These cases warrants investigations to look for aneurysms that can cause such bleeding. Non-traumatic
Hypertensive bleed
Intracranial bleed in hypertensive subjects usually occurs at 50 to 60 years of life with 30 to 50% chance of death. Such hemorrhages are typically located in the basal ganglia, cerebellum, or occipital lobes. Other location such as bleed within the cerebral cortex and intracranial bleed in people younger than 50 years should prompt further investigations on other causes of bleed such as brain tumour or cerebral arteriovenous malformation. The bleed can be very small without any significant effect on surrounding brain or large hemorrhage that exerts mass effecct on adjacent brain. Follow up CT scan is recommended. Those with extension of bleed into the ventricular system, expansion of bleeding, or increasing cerebral oedema on CT scan gives poorer prognosis. CT angiography (CTA) of brain can be performed to investigate the source of bleeding. An image during the delayed phase of the CTA may be taken to look for pooling of contrast that signifies active bleeding (known as "Spot sign"). Presence of "Spot sign" signifies poor clinical outcome for the subject. Cerebral amyloid angiopathy
Cerebral amyloid angiopathy (CAA) is the deposition of Amyloid beta peptide protein within the brain. Accumulation of such peptide proteins within the walls of the arteries can cause weakening of the walls and causes microhemorrhages, SAH within the cerebral sulci or large cerebral intraparenchymal bleed. SAH in CAA can be differentiated from vasculitis by its presentations.
These are pseudoaneurysm, caused by thrombus clogging the distal arteries, which results in inflammation and small tears at the site of occlusion. These inflammation and thrombis can caused by infective endocarditis, artificial heart valve or other heart problems. Similar to vasculitis, rupture of mycotic aneurysm also causes SAH in cerebral sulci, mostly located in the vertex. If mycotic aneurysm is located more proximally, it will produce diffuse SAH pattern. CTA or MRA would produce focal outpouching or increase in diameter of the vessel. Meanwhile, GRE/SWI MRI sequence would produce focal hypointensity. Small mycotic aneurysms are difficult to be seen on CT or MRI. Thus, DSA is useful in identifying these lesions. Management
For those who is already on blood thinners such as aspirin or clopidogrel for prevention of myocardial infarction or stroke, traumatic intracranial hemorrhage should prompt the use of platelet function assays (PFA-100) to assess the effect of these antiplalelet agents. After that, plateletpheresis can be started to increase the aggregation of platelets, thus stopping the intracranial bleed. In those with impaired kidney functions, desmopressin or cryoprecipitate can be used instead.From limited observational data, it may be relatively safe to restart blood thinners after an ICH as it is asscoated with reduced thromboembolic complications with similar risk of recurrent hemorrhage when compared to those did not start blood thinners after an ICH. Comparison
References
Further reading
Shepherd S. 2004. "Head Trauma." Emedicine.com. Vinas FC and Pilitsis J. 2004. "Penetrating Head Trauma." Emedicine.com. Julian A. Mattiello, M.D., Ph.D. Michael Munz, M.D. 2001.