Current Neurology and Neuroscience Reports

, Volume 1, Issue 6, pp 587–592 | Cite as

Critical care of acute ischemic stroke

  • Richard A. Bernstein
  • J. Claude Hemphill
Article

Abstract

Advances in neurologic therapeutics and intensive care medicine have expanded the arsenal of treatments available for the critical care of ischemic stroke. Several agents are available for acute reperfusion of the ischemic brain. These include intravenous recombinant tissue-plasminogen activator (rtPA), which is effective in a 3-hour time window, and intra-arterial thrombolytics, which may be effective within 6 hours. In addition, newer agents such as Ancrod and abciximab may be effective within the acute time period. Efforts to prevent secondary brain injury in critically ill patients with stroke often include prevention and reduction of fever, induced hypertension, and mechanical ventilation. Finally, death due to severe brain edema after massive hemispheric infarction can often be prevented with surgical or medical intervention. Unfortunately, there is a critical lack of well-designed clinical studies to guide the clinician in the use of these interventions. In addition, there is concern that some of these interventions may preserve life at the cost of quality of life. This article reviews the evidence behind these approaches to the critical care of ischemic stroke.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References and Recommended Reading

  1. 1.
    DeGraba TJ, Pettigrew LC: Why do neuroprotective drugs work in animals but not humans? Neurol Clin 2000, 19:475–493.CrossRefGoogle Scholar
  2. 2.
    The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995, 333:1581–1587.CrossRefGoogle Scholar
  3. 3.
    Albers GW, Bates VE, Clark WM, et al.: Intravenous tissuetype plasminogen activator for treatment of acute stroke: the standard treatment with alteplase to reverse stroke (STARS) study. JAMA 2000, 283:1145–1150.PubMedCrossRefGoogle Scholar
  4. 4.
    Hacke W, Kaste M, Fieschi C, et al.: Randomized doubleblind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischemic stroke (ECASS II). Lancet 1998, 352:1245–1251.PubMedCrossRefGoogle Scholar
  5. 5.
    Clark WM, Wissman S, Albers GW, et al.: Recombinant tissue-type plasminogen activator (alteplase) for ischemic stroke 3 to 5 hours after symptom onset. JAMA 1999, 282:2019–2026.PubMedCrossRefGoogle Scholar
  6. 6.
    Furlan A, Higashida R, Wechsler L, et al.: Intra-arterial prourokinase for acute ischemic stroke. JAMA 1999, 282:2003–2011. Pivotal study of angiographically guided intra-arterial thrombolysis for middle cerebral artery occlusions. This trial, which had a 6-hour time window, describes an alternative therapy to intravenous tissue plasminogen activator for a limited subset of ischemic stroke patients. Unfortunately, the thrombolytic agent used in the study is not approved by the Food and Drug Administration, nor is it currently available. In addition, the intra-arterial modality requires a large, specialized team to administer, which can be difficult to accomplish at night or at nontertiary care hospitals.PubMedCrossRefGoogle Scholar
  7. 7.
    Katzan IL, Masaryk J, Furlan AJ, et al.: Intra-arterial thrombolysis for perioperatve stroke after open heart surgery. Neurology 1999, 52:1081–1084.PubMedGoogle Scholar
  8. 8.
    Gruber A, Nassel C, Lang W, et al.: Intra-arterial thrombolysis for the treatment of perioperative childhood cardioembolic stroke. Neurology 2000, 54:1684–1686.PubMedGoogle Scholar
  9. 9.
    Ueda T, Sakaki S, Nochide I: Angioplasty after intra-arterial thrombolysis for acute occlusion of intracranial arteries. Stroke 1998, 29:2568–2574.PubMedGoogle Scholar
  10. 10.
    Christou I, Alexandrov AV, Burgin S, et al.: Timing of recanalization after tissue plasminogen activator therapy determined by transcranial doppler correlates with clinical recovery from ischemic stroke. Stroke 2000, 31:1812–1816.PubMedGoogle Scholar
  11. 11.
    Lewandowski CA, Frankel M, Tomsick TA, et al.: Combined intravenous and intra-arterial rTPA versus intraarterial therapy of acute ischemic stroke. Stroke 1999, 30:2598–2605. This pilot trial combined a lower dose of intravenous tissueplasminogen activator (tPA) followed by intra-arterial tPA. Although the study does not prove efficacy, it likely represents a future modality for urgent stroke treatment. It may expand the number of patients treated, as a local emergency room could initiate intravenous thrombolysis and then transfer patients to a tertiary care institution for intra-arterial, if necessary.PubMedGoogle Scholar
  12. 12.
    Sherman DG, Atkinson RP, Chippendale T, et al.: Intravenous ancrod for treatment of acute ischemic stroke. JAMA 2000, 283:2395–2403. A randomized, double-blind, placebo-controlled trial of the defibrinogenating agent Ancrod, derived from Malaysian pit viper venom. This trial demonstrated efficacy in the treatment of ischemic stroke within 3 hours. However, Ancrod is not yet approved by the Food and Drug Administration for treatment of stroke. Also, it is unclear whether Ancrod is superior to intravenous tissue plasminogen activator for treatment within the 3-hour time window.PubMedCrossRefGoogle Scholar
  13. 13.
    The Abciximab in Ischemic Stroke Investigators: Abciximab in acute ischemic stroke. Stroke 2000, 31:601–609.Google Scholar
  14. 14.
    Winkley JM, Adams HP: Potential role of abciximab in ischemic cerebrovascular disease. Am J Cardiol 2000, 85:47C-51C.PubMedCrossRefGoogle Scholar
  15. 15.
    Mayer SA, Copeland D, Bernardini GL, et al.: Cost and outcome of mechanical ventilation for life threatening stroke. Stroke 2000, 31:2346–2353.PubMedGoogle Scholar
  16. 16.
    Coplin WM, Pierson DJ, Cooley KD, et al.: Implications of extubation delay in brain-injured patients meeting standard weaning criteria. Am J Respir Crit Care Med 2000, 161:1530–1536.PubMedGoogle Scholar
  17. 17.
    Castillo J, Davalos A, Marrugat J, et al.: Timing for fever related brain damage in acute ischemic stroke. Stroke 1998, 29:2455–2460.PubMedGoogle Scholar
  18. 18.
    Ginsberg MD, Busto R: Combating hyperthermia in acute stroke. Stroke 1998, 29:529–534.PubMedGoogle Scholar
  19. 19.
    Hajat C, Hajat S, Sharma P: Effects of poststroke pyrexia on stroke outcome. Stroke 2000, 31:410–414. A meta-analysis of the effect of post-stroke fever on outcome, in which the authors review nine studies that included 3790 patients. They find evidence that there is a marked increase in morbidity and mortality in stroke patients with fever, and suggest that efforts should be undertaken to combat fever in patients with stroke. It remains possible, however, that fever indicates, rather than causes, severe neurologic damage.PubMedGoogle Scholar
  20. 20.
    Boysen G, Christensen H: Stroke severity determines body temperature in acute stroke. Stroke 2001, 31:413–417.Google Scholar
  21. 21.
    Morfis L, Schwartz RS, Poulos R, et al.: Blood pressure changes in acute cerebral infarction and hemorrhage. Stroke 1997, 28:1401–1405.PubMedGoogle Scholar
  22. 22.
    Lisk DR, Grotta JC, Lamki LM, et al.: Should hypertension be treated after acute stroke? A randomized controlled trial using single photon emission computed tomography. Arch Neurol 1993, 50:855–862.PubMedGoogle Scholar
  23. 23.
    Mayerg MR, Batjer HH, Dacey R, et al.: Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Circulation 1994, 90:2592–2605.Google Scholar
  24. 24.
    Rordorf G, Cramer SC, Efird JT, et al.: Pharmacologic elevation of blood pressure in acute stroke. Stroke 1997, 28:2133–2138.PubMedGoogle Scholar
  25. 25.
    Schwab S, Spranger M, Schwarz et al.: Barbiturate coma in severe hemispheric stroke: useful or obslete? Neurology 1997, 48:1608–1613.PubMedGoogle Scholar
  26. 26.
    Frank JI: Large hemispheric infarction, deterioration, and intracranial pressure. Neurology 1995, 45:1286–1290.PubMedGoogle Scholar
  27. 27.
    Schwab S, Steinber T, Aschoff A, et al.: Early hemicraniectomy inpatients with complete middle cerebral artery infarction. Stroke 1998, 29:1888–1893. Review of a single center’s experience with hemicraniectomy for massive hemispheric edema after middle cerebral artery (MCA) occlusion (“malignant” MCA occlusion). They found that patients with hemicraniectomy within 24 hours of stroke onset seem to have a better outcome than those whose surgery is delayed beyond this time. Hemicraniectomy may significantly improve the outcome of patients with massive cerebral edema due to stroke.PubMedGoogle Scholar
  28. 28.
    Manno EM, Adams RE, Derdeyn CP, et al.: The effects of mannitol on cerebral edema after large hemispheric cerebral infarct. Neurology 1999, 52:583–587. This study used serial magnetic resonance imaging scans to determine whether a single large bolus of intravenous mannitol worsened midline shift in massive hemispheric infarction, as had been hypothesized by other studies. They found that this did not occur, suggesting that worsened herniation and shift should not be a concern when deciding whether to initiate osmotherapy for severe hemispheric edema in the setting of stroke.PubMedGoogle Scholar
  29. 29.
    Bereczki D, Liu M, Fernandes do Prado G, et al.: Cochrane report: a systematic review of mannitol therapy for acute ischemic stroke and cerebral parenchymal hemorrhage. Stroke 2000, 31:2719–2722.PubMedGoogle Scholar
  30. 30.
    Carter BS, Ogilvy CS, Candia GJ, et al.: One year outcome after decompressive surgery for massive non-dominant hemispheric infarction. Neurosurgery 1997, 40:1168–1176.PubMedCrossRefGoogle Scholar
  31. 31.
    Oppenheim C, Samson Y, Manai R, et al.: Prediction of malignant middle cerebral artery infarction by diffusion weighted imaging. Stroke 2000, 31:2175–2181.PubMedGoogle Scholar
  32. 32.
    Schwab S, Schwarz S, Spranger M, et al.: Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998, 29:2461–2466. A review of the experience with 25 patients with ldmalignant" middle cerebral artery occlusion treated with moderate hypothermia. These patients had body temperature lowered to 33° C for 48 to 72 hours, followed by passive rewarming. Although the patients outcomes were better than control patients, the rewarming phase proved to be critical. Those patients who died (44%) tended to have uncontrollable increases in intracranial pressure (ICP) during rewarming, despite improved ICP during the hypothermia period itself. Additionally, 40% of the patients developed pneumonia.PubMedGoogle Scholar
  33. 33.
    Kammergaard LP, Rasmussen BH, Jorgenson HS, et al.: Feasibility and safety of inducing modest hypothermia in awake patients with acute stroke through surface cooling: a case control study. Stroke 2000, 31:2251–2256.Google Scholar

Copyright information

© Current Science Inc. 2001

Authors and Affiliations

  • Richard A. Bernstein
    • 1
  • J. Claude Hemphill
    • 1
  1. 1.Department of NeurologySan Francisco General HospitalSan FranciscoUSA

Personalised recommendations