Hemorrhagic stroke management
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Hemorrhagic stroke Microchapters |
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Diagnosis |
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Treatment |
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AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage (2015) |
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AHA/ASA Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (2012) |
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AHA/ASA Guideline Recommendation for the Primary Prevention of Stroke (2014) |
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AHA/ASA Guideline Recommendations for Prevention of Stroke in Women (2014) Sex-Specific Risk Factors
Risk Factors Commoner in Women |
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Case Studies |
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Hemorrhagic stroke management On the Web |
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American Roentgen Ray Society Images of Hemorrhagic stroke management |
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Risk calculators and risk factors for Hemorrhagic stroke management |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Medical therapy
Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
Coagulation factor deficiency or platelet disorder treatments
Patients with a known coagulation factor deficiency or platelet disorder:[1][2]
- Replacement of the appropriate factor or platelets
- Hematology consult
patient undergoing an IV heparin infusion
- Protamine sulfate IV injection at a dose of 1 mg per 100 U of heparin (maximum dose 50 mg) with adjustment based on time elapsed since discontinuation of heparin infusion
Patients who are receiving low-molecular-weight heparin (reversal may be incomplete)
- Protamine sulfate IV injection at a dose of 1 mg per 100 U of heparin (maximum dose 50 mg)
Vitamin K antagonists (VKAs)
Rapid correction of the international normalized ratio (INR) is recommended.
- Fresh frozen plasma (FFP), along with vitamin K (5 to 10 mg, usually given slowly via the IV route) has been the mainstay of treatment
Recently new treatments have emerged as potential therapies such as:[3][4]
- Prothrombin complex concentrates (PCCs) contains factors II, IX, X, and VII. PCC does not require cross matching, can be reconstituted and administered rapidly in a small volume (20–40 mL) and Several studies have shown that PCCs rapidly normalize the INR (within minutes) in patients taking VKAs.
- Activated PCC FEIBA (factor VIII inhibitor bypassing activity)
- Recombinant activated factor VIIa (rFVIIa)
New Anticoagulant Medication–Related ICH
There are no randomized trials of reversing agents for newer anticoagulants among patients with ICH or other major bleeding complications. Currently available agents in the United States (dabigatran, rivaroxaban, and apixaban) have relatively short half-lives ranging from 5 to 15 hours. Evaluation of the activated partial thromboplastin time and prothrombin time and consultation with a hematologist are reasonable to individualize care. Potential reversal strategies using FEIBA, other PCCs, or rFVIIa might be considered.
- Activated charcoal can be used if the most recent dose of dabigatran, apixaban, or rivaroxaban was taken within the previous couple of hours[5]
- FFP is of unclear utility, and vitamin K is not useful
- FEIBA or rFVIIa may be better for the direct thrombin inhibitor (dabigatran)
- PCCs may be better for the factor Xa inhibitors (rivaroxaban and apixaban)[6][7]
- Hemodialysis has been noted as an option for dabigatran, but less so for rivaroxaban or apixaban[8]
Antiplatelet Medication–Related ICH
Studies addressing the effect of prior antiplatelet agent use or platelet dysfunction on ICH growth and outcome have found conflicting results.[9][10][11][12]
Thromboprophylaxis in ICH Patients
Patients with ICH have a high risk of thromboembolic disease.[13]
- intermittent pneumatic compression begun as early as the day of hospital admission reduced the occurrence of proximal DVT[14]
- ICH patients who develop DVT or PE may be considered for full systemic anticoagulation or placement of an inferior vena cava (IVC) filter[15]
BP-Lowering Treatment
- Overall, current evidence indicates that early intensive BP lowering is safe and feasible in patients with [intracerebral hemorrhage|intracerebral hemorrhage (ICH) and that surviving patients show modestly better functional recovery, with a favorable trend seen toward a reduction in the conventional clinical end point of death and major disability.
- It is reasonable for intracerebral hemorrhage (ICH) patients to receive early treatment targeted to an SBP level <140 mmHg to improve their chances of achieving better functional recovery if they survive the condition.
- There are fewer data available pertaining to the safety and effectiveness of treatment in patients with very high BP (sustained SBP >220 mm Hg) on presentation, large and more severe ICH, and those requiring surgical decompression.
2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage[16]
Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis: Recommendations
Patients with a severe coagulation factor deficiency or severe thrombocytopenia
| Class I |
| "1.Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectivel (Level of Evidence: C)" |
Patients with ICH whose INR is elevated because of VKA
| Class I |
| "1.Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Level of Evidence: C)" |
| Class III (Harm) |
| "1.rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Level of Evidence: C)" |
| Class IIb |
| "1.PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP (Level of Evidence: B)" |
Patients with ICH who are taking dabigatran, rivaroxaban, or apixaban
| Class IIb |
| "1.For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA, other PCCs, or rFVIIa might be considered on an individual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or riva- roxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Level of Evidence: C)" |
Reverse heparin in patients with acute ICH
| Class IIb |
| "1. Protamine sulfate may be considered to reverse heparin in patients with acute ICH (Level of Evidence: C)" |
Patients with a history of anti platelet and ICH
| Class IIb |
| "1.The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is uncertain (Level of Evidence: C)" |
Hematoma expansion
| Class III (Harm) |
| "1. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Level of Evidence: A)" |
prevention of venous thromboembolism
| Class I |
| "1.Patients with ICH should have intermittent pneu- matic compression for prevention of venous throm- boembolism beginning the day of hospital admission (Level of Evidence: A)" |
| Class III (Harm) |
| "1.Graduated compression stockings are not beneficial to reduce DVT or improve outcome (Level of Evidence: A)" |
| Class IIb |
| "1.After documentation of cessation of bleeding, low- dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for pre- vention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Level of Evidence: B)" |
ICH patients with symptom- atic DVT or PE
| Class IIa |
| "1.Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptom- atic DVT or PE (Level of Evidence: C)" |
| "2. The decision between these 2 options should take into account several factors, including time from hem- orrhage onset, hematoma stability, cause of hemor- rhage, and overall patient condition (Level of Evidence: C)" |
References
- ↑ Schulman S, Bijsterveld NR. Anticoagulants and their reversal. Transfus Med Rev. 2007;21:37–48. doi: 10.1016/j.tmrv.2006.08.002.
- ↑ Andrews CM, Jauch EC, Hemphill JC 3rd, Smith WS, Weingart SD. Emergency neurological life support: intracerebral hemorrhage. Neurocrit Care. 2012;17(suppl 1):S37–S46. doi: 10.1007/s12028-012-9757-2.
- ↑ Holbrook A, Schulman S, Witt DM, Vandvik PO, Fish J, Kovacs MJ, Svensson PJ, Veenstra DL, Crowther M, Guyatt GH; American College of Chest Physicians. Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e152S–e184S. doi: 10.1378/ chest.11-2295.
- ↑ Hanley JP. Warfarin reversal. J Clin Pathol. 2004;57:1132–1139. doi: 10.1136/jcp.2003.008904.
- ↑ Kaatz S, Kouides PA, Garcia DA, Spyropolous AC, Crowther M, Douketis JD, Chan AK, James A, Moll S, Ortel TL, Van Cott EM, Ansell J. Guidance on the emergent reversal of oral thrombin and factor Xa inhibitors. Am J Hematol. 2012;87 Suppl 1:S141–S145. doi: 10.1002/ ajh.23202.
- ↑ Dager WE, Gosselin RC, Roberts AJ. Reversing dabigatran in life-threat- ening bleeding occurring during cardiac ablation with factor eight inhibi- tor bypassing activity. Crit Care Med. 2013;41:e42–e46. doi: 10.1097/ CCM.0b013e31827caaa3.
- ↑ Oh JJ, Akers WS, Lewis D, Ramaiah C, Flynn JD. Recombinant factor VIIa for refractory bleeding after cardiac surgery secondary to antico- agulation with the direct thrombin inhibitor lepirudin. Pharmacotherapy. 2006;26:569–577. doi: 10.1592/phco.26.4.576.
- ↑ Veshchev I, Elran H, Salame K. Recombinant coagulation factor VIIa for rapid preoperative correction of warfarin-related coagulopathy in patients with acute subdural hematoma. Med Sci Monit. 2002;8:CS98–CS100.
- ↑ Sansing LH, Messe SR, Cucchiara BL, Cohen SN, Lyden PD, Kasner SE; CHANT Investigators. Prior antiplatelet use does not affect hem- orrhage growth or outcome after ICH. Neurology. 2009;72:1397–1402. doi: 10.1212/01.wnl.0000342709.31341.88.
- ↑ Naidech AM, Jovanovic B, Liebling S, Garg RK, Bassin SL, Bendok BR, Bernstein RA, Alberts MJ, Batjer HH. Reduced platelet activity is associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage. Stroke. 2009;40:2398–2401. doi: 10.1161/ STROKEAHA.109.550939.
- ↑ de Gans K, de Haan RJ, Majoie CB, Koopman MM, Brand A, Dijkgraaf MG, Vermeulen M, Roos YB; PATCH Investigators. PATCH: Platelet Transfusion in Cerebral Haemorrhage: study protocol for a multi- centre, randomised, controlled trial. BMC Neurol. 2010;10:19. doi: 10.1186/1471-2377-10-19.
- ↑ Naidech AM, Bernstein RA, Levasseur K, Bassin SL, Bendok BR, Batjer HH, Bleck TP, Alberts MJ. Platelet activity and outcome after intracerebral hemorrhage. Ann Neurol. 2009;65:352–356. doi: 10.1002/ ana.21618.
- ↑ Gregory PC, Kuhlemeier KV. Prevalence of venous thromboembolism in acute hemorrhagic and thromboembolic stroke. Am J Phys Med Rehabil. 2003;82:364–369. doi: 10.1097/01.PHM.0000064725.62897.A5.
- ↑ Dennis M, Sandercock P, Reid J, Graham C, Forbes J, Murray G; CLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicentre randomised controlled trial [published corrections appear in Lancet. 2013;382:506 and Lancet. 2013;382:1020]. Lancet. 2013;382:516–524. doi: 10.1016/S0140-6736(13)61050-8.
- ↑ Kelly J, Hunt BJ, Lewis RR, Rudd A. Anticoagulation or inferior vena cava filter placement for patients with primary intracerebral hemorrhage developing venous thromboembolism? Stroke. 2003;34:2999–3005. doi: 10.1161/01.STR.0000102561.86835.17.
- ↑ 2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhagehttp://stroke.ahajournals.org/content/early/2015/05/28/STR.0000000000000069 Accessed on November 10, 2016