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Three Part Question

In [adults with spontaneous intracerebral hemorrhage], does [early blood pressure control] improve [long term outcome]

Clinical Scenario

An 56 year old female presents to the emergency department with altered level of consciousness. She if found to have a systolic blood pressure of 200/100 and the CT confirms your suspicions of a intracerebral hemorrhage. You wonder how aggressive should I be in lowering her blood pressure acutely.

Search Strategy

Medline 1950 – 4/10 using OVID interface, Cochrane Library (2010)
[Exp intracranial hemorrhage , Hypertensive/drug Therapy] OR [Exp intracranial hemorrhage , Hypertensive/drug Therapy])
Using PubMed clinical queries, category: therapy, and scope: broad
[(intracerebral hemorrhage) AND (blood pressure)]

Search Outcome

176 papers were located with only two RCTs fulfilling the three part question.

Relevant Paper(s)

Author, date and country	Patient group	Study type (level of evidence)	Outcomes	Key results	Study Weaknesses
Anderson, C.S., et.al. 2010 Australia, China and South Korea	Adults with CT confirmed intracerebral hemorrhage, elevated systolic blood pressure and capacity to start lowering blood pressure within 6 hours of start of hemorrhage.	Prospective Randomized Control Trial	Over a two year period, 404 patients over the age of 18 were enrolledwith a total of 296 patients making it through to the final analysis. Patients were randomly assigned to recieve either intensive blood pressure lowering or standard of care blood pressure lowering. The outcome that was evaluated was absolute or proportional increases in hematoma and perihematomal edema.	The patients in the intensive blood pressure lowering group showed a decrease in hematoma growth of 3.15ml and 2.45ml at 24 and 72 hours, respectively. There was no significant difference in perihematomal edema in the two groups.	This study was not completely blinded. This was a pilot study with recruitment for the next phase beginning in 2008.
Koch, S., et.al. June 2008 United States	Adults with CT confirmed intracerebral hemorrhage	Prospective Randomized Control Trial	42 patients were enrolled and randomly assigned to receive aggressive blood pressure lowering (MAP<110mmHg) or standard blood pressure lowering (MAP 110-130mmHg). The clinical endpoint that was evaluated was clinical deterioration within the first 48 hours. The secondary endpoint that was evaluated was hematoma enlargement at 24 hours.	The was no significant difference in early neurological deterioration, hematoma and edema growth, and clinical outcome at 90 days.	This study was not completely blinded. The sample size in the study was small.

Comment(s)

Spontaneous intracerebral hemorrhage is a condition that is seen in emergency departments across the United States. Many patients with intracerebral hemorrhage also have an elevated systolic blood pressure. Standard of care in many, if not all, emergency departments is to lower the systolic blood pressure using intravenous agents. One of the above papers reaffirms the current standard of care by showing that intensive blood pressure lowering is successful at attentuating hematoma growth while the other was unable to statistically show that. The Koch, et.al paper did, however, show that strict blood pressure control in acute intracerebral hemorrhage is accepted standard of care in hospitals around the United States.

Clinical Bottom Line

Intensive blood pressure lowering to a systolic blood pressure below 140 within 1 hour shows a decrease in hematoma growth over 72 hours according to one study that was evaluated. The other study evaluated did not show a statistical significance. Both papers reaffirmed the standard of care of blood pressure lowering in acute intracerebral hemorrhage.

References

1. Anderson S.C. , et.al Effects of Early Intensive Blood Pressure-Lowering Treatment on the Growth of Hematoma and Perihematomal Edema in Acute Intracerebral Hemorrhage. Stroke 2010;41:307-312
2. Koch, S., et.al. Rapid Blood Pressure Reduction in Acute Intracerebral Hemorrhage: Feasibility and Safety Neurocritical care 2008; 8(3):316-321