Neuro Critical Care - Blood pressure and Intracranial Haemorrhage: Celia Bradford
Join Celia Bradford as she discusses blood pressure control in intracranial haemorrhage in neuro critical care. Intracranial haemorrhage risk factors include hypertension. The question becomes, what do you do with hypertension in the management of intracranial haemorrhage? Does blood pressure being high cause the bleed to be more severe or does a severe bleed cause increased blood pressure? It is a classic chicken or egg scenario. Celia takes you through two prominent trials in the area and gives you valuable and practical tips on how to manage these patients. The INTERACT-1 trial looked at haematoma expansion in two groups randomised to blood pressures of <180mmHg or <140mmHg systolic. This trial suggested benefit in patients treated with more aggressive blood pressure control. INTERACT-2 was a much larger trial looked at controlling blood pressure within 6 hours in patients with blood pressures between 150-220mmHg systolic. They used the same parameters for two groups (<180mmHg or <140mmHg systolic) and the results were less clear when comparing intensive and standard blood pressure control targets. ATACH-2 also looked at outcomes of tight control of blood pressure control. Two groups were randomised to 110-140mmHg or 140-180mmHg. This study demonstrated no benefit to more aggressive control of blood pressure and the group with more intensive treatment had worse renal outcomes. There were also some issues with the study that Celia discusses. There is an unanswered question in that controlling blood pressure too aggressively may impact the penumbra (which may or may not exist!) Celia’s thinking from all of this? Aim blood pressure targets low but not too low (130-150mmHg). Aim for smooth control. Chose agents with a rapid onset of action and avoid agents such as SNP/GTN. For more like this, head to our podcast page. #CodaPodcast
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Neuro Critical Care - Blood pressure and Intracranial Haemorrhage: Celia Bradford
- 1. PRESSURE DOWN B L O O D P R E S S U R E M A N A G E M E N T A F T E R I N T R A C E R E B R A L H A E M O R R H A G E Dr Celia Bradford Intensivist Royal North Shore Hospital Sydney Australia @celiabradford
- 2. C A S E C O U R T E S Y O F A . P R O F F R A N K G A I L L A R D, R A D I O PA E D I A . O R G , R I D : 2 7 6 4
- 4. BP???
- 7. H A E M ATO M A G R O W T H K A Z U I E T A L S T R O K E 1 9 9 6 2 7 : 1 7 8 3
- 10. INTERACT I N T E R A C T - 2 N E J M 3 6 8 ; 2 5 J U N E 2 0 2 0 1 3 INTERACT 2 -within 6 hours -BP 150-220mmHg -2839 patients -anti-HT Rx intravenous treatment and therapy with oral agents were to be initiated according to prespecified treatment protocols BP < BP <
- 11. INTERACT-2 90-day mRS 3–6 (52.0% vs. 55.6%, OR 0.87, 95% CI 0.75–1.01),
- 12. ATACH ATA C H - 2 N E J M 3 7 5 : 1 1 S E P T 2 0 1 6 ATACH-2 -within 4.5 hours (changed) -iv nicardipine -baseline BP >150mmHg BP 110-139mmHg BP 140- 179mmHg
- 13. 1 2 % I N I N T E N S I V E G R O U P D I D N OT A C H I E V E TA R G E T
- 14. ATA C H – 2 R E S U LT S 9 0 D AY M R S 4 - 6 ( 3 8 . 7 % V S 3 7 . 7 % , R R 1 . 0 4 C I 0 . 8 5 - 1 . 2 7 )
- 15. ATACH-2 *CHANGED ENTRY CRITERIA *STOPPED EARLY DUE TO FUTILITY *INTENSE GROUP HAD HIGHER RATES OF ADVERSE RENAL EVENTS (9% VS 4%)
- 16. WHAT TO DO WITH THE BP
- 17. 1 / A I M L O W B U T N O T T O O L O W ( 1 3 0 - 1 5 0 M M H G ) 2 / A I M F O R S M O O T H C O N T R O L ( A C H I E V E D B E S T W I T H I V A G E N T S , E G N I C A R D I P I N E , H Y D R A L A Z I N E ) 3 / R A P I D O N S E T O F A C T I O N 4 / A V O I D A G E N T S S U C H A S S N P/ G T N SUMMARY
Editor's Notes
- TODAY I’d like to give you a brief summary of blood pressure management in patients following ICH
- You’re on duty in the Intensive Care and a case is being referred up from the Emergency Department. The patient has an Intracerebral Haemorrhage in the classic basal ganglia territory.
- You recall that haemorrhagic stroke accounts for about 20% of strokes This is higher in Asian populations and may be up to 50%
- You realise that high blood pressure is associated with higher mortality following ICH but the question is: Does reducing the blood pressure improve outcome
- In addition high BP is associated with increase haematoma size AND Variability in systolic BP is also associated with increased haematoma size But which is the chicken, which is the egg? It is not known whether the increase in bleed size causes higher BP OR if the higher BP causes increased clot size
- Imaging studies suggest that growth in haematoma is most likely to occur early after symptom onset
- Does controlling BP following ICH help? 1/Does it improve survival and functional status 2/Is it safe? Concerns about reducing regional cerebral blood flow do not seem to be warranted 3/Is it feasible?
- Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial The pilot trial enrolled 404 patients with ICH within 6 hours showed that early intensive BP lowering (target SBP 140 mm Hg) vs. SBP<180 mm Hg was safe and might reduce the risk of hematoma expansion INTERACT2;phase III trial enrolling 2,839 patients with ICH within 6 hours. Intensive SBP lowering <140 mm Hg compared to SBP<180 mm Hg did not significantly reduce the primary endpoint of 90-day mRS 3–6 (52.0% vs. 55.6%, OR 0.87, 95% CI 0.75–1.01), but had a favorable shift on the 90-day mRS distribution (OR 0.87, 95% CI 0.77–1.00), which was a prespecified analysis. Between the two groups, the rate of all-cause death was comparable (0.99, 0.79–1.25), and the contribution of ICH to death was also comparable. Intenisve BP lowering increased neither neurological deterioration within 24 hours (0.95, 0.77–1.17) nor non-fatal serious adverse events
- No difference in primary endpoint of a MRS of 3-6 at Day 90 When an ordinal analysis conducted (which was a prespecified endpoint) the difference was marginally significant)
- The Antihypertensive Treatment of Acute Cerebral Haemorrhage (ATACH) feasibility trial also showed that acute BP lowering down to SBP 110–140 mm Hg with intravenous nicardipine was safe and feasible
- No difference in the primary endpoint of 90-day mRS 4–6 (38.7% vs. 37.7%, RR 1.04, 95% CI 0.85–1.27) and the rate of hematoma expansion >33% at 24 hours (18.9% vs. 24.4%; 0.78, 0.58–1.03). The intensive BP lowering group had more renal adverse events within 7 days (9.0% vs. 4.0%, P=0.002). The achieved SBP at 2–3 hours after randomization was around 120 mm Hg in the intensive arm and 140 mm Hg in the standard arm. Therefore, the ATACH-2 results suggest that a desirable SBP target would be 140 mm Hg and very aggressive SBP lowering down to 120 mm Hg seems unnecessary
- SNP: can increase ICP, may increase size of haematoma due to venodilation, BP variability more likely