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G id li f BP t i ti t ith
AMOHOTOBAMOHOTOBKASR ALAINY KASR ALAINY 18271827
MEDICAL SCHOOLMEDICAL SCHOOL 3000 B.C.
Guidelines of BP management in patients with
acute stroke (neurologist perspectives)
PROF. SHERIF HAMDYKASR ALAINY
CAIRO UNIVERSITYCAIRO UNIVERSITY 1908
Incidence & Prevalence of Strokes in Upper Egypt
• Incidence found to be about ABOUT 1.8 PER 1000 PER YEAR , URBAN 1.5, SUBURBAN 1.8, RURAL 2.1 per 1000 per year
• Prevalence of Strokes: 5.08 per 1000 per 4
5
6
I id
5.085.85.4
4.1p p
year, URBAN 4.1, SUBURBAN 5.8, RURAL 5.4 per 1000 per year
0
1
2
3
URBAN Rural Suburban Total
IncidencePrevalence
Incidence Kandil et al. 2006
Dennis et al. 1989
Fogelholm et al. 1992
5
10
15
20
25
30
35
WINTERSPRINGSUMMERAUTUMN
31.7%27.7%
24.7%
13.8%
1.81.82.1
1.5
M.R. Kandil, H.N El-Tallawy, H.M Farawez, G. Khalifa, M. A. Ahmed, A. Hamed & A.M. Ali, EJNPN, 2006, META-ANALYSIS OF STROKE STUDIES IN EGYPT, EL-TAMAWY et al. ,EJNPN, 2007
Thromboembolic stroke
1.24/1000 1.3/1000 -
Cerebral hemorrhage
0.43/1000 0.43/1000
0.31/1000
Subarachnoid hemorrhage
0.19/1000 0.1/1000 -
TIAs 0.25/1000 0.35/1000
-
0
5
Winter Spring Summer Autumn
The Percentage of Strokes by season In Egypt
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Distribution of different stroke subtypes in Egypt
Hemorrhage MCAHemorrhageIschemiaThromboticEmbolic
Ischemia 78%Thrombotic 67.86%Embolic 10.14%
Cerebral Hemorrhage 22%Capsular 12%Lobar 4.5%Intraventricular 3%Subarachnoid 2.8%
MCAACAVBLacunar
MCA 73.7%ACA 10.5%Vertebro-basilar & Lacunar 15.8%
39
30
35
40
SexDistributionMaleFemale
MALES59.5%
FEMALES40.5%
2.1 3.8
13
26.5
16.1
0
5
10
15
20
25
% o
f pat
ient
s
<30 30-40 40-50 50-60 60-70 >70years
Sex Distribution in Egyptian Stroke patientsAge at Onset of Stroke
META-ANALYSIS OF STROKE STUDIES IN EGYPT, EL-TAMAWY & ,ABDGHANY. ,EJNPN, 2007
HIGH BLOOD PRESSURE in Egypt,
• The Epidemiology of intermediate phenotype 60
– Hypertension– Hyperlipidemia– Diabetes mellitus– Carotid stenosis
01020304050
HYPE25y
75yFEMA
MALE
Hypertension
Prevalence of Hypertension in Egypt 26.3% PERTENSION
y y MALES
LES26.3%– Prevalence in 25-34 years old is 7.8%– Prevalence in > 75 years old is 56.6%– Prevalence in females is 26.9%– Prevalence in males is 25.7%
Ibrahim M., Rizk H., Appel L. J., Results of the Egyptian National Hypertension Project NHP,1995
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The difference between stroke patients and controls as regard risk factors in Egypt
46%, 31.3%, 24,7%, 39.3%, 42%, 64%
17% 31 7%
Family History OR 11.925, 95%CI 6.84-20.79HYPERTENSION
10
20
30
40
50
60
70
patientscontrols
3
4
5
6
7 HTNHDSmokersDMTIAsHypercholesteremiaOb it U b
6.4% 18% 18.3%17% 31.7% HYPERTENSION
OR 3.836, 95%CI 2.539-5.796
0 FH PAS TIA DM HD HTN
Epidemiological profile in EgyptShalaby E., Helmy S., Douaa Elderwi, Naglaa Elsherbiny. 2004, Cairo university
0 20 40 60 80
1
2 Obesity UrbanObesity Rural
450 subjects150 stroke patients300 normal subjects
OR=11.925 2.07 2.89 3.53 3.84
METANALYSIS , ELTAMAWY et al., EJNPN 2007
Immediate outcome (at discharge) of cerebrovascular stroke patients admitted to neurology Department of Assiut University during one year (2003).
Total ImprovementOR
StationaryOR
DeteriorationOR
Death0R
100
200
300
400
500
600
700
800
900CVS
Ischemic
hemorrhagic
Outcome
No. % No % No % No % No %
Cerebrovascular stroke
825 100 474 57.4 50 6.1 80 9.7 221 26.8
Ischemic stroke 581 70.4 348 59.9OR
33 5.6 52 9.0 148 25.4
0
100
Total Improve Stationary Deteriorate Death
OR 1.398
Hemorrhagic Stroke
244 29.6 126 51.6 17 6.9 28 11.5 73 30.0OR
1.248
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RISK FACTORS
Sherif Hamdy 2010
AGE GENDER OBESITY CORNEAL ARCUSSEX EAR LOBE
CREASE
CERVICALBRUIT &
STENOSISPVDFAMILY H
STROKES
VON
SOCIALDEPRIVATION
PSYCHO-FACTORS
PHYSICAL HCT SEX ALCOHOL
INFECTION
LIPIDS
SNORING
DM
HOMO-CYSTEINE
HTN
VENTILATFUNCTION
FIBRINOGEN
SERUM ALBUMIN
DIET -WILLIBRANDFACTOR
TIAVASECTOMY
PHYSICALACTIVITY
AF
HCTVALUE
LVH
SEX HORMONES
HF
ALCOHOL INTAKE
MI
WBC
CONTROVERSIAL VIEWS• Hypertension occurs commonly after stroke even in patients without
history of HTN• BP is often elevated acutely and typically returns to baseline
spontaneously over the first week.• Both elevated and low BP are associated with high rates of early and
late death, A U shaped relationship between admission BP and death– Castillo et al. Stroke 2004; 35,2:520-526.
• Theoretical reasons in favor of lowering BP acutely are to reduce cerebral edema and to lessen the risk of hemorrhagic transformation
• Allowing BP to remains high, risks of develop the following in population already prone to
M di l i f ti– Myocardial infarction– Pulmonary edema– Renal failure
• However the acute management of BP is controversial.
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Hypertension within the first week of stroke
• Concerns of the impaired auto-regulation in the peri-infarct area will result in further reduction ofperi infarct area will result in further reduction of CBF with lowering BP
• PET within the first week after stroke, showed focal impairment of auto-regulationand reduction in MABP in the peri-infarct area
• CBF did fall in some patients with lowering BP• There was an upward shift of the auto-regulatory
curve as a consequence of chronic HTN– Powers et al. Stroke 2007; 38,2:506
AUTOREGULATORY CURVEBelow the lower level of autoregulation the brain loses its ability to maintain constant CBF and flow become pressure passive
CBF
HTN
p p
CPP
Diringer M.N. Continuum June 2009. vol15;3:121-137
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BP reduction• Larger BP reduction have been associated with
– early neurological worsening, ea y eu o og ca o se g,– larger infarct volumes, – Higher rates of poor outcome– Death
• American Heart Association guidelines for early management of ischemic stroke,
– Recommend treating – SBP > 220mm Hg or
DBP> 120mm HgAdams et al. Stroke 2007;38,5:1655-1711
Chronic BP
• Risk of exceeding an upward shifted lower li it f t l ti i th tti flimits of auto regulation in the setting of poorly controlled chronic hypertension , pre stroke BP status control data should to be used in decision making
• Continuing the anti-hypertensiveContinuing the anti hypertensive medications used for treatment of chronic HTN before stroke may be recommended
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Diffusion/Perfusion Mismatch
Red: Ischemic Red: Ischemic coreOrange: Diffusion wt imageBlue: Ischemic penumbraLight Blue: Perfusion wt image
Lee, et al., 2005
Early CT may be essential ELTOUKHY, et al., 2006 ,KASR ALAINY CAIRO UNIVERSITY
• Non-contrast CT scan is regarded as the most important early diagnostic tool in assessment of suspected acute stroke, to exclude hemorrhage and to demonstrateexclude hemorrhage and to demonstrate early infacrts
• CT perfusion scan CBF in grey matter 50-60mL/100g/min
• CBF 35mL/100g/min 50-60% of normal values: protein synthesis within neurons ceases
• CBF 20mL/100g/min 30-40% of normal values: synaptic transmission is disturbed, loss of function of neurons, Tissue At Risk
• CBF 10mL/100g/min <20% of normal values, leads to irreversible cell death
• REPERFUSION of Tissue At Risk , can ,lead to complete regeneration of neuronal function
• MRI is more sensitive and superior, FLAIR study , Diffusion-Perfusion wt images should be included in a rapid protocol in assessment of patients with suspected acute stroke
CBF CBV
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--Avoid dropping of BPAvoid dropping of BP
--Loss of autoregulation of Loss of autoregulation of cerebral blood pressurecerebral blood pressure
--Drop of BP will result in Drop of BP will result in decrease cerebral blood decrease cerebral blood flow.flow.
--Drop of BP will lead to Drop of BP will lead to
National Stroke Research Institute
increase infarction size more increase infarction size more marked in marked in PENUMBRAPENUMBRA areaarea
BP MANAGEMENT• Low BP (< 120/80 mmHg):
• withhold antihypertensive treatment
• Extreme hypertension (>200/120 mmHg):
• optimize environment, bed rest, • IV fluids
• Normal BP – mild elevation (120-160 / 80-95 mmHg):
• optimize environment, bed rest, pain control if appropriate
• no pharmacological intervention needed
• Moderate to severe elevations (160-200 / 95-120 mmHg):
optimi e en ironment bed rest
ppain control if appropriate
• cautious lowering of BP, consider:
» IV labetalol, atenolol» IV enalapril» IV verapamil» IV hydralazine» transdermal GTN» continuos infusion (GTN,
sodium nitroprusside, fenoldopam)
» review for other drugs with possible effects on
• optimize environment, bed rest, pain control if appropriate
• consider additional oral antihypertensives
BP
Geoffrey A. 2003
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Handling blood pressureHandling blood pressure
--The general advice is to avoid to lower blood The general advice is to avoid to lower blood pressure at the initial period of an ischemic stroke.pressure at the initial period of an ischemic stroke.
--The sole exceptions are:The sole exceptions are:
--Cardiac insufficiency or ischemiaCardiac insufficiency or ischemia
--Aortic dissectionAortic dissection
Acute Renal shutAcute Renal shut down & failuredown & failure--Acute Renal shutAcute Renal shut--down & failuredown & failure
--Hypertensive encephalopathyHypertensive encephalopathy
--Maintain the antihypertensive drugs which Maintain the antihypertensive drugs which
were used before.were used before.
Antihypertensive treatment in Antihypertensive treatment in acute ischemic strokeacute ischemic stroke
•• STRATEGYSTRATEGY11--SBP > SBP > 220 220 mm Hg and ormm Hg and orgg
DBP > DBP > 120 120 mm Hgmm Hgaa-- Capopril Capopril 66..2525--1212..5 5 mg orally parenterallymg orally parenterallybb-- Labetol Labetol 55--20 20 mg I.V.mg I.V.cc-- Urapidil Urapidil 1010--20 20 mg I.V. followed bymg I.V. followed by
44--8 8 mg I.V. mg I.V. 22-- DBP > DBP > 140 140 mm Hgmm HgNitroglycerin Nitroglycerin 5 5 mg I.V. followed by mg I.V. followed by 11--4 4 mg/h I.V.mg/h I.V.
33-- NO TREATMENTNO TREATMENT Systolic BP Systolic BP 220220--240 240 mmHgmmHgDiastolic BP Diastolic BP 120120--130 130 mmHgmmHg
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Management of BP after treatment with rt-PA
• Monitor BP– Every 15 min for 2 hrs after treatmente y 5 o s a te t eat e t– Then every 30 min for 16 hrs
• Treat HTN if– SBP > 180 mm Hg OR– DBP >105 mm Hg
• Choice of agents – Labetalol 10 mg IV over 1-2 min up to 2.5-5 mg everyLabetalol 10 mg IV over 1 2 min up to 2.5 5 mg every
5 min to max 15mg/hr– Nicardipine infusion– Hydralazine– Enalapril
Hypertensive encephalopathy, Eclampsia & reversible posterior Leukoencephalopathy
in hypertensive crisis BP should be lowered but,hypertension should not be lowered unless– End organ failure e.g.
microscopic hematuria, oliguria, congestive heart failure, cardiac ischemia
– Administration of tissue plasminogen activatorplasminogen activator
– MABP should be lowered no more than 20-25% in 1-2 hrs over the ensuing hrs to days
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INTRACEREBRAL HEMORRHAGE
• Chronic HTN is a major risk factor for spontaneous ICH in most patients even inspontaneous ICH in most patients, even in absence of a history of HTN
• Systemic HTN is commonly seen in the first 24hrs and associated with poor outcome
• While HTN is easily measured and treated, it is unclear whether its treatment will lead tois unclear whether its treatment will lead to improve the outcome or not
BLOOD PRESSURE & INTRACEREBRAL HAEMORRHAGE
• Elevated BP is also observed with intra b l h t i b t it icerebral hematoma expansion, but it is
not known whether it a cause or effect• While a lower BP may decrease the rate
of bleeding, it may also reduce the rate of CBF to ischemic or hypo-perfusedof CBF to ischemic or hypo perfused neurons
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Intra-cerebral hemorrhageCerebellum
ThalamusPONS
BG LOBAR
CPP, ABP, ICP , CVR and vessel caliber
• Cerebral perfusion pressure CPP
• CPP = MABP ICP
CRITICAL CARE NEUROLOGYVolume 12 Number 1 February 2006
• CPP = MABP – ICP• Normotensive autoregulate
between CPP between 50-150mm Hg
• CVR cerebrovascular resistance is primarily at arteriole level
• CBF = CPP / CVR cerebro-vascular resistance
• CCP should be maintained 70-100mm Hg
• The goal of therapy is to lower to a mean BP to 100-130 mm Hg
• Lower blood pressure may be poorly tolerated
Becker K, Continuum, 2006;12,1: 30-45
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Mean ABP
• Although, it may be a cause of the hemorrhage , it is simply may be a reflection of chronic ofit is simply may be a reflection of chronic of – Chronic HTN– The brain attempt to maintain cerebral perfusion
pressure CPP in response to sudden ICT– Pain, anxiety and sympathetic activation
• Even without treatment BP tends to decline toEven without treatment, BP tends to decline to baseline levels during the first 7-10 days after hemorrhage
MABP is > 120mm Hg in over than 2/3 of patients with ICH, > 140mm Hg in over than 1/3 of patients with ICH
Carlberg et al. 1993
Controversy
• Reasons to treat HTN– Risk of hematoma expansion– Systemic risks, Heart , kidney , blood vessels
• Reasons not to treat HTN– Ongoing peri- hematoma ischemia
Risk of inducing ischemia– Risk of inducing ischemia– Impaired autoregulation
Diringer M.N. Continuum June 2009. vol15;3:121-137
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AUTOREGULATORY CURVEBelow the lower level of autoregulation the brain loses its ability to maintain constant CBF and flow become pressure passive
CBF
HTN
p p
CPP
Diringer M.N. Continuum June 2009. vol15;3:121-137
ISCHEMIC PENUMBRA IN HEMATOMA EXPANSION
• Concepts was believed that ischemic penumbra may be a consequence of hematoma
• Determinant factors– Level of HTN
consequence of hematoma compresses surrounding tissues with reduced CBF
• PET, SPECT & MRI Findings , it was not associated with increased oxygen extraction , findings indicative of metabolic suppression rather than ischemia
– LABILITY of BP– Staff familiarity of
antihypertensive agents – Co-morbidity– Chronicity of HTN & left LVH– Retinopathy– Signs of acute cardiac ischemia– HFischemia
• Goal should be optimizing perfusion, not treating hypertension, and treating increased ICP
Diringer M.N. Continuum June 2009. vol15;3:121-137, Anderson et al., Lancet Neurol. 2008; 7,5:391-399
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ATACH, INTERACT, INTERACT 2
– ATACH• HTN after ICH
– Early aggressive reduction BP may
• PILOT , 60 PTS• NICARDIPINE
– INTERACT• Randomized, open label• 400 PTS• Intensive BP reduction
– INTERACT 22800 PTS
reduce risk of hematoma expansion
– MAP 100mm Hg AVOIDE REDUCTION
– MAP over 120mm Hg 10-15% may be reasonable
• 2800 PTS• AGGRESSIVE BP
reduction • Furosemide, urapidil,
phentolamine
– Modest reduction of BP 15%-20% may not increase ischemia
Anderson et al., Lancet Neurol. 2008; 7,5:391-399
Recommendations differs from American Stroke
Association Guidelines– Bolus administrationBolus administration
of Labetalol, Furosemide , urapidil, enalaprilat , metoprolol, hydralazine, phentolamineContinuous drip Ca
–– Agents that are Agents that are Venodilators such as Venodilators such as Na Nitroprusside or Na Nitroprusside or nitrates should not be nitrates should not be used because their used because their tendency to increase ICPtendency to increase ICP– Continuous drip Ca
Channels Blockers nicardipine , clevidipine NEW‼
Anderson et al., Lancet Neurol. 2008; 7,5:391-399
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Guidelines in the first few hours of acute stroke with intracerebral
hemorrhage • Hypertension
– SBP > 230mm Hg or DBP >140 mm Hg on two– SBP > 230mm Hg or DBP >140 mm Hg on two readings 5 min apart
• Institute nitroprusside or nicardipine – SBP 180-230mm Hg or DBP 105-140mm Hg or
MABP 130mm Hg or greater on two readings 20 min apart
• Institute labetolol, esmolol, nicardipine or enalapril• avoid oral or sublingual nifedipine
– SBP > 180mm Hg or DBP > 105 mm Hg• Defer anti-hypertensive unless coronary ischemia suspected
– CPP should be maintained > 70mm Hg at all times
American stroke association guidelines
Hypotension in ICH• The etiology of hypotension should be
establishedestablished• Volume replenishment is the first approach• If hypotension persists after correction of volume
deficit, continuous perfusion of vasopressors should be considered, particularly for SBP less than 90 mm Hg– Phenylephrine 2mcg/kg/min to 10mcg– Dopamine 2mcg/kg/min to 20mcg– Noepinephrine 0.05mcg/kg/min to 0.2mcg
American stroke association guidelines
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Conclusions •• Avoid dropping of BPAvoid dropping of BP• BP is often elevated acutely and typically returns toBP is often elevated acutely and typically returns to
baseline spontaneously over the first week in strokes.
• Even without treatment, BP tends to decline to baseline levels during the first 7-10 days after cerebral hemorrhage
• Choice of agents e.g. Labetalol, Hydralazine, Enalapril, or Nicardipine infusion
• Venodilators such as nitrates should not be used because their tendency to increase ICP
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