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An 11 year old boy walked into our accident and emergency department with his mother having woken up with headache four hours ago. He was known to have mild learning difficulties for speech and language, but was otherwise previously fit and healthy. He was not on any medications, and he did not have any history of trauma. He had vomited twice at home. On initial examination, he did not have a high temperature, rash, or meningeal symptoms, and his Glasgow Coma Scale score was E4 M6 V5. He had no neurological signs or papilloedema and the pupils were normal. He had no neck stiffness or meningeal signs. His pulse rate was 60 per minute and a subsequent electrocardiogram showed sinus bradycardia. His blood pressure was normal.
During further examination his conscious level deteriorated. He became vague and disinterested, and then he began babbling. He had a fluctuating conscious level, at best occasional spontaneous eye opening, localising to pain with inappropriate words. His respiratory rate was normal and he was maintaining his airway. At this point, the most likely clinical diagnosis was acute encephalitis and he was treated with intravenous cefotaxime and aciclovir. Investigations including full blood count, urea and electrolytes, C-reactive protein, glucose, liver function tests, and clotting profiles were normal. An urgent computed tomography (CT) scan of brain revealed recent haemorrhage in predominantly the right lateral, third, and fourth ventricles (fig 1). There was no evidence of acute hydrocephalus. Following our initial management he was transferred to the neurosurgical unit for continuing care. He then developed mild weakness of his left limbs. He underwent further CT scanning of brain and was treated conservatively. The CT scan and a cerebral angiogram performed at a later date did not reveal any underlying cause, such as an arteriovenous malformation or aneurysm.
Four months later the mild left sided weakness persists and it was planned to carry out magnetic resonance imaging (MRI) after six months of the haemorrhage to exclude an angiographically occult lesion such as cavernoma. The MRI confirmed the findings of the CT scan performed previously.
Spontaneous intracranial haemorrhage is rare in adolescence. Primary intraventricular haemorrhage is an uncommon subgroup. Little is known about the clinical and imaging features of primary intraventricular haemorrhage. Livingston et al reported that the clinical features in this condition were not specific, but that altered consciousness, headache, vomiting, and focal signs were common.1 Vascular malformations may result in intraventricular haemorrhage in children. Such presentation accounts for 3% of adult intracranial bleeds but relevant data about this association have not been reported in children.2 Certain prognostic factors like initial level of consciousness,3 early hydrocephalus,4 and delay in diagnosing intracranial aneurysms5 may adversely affect the outcome with severe neurological deficits and high mortality. In our case an early cranial CT scan ensured urgent neurosurgical referral. The absence of the abovementioned adverse prognostic factors might explain the reasonable outcome in our patient with little in the way of neurological deficit. Therefore to diagnose this serious condition, a high degree of clinical suspicion and a low threshold for early use of CT is essential, particularly in children who have difficulties with expression and speech.
Competing interests: none declared
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