOC), on the other hand, is itself a common presenting symptom with a wide range of causes and is an established source of diagnostic difficulty.1 It is therefore vital not to miss SAH as a potential diagnosis.

The frequency of misdiagnosis of SAH has been widely reported, with two more recent cohort studies quoting between 5% and 12%.2 3 Identified risk factors for misdiagnosis were smaller aneurysm, no major neurological deficit or reduced consciousness and being triaged as ‘low acuity’.2–4

We describe a case of SAH presenting with TLOC during oral sex, with normal consciousness and no neurological deficit. Headache, although present, was only moderate and the patient was initially triaged as a seizure episode. CT head revealed a trace of subarachnoid blood, and she was transferred to the local neurosurgical unit for further intervention.

Case presentation

A 44-year-old woman was brought to the ED by an ambulance. Her partner had called the emergency services after an episode of unresponsiveness, estimated to last 2–3 min. On arrival of the ambulance services, she had a Glasgow Coma Scale score (GCS) of 15/15 with normal vital signs. She was conveyed to hospital with a possible seizure episode, as her partner initially reported her body was stiff during the episode.

On arrival in the ED, she remained GCS 15/15 with normal vital signs. She felt nauseous but did not vomit in the ED. Headache was described as frontal and rated 6/10 on a pain scale. There were no other positive symptoms. On closer history taking, the patient reported nearing orgasm while receiving oral sex from her partner before losing consciousness. Her partner estimated she was unconscious for 2–3 min, with no convulsive activity reported. She was not reported to be postictal. She had been otherwise well preceding the event.

The patient had a medical history of asthma and urticaria and reported an episode of cerebral malaria 20 years prior, with no neurological sequelae. Regular medications comprised inhalers and an antihistamine. She drank occasional alcohol, smoked 10 cigarettes daily and did not use recreational drugs.

Physical examination was unremarkable with no focal neurological deficit nor nuchal rigidity. She was normotensive. ECG showed normal sinus rhythm and blood results, including lactate, were all within the normal range.

At this point, the differential diagnoses included reflex-mediated syncope related to sexual activity, seizure and—given the ongoing headache and nausea—an intracerebral haemorrhage. We proceeded to perform CT imaging.

Unenhanced CT head was reported as: ’There is suspicion of a trace of acute subarachnoid blood. No acute intra-axial haemorrhage, mass, acute infarct or acute subdural haematoma. Ventricles and CSF spaces are within normal limits for age. Unremarkable paranasal sinuses and mastoid air cells. No bony lesion.’

She was subsequently transferred to a neurosurgical centre where she underwent CT angiography, revealing a right-sided 7 mm anterior communicating artery aneurysm. The patient underwent endovascular coiling the following day. Figure 1 shows the aneurysm prior to coiling. She remained an inpatient for a further 14 days and was discharged with no residual neurological deficit.

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Figure 1

Anterior communicating artery aneurysm.

Outcome and follow-up

As described above, our patient successfully underwent endovascular coiling of the aneurysm the following day at our local neurosurgical centre. Her subsequent 2-week admission was complicated by vasospasm; however, there was no further bleeding. She had no neurological deficit at discharge. At the time of writing, 4 months postdischarge, she remains well and under outpatient neurosurgical follow-up.

Discussion

Transient loss of consciousness is a common presentation to the ED and is usually defined as a sudden, spontaneous loss of consciousness with complete recovery and no residual neurological deficit.5 When considering the cause, it is important to try to distinguish syncope—which is a result of a cerebral perfusion deficit—from seizures and neuropsychiatric causes.6

Syncope has a well-described wide range of aetiologies but can still prove to be a diagnostic conundrum.1 Previously described is the ‘rule of 15 s’—an approximately 15% of the following conditions present with syncope: ruptured ectopic pregnancy, aortic dissection, aortic aneurysm, acute coronary syndrome, pulmonary embolism and cerebral haemorrhage.7 8 Although this may not be an accurate proportion, it serves as a reminder for the potentially immediately deadly causes—the majority of which are vascular in origin.9 Of note, pulmonary embolism has been the source of two recent multicentre investigations into admissions with syncope.10 11 We will discuss SAH further.

Loss of consciousness has been shown to be present in around 40% of those with spontaneous SAH.12 The mechanism is likely to be related to a rise in intracranial pressure secondary to bleeding. As might be expected, loss of consciousness (LOC) in the context of SAH is not necessarily transient and has been associated with poorer clinical grade and larger volumes of blood.12 However, in the same retrospective analysis, 38% of those with LOC at ictus had duration <10 min.12 Furthermore, of those with TLOC, that is, <10 min, nearly half were of Hunt and Hess Grade (HH) 1 or 2 at presentation—a commonly used prognostic scoring tool in SAH. HH 1 or 2 implies normal consciousness with headache only and no neurological deficit (except a single cranial nerve palsy).13 Of the 1460 enrolled patients with SAH in the analysis, there were only 80 patients with TLOC and HH 1 or 2 (5.4%). Our patient would fit into this subgroup.

The European Society of Cardiology guidelines for syncope regard SAH as an incorrect diagnosis of syncope as LOC may be ‘progressive or there may not be complete neurological recovery’.6 In addition, the 2010 NICE guideline for TLOC does not discuss cerebrovascular causes of TLOC.5While a rare cause, as previous studies and our case demonstrate, SAH should be considered even in those with textbook syncope.

Non-traumatic SAH is a result from aneurysmal bleeding in the majority of cases. Known risk factors for rupture include activities that involve sudden increases in blood pressure and sexual activity is well described as a precipitant.14 15 Older studies with intra-arterial monitoring during coitus demonstrate that during sexual activity blood pressure, as well as heart rate, is very labile, with particular rises during orgasm.16 17 It is worth noting, however, that these were studying penetrative sex, rather than oral sex.

There are several factors to consider in our case that may have contributed to the patient’s good clinical grade. First, our patient had rupture of a 7 mm anterior communicating artery aneurysm, generally regarded as small in size.18 As a result, there was only a small amount of blood seen on initial CT scan, so focal neurology and features of raised intracranial pressure were less likely to be evident. Finally, she was triaged in the ED within 2 hours of onset of symptoms, which may mean that features of meningeal irritation were not yet evident. These, in conjunction with her atypical presentation with TLOC, make her a higher risk candidate for misdiagnosis. Indeed, previous studies analysing cases of misdiagnosis demonstrated that seizures and syncope were both given as the discharge diagnosis at first contact.3 19

Misdiagnosis is well studied in SAH.20 It has previously been shown to be a large source of litigation in the USA, due to the potentially catastrophic outcomes.21 One of the strongest demonstrated risk factors for misdiagnosis is good clinical grade at presentation, and thus lower triage acuity.2–4 Alongside this, smaller volumes of blood and right-sided aneurysm have also been identified as independent risk factors.2 Interestingly, one previous retrospective analysis of missed SAH identified over half (57%) were from aneurysms <10 mm in size.19 As described, her case possesses several risk factors for misdiagnosis.

We have presented the case of a young female patient presenting with TLOC and moderate headache, with normal GCS and neurology, who was initially triaged ‘?seizure’ and for whom SAH was not a standout diagnosis. Detailed history taking revealed a known risk factor at ictus. She was accurately diagnosed and treated with favourable outcome but represents a small subgroup of atypical presenters with TLOC who may well have additional risk factors for misdiagnosis.

This case highlights the importance of thorough history taking and examination in the presentation of TLOC with careful consideration of CT head imaging if there is any suspicion of SAH.