Chinese Medical Journal, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 10, 2024

Spontaneous intracerebral hemorrhage (ICH) accounts for 10–30% of all strokes worldwide and is more prevalent in Asians, Hispanics, African Americans.[1–3] Uncontrolled hypertension anticoagulant use are the common causes spontaneous ICH.[4–6] Non-contrast head computed tomography (CT) very sensitive diagnosis ICH. CT angiography (CTA), magnetic resonance (MRA), or catheter indicated to rule out vascular abnormalities other underlying etiologies, particularly younger patients.[3] Depressed level consciousness, large ICH volume, intraventricular extension, hematoma expansion predictors poor outcomes after ICH.[7–11] Although early pioneering studies surgical treatment showed promising results,[12,13] subsequent landmark randomized controlled trials (RCTs) including (STICH), STICH II, Minimally Invasive Surgery plus Alteplase Intracerebral Hemorrhage Evacuation Phase III (MISTIE III) failed show definitive outcome benefit from evacuation.[14–17] Medical therapies targeting expansion, such as intensive lowering systolic blood pressure (SBP) less than 140 mmHg, reversal anticoagulation hemostatic therapy with Andexanet alfa, recombinant activated factor VII (rFVIIa), tranexamic acid, a reduction without significant benefit.[18–23] Recent Advances Management In patients ICH, major determinants functional include location, size, expansion. Hematoma occurs approximately 30% patients.[9,10] It mostly during first 3 h ICH.[24–26] Several imaging markers, spot signs, may predict good accuracy on contrast CTA.[25,26] Intensive BP control Two landmark, phase III, multicenter, prospective RCTs evaluated effect (BP) ICH.[19,20] The rapid blood-pressure acute (INTERACT-2) trial compared SBP <140 mmHg vs. <180 within 6 onset. no differences adverse events, mortality, severe disability at 90 days.[19] An ordinal analysis modified Rankin Scale (mRS) scores improved control. antihypertensive cerebral (ATACH-2) used intravenous nicardipine onset target mmHg.[20] There was difference days. group, however, had higher rate renal events standard group (9.0% 4.0%, P = 0.002). contradictory results were likely attributable study design overly aggressive ATACH-2 (i.e., mean minimum 128.9 141.1 2 h, 150 164 1 INTERACT-2 trial). A pooled individual patient data that achieving stable 120–130 associated favorable mild-to-moderately whereas drops >60 hour harmful.[27] registered Blood Pressure Acute Stroke Collaboration earlier 120–140 over 24 lower risk better outcomes, especially volume >10 mL.[28] INTERACT-3 effectiveness care bundle strict glucose control, fever 7036 presenting symptom onset.[29] likelihood months (odds ratio [OR], 0.86; 95% CI, 0.76–0.97; 0.015). INTERACT-4 ultra-early ambulance.[30] Suspected stroke motor deficit elevated ≥150 receive immediate 130–140 (intervention group) usual management (usual-care group). At hospital arrival, 159 intervention 170 usual-care group. Prehospital decrease odds among hemorrhagic (common OR, 0.75; 0.60–0.92). summary, 2–6 reduce improve Reversal oral Anticoagulant-associated increases outcome, death.[5,6,31] Early crucial prevent current guidelines summarized Figure 1.[11,32] anticoagulant-associated should be discontinued immediately. dose charcoal recommended absorption direct anticoagulants (DOAC) if agent taken previous h. Specific agents administered soon possible respect different anticoagulants.[24,33]Figure 1: Current approaches anticoagulation. 4F-PCC: 4-factor prothrombin complex concentrate; ICH: hemorrhage; INR: International normalized ratio; IV: Intravenous injection.4-factor concentrate (4F-PCC) vitamin K antagonist (VKA)-related includes quick its by 4F-PCC K, goal international (INR) <1.3 4 h.[32] superior fresh frozen plasma (FFP) normalizing INR. Faster INR normalization smaller these studies.[33,34] PCC later increase expansion.[32] retrospective 67 intracranial hemorrhage, (aPCC) found equally effective apixaban rivaroxaban effect.[35] efficacy (P 0.362) mortality 0.838) between groups. Idarucizumab Dabigatran (Pradaxa) thrombin inhibitor. monoclonal antibody fragment developed reverse dabigatran effect.[36] prospective, open-label study, 235 (137 gastrointestinal bleeding 98 hemorrhage) received idarucizumab (administered two 2.5 g dose) complete effect. days, thrombotic occurred 6.3% patients. 30-day 16.4% hemorrhage. available Of note, excreted kidneys. When not available, dialysis can considered concentration impairment.[37] human Xa decoy protein designed inhibitors.[38] single-group 479 (69% 23% gastrointestinal), an bolus (400 mg 800 mg) 15–30 min followed 2-h infusion (480 960 resulted excellent 80% treated four inhibitors.[39] FXa inhibitor-associated (ANNEXA-1) randomized, multicenter clinical evaluating safety 15 taking inhibitor.[23] primary endpoint efficacy, defined 35% 12 baseline, National Institutes Health (NIHSS) score seven points rescue randomization. rates (67.0% 53.1%; 0.003), (10.3% 5.6%; 0.048), ischemic (6.5% 1.5%). 30 days Given lack additional warranted prove Andexanet. Hemostatic uses medications stop when body's natural system cannot. baseline volume.[23] Factor VIIa rFVIIa directly activates X surface platelets, resulting acceleration coagulation. (FAST) trial, 841 non-coagulopathic randomly assigned placebo, 20 μg/kg rFVIIa, 80 reduced survival ICH.[18]A secondary FAST suggested age ≤70 years, <60 mL, (IVH) <5 onset-to-treatment time ≤2.5 almost 50% growth (7.3 ± 3.2 3.8 1.5; 0.02) trend toward (adjusted 0.28; 0.08–1.06).[40] (FASTEST) currently enrolling earliest placebo (https://classic.clinicaltrials.gov/ct2/show/NCT03496883). will determined 180 Tranexamic acid synthetic lysine analog competes residues fibrin effectively inhibits interaction fibrinolytic enzymes fibrin. prevents dissolution clots hyperacute (TICH-2) 2325 8-h 8 0.88; 0.76–1.03; 0.11) groups.[21] subgroup TICH-2 data, there also groups spot-sign positive (OR, 0.85; 0.29–2.46) negative 0.77; 0.41–1.45) participants (Pheterogenity 0.88).[41] Recently, based assessment (TRAIGE) non-vitamin (TICH-NOAC) expansion.[22,42] Platelet transfusion Antiplatelet drugs interfere platelet aggregation antiplatelet (PATCH) 190 prior diagnostic brain imaging.[43] death dependence 2.05; 1.18–3.56; 0.0114). addition, serious (42% 29%). Therefore, transfusions potentially harmful unless requires emergency surgery.[11] Desmopressin (DDAVP) DDAVP induces synthesis von Willebrand (VWF) endothelial cells commonly pro-hemostatic drug inherited disorders. recent comparing (n 118) 91), (16.1% 17.6%; 0.78) groups.[44] Surgical Treatment evacuation mass effect, (ICP), midline shift, herniation. Additionally, it injury. (1) craniotomy evacuation, (2) minimally invasive surgery (MIS) (3) external ventricular drain (EVD) IVH hydrocephalus. Craniotomy investigate evacuation.[14] total 1033 supratentorial lobar basal ganglia conservative main inclusion criteria 72 ictus, diameter ≥2 cm, Glasgow Coma (GCS) ≥5. (26% 24%, 0.414) (36% 37%, 0.707) II performed same investigators test ICH.[15] 601 10–100 best GCS 5 6, eye 48 ictus management. unfavorable (62% 59%, 0.367) (18% 0.095) revealed small superficial IVH. limitations delayed median (30 26 respectively) massive (a cm mL). MIS bone flap, parenchyma dissection, retraction normal tissue reach hematoma. has advantage causing injury through openings peri-fascicular tract formation. Auer et al[12] report endoscopic medical 1989. 100 focal deficits altered ≥10 mL ictus. hematomas evacuated burr hole neuro-endoscope. 140–160 both significantly 70%, <0.01) only minimal (40% 25%, <0.05). 50 mL. 2009, Wang al[13] published RCT craniopuncture 25–40 ≥9, 377 195) 182). Craniopuncture dependent survivors (mRS >2) (40.9% 63.0%, <0.01). (6.7% 8.8%) thrombolysis open-label, conducted 78 hospitals North America, Europe, Australia, Asia.[17] procedure included stereotactic image-guided placement inside hematoma, intra-hemorrhage aspiration 1.0 tissue-type plasminogen activator (r-tPA) every maximum nine doses. 506 ≥30 ≤14 NIHSS ≥6, least scan either MISTIE led size 69% 3% treatment, 0–3) (45% 41%, 0.33). meta-analysis residual <15 Xu al[45] investigated small-bone flap hypertensive (MISICH 16 centers China, 733 ≥25 surgery, aspiration, 1:1:1 ratio. (33.3% endoscopy 32.7% (22.2%, 0.017). analysis, thalamic craniotomy. three limitation recently removal (ENRICH) trial,[46] 300 anterior 30–80 last-known (surgery alone (control utility-weighted mRS demonstrated (the 0.458 0.374; difference, 0.084; Bayesian credible interval, 0.005–0.163; posterior probability superiority 0.981). percentage who died 9.3% 18.0% While ENRICH MIS, beneficial appeared hemorrhages (+0.1418). fared worse (−0.0406). These findings RCTs, which hemorrhage.[13,45] inconsistent due criteria, techniques, endpoint, statistical analysis. Additional deep subcortical hematomas. EVD seen up 45% ICH.[47] outcomes. addition clotting aqueduct obstructive hydrocephalus, breakdown products cause inflammation ependymal subependymal tissue.[48] fibrosis arachnoid granulations, communicating Clot lysis: accelerated resolution (CLEAR 500 ≤30 obstructing 3rd 4th ventricles, pathology r-tPA doses 249) 0.9% saline 251) via EVD.[16] ≤3) (48% 45%; 0.554). (20–50 mL) appear have treatment. Critical Thinking Future Clinical Trial Design Timing post hoc combined trials, reaching one outcome.[49,50] supported finding.[30] comprehensive 6-h strongly support therapy, anticoagulation, future designs. timing Patients procedure, contrast, could futile (hematoma volumes >90 irreversible damage.[7] intervention, Table 1. Among CLEAR most delay randomization (47 51.8 respectively).[17,18] (minimal diameters 26–30 h.[15,16] trial[46] Both selection (with surgery. 2186) eight those ictus.[51] select 25–80 2–8 - Summary Study Inclusion Sample size: (n) Median (h) Primary Favorable Mortality: (%) Limitation Mendelow al [14] 2005 Minimal cmGCS ≥5, 503 530 (16–49) GOS 26% 0.414 36% 0.707 included, [13] 2009 Motor strength 0–3, >9, ganglion 195 182 21.1 (4–72) Death dependency 59.1% 37.0%, <0.0001 6.7% 8.8%, 0.44 Relatively sample unable compare late [15] 2013 Conscious, IVH, ictal 305 292 (15.3–25.3) GOSE 41% 38%, 0.367 18% 0.095 47% ≥21 Hanley [16] 2017 ventricles 246 245 (36.4–65.8) 0–3 48% 45%, 0.554 29%, 0.007 Most [17] 2019 255 251 47 (33–60) 0.33 19% 26%, 0.08 Very Pradilla [46] 2024 5–14, >5, 16.75 (10.7–21.3) Utility weighted-mRS 0.374. Significant 20% 23%, 0.669 ENRICH: GCS: Scale; GOS: Outcome GOSE: Extended IVH: Intraventricular mRS: Modified NIHSS: RCTs: Randomized trials; STICH: Validated measurement endpoint.[23,36,39] As shown Annexa-I necessarily outcomes.[23] long-term endpoint. endpoint,[46] been validated trials.[46] contributed score. Finally, recovery slow gradual. 715 4–5) CLEAR-III 43% achieved months.[52] optimal months. "Time brain" apply hours, critical design. Conflicts interest None.

Language: Английский