STRATEGIES FOR BP MANAGEMENT

Akshal S. Patel, MD

Swedish Neuroscience Institute

No disclosures, no conflicts of interest

■ Not bought and paid for

GOALS

Review BP management in the setting of ICH

Review BP management in the setting of MT

Overview of ICH

■ Hemorrhagic, intraparenchymal

■ Non-traumatic

■ Distinct from SAH or IVH

Not All Hemorrhages are Created Equal

Primary

■ HTN (60-70%)

■ CAA

■ CADASIL

■ Coagulopathy

■ Drug abuse

Secondary

▪ Vascular lesions

▪ AVM, DAVF

▪ Vasculopathy

▪ Ischemic stroke

▪ Post-tPA

▪ HT

▪ CVST

▪ Trauma

▪ Tumor

Hypertensive ICH

■ Rupture of small arterioles (<100 micron)

■ Typically in penetrating arteries

■ Deep structures

Thalamic Cerebellar Pontine Ganglionic

Mechanisms of Injury

▪ Primary

– Tissue dissection

– Displacement and brain herniation

▪ Secondary

▪ Perihematomalinjury

▪ Hematoma expansion

▪ Cellular toxicity

Hematoma Expansion

Hemphill, 2008

Hematoma Expansion

▪ Expansion not uncommon

▪ No longer just seen with AVMs or coagulopathy

▪ 72% have some expansion over 24h

▪ 38% have more than 33% expansion first 24h

▪ Usually clinically significant

▪ Within 1 hr in ¼ of cases

▪ Hematoma expansion worsens outcome

Davis et al., Neurology 2006

Brott et al., Stroke 1997

Hematoma Expansion

Kazui et al., Stroke 1997

Jauch et al., Stroke 2006

Powers et al., Neurology 2001

■ Mechanism unknown

– Elevated BP?

■ Elevated GLU on admission & SBP>200 mm Hg

■ Acute NCP gtt in small-to-med ICH

– MAP lowering of 15% does not affect global or peri-hematomal PET-CBF

– Preserved autoregulation– Perihematoma coagulopathy/DIC?

“Spot Sign”

Goldstein et al., Neurology 2007

CTA or CECT

BP Control

Anderson et al., Lancet Neurol 2008

•95% of 404 pts in China

•SBP<180 vs. SBP<140 if SBP 150-220 on presentation x2

•Decreased hematoma expansion

•No clinical efficacy signal

INTERACT

ATACH, Crit Care Med 2010

■ 170-200 (n=18)

– One (6%) deterioration; three (17%) died

■ 140-170 (n=20)

– Two (10%) deterioration; one (5%) SAE; two (10%) died

■ 110-140 (n=22)

– Four (18%) neuro deterioration, three (14%) SAE; five (23%) died

BP Control

Anderson et al., NEJM 2013

BP Control

•2794 pts, multicenter

•SBP<140 (intensive) v SBP<180 within first hour

•mRS 3-6 was primary outcome

•719 of 1382 (52.0%) v 785 of 1412 (55.6%) had a primary outcome event (OR 0.87; 95% CI 0.75 to 1.01)

•Same mortality

•Ordinal analysis showed improved functional outcomes with intensive treatment (mRS shift)

INTERACT 2

Anderson et al., NEJM 2013

BP Control

Qureshi et al., NEJM 2016

BP Control

•1000 pts, multicenter, GCS >4

•SBP<140 (intensive) v SBP<180 within 4.5 hours of symptom onset with IV nicardipine

•mRS 4-6 was primary outcome

•38.7% (186 of 481) v 37.7% (181 of 480), RR 1.04; 95% CI 0.85 to 1.27

•More renal adverse events in intensive group (9.0% vs. 4.0%, P=0.002)

ATACH 2

Qureshi et al., NEJM 2016

The Devil in the Details

Blood Pressure Variability (BPV)

■ Failure of two RCTs to answer the

question

■ The question was maybe too simple

■ FAST-MAG trial

INCREASED VARIABILITY

F

A

v

O

R

A

B

L

E

O

U

T

O

C

M

E

A decade agoIV tPA (tissue

type plasminogen

activator)

Administered within 4.5%

hours of symptom onset

Devices successful 30-

45% of the time

IV tPAsuccessful 30-

40% of the time

49 yo M, Pre-stoke mRS 0, LKN 3h, ASPECTS 8

0

10

20

30

40

50

60

70

80

90

100

MR RESCUE IMS III MR CLEAN REVASCAT ESCAPE EXTEND-IA SWIFT PRIME

Outcomes and Revascularization

%TICI 2b/3 %mRS 0-2 % Strever Use

BP Control

■ 217 acute ischemic patients with LVO, retrospective analysis

Goyal et al. Neurology 2017

BP Control

Fluctuations in BP or “BPV” during and shortly after MT maybe critical

GA vs. Conscious sedation

Bennet et al. JNIS 2017 and Simonsen et al. JAMA 2018

Future Directions: Transcranial Doppler Monitoring

Representative images of a middle-aged patient with acute middle cerebral artery (MCA)

occlusion.

Kneihsl et al. JNIS 2017

BP control

■ What’s next?