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    Home > Active Ingredient News > Study of Nervous System > This article explains in detail the prediction and coping strategies of thrombolytic bleeding complications

    This article explains in detail the prediction and coping strategies of thrombolytic bleeding complications

    • Last Update: 2022-10-26
    • Source: Internet
    • Author: User
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    *For medical professionals only

    Can the risk of bleeding before thrombolysis be predicted in advance?


    Post-thrombolytic hemorrhagic transformation (HT) refers to a hemorrhagic stroke that occurs for a period of time after intravenous thrombolysis in patients with acute ischaemic stroke
    .
    In general, the earlier thrombolytic therapy, the lower
    the risk of HT.

    Common complications of thrombolytic therapy include HT, systemic bleeding, vascular reocclusion, vasogenic oedema, and allergies
    .
    Predicting and responding to these complications in advance can help guide our clinical work and improve thrombolysis rates
    .
    01 Classification of secondary blood associated with thrombolysis ➤ Superficial bleeding: common, often bleeding
    at the puncture site or at the site of vascular injury.

    ➤ Internal bleeding: intestinal (common), genitourinary (common), central nervous system (common), posterior peritoneum (uncommon), or parenchymal organ bleeding (rare).



    02Pathogenesis of HT







    The pathogenesis of HT is not fully understood, and most studies believe that it is caused by
    occlusive vascular recanalization, reperfusion injury, and collateral circulation establishment.


    ➤ Occlusive vascular recanalization: after the occlusive emboli blocks the blood vessel, its distal vessel ischemia paralysis, after the emboli disintegrate or migrate distally, the vascular permeability increases and causes blood exudation
    .


    ➤ Reperfusion injury: mass effect of large-scale infarction and edema of surrounding tissues, compression of blood vessels around infarction causing blood retention, reperfusion of small blood vessels after edema decreases, rupture of small blood vessels that have occurred necrosis, resulting in spotty and flaky bleeding
    .


    ➤ Collateral circulation establishment: Due to the incomplete development of the newly built collateral circulation blood vessel wall, bleeding is caused by blood impact during recanalization
    .



    03HT typing after thrombolysis



    HT can be classified
    according to clinical and imaging.


    (Click to view larger image)



    04Risk factors for HT



    (Click to view larger image)



    05Risk prediction of bleeding before thrombolysis



    ➤ HT's image prediction model


    CTA+ASPECTS SCORE + CBA
    .


    (1) No collateral (score: 0 points); (2) less than 50% of the collateral (score: 1 point); (3) More than 50% of collateral (score: 2 points) (4) 100% of collateral (score: 3 points).


    ➤ Prediction of biochemical indicators of HT


    (1) Ribonucleic acid (RNA): Jickling et al.
    found the differential expression of 29 RNAs in the peripheral blood of HT patients, including SMAD4 protein (SMAD4), phosphoinositol-5-phosphatase (INPP5D), vascular endothelial growth inhibitory factor (VEGI), bidirectional regulatory protein (AREG), human coagulation factor deficiency protein 2 (MCFD2) and membrane-associated zinc finger protein 7 (MARCH7).

    Among them, the expression increased SMAD4, AREG, MARCH7, and the expression decreased VEGI and MCFD2
    .


    (2) Matrix metalloproteinase (MMP): MMP, especially MMP-9, plays an important role
    in the occurrence of HT in rt-PA thrombolysis patients.
    RT-PA has been found to increase MMP-9 levels and then participate in mediating the occurrence
    of HT.


    (3) Serum albumin: Domestic Che et al.
    proposed that low serum albumin is an independent predictor of HT after rt-PA thrombolysis, and it is recommended that the serum albumin level be evaluated within 24 hours of thrombolysis, and the occurrence of HT is reduced by correcting hypoalbuminemia in the acute phase by transfusion of albumin and improving the prognosis
    of patients.


    (4) Serum ion level: calcium ions, as a cofactor of coagulation cascade, play an important role
    in the conversion of prothrombin into thrombin.
    It has been found that low serum calcium levels within 24 hours after thrombolysis are independently associated with HT, and PH type is more common in thrombolytic patients less than 2.
    16 mmol/L, suggesting that serum calcium levels may also be used as one of
    the predictive indicators of HT.


    (5) Neutrophil-to-lymphocyte ratio: In recent years, studies have shown a correlation
    between the neutrophil-to-lymphocyte ratio (NLR) and НТ.
    Domestic Guo et al.
    proposed that the NLR in the post-thrombolysis bleeding group was higher than that in the non-bleeding group, and NLR was a dynamic process, pointing out that NLR higher than 10.
    59 12~18 h after treatment was independently related
    to the occurrence of PH and SICH.


    (6) Serum alkaline phosphatase: A study of stroke patients with atrial fibrillation and/or rheumatic heart disease found that serum alkaline phosphatase (ALP) predicts the occurrence of SICH, and the incidence of SICH in the high-level ALP group (>92 IU/L) is 8.
    96 times that in the low-level ALP group (<70 IU/L), but the researchers did not find a correlation between ALP levels and HT, HI, PH, and whether ALP can be used as a predictor of HT.
    Rely on further research to confirm.


    ➤ HT risk prediction model


    (Click to view larger image)



    06 How to prevent post-thrombolytic HT



    (1) Evaluation according to predictors: advanced age, diabetes, severe stroke, imaging changes, time, prethrombolytic blood pressure, low platelets, previous antithrombotic drugs, etc
    .


    (2) Grasp the treatment time window: 4.
    5 h (the earlier the better), → need to ask a detailed medical history and carefully identify
    .


    (3) Control blood pressure: SBP>185 mmHg, DBP>110 mmHg is contraindicated
    .


    (4) Control of hyperglycemia: blood sugar < 2.
    7 mmol or > 22.
    2 mmol is contraindicated
    .


    Thrombolytic monitoring


    During thrombolysis: (1) closely monitor neurological status, blood pressure, and heart rate; (2) Closely observe the changes in the condition, and resume CT in time after the deterioration of the condition, otherwise repeat CT
    at 24 hours.


    (1) Blood pressure: q15 minx2 h, followed by q30 minx6 h, followed by q60 minx16 h
    .


    (2) Pulse measurement and breathing: Q1 Hx12 h, followed by Q2 Hx12 h
    .


    (3) Neurological function score: Q1 Hx6 h, followed by Q3 Hx72 h
    .


    ➤ Blood pressure management


    There are no guidelines for the management of blood pressure in patients with symptomatic intracranial haemorrhage (SICH) after thrombolysis, so guidelines for blood pressure management in spontaneous intracerebral hemorrhage can be followed; It is recommended to maintain the target blood pressure at 160/90 mmHg, and if the patient's systolic blood pressure (SBP) rises to 150~220 mmHg, it is reasonable
    to reduce it to 140 mmHg.


    Recommended regimen for blood pressure management in patients with SICH after thrombolysis:


    (1) If SBP > 200 mmHg or mean arterial pressure (MAP) > 150 mmHg, consider aggressive antihypertensive treatment
    with continuous intravenous infusion therapy.


    (2) If SBPs > 180 mmHg or MAP> 130 mmHg and increased intracranial pressure (ICP) is suspected at the same time, ICP monitoring is required and intermittent or continuous intravenous antihypertensive drugs are used while maintaining CPP (cerebral perfusion pressure) > 60 mmHg
    .


    (3) If SBP > 180 mmHg or MAP > 130 mmHg, but there are no signs of ICP elevation, moderate blood pressure lowering (such as reducing MAP to 110 mmHg or maintaining it at 160/90 mmHg) can be considered, and blood pressure
    can be monitored every 15 minutes.



    07 Treatment (there are currently no unified standardized guidelines).



    (1) Including condensed protein, platelet transfusion, fresh frozen plasma, platelet transfusion and 6-aminocaproic acid
    .


    (2) Because the half-life of alteplase is short, the image of the coagulation system is slight, so it is generally not necessary to give coagulation factors
    .


    (3) Most patients with cerebral hemorrhage can control bleeding
    by interrupting thrombolytic and anticoagulant therapy.
    If heparin has been used within 4 hours of bleeding, protamine
    should be considered.


    (4) For a small number of patients who do not respond to conservative treatment, blood products can be transfused, including cryoprecipitate, fresh frozen plasma and platelets, and clinical and laboratory re-evaluation
    should be done after each use.


    (5) The target value of fibrinogen was 1 g/L
    by infusion of cryophediment.
    Antifibrin hemolytics may be the last option
    .


    Where to see more thrombolysis knowledge?
    Come to the "Doctor Station" and take a look 👇


    Source of this articleResponsible Editor of NeuroTimesMr.
    Lu Li Xiang Yu

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