Peter Birkeland

Intracranial Aneurysms in Sickle-Cell Disease Are Associated With the Hemoglobin SS Genotype But Not With Moyamoya Syndrome

Background and Purpose— Intracranial aneurysms and aneurysmal subarachnoid hemorrhage may occur more frequently in sickle-cell disease (SCD), and this could be related to the sickle genotype and moyamoya syndrome seen in SCD. Methods— Records from a total of 1002 patients with SCD attending 2 specialized adult hematologic services were retrospectively reviewed. We analyzed data of a cohort of 767 patients attending 1 SCD clinic between 2002 and 2013 and of 235 patients from the other clinic who have had neurovascular imaging between 2007 and 2014. Results— We identified 4 patients in the cohort who had an aneurysmal subarachnoid hemorrhage during 9063 patient-years. The highest incidence rate was seen among women in the age group 30 to 39 years with the hemoglobin SS (HbSS) genotype (440 per 100 000 patient-years). Unruptured intracranial aneurysms were found in 20 of the 324 patients, who had imaging data; the prevalence was significantly higher in patients with HbSS genotype compared with other sickle genotypes with the highest prevalence (15%) observed in women in the age group 30 to 39 years. Fifty-one HbSS patients had a moyamoya vasculopathy, but only 3 of these had concomitant intracranial aneurysms. Conclusions— Intracranial aneurysms are common in HbSS SCD. There was also a trend toward more common occurrence of aneurysmal subarachnoid hemorrhage in HbSS; women in the age group 30 to 39 years were most at risk. There was no correlation between the occurrence of intracranial aneurysms and moyamoya syndrome.

Aspirin is associated with an increased risk of subdural hematoma in normal-pressure hydrocephalus patients following shunt implantation

OBJECT In this paper the authors investigate whether shunt-treated patients with normal-pressure hydrocephalus receiving aspirin therapy are at increased risk of developing subdural hematoma (SDH). METHODS Records from 80 consecutive patients who had undergone implantation of a cerebrospinal fluid shunt for the treatment of normal-pressure hydrocephalus were retrospectively reviewed. RESULTS Eleven cases of symptomatic SDH occurred, all among patients receiving aspirin or clopidogrel. The 5-year survival estimate was 0.3 (p < 0.0001) for users of aspirin and the hazard ratio was 12.8 (95% CI 3.1-53). CONCLUSIONS Patients on an aspirin therapy regimen have a markedly increased risk of SDH after a shunt has been implanted for the treatment of normal-pressure hydrocephalus. Users of clopidogrel may have an even greater risk.

Subdural haematoma complicating shunting for normal pressure hydrocephalus in the setting of concomitant antiplatelet medication – a report of 11 cases

Abstract Objective: To report on the occurrence and management of subdural haematoma after shunt implantation for normal pressure hydrocephalus and to determine the risk of recurrence in the setting of antiplatelet medication. Methods: From a consecutive series of 80 patients implanted with a cerebrospinal fluid shunt for normal pressure hydrocephalus, records from 11 patients taking antiplatelet drugs, who subsequently had surgery for subdural haematoma were extracted and retrospectively reviewed. Results: Patients were followed up for a mean of 1819 days after shunt implantation. Subdural haematomas occurred at a median of 335 days after shunt implantation – four ipsilateral, five contralateral and two bilateral with respect to the ventricular catheter. Three patients had reoperations done within a week without having resumed antiplatelet medication in the interim. One of them had three further reoperations done before the subdural collection disappeared. Only one patient had a late recurrence almost 11 years after shunt implantation. Conclusions: Subdural haematoma in the setting of a ventriculoperitoneal implantation for normal pressure hydrocephalus and concomitant antiplatelet medication can be managed along usual lines. Antiplatelet medication can be recommenced in due course with a low risk of recurrence.

An expanding intracerebral haematoma

A 44 year old man presented to the emergency department with a sudden onset headache. He had no medical history of note and took no drugs. Urgent computed tomography of the head was performed (fig 1⇓). A repeat scan (eight minutes later) was performed after administration of intravenous contrast (OptiRay) (fig 2⇓). Upon return from the radiology department, he developed left sided hemiplegia. His blood pressure was 179/90 mm Hg. After another 46 minutes, computed tomography (fig 3⇓) with angiography (not shown) was performed; no abnormal vessels were seen. Blood tests did not show an underlying coagulopathy. He subsequently deteriorated to localising to pain and making incomprehensible sounds to pain without opening his eyes (Glasgow coma score 8). His pupils remained equal and reactive to light. Fig 1 The patient’s initial computed tomogram of the head Fig 2 Repeat computed tomogram (eight minutes later) after administration of intravenous contrast Fig 3 Repeat computed tomogram (54 minutes after the first) The sequence of scans (figs 1-3) depicts an expanding intracerebral haematoma. ### 1. What causes of this bleed should be considered? #### Short answer Aneurysmal subarachnoid haemorrhage should first be suspected in patients with a history of sudden onset headache. However, in this case the initial scan shows a small haematoma in the right basal ganglia rather than a subarachnoid haemorrhage. In patients with haemorrhage in the basal ganglia hypertension is the most common cause. Other causes include ruptured arteriovenous malformation, cavernoma, and tumour related haemorrhage. #### Discussion Aneurysmal subarachnoid haemorrhage should be at the top of the list of differential diagnoses in patients with a …