Blood Pressure Management After Intracerebral and Subarachnoid Hemorrhage

The Knowns and Known Unknowns

Jatinder S. Minhas, MD; Tom J. Moullaali, MD, PhD; Gabriel J.E. Rinkel, MD, PhD; Craig S. Anderson, MD, PhD

Disclosures

Stroke. 2022;53(4):1065-1073. 

In This Article

Rationale for Early BP Lowering After ICH and SAH

Elevated BP is common in acute stroke, but particularly so for hemorrhagic forms because of greater sympathomimetic activation which contributes to a worse outcome.[11] In ICH, high BP is related to greater hematoma growth, most of which occurs in the first few hours after onset and is more likely in patients presenting with large hematomas and in the context of using antithrombotic medications.[12] Clinically, larger parenchymal hematomas in the cerebral hemispheres are more likely to compress vital structures and thus cause greater neurological deficits, and with extension into ventricular and subarachnoid spaces lead to hydrocephalus, which further compromises neurological function and functional recovery.[13,14] It is plausible, therefore, that a key therapeutic mechanism of action for BP control in ICH is to attenuate hematoma growth,[15] and thus BP should be controlled as early as possible in ICH, ideally within the first few hours of onset. Lower BP levels over the subsequent hours and several days could promote the reabsorption of hematoma and perihematomal edema and reduce the risks of recurrent ICH and serious ischemic events.

A similar biphasic pattern of therapeutic action is also apparent for SAH. As high BP is associated with rebleeding[3] and poor outcome,[16] guidelines recommend to reduce high BP in the acute phase of SAH, but there is disagreement on an upper threshold for treatment, approach, and target.[17,18] Among the various potential triggers identified for SAH is a sudden surge in BP being responsible for rapid aneurysm growth and rupture,[19] although this may have little relevance to clinical practice other than supporting the need to ensure good long-term BP control in hypertensive patients.[20] Consequently, and as in ICH, patients often present with high BP after aneurysmal SAH, with increasing intracranial pressure (ICP) as a contributing factor, which can present a Scylla and Charybdis dilemma for clinicians: leaving the patient with untreated high BP runs the risk rebleeding, while reducing BP may increase the risk of DCI, which typically arises within several days and is the main contributor to death and disability in patients with SAH and secured aneurysms.[16] Despite decades of research, the cause and treatment of DCI have not been fully resolved, and nimodipine is the only proven strategy for prevention. The mechanisms by which nimodipine exerts its beneficial effects have not been fully clarified, but its (modest) BP lowering effects may contribute.

Thus, given that early assessments of the effects of BP lowering in ICH are made within 24 hours (ie, on hematoma growth and early neurological deterioration), and that guidelines recommend an early occlusion of ruptured aneurysms in SAH, preferably within 24 hours (ie, to eliminate the risk of rebleeding, and as DCI occurs later), it seems reasonable to consider BP management in both forms of hemorrhagic stroke according to acute and subacute phases, defined by a 24 hour cut point.

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