Journal of ISSN: 2373-6410JNSK

Neurology & Stroke
Editorial
Volume 4 Issue 4 - 2016
Newer Nuances in the Management of Acute Stroke
Arun Oommen*
Consultant Neurosurgeon, Lakeshore Hospital and Research Centre, India
Received:March 11, 2016 | Published: March 15, 2016
*Corresponding author: Dr. Arun Oommen, MBBS, MS (Gen Surg), Mch ( Neurosurgery), MRCS Ed, MBA, Consultant Neurosurgeon, Lakeshore Hospital and Research Centre, Kochi, India, Website: www.arunoommen.com, Email:
Citation: Oommen A (2016) Newer Nuances in the Management of Acute Stroke. J Neurol Stroke 4(4): 00135. DOI: 10.15406/jnsk.2016.04.00135

Editorial

Acute stroke can result in significant catastrophic neurological events and hence require immediate recognition and treatment to prevent irreversible injury and death. Efficient and appropriate management of the early stages of a neurological emergency has substantial impact on patient outcome and it is critical to have site-specific protocols to drive care quickly and efficiently. Emergency neurological life support (ENLS) is an educational program designed to provide caretakers advisory instruction regarding management for the first few hours of a neurological emergency [1].

Intracerebral haemorrhage protocol of ENLS is mainly concerned with the initial evaluation and treatment period and it is important to determine optimal treatment required in the initial 72 hours as part of health care planning. The first 24h are vital for managing BP, identifying and controlling seizures, ICP management and maintaining a secure airway. Avoiding hyperglycemia/ hypoglycemia, fever and hypoxia are also vital, as these may have deleterious effects on the outcomes [2-4].

The recent release of the American Heart Association Guidelines for Spontaneous Hemorrhage addresses new treatment goals for blood pressure control and coagulation reversal [2]. Even though blood pressure management has been controversial, recent guidelines favor rapid control of moderately high blood pressure [5,6]. Two pilot randomized clinical trials, the INTERACT trial and the ATACH trial, have suggested that the systolic blood pressure being reduced to below 140mmHg is safe [7,8]. INTERACT2 was a phase III clinical trial of acute blood pressure lowering in ICH patients presenting with a systolic blood pressure between 150 and 220mmHg [9]. The patients were randomized to two different blood pressure thresholds: a standard regular threshold of <180mmHg and an intensive threshold of lesser than 140mmHg. Patients in the intensive arm had better outcomes with about 4 % fewer patients having death or severe disability (modified Rankin Scale score of 3–6). However, we could not find any difference in haematoma expansion between the two groups. So current guidelines do not recommend the blood pressure to remain high without treatment [2,5,6]. The current American Heart Association and the American Stroke Association Guidelines for the Management of ICH and the European Stroke Organization guidelines have recommended a target blood pressure of less than 140mmHg similar to the INTERACT2 trial [2,6]. So in patients presenting with very high blood pressure, acute lowering of blood pressure is justifiable, but less is known about the specific safety and efficacy of treatment [2].

Basic principles of blood pressure lowering in ICH are that management should be started immediately and a drug that can be easily titratable should be used so that the target value is quickly attained and without any potential for overshoot. IV beta-blockers and calcium-channel blockers are the commonly used medications for this indication in the ED and the intensive care unit (ICU).

Current guidelines for warfarin reversal [2,10], recommend the use of vitamin K 5–10 mg administered intravenously by slow IV infusion, along with another more rapidly acting agent such as FFP or PCC, as it typically takes a few hours after vitamin K administration for the warfarin-induced coagulopathy to revert, but it has a more long-lasting effect than PCC or FFP [11].

Both CHEST and American Heart Association / American Stroke Association guidelines recommend the use of prothrombin complex concentrate (PCC) agents over fresh frozen plasma (FFP) [12,13]. PCCs can correct the INR within minutes, faster than FFP, and with fewer cardiopulmonary complications [14]. PCCs have better tolerance than FFP due to lower fluid volumes and reduced risk for transfusion associated circulatory overload or transfusion related acute lung injury [15,16]. INR may be checked 30 min after the end of PCC infusion to check if it is within normal range [15-19]. A second dose of the PCC may be considered if INR remains elevated and risk of continued bleeding is high. In patients who require volume resuscitation FFP can be a better choice and it may be used in combination with PCC if reversal is inadequate. It may be also noted that in a study where PCC and FFP were compared, no difference in hematoma growth was noted in patients whose INR was corrected within 2h [20]. Hence it may be inferred that it is the timing of coagulopathy reversal and not the specific agent that makes the greatest impact.

Newer anticoagulants, like direct Xa inhibitors (e.g. rivaroxaban, edoxaban or apixaban) or direct thrombin inhibitors (e.g. dabigatran) at present do not have a specific reversal agent. Moreover, experience with ICH in patients taking these medications is limited. PCCs may have limited effectiveness in reversing the effect of rivaroxaban and apixaban, but not of dabigatran [21].

The reversal agent for UFH is protamine sulfate, Administered dose is based on the time since last UFH was administered. Administered dose is 0-25 -1mg for every 100U of UFH IV received within 2 hours with a maximum dose of 50mg [22]

Current American Heart Association ICH guidelines recommend that patients with cerebellar hemorrhage having brainstem compression or are deteriorating neurologically should be considered for surgical removal of the hemorrhage at the earliest. Initial treatment of these patients with ventricular drainage alone rather than surgical evacuation is not recommended [2]. Supratentorial hematoma with neurological deterioration can be considered for surgical evacuation or decompressive hemicraniectomy as a life-saving measure. Correction of coagulopathy is critical in patients undergoing surgical hematoma evacuation [23,24].

Acute ischemic stroke is a neurological emergency that can be treated with time-sensitive interventions, including intravenous thrombolysis and endovascular approaches. Extensive studies have suggested that rapid clinical/ radiological assessment and treatment are essential for improving neurological outcome.

The latest version of ENLS is supported by remarkable advancements developing in the field of emergency neurology during the past few years. The recent success of endovascular trials for management of acute ischemic stroke has impacted the time course and treatment options needed for these patients and stresses the necessity for improved communication and collaboration among treating facilities [25-27].

A potential tPA candidate (stroke onset within 3 hours) should be subjected to interventions for immediate BP control. The target BP for IV tPA candidates is less than 185/110mmHg, and once tPA has been initiated, BP must be kept below 180/105mmHg to reduce the risk of intracranial hemorrhage [26]. BP should be lowered carefully and strategically while being careful not to drop the BP too much once the patient is at goal. Chronic antihypertensive medications should be reduced or temporarily withheld. tPA has not yet been approved by the Food and Drug Administration for use in patients presenting with stroke between 3 and 4.5 hours in the US, though it has been approved in Europe and Canada. However, tPA use in this timeframe has been endorsed by the American Stroke Association and is widely used [26].

For patients with large vessel occlusion like middle cerebral artery (MCA), intracranial internal carotid artery (ICA), basilar or vertebral artery and presenting within 6 h of the stroke onset, intra-arterial (IA) thrombolysis may be an option [28,29]. If the patient presents within 8 h, mechanical embolectomy may be considered. Numerous recent randomized trials of embolectomy in acute, large vessel ischemic stroke have shown much superior clinical efficacy and even reduction in mortality with or without IV tPA pre treatment [30-34]. IA thrombolysis or embolectomy may be avoided in the absence of a large vessel occlusion on CTA or MRA, or with large area of infarction already present on the brain imaging study.

References

  1. Smith WS, Weingart S (2012) Emergency neurological life support (ENLS): what to do in the first hour of a neurological emergency. Neurocrit Care 17(Suppl 1): S1-S3.
  2. Hemphill JC, Greenberg SM, Anderson C, Becker K, Bendok BR, et al. (2015) Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 46(7): 2032-2060.
  3. Schwarz S, Hafner K, Aschoff A, Schwab S (2000) Incidence and prognostic significance of fever following intracerebral hemorrhage. Neurology 54(2): 354-361.
  4. Vespa PM (2008) Intensive glycemic control in traumatic brain injury: what is the ideal glucose range? Crit Care 12(5): 175.
  5. Kothari R, Brott T, Broderick J, Barsan W, Sauerbeck L, et al. (1996) The ABCs of measuring intracerebral hemorrhage volume. Stroke 27(8): 1304-1305.
  6. Steiner T, Al-Shahi Salman R, Beer R, Christensen H, Cordonnier C, et al. (2014) European Stroke Organisation (ESO) guidelines for the management of spontaneous intracerebral hemorrhage. Int J Stroke 9(7): 840-855.
  7. Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) investigators (2010) Antihypertensive treatment of acute cerebral hemorrhage. Crit Care Med 38(2): 637-648.
  8. Anderson CS, Huang Y, Wang JG, Arima H, Neal B, et al. (2008) Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol 7(5): 391-399.
  9. Anderson CS, Heeley E, Huang Y, Wang J, Stapf C, et al. (2013) Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 368(25): 2355-2365.
  10. Ageno W, Gallus AS, Wittkowsky A, Crowther M, Hylek EM, et al. (2012) Oral Anticoagulant Therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 141(2 Suppl): e44S-e88S.
  11. (1998) Guidelines on oral anticoagulation: third edition. Br J Haematol 101(2): 374-387.
  12. Leissinger CA, Blatt PM, Hoots WK, Ewenstein B (2008) Role of prothrombin complex concentrates in reversing warfarin anticoagulation: a review of the literature. Am J Hematol 83(2): 137-143.
  13. Tran H, Collecutt M, Whitehead S, Salem HH (2011) Prothrombin complex concentrates used alone in urgent reversal of warfarin anticoagulation. Intern Med J 41(4): 337-343.
  14. Sarode R, Milling TJ, Refaai MA, Mangione A, Schneider A, et al. (2013) Efficacy and safety of a 4-factor prothrombin complex concentrate in patients on vitamin K antagonists presenting with major bleeding: a randomized, plasmacontrolled, phase IIIb study. Circulation 128(11): 1234-1243.
  15. van Aart L, Eijkhout HW, Kamphuis JS, Dam M, Schattenkerk ME, et al. (2006) Individualized dosing regimen for prothrombin complex concentrate more effective than standard treatment in the reversal of oral anticoagulant therapy: an open, prospective randomized controlled trial. Thromb Res 118(3): 313-320.
  16. Crawford JH, Augustson BM (2006) Prothrombinex use for the reversal of warfarin: is fresh frozen plasma needed? Med J Aust 184(7): 365-366.
  17. Dager WE (2011) Using prothrombin complex concentrates to rapidly reverse oral anticoagulant effects. Ann Pharmacother 45(7-8): 1016-1020.
  18. Bershad EM, Suarez JI (2010) Prothrombin complex concentrates for oral anticoagulant therapy-related intracranial hemorrhage: a review of the literature. Neurocrit Care 12(3): 403-413.
  19. Holland L, Warkentin TE, Refaai M, Crowther MA, Johnston MA, et al. (2009) Suboptimal effect of a three-factor prothrombin complex concentrate (Profilnine-SD) in correcting supratherapeutic international normalized ratio due to warfarin overdose. Transfusion 49(6): 1171-1177.
  20. Huttner HB, Schellinger PD, Hartmann M, Köhrmann M, Juettler E, et al. (2006) Hematoma growth and outcome in treated neurocritical care patients with intracerebral hemorrhage related to oral anticoagulant therapy: comparison of acute treatment strategies using vitamin K, fresh frozen plasma, and prothrombin complex concentrates. Stroke 37(6): 1465-1470.
  21. Eerenberg ES, Kamphuisen PW, Sijpkens MK, Meijers JC, Buller HR, et al. (2011) Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate: a randomized, placebo-controlled, crossover study in healthy subjects. Circulation 124(14): 1573-1579.
  22. Schulman S, Bijsterveld NR (2007) Anticoagulants and their reversal. Transfus Med Rev 21(1): 37-48.
  23. Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, et al. (2005) Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomized trial. Lancet 365(9457): 387-397.
  24. Mendelow AD, Gregson BA, Rowan EN, Murray GD, Gholkar A, et al. (2013) Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet 382(9890): 397-408.
  25. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, et al. (2015) Heart disease and stroke statistics-2015 update: a report from the American Heart Association. Circulation 131(4): e29-e322.
  26. Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ, et al. (2013) Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 44(3): 870-947.
  27. (1997) Intracerebral hemorrhage after intravenous t-pa therapy for ischemic stroke. The ninds t-pa stroke study group. Stroke 28(11): 2109-2118.
  28. Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, et al. (1999) Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA 282(21): 2003-2011.
  29. Ogawa A, Mori E, Minematsu K, Taki W, Takahashi A, et al. (2007) Randomized trial of intraarterial infusion of urokinase within 6 hours of middle cerebral artery stroke: the middle cerebral artery embolism local fibrinolytic intervention trial (Melt) japan.  Stroke 38(10): 26339-2639.
  30. Berkhemer OA, Fransen PS, Beumer D, van den Berg LA, Lingsma HF, et al. (2015) A randomized trial of intraarterial treatment for acute ischemic stroke. New Engl J Med 372(1): 11-20.
  31. Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, et al. (2015) Endovascular therapy for ischemic stroke with perfusion-imaging selection. New Engl J Med 372(11): 1009-1018.
  32. Goyal M, Demchuk AM, Menon BK, Eesa M, Rempel JL, et al. (2015) Randomized assessment of rapid endovascular treatment of ischemic stroke. New Engl J Med 372(11): 1019-1030.
  33. Jovin TG, Chamorro A, Cobo E, de Miquel MA, Molina CA, et al. (2015) Thrombectomy within 8 hours after symptom onset in ischemic stroke. New Engl J Med 372(24): 2296-2306.
  34. Saver JL, Goyal M, Bonafe A, Diener HC, Levy EI, et al. (2015) Stent-retriever thrombectomy after intravenous t-pa vs T-pa alone in stroke. New Engl J Med 372(24): 2285-2295.
© 2014-2016 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at http://medcraveonline.com
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy