Spontaneous Intracerebral Hemorrhage Risk Factors

Spontaneous Intracerebral Hemorrhage Risk Factors

Psychosocial, ethnic, and economic factors play a role in the prevalence of cerebral hemorrhage, with ICH being twice as common in low-income and middle-income countries compared with high-income countries. Other identified risk factors for ICH include age (i.e., each decade from 50 years of age is associated with a 2-fold increase in the incidence of ICH) and an elevated alcohol intake.

Etiologies of ICH to always consider include intracranial aneurysms (typically presenting as subarachnoid hemorrhage); arteriovenous malformations (ICH is the first presentation of AVMs in 60 % of cases); cerebral venous sinus thrombosis and venous infarction; brain tumors (<5 % of all ICH cases) including cerebral metastases (e.g., lung cancer, melanoma, renal cell carcinoma, thyroid carcinoma, and choriocarcinoma) and primary CNS tumors (e.g., glioblastoma multiforme and oligodendrogliomas); and drugs of abuse (e.g., cocaine, amphetamines). Because of the differing etiologies of ICH, a rapid and accurate diagnosis of the underlying etiology of ICH is essential to direct appropriate management strategies.

The most important modifiable risk factor in spontaneous ICH is chronic arterial hypertension:

see Hypertensive intracerebral hemorrhage.

Besides hypertension, cerebrovascular amyloid deposition (i.e., cerebral amyloid angiopathy) is associated with ICH in older patients.


Although cerebral amyloid angiopathy (CAA), which is Aβ deposition in the cerebral vessels, related cerebral hemorrhage rarely develops in young people, several patients with CAA-related cerebral hemorrhage under the age of 55 with histories of neurosurgeries with and without dura mater graft in early childhood have been reported. These patients might show that Aβ pathology is often recognized as Aβ-CAA rather than parenchymal Aβ deposition in the transmission of cerebral β-amyloidosis in humans, and Hamaguchi et al. proposed an emerging concept, “acquired CAA”. Considering that there have been several patients with acquired CAA with an incubation period from neurosurgery and the onset of CAA-related cerebral hemorrhage of longer than 40 years, the number of cases is likely to increase in the future, and detailed epidemiological investigation is required. It is necessary to continue to elucidate the pathomechanisms of acquired CAA and urgently establish a method for preventing the transmission of cerebral β-amyloidosis among individuals 1).

It is a common initial symptom of intracranial vascular malformations.

see Intracerebral hemorrhage from ruptured cerebral arteriovenous malformation.

see Aneurysmal intracerebral hemorrhage.

see Cerebral venous sinus thrombosis and venous infarction.

see Spontaneous intracranial hematoma caused by neoplasm.

Vasculitis.

Complication of AIDS.

Shunting for NPH

Coagulopathies (i.e., the use of antithrombotic or thrombolytic agents, congenital or acquired factor deficiencies) and systemic diseases, such as thrombocytopenia, are possible causes of ICH. The use of oral anticoagulants, especially vitamin K inhibitors (i.e., warfarin), has increased coagulopathy-associated ICH in recent years, accounting for more than 15 % of all cases.

Severe thrombocytopenia can result in petechial hemorrhages or spontaneous intracerebral hemorrhage (ICH).

see Anticoagulant Related Intracerebral Hemorrhage.


Intracerebral hemorrhage risk is increased with higher doses than the recommended 100 mg of alteplase (Activase®, recombinant tissue plasminogen activator (rt-PA)) 2) in older patients, in those with anterior MI or higher Killip class, and with bolus administration (vs. infusion) 3).

When heparin was used adjunctively, higher doses were associated with a higher risk of ICH 4) ICH is thought to occur in those patients with some preexisting underlying vascular abnormality 5). Immediate coronary angioplasty is safer than rt-PA when available 6).

Remote supratentorial hematoma soon after posterior fossa surgery for the removal of a space-occupying lesion is a rare but dramatic and dreaded complication, carrying significant morbidity and mortality 7) 8) 9) 10) 11) 12) 13) 14).

see Posterior reversible encephalopathy syndrome.

Ethanol

Cocaine

Inadvertent intrathecal injection of unapproved contrast agents.

The evidence linking vitamin D (VitD) levels and Spontaneous Intracerebral Hemorrhage Risk Factors remains inconclusive. Szejko et al. tested the hypothesis that lower genetically determined VitD levels are associated with a higher risk of ICH. They conducted a 2-sample Mendelian Randomization (MR) study using publicly available summary statistics from published genome-wide association study of VitD levels (417 580 study participants) and ICH (1545 ICH cases and 1481 matched controls). They used the inverse variance-weighted average method to generate causal estimates and the MR Pleiotropy Residual Sum and Outlier and MR-Egger approaches to assess for horizontal pleiotropy. To account for known differences in their underlying mechanism, we implemented stratified analysis based on the location of the hemorrhage within the brain (lobar or nonlobar). Our primary analysis indicated that each SD decrease in genetically instrumented VitD levels was associated with a 60% increased risk of ICH (odds ratio [OR], 1.60; [95% CI, 1.05-2.43]; P=0.029). They found no evidence of horizontal pleiotropy (MR-Egger intercept and MR Pleiotropy Residual Sum and Outlier global test with P>0.05). Stratified analyses indicated that the association was stronger for nonlobar ICH (OR, 1.87; [95% CI, 1.18-2.97]; P=0.007) compared with lobar ICH (OR, 1.43; [95% CI, 0.86-2.38]; P=0.17). Lower levels of genetically proxied VitD levels are associated with higher ICH risk. These results provide evidence for a causal role of VitD metabolism in ICH 15).

COVID-19 and Intracerebral Hemorrhage


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Hamaguchi T, Ono K, Yamada M. Transmission of Cerebral β-Amyloidosis Among Individuals. Neurochem Res. 2022 Mar 11. doi: 10.1007/s11064-022-03566-4. Epub ahead of print. PMID: 35277809.
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Public Health Service. Approval of Thrombolytic Agents. FDA Drug Bull. 1988; 18:6–7
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Mehta SR, Eikelboom JW, Yusuf S. Risk of intracranial hemorrhage with bolus versus infusion thrombolytic therapy: a meta-analysis. Lancet. 2000; 356:449–454
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Tenecteplase (TNKase) for thrombolysis. Med Letter. 2000; 42:106–108
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DaSilva VF, Bormanis J. Intracerebral Hemorrhage After Combined Anticoagulant-Thrombolytic Therapy for Myocardial Infarction: Two Case Reports and a Short Review. Neurosurgery. 1992; 30:943–945
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Grines CL, Browne KF, Marco J, et al. A Comparison of Immediate Angioplasty with Thrombolytic Therapy for Acute Myocardial Infarction. N Engl J Med. 1993; 328:673–679
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Bucciero A, Quaglietta P, Vizioli L. Supratentorial intracerebral hemorrhage after posterior fossa surgery: Case report. J Neurosurg Sci. 1991;35:221–4.
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Haines SJ, Maroon JC, Jannetta PJ. Supratentorial intracerebral hemorrhage following posterior fossa surgery. J Neurosurg. 1978;49:881–6.
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Harders A, Gilsbach J, Weigel K. Supratentorial space occupying lesions following infratentorial surgery early diagnosis and treatment. Acta Neurochir (Wien) 1985;74:57–60.
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Seiler RW, Zurbrugg HR. Supratentorial intracerebral hemorrhage after posterior fossa operation. Neurosurgery. 1986;18:472–4.
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Tondon A, Mahapatra AK. Superatentorial intracerebral hemorrhage following infratentorial surgery. J Clin Neurosci. 2004;11:762–5.
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Vrettou CS, Stavrinou LC, Halikias S, Kyriakopoulou M, Kollias S, Stranjalis G, et al. Factor XIII deficiency as a potential cause of supratentorial haemorrhage after posterior fossa surgery. Acta Neurochir (Wien) 2010;152:529–32.
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Pandey P, Madhugiri VS, Sattur MG, Devi BI. Remote supratentorial extradural hematoma following posterior fossa surgery. Childs Nerv Syst. 2008;24:851–4.
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Wolfsberger S, Gruber A, Czech T. Multiple supratentorial epidural haematomas after posterior fossa surgery. Neurosurg Rev. 2004;27:128–32.
15)

Szejko N, Acosta JN, Both CP, Leasure A, Matouk C, Sansing L, Gill TM, Hongyu Z, Sheth K, Falcone GJ. Genetically-Proxied Levels of Vitamin D and Risk of Intracerebral Hemorrhage. J Am Heart Assoc. 2022 Jun 22:e024141. doi: 10.1161/JAHA.121.024141. Epub ahead of print. PMID: 35730641.

Spontaneous intracerebral hemorrhage outcome

Spontaneous intracerebral hemorrhage outcome

ICH is a potentially devastating neurologic emergency with long-term functional independence achieved in only 12-39% of cases and mortality rates of 54% at 1 year 1).

Patients with spontaneous intracerebral hemorrhage have high mortality and poor outcome. It is the most serious, least treatable and more variable in incidence and management compared to other stroke subtypes 2) 3).

Although this is a heterogeneous disorder with a wide range of outcomes, overall mortality at 1 month is approximately 40%, and only 25% of patients have a favorable outcome 4) 5).

Case fatality is extremely high (reaching approximately 60 % at 1 year post event). Only 20 % of patients who survive are independent within 6 months 6).


Anion gap level is a potential predictive biomarker for the long-term outcomes of spontaneous intracerebral hemorrhage patients, and rectifying AG at admission improves the spontaneous intracerebral hemorrhage outcome7).


In a cohort (n=1094), there were 306 deaths (per 100 patient-years: absolute event rate 11.7, 95% CI 10.5 to 13.1); 156 were “early” and 150 “late”. In multivariable analyses, early death was independently associated with age (per year increase, HR 1.05, p=0.003), history of hypertension (HR 1.89, p=0.038), pre-event mRS (per point increase, HR 1.41, p<0.0001), admission NIHSS (per point increase, HR 1.11, p<0.0001), and hemorrhage volume > 60ml (HR 4.08, p<0.0001). Late death showed independent associations with age (per year increase, HR 1.04, p=0.003), pre-event mRS (per point increase, HR 1.42, p=0.001), prior anticoagulant use (HR 2.13, p=0.028) and the presence of intraventricular hemorrhage (HR 1.73, p=0.033) in multivariable analyses. In further analyses where time was treated as continuous (rather than dichotomized), the hazard ratio of previous cerebral ischaemic events increased with time, whilst those for GCS, NIHSS and ICH volume decreased over time.

They provided new evidence that not all baseline factors associated with early mortality after intracerebral hemorrhage are associated with mortality after 6 months, and that the effects of baseline variables change over time. The findings could help design better prognostic scores for later death after intracerebral hemorrhage 8).


As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can produce intracranial hypertension, which if left untreated can lead to coma and death.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking.

It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause intracranial hypertension and potentially fatal brain herniation syndromes.

They have high rates of morbidity and rates of mortality of up to 50%. Initial hematoma size and subsequent hematoma expansion are among the most important predictors of poor outcome.

Efforts to improve clinical outcome through mitigation of hematoma expansion have so far been unsuccessful.

Data suggest that outcomes can be improved with standardized medical care.

A strong association exists between the amount of intraventricular hemorrhage (IVH) and poor outcome in intracerebral hemorrhage. An IVH volume of 5 to 10 mL emerges as a significant threshold for decision making on prognosis in these patients 9).

The ICH score is a simple and reliable clinical grading scale that is used for predicting the early mortality of patients with ICHs.

Neurological deterioration (ND) occurs frequently and predicts poor outcomes. Hematoma expansion and intraventricular hemorrhage in early ND, and cerebral edema, fever, and medical complications in later ND 10).


Hematoma expansion is a potentially modifiable predictor of poor outcome following an acute intracerebral hemorrhage (ICH). The ability to identify patients with ICH who are likeliest to experience hematoma expansion and therefore likeliest to benefit from expansion-targeted treatments remains an unmet need. Hypodensities within an ICH detected by noncontrast computed tomography (NCCT) have been suggested as a predictor of hematoma expansion.

There have been no dramatic advances in the development of interventions to improve the functional outcomes after ICH 11).

The purpose of a study was to establish and validate a nomogram to estimate the 30-day probability of death in patients with spontaneous intracerebral hemorrhage.. From January 2015 to December 2017, a cohort of 450 patients with clinically diagnosed cerebral hemorrhage was collected for model development. The minimum absolute contraction and the selection operator (lasso) regression model were used to select the strongest prediction of patients with cerebral hemorrhage. Discrimination and calibration were used to evaluate the performance of the resulting nomogram. After internal validation, the nomogram was further assessed in a different cohort containing 148 consecutive subjects examined between January 2018 and December 2018. The nomogram included five predictors from the lasso regression analysis, including Glasgow coma scale (GCS), hematoma locationhematoma volumewhite blood cells, and D-dimerInternal verification showed that the model had good discrimination, (the area under the curve is 0.955), and good calibration [unreliability (U) statistic, p = 0.739]. The nomogram still showed good discrimination (area under the curve = 0.888) and good calibration [U statistic, p = 0.926] in the verification cohort data. Decision curve analysis showed that the prediction nomogram was clinically useful. The current study delineates a predictive nomogram combining clinical and imaging features, which can help identify patients who may die of a cerebral hemorrhage 12).

The ICH Score is a valid clinical grading scale for long-term functional outcome after acute intracerebral hemorrhage (ICH) 13).

Based on the viewpoint that increased BP causes greater tearing of blood vessels and flow-out of blood through these vessels and eventually leads to the expansion of the hematoma, high BP is considered to be associated with hematoma expansion and poor outcomes, especially early neurological deterioration, mortality, and dependency 14) 15) 16).


The 2015 American Heart Association/American Stroke Association guidelines for the management of spontaneous ICH recommend early BP reduction with an SBP target of 140 mmHg for patients with ICH presenting with an SBP between 150 and 220 mmHg and without any contraindication to acute BP treatment 17).

Spontaneous intracerebral hemorrhage (SICH) survivors are at risk of hospital readmissions. Data on readmissions after SICH is scarce. We aimed to study the frequency and predictors of readmissions after SICH in Algarve, Portugal.

A retrospective study of a community representative cohort of SICH survivors (2009-2015). The first unplanned readmission in the first year after discharge was the outcome. Cox regression analysis was performed to identify predictors of 1-year readmission.

Of the 357 SICH survivors followed, 116 (32.5%) were readmitted within the first-year. Sixty-seven (18.8%) of the survivors were early readmitted (<90 days), corresponding to 57.8% or all readmissions. Common causes were pneumonia, endocrine/nutritional/metabolic and cardiovascular complications. The risk of readmission was increased by prior to index SICH history of ≥ 3 previous emergency department visits (hazards ratio (HR) = 2.663 (1.770-4.007); P < 0.001), pneumonia during index hospitalization (HR = 2.910 (1.844-4.592); P < 0.001) and reduced in patients discharge home (HR = 0.681 (0.366-0.976); P = 0.048).

The rate of readmissions after SICH is high, predictors are identifiable and causes are potentially preventable. Improvement of care can potentially reduce this burden 18).


1)

van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010 Feb;9(2):167-76. doi: 10.1016/S1474-4422(09)70340-0. Epub 2010 Jan 5. PMID: 20056489.
2)

Van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol 2010;9:167–76.
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Krishnamurthi RV, Feigin VL, Forouzanfar MH, et al. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990–2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health 2013;1:e259–81.
4)

van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of Intracerebral hemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9(2):167–176.
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Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurol. 2003;2(1):43–53.
6)

de Oliveira Manoel AL, Goffi A, Zampieri FG, Turkel-Parrella D, Duggal A, Marotta TR, Macdonald RL, Abrahamson S. The critical care management of spontaneous intracranial hemorrhage: a contemporary review. Crit Care. 2016 Sep 18;20:272. doi: 10.1186/s13054-016-1432-0. Review. PubMed PMID: 27640182; PubMed Central PMCID: PMC5027096.
7)

Shen J, Li DL, Yang ZS, Zhang YZ, Li ZY. Anion gap predicts the long-term neurological and cognitive outcomes of spontaneous intracerebral hemorrhage. Eur Rev Med Pharmacol Sci. 2022 May;26(9):3230-3236. doi: 10.26355/eurrev_202205_28741. PMID: 35587074.
8)

Banerjee G, Ambler G, Wilson D, Hostettler IC, Shakeshaft C, Lunawat S, Cohen H, Yousry T, Al-Shahi Salman R, Lip GYH, Houlden H, Muir KW, Brown MM, Jäger HR, Werring DJ; CROMIS-2 collaborators. Baseline factors associated with early and late death in Intracerebral hemorrhage survivors. Eur J Neurol. 2020 Mar 29. doi: 10.1111/ene.14238. [Epub ahead of print] PubMed PMID: 32223078.
9)

Chan E, Anderson CS, Wang X, Arima H, Saxena A, Moullaali TJ, Heeley E, Delcourt C, Wu G, Wang J, Chen G, Lavados PM, Stapf C, Robinson T, Chalmers J, Huang Y; INTERACT2 Investigators. Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: intensive blood pressure reduction in acute cerebral hemorrhage trial results. Stroke. 2015 Mar;46(3):653-8. doi: 10.1161/STROKEAHA.114.008470. Epub 2015 Feb 12. PubMed PMID: 25677598.
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Lord AS, Gilmore E, Choi HA, Mayer SA; VISTA-ICH Collaboration. Time course and predictors of neurological deterioration after intracerebral hemorrhage. Stroke. 2015 Mar;46(3):647-52. doi: 10.1161/STROKEAHA.114.007704. Epub 2015 Feb 5. PubMed PMID: 25657190.
11) , 17)

Hemphill JC 3rd, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M, Fung GL, Goldstein JN, Macdonald RL, Mitchell PH, Scott PA, Selim MH, Woo D; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015 Jul;46(7):2032-60. doi: 10.1161/STR.0000000000000069. Epub 2015 May 28. PubMed PMID: 26022637.
12)

Han Q, Li M, Su D, Fu A, Li L, Chen T. Development and validation of a 30-day death nomogram in patients with spontaneous cerebral hemorrhage: a retrospective cohort study. Acta Neurol Belg. 2021 Feb 10. doi: 10.1007/s13760-021-01617-1. Epub ahead of print. PMID: 33566335.
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Hemphill JC 3rd, Farrant M, Neill TA Jr. Prospective validation of the ICH Score for 12-month functional outcome. Neurology. 2009 Oct 6;73(14):1088-94. doi: 10.1212/WNL.0b013e3181b8b332. Epub 2009 Sep 2. PubMed PMID: 19726752; PubMed Central PMCID: PMC2764394.
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Rodriguez-Luna D, Pineiro S, Rubiera M, Ribo M, Coscojuela P, Pagola J, et al. Impact of blood pressure changes and course on hematoma growth in acute intracerebral hemorrhage. Eur J Neurol. 2013;20:1277–1283.
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Sakamoto Y, Koga M, Yamagami H, Okuda S, Okada Y, Kimura K, et al. Systolic blood pressure after intravenous antihypertensive treatment and clinical outcomes in hyperacute intracerebral hemorrhage: the stroke acute management with urgent risk-factor assessment and improvement-intracerebral hemorrhage study. Stroke. 2013;44:1846–1851.
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Zhang Y, Reilly KH, Tong W, Xu T, Chen J, Bazzano LA, et al. Blood pressure and clinical outcome among patients with acute stroke in Inner Mongolia, China. J Hypertens. 2008;26:1446–1452.
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Nzwalo H, Nogueira J, Guilherme P, Abreu P, Félix C, Ferreira F, Ramalhete S, Marreiros A, Tatlisumak T, Thomassen L, Logallo N. Hospital readmissions after spontaneous intracerebral hemorrhage in Southern Portugal. Clin Neurol Neurosurg. 2018 Apr 12;169:144-148. doi: 10.1016/j.clineuro.2018.04.015. [Epub ahead of print] PubMed PMID: 29665499.

Spontaneous intracerebral hemorrhage surgery

Spontaneous intracerebral hemorrhage surgery

Based on the MIMIC-III database, Yi et al. from the Guangzhou Overseas Chinese Hospital firstly described the dissimilarities in survival probabilitymortality, and neurological recovery among mainstream treatments for intracerebral hemorrhage; secondly, patient classification was determined by important clinical features; and outcome variations among treatment groups were compared. The 28-day, 90-day, and in-hospital mortality in the craniotomy group were significantly lower than minimally invasive surgery (MIS) and non-surgical group patients; and, the medium/long-term mortality in the MIS group was significantly lower than the non-surgical group. The craniotomy group positively correlated with short-term GCS recovery compared with the MIS group; no difference existed between the non-surgical and MIS groups. The craniotomy group’s 90-day survival probability and short-term GCS recovery were superior to the other two treatments in the subgroups of first GCS 3-12; this tendency also presented in the MIS group over the non-surgical group. For milder patients (first GCS > 12), the three treatment regimens had a minimal effect on patient survival, but the non-surgical group showed an advantage in short-term GCS recovery. Craniotomy patients have lower mortality and a better short-term neurological recovery in an ICH population, especially in short-to-medium term mortality and short-term neurological recovery over MIS patients. In addition, surgical treatment is recommendable for patients with a GCS ≤ 12. 1).

see STITCH.

see Intracerebral hemorrhage treatment randomized controlled trials.


A better understanding of the pathophysiology of intracerebral hemorrhage (ICH) has led to the identification of several new mechanisms of injury that could be potential therapeutic targets 2).

Minimally invasive surgery (MIS) for the treatment of ICH is the main clinical method that is currently used, despite the lack of large-scale, clinical, multi-center, randomized controlled trials 3).

see Intracerebral hemorrhage surgery indications.

Open craniotomy is the most widely studied surgical techniques in patients with supratentorial ICH. Other methods include endoscopic hemorrhage aspiration, use of fibrinolytic therapy to dissolve the clot followed by aspiration, and CT-guided stereotactic aspiration 4) 5).

see Intracerebral hemorrhage minimally invasive surgery

see Endoscopic surgery for intracerebral hemorrhage

Decompressive hemicraniectomy with hematoma evacuation for large ICH might be a safe and effective procedure in patients with severely disturbed consciousness and large hematoma volume 6).

Decompressive hemicraniectomy without clot evacuation appears feasible in patients with large ICH and deserves further investigation, preferably in a randomized controlled setting 7) 8)

Early decompressive hemicraniectomy (DH) with or without clot evacuation is feasible and safe for managing spontaneous ICH. The experience of Esquenazi et al. in a uncontrolled retrospective series, the largest such series in the modern era, suggests that it may be of particular benefit in patients with large non-dominant hemisphere ICH who are not moribund at presentation. These findings suggest that a prospective randomized trial of DH vs. craniotomy for ICH be conducted.

Over 7 years, DH was performed in 73 patients with clot evacuation in 86% and DH alone in 14%. The average ICH volume was 81 cc and the median DH surface area was 105 cm(2). 26 patients were comatose at initial presentation. Three-month functional outcomes were favorable in 29%, unfavorable in 44% and 27% of patients expired. Admission Glasgow Coma Scale (p=0.003), dominant hemisphere ICH location (p=0.01) and hematoma volume (p=0.002) contributed significantly to the outcome, as estimated by a multivariate analysis. Eight surgical complications occurred. 9).

Intracerebral hemorrhage surgery meta-analysis


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Yi Y, Che W, Cao Y, Chen F, Liao J, Wang X, Lyu J. Prognostic data analysis of surgical treatments for intracerebral hemorrhage. Neurosurg Rev. 2022 Apr 19. doi: 10.1007/s10143-022-01785-5. Epub ahead of print. PMID: 35441246.
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Aiyagari V. The clinical management of acute intracerebral hemorrhage. Expert Rev Neurother. 2015 Dec;15(12):1421-32. doi: 10.1586/14737175.2015.1113876. Epub 2015 Nov 13. PubMed PMID: 26565118.
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Wang WM, Jiang C, Bai HM. New Insights in Minimally Invasive Surgery for Intracerebral Hemorrhage. Front Neurol Neurosci. 2015 Nov;37:155-65. doi: 10.1159/000437120. Epub 2015 Nov 12. PubMed PMID: 26588789.
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Hersh EH, Gologorsky Y, Chartrain AG, Mocco J, Kellner CP. Minimally Invasive Surgery for Intracerebral Hemorrhage. Curr Neurol Neurosci Rep. 2018 May 9;18(6):34. doi: 10.1007/s11910-018-0836-4. Review. PubMed PMID: 29740726.
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Hanley DF, Thompson RE, Muschelli J, Rosenblum M, McBee N, Lane K, Bistran-Hall AJ, Mayo SW, Keyl P, Gandhi D, Morgan TC, Ullman N, Mould WA, Carhuapoma JR, Kase C, Ziai W, Thompson CB, Yenokyan G, Huang E, Broaddus WC, Graham RS, Aldrich EF, Dodd R, Wijman C, Caron JL, Huang J, Camarata P, Mendelow AD, Gregson B, Janis S, Vespa P, Martin N, Awad I, Zuccarello M; MISTIE Investigators. Safety and efficacy of minimally invasive surgery plus alteplase in intracerebral haemorrhage evacuation (MISTIE): a randomised, controlled, open-label, phase 2 trial. Lancet Neurol. 2016 Nov;15(12):1228-1237. doi: 10.1016/S1474-4422(16)30234-4. Epub 2016 Oct 11. PubMed PMID: 27751554; PubMed Central PMCID: PMC5154627.
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Takeuchi S, Wada K, Nagatani K, Otani N, Mori K. Decompressive hemicraniectomy for spontaneous intracerebral hemorrhage. Neurosurg Focus. 2013 May;34(5):E5. doi: 10.3171/2013.2.FOCUS12424. Review. PubMed PMID: 23634924.
7)

Heuts SG, Bruce SS, Zacharia BE, Hickman ZL, Kellner CP, Sussman ES, McDowell MM, Bruce RA, Connolly ES Jr. Decompressive hemicraniectomy without clot evacuation in dominant-sided intracerebral hemorrhage with ICP crisis. Neurosurg Focus. 2013 May;34(5):E4. doi: 10.3171/2013.2.FOCUS1326. PubMed PMID: 23634923.
8)

Bösel J, Zweckberger K, Hacke W. Haemorrhage and hemicraniectomy: refining surgery for stroke. Curr Opin Neurol. 2015 Feb;28(1):16-22. doi: 10.1097/WCO.0000000000000167. PubMed PMID: 25490194.
9)

Esquenazi Y, Savitz SI, Khoury RE, McIntosh MA, Grotta JC, Tandon N. Decompressive hemicraniectomy with or without clot evacuation for large spontaneous supratentorial intracerebral hemorrhages. Clin Neurol Neurosurg. 2015 Jan;128:117-22. doi: 10.1016/j.clineuro.2014.11.015. Epub 2014 Nov 27. PubMed PMID: 25496934.
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