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 outcomes 7).


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 location, hematoma volume, white blood cells, and D-dimer. Internal 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.
3)
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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.
5)
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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)
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9)
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11) , 17)
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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.
13)
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18)
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.
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