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CME
Year : 2013  |  Volume : 25  |  Issue : 2  |  Page : 111-115

Hypertension in acute stroke ( a management dilemma Hypertension in acute stroke)


Department of Internal Medicine, Emergency Unit, Cairo University, Cairo, Egypt

Date of Submission29-Mar-2013
Date of Acceptance17-Apr-2013
Date of Web Publication4-Jul-2014

Correspondence Address:
Amany A.M. Sholkamy
Department of Internal Medicine, Emergency Unit, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.7123/01.EJIM.0000431462.25347.09

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How to cite this article:
Sholkamy AA, Salem M, Bahgat M. Hypertension in acute stroke ( a management dilemma Hypertension in acute stroke). Egypt J Intern Med 2013;25:111-5

How to cite this URL:
Sholkamy AA, Salem M, Bahgat M. Hypertension in acute stroke ( a management dilemma Hypertension in acute stroke). Egypt J Intern Med [serial online] 2013 [cited 2019 Jul 23];25:111-5. Available from: http://www.esim.eg.net/text.asp?2013/25/2/111/135872

Hypertension in acute stroke

Amany A.M. Sholkamy, Mohamad Salem and Magy Bahgat

Department of Internal Medicine, Emergency Unit, Cairo University, Cairo, Egypt

Correspondence to Amany A.M. Sholkamy,

Department of Internal Medicine, Emergency Unit, Cairo, Egypt

Tel: + 20 122 356 7784;

e-mail: doc_amany@yahoo.com

Received 29 March 2013 Accepted 17 April 2013

A 55-year-old patient presented to the emergency depart­ment with acute right-sided hemiparesis and drowsiness. His pulse was 100 bpm and blood pressure (BP) was 220/ 120 mmHg. He had no history of ischemic heart disease or renal impairment and was not diabetic.

What would be the initial approach in view of this marked elevation in BP?

To manage any patient with acute stroke you have to answer two important questions:

  1. Does this patient have ischemic or hemorrhagic stroke?
  2. If the patient has ischemic stroke, is he a candidate for thrombolytic therapy or not? and if he has a hemorrhagic stroke, what are the indications for surgery?


Management of hypertension in acute ischemic stroke

Magy Bahgat

Department of Internal Medicine, Emergency Unit, Cairo University, Egypt

The treatment of arterial hypertension immediately after stroke is problematic. Observational studies have found that a rapid and steep reduction in BP during the first 24 h after stroke onset might be harmful [1,2].


  Pathophysiologic basis Top


Two important pathophysiologic processes should be con­sidered during management of acute stroke. These are:

  1. Impaired cerebral autoregulation.
  2. Increased intracranial pressure (ICP).


(a) Impaired cerebral autoregulation

CBF=(CAP - JVP)/CVR,

where CBF is the cerebral blood flow, CAP is the carotid

artery pressure, JVP is the jugular venous pressure, and CVR is the cerebrovascular resistance.

CBF is maintained relatively constant through autoregu­lation of CVR. Autoregulation of CVR can become dysfunctional during stroke. Under this condition, the brain will be very sensitive to even minor changes in cerebral perfusion pressure (CPP) [3,4].

Another important consideration is that the set-point for cerebral autoregulation is altered in chronic hypertension and the cerebral autoregulation curve is shifted toward the right. This means that CBF can be maintained at a constant level at higher BPs. Acute reductions in BP, even if in within the normal ranges, will lead to a decrease in CBF [as mean arterial pressure (MAP) will lie on the steep part of the cerebral autoregulation curve] and the development of ischemic symptoms in patients with chronic hypertension [3].

(b) Increased ICP

ICP is often increased in cases of intracerebral hemor­rhage, large infarction, or brain edema. An increase in MAP may be the only means of maintaining CPP above 60-70 mmHg, the level necessary to maintain perfu­sion [5].

CPP=MAP-ICP,

where CPP is cerebral perfusion pressure, MAP is the mean arterial pressure, and ICP is the intra-cranial pressure.

In patients with ischemic stroke, perfusion pressure distal to the obstructed vessel is low, and the distal vessels are dilated. Thus, elevated BP is necessary to maintain brain perfusion in borderline ischemic areas [6]. Lowering of BP in patients with acute ischemic stroke has been associated with clinical deterioration.


  The guidelines Top


For patients with acute ischemic stroke who are not eligible for thrombolytic therapy, the November 2010

DOI: 10.7123/01.EJIM.0000431462.2534 7.09

American Heart Association/American Stroke Association guidelines [7] are as follows:

  1. For patients with a systolic blood pressure (SBP) of 220 mmHg or less and a diastolic blood pressure (DBP) of 120 mmHg or less, BP should 'not' be treated acutely unless hypertension is extreme (SBP4220mmHg or DBP4120mm Hg) or the patient has active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalo-pathy, acute renal failure, or preeclampsia/eclampsia.
  2. For patients with SBP greater than 220mmHg or DBP between 121 and 140 mmHg, a cautious attempt at lowering the BP by B15% during the first 24h after stroke onset should be made. Guidelines suggest that antihypertensive medications should be restarted at B24h after stroke onset in patients with pre-existing hypertension who are neurologically stable.



  Further management Top


If BP is not maintained at or below 185/110 mmHg, do not consider administering recombinant tissue plasmino-gen activator (rtPA).

During and after thrombolytic therapy, BP should be maintained below 180/105mmHg for at least 24h.

Thrombolytic therapy [7]:

The sooner the rtPA is initiated the more likely it is to be

beneficial.

Indications for thrombolytic therapy in acute stroke



(1) Acute ischemic stroke within 4.5h of symptom onset.

(2) Exclusion of hemorrhage through a baseline com­puted tomography scan obtained before initiation of therapy.

  1. The only Food and Drug Administration-approved thrombolytic therapy for ischemic stroke is rtPA at a dose of 0.9 mg/kg (max. 90 mg): 10% as an intra­venous bolus, followed by 90% as a 60-min infusion. Antiplatelets and anticoagulants should be avoided for 24h after lytic therapy.
  2. The main concern as regards thrombolytic therapy is the risk for bleeding, and the most feared complication is symptomatic intracranial hemorrhage. Before lytic therapy is initiated, treatment is recommended so that BP is less than 185/110 mmHg.
  3. Criteria for thrombolytic therapy are restrictive, and only 1-2% of patients with acute stroke receive thrombolytic therapy.



  Remember Top


  1. BP management in the acute phase of stroke is different from chronic therapy.
  2. Acute BP lowering due to impaired cerebral auto-regulation and, often, increased ICP should be avoided.
  3. BP should be cautiously reduced by B15% within the first 24h after stroke onset.
  4. Short-acting nifedipine should be avoided because it can cause a prolonged and precipitous decline in BP [8].


References

  1. Castillo J, Leira R, Garc΄ύa MM, Serena J, Blanco M, Da΄valos A. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke 2004; 35:520-527.
  2. Oliveira Filho J, Silva SCS, Trabuco CC, Pedreira BB, Sousa EU, Bacellar A. Detrimental effect of blood pressure reduction in the first 24 h of acute stroke onset. Neurology 2003; 61:1047-1051.
  3. Goldstein LB. Acute ischemic stroke treatment in 2007. Circulation 2007; 116:1504-1514.
  4. Kaplan NM. Management of hypertensive emergencies. Lancet 1994; 344:1335-1338.
  5. Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF. Spon­taneous intracerebral hemorrhage. N Engl J Med 2001; 344:1450-1460.
  6. Aiyagari V, Gorelick PB. Management of blood pressure for acute and recurrent stroke. Stroke 2009; 40:2251-2256.
  7. Jauch EC, Cucchiara B, Adeoye O, Meurer W, Brice J, Chan YYF, et al. Part 11: Adult stroke: 2010 American Heart Association Guidelines for Cardio-pulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122 (Suppl 3): S818-S828.
  8. Adams HP Jr, Del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and quality of Care Outcomes in Research Interdisciplinary Working Groups. Stroke 2007; 38:1655-1711.


Management of hypertension in hemorrhagic stroke

Amany A.M. Sholkamy

Department of Internal Medicine, Emergency Unit, Cairo University, Cairo, Egypt

In reference to the above-mentioned presented case:

  1. The patient presented to the emergency department with acute right-sided hemiparesis, drowsiness, and a marked elevation in blood pressure (BP).
  2. The differential diagnosis in the presence of lateralization is usually either hemorrhagic stroke or ischemic stroke.
  3. Elevation of the BP frequently occurs in patients with acute intracerebral hemorrhage (ICH). The degree of elevation in BP is usually greater than that seen in patients with ischemic stroke [1].
  4. Potential pathophysiologic mechanisms for this marked elevation in BP include stress activation of the neuroendocrine system (sympathetic nervous system, renin-angiotensin axis, or glucocorticoid system) and increased intracranial pressure [2].
  5. In view of the marked BP elevation in the present case; the diagnosis may be a hemorrhagic stroke. However, until brain computed tomography (CT) is performed, there is no clear evidence that will help us differentiate between hemorrhagic and ischemic stroke.


(1) Pathophysiologic basis

Mechanisms of brain injury in ICH


Several mechanisms contribute to brain injury:

  1. Primary direct mechanical injury to the brain parenchyma by the expanding clot.
  2. Increased intracranial pressure (ICP).
  3. Herniation secondary to mass effect.


Both clot volume and secondary perilesional edema contribute to the mass effect [3].

Serial CTscans in patients with hypertensive hemorrhage have shown that the hemorrhage enlarges in the first 6 h after presentation in a subset of patients. In a prospective series of 103 patients with ICH, significant hematoma growth (a >33% volume increase) occurred in 38% of patients over the first 24 h.

Pathologic studies before CT scanning found that bleeding points occurred at the rim of the hemorrhage and postulated that this new recruitment of bleeding sites would lead to enlargement of the clot. As the clot expands, surrounding vessels are stretched, causing new sites of vessel rupture. Although the precise mechanism of hematoma enlargement is not yet defined and may be heterogeneous; blood-brain barrier breakdown and dysre-gulation of hemostasis through inflammatory cascade activation is common. Overexpression of IL-6 and matrix metalloproteinases, are probably important pathways.

In addition, the volume of the clot is very important in determining the outcome in patients with ICH, espe­cially during the first 24 h [4].

The conflict:

Severe elevations in BP may worsen ICH by causing bleeding and hematoma enlargement [5].

Enlargement of the hematoma is associated with neurologic deterioration and worse outcomes. These observations indicate that significant improvements in patient outcome from ICH can be achieved by minimizing hematoma enlargement [6].

However,

(1) An increased mean arterial pressure may be necessary to maintain cerebral perfusion in some patients, and lowering the arterial pressure [e.g. to a systolic blood pressure (SBP) <130 mmHg] may cause ischemic changes in the area surrounding the hematoma and worsen neurologic injury. Decreased blood flow to the area surrounding the clot causes local neuronal ischemia, which leads to further cytotoxic edema and release of toxic excitatory amino acids and inflammatory mediators [7,8].

Studies have been carried out in that respect:

  1. Limited prospective data are available on BP manage­ment in ICH.
  2. In a randomized controlled trial [INTensive Blood Pressure Reduction in Acute Cerebral Hemorrhage
  3. trial (INTERACT)] on 404 patients with acute spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg), compared with traditional management (target SBP 180 mmHg), was associated with a reduction in hematoma growth at 24 h (14 vs. 26%). The study showed that SBP greater than 140-150 mmHg within 12h of ICH is associated with more than double the risk of subsequent death or dependency [9,10].
  4. The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial further confirmed these findings [11].
  5. Smaller, nonrandomized studies have also found that more aggressive BP lowering is associated with strong trends toward reduced hematoma enlargement. Some studies also showed trends toward reduced peri-lesional edema and better clinical outcomes [12].


The guidelines

The INTERACT and ATACH studies now represent the best available evidence to help guide decisions on BP lowering in ICH. Although these studies have shown that intensive BP lowering is clinically feasible and potentially safe, the BP pressure target, duration of therapy, and whether such treatment improves clinical outcomes remain unclear ([Table 1]).
Table 1: Suggested recommended guidelines for treating elevated BP in spontaneous ICH

Click here to view


(1) These guidelines also concluded that in patients presenting with an SBP of 150-200 mmHg, acute lowering to 140 mmHg is probably safe. They stated that the target for SBP should be 140 mmHg. However, this recommendation was labeled as Class IIa; Level of Evidence: B [13].


  Further management of acute hemorrhagic stroke: Top


(1) Antihypertensive drugs: labetalol is the drug of choice [14].

(2) Surgical management: the indications for surgery in patients with ICH vary with the site of the bleed. Intracerebral hemorrhage may be:

  1. Cerebellar.
  2. Supratentorial.
  3. Intraventricular.


Cerebellar hemorrhage

(1) Surgical removal of the hemorrhage by cerebellar decompression should be performed under the following conditions:

  1. If the hemorrhage is greater than 3cm in diameter.
  2. If there is clinical deterioration.
  3. If there is brainstem compression and/or hydro-cephalus due to ventricular obstruction [13].


Surgery decreases the risk for brainstem compression and obstructive hydrocephalus [13].

Supratentorial hemorrhage

  1. Surgery is controversial.
  2. It should not be considered either for patients who are fully alert or for those who are deeply comatose.
  3. It should only be considered as a life saving procedure to treat refractory increases in intracranial pressure; even under these circumstances, decisions should be addressed on a per patient basis [15].


Features that support performance of surgery include:

  1. Recent onset of hemorrhage.
  2. Ongoing clinical deterioration.
  3. Location of the hematoma near the cortical surface.


Features in favor of less aggressive therapy include:

  1. Serious concomitant medical problems.
  2. Advanced age.
  3. Stable clinical condition.
  4. Remote onset of hemorrhage.
  5. Inaccessibility of the hemorrhage.


Open craniotomy is the method of choice [16].

Intraventricular hemorrhage

Patients with neurologic deterioration in the setting of ventricular enlargement may be candidates for ventriculo-stomy and external ventricular drainage [17].


  Conclusion Top


The management should be rapid and decisive. As stated before 'time is brain'. The management dilemma on whether to lower the BP or keep it as such will continue until we perform CTscanning of the brain for this patient

to determine whether he has ischemic (do not lower the BP) or hemorrhagic stroke (aggressively lower the BP).

Diagnosing intracranial hemorrhage on clinical grounds is very imprecise; hence, neuroimaging studies using CT or MRI are critical to help guide BP therapy in stroke patients. According to the 2010 American Heart Associa­tion/American Stroke Association guidelines, CT should be performed within 25 min and CT interpretation should be available within 45 min of the patient's arrival at the emergency room [7].

The question on whether we are allowed to intervene or manage BP before obtaining a CT scan of the brain remains. In this case, the marked elevation in BP points toward a high possibility of a hemorrhagic rather than an ischemic stroke. Besides, all the previously mentioned guidelines still had their level of evidence 'B'. However, obtaining an answer to this question requires further studies.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

References

  1. Qureshi AI, Ezzeddine MA, Nasar A, Suri MFK, Kirmani JF, Hussein HM, et al. Prevalence of elevated blood pressure in 563704 adult patients with stroke presenting to the ED in the United States. Am J Emerg Med 2007; 25: 32-38.
  2. Zhang Y, Reilly KH, Tong W, Xu T, Chen J, Bazzano LA, et al. Blood pressure and clinical outcome among patients with acute stroke in Inner Mongolia, China. J Hypertens 2008; 26:1446-1452.
  3. Xu BN, Yabuki A, Mishina H, Miyazaki M, Maeda M, Ishii S, et al. Patho-physiology of brain swelling after acute experimental brain compression and decompression. Neurosurgery 1993; 32:289-296.
  4. Rodriguez Luna D, Rubiera M, Ribo M, Coscojuela P, Pin˜eiro S, Pagola J, et al. Ultraearly hematoma growth predicts poor outcome after acute intracerebral hemorrhage. Neurology 2011; 77:1599-1604.
  5. Broderick JP, Diringer MN, Hill MD, Brun NC, Mayer SA, Steiner T, et al. Determinants of intracerebral hemorrhage growth: an exploratory analysis. Stroke 2007; 38:1072-1075.
  6. Rordorf G, McDonald C, Kasner SE, Wilterdink JL. Spontaneous intracerebral hemorrhage: pathogenesis, clinical features and diagnosis. UpToDate 2012.
  7. Menon RS, Burgess RE, Wing JJ, Gibbons MC, Shara NM, Fernandez S, et al. Predictors of highly prevalent brain ischemia in intracerebral hemor­rhage. Ann Neurol 2012; 71:199-205.
  8. Garg RK, Liebling SM, Maas MB, Nemeth AJ, Russell EJ, Naidech AM. Blood pressure reduction, decreased diffusion on MRI and outcomes after intracerebral hemorrhage. Stroke 2012; 43:67-71.
  9. Anderson CS, Huang Y, Wang JG, Arima H, Neal B, Peng B, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol 2008; 7:391-399.
  10. Anderson CS, Huang Y, Arima H, Heeley E, Skulina C, Parsons MW, et al. Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: The intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT). Stroke 2010; 41:307-312.
  11. Qureshi AI. Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH): rationale and design. Neurocrit Care 2007; 6:56-66.
  12. Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, et al. Guidelines for the management of spontaneous intracerebral hemor­rhage in adults: 2007 update. Guideline from the American Heart Asso­ciation/American Stroke Association Stroke Council, High Blood P ressure Research Council and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38: 2001-2023.
  13. Morgenstern LB, Hemphill JC III, Anderson C, Becker K, Broderick JP, Connolly ES Jr, et al. Guidelines for the management of spontaneous




 
 
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