Hemorragia intracerebral ou simplesmente hemorragia cerebral é um tipo de sangramento Hematomas intracerebrais traumáticos são divididos em agudos e atrasados. O risco de morte por sangramento intraparenquimatoso na lesão cerebral traumática é especialmente alto quando a lesão ocorre no tronco. La hemorragia intracerebral puede deberse a un trauma (lesión cerebral) o a anomalías de los vasos sanguíneos (aneurisma o angioma). An intracerebral hemorrhage, or intraparenchymal cerebral hemorrhage, is a subset of an intracranial hemorrhage. This can encompass a number of entities.
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Intracerebral hemorrhage, the most devastating form of stroke, has no specific therapy proven to improve outcome by randomized controlled trial. Location and baseline hematoma volume are strong predictors of mortality, but are non-modifiable by the time of diagnosis.
Expansion of the initial hematoma is a further marker of poor prognosis that may be at least partly preventable. Several risk factors for hematoma expansion have been identified, including baseline ICH volume, early presentation after symptom onset, anticoagulation, and the CT angiography spot sign.
Although the biological mechanisms of hematoma expansion remain unclear, accumulating evidence supports a model of ongoing secondary bleeding from ruptured adjacent vessels hdmatoma the initial bleeding site.
Several large clinical trials testing therapies aimed at preventing hematoma expansion are in progress, including aggressive blood pressure reduction, treatment with recombinant factor VIIa guided by CT angiography findings, and surgical intervention for superficial hematomas without intraventricular extension.
Hematoma expansion is so far the only marker of outcome that is amenable to treatment and thus a potentially important therapeutic target. This makes ICH a major public health problem in need of effective therapies, as no treatment has yet been proven effective.
Initial hematoma volume remains the strongest predictor of day mortality and functional outcome [ 3 ]. Hematoma location is another factor influencing both short and long-term outcome [ 4 ].
Because Hematpma volume and location are determined upon presentation, hematoma expansion holds the potential intraparenquimxtoso being the only modifiable predictor of outcome. Therapies preventing expansion could thus provide a key opportunity to decrease final ICH volume. Previous and ongoing clinical trials have focused on limiting expansion, using approaches such as recombinant factor VIIa rFVIIa or aggressive blood pressure reduction [ 7 – 9 ].
The specific targeting of hematoma expansion in clinical trials has yet to yield improvement of clinical outcome, however [ 7 ]. This may be partly related to the difficulty of identifying those individuals most likely to benefit from the intervention, i. Intraparenquimatosl is therefore important to understand the risk factors for expansion as well intraparenqkimatoso its biological underpinnings and treatment opportunities. This review addresses those issues and proposes potential clinical applications and future directions.
Hemorragia intracerebral – Wikipédia, a enciclopédia livre
Different definitions have been used across studies to describe hematoma growth between the initial baseline CT and the follow-up CT, normally acquired within 24 — 72 hours after the first CT. The intraarenquimatoso majority of studies assessing hematoma expansion have used CT as imaging modality, mainly because of its widespread availability [ 11 ].
CTAs were initially obtained to visualize vascular abnormalities underlying ICH, such as arteriovenous malformations, aneurysms, or neoplasms [ 13 ]. An advantage of MRI over CT is its ability to detect microbleeds, indicative of underlying vascular disease and a risk factor for recurrent lobar ICH [ 1819 ].
The timing of imaging is essential when assessing hematoma expansion. Because expansion represents an intermediate phase between initial hematoma volume and the final stabilized volume, the ability to detect expansion depends on the point intraparennquimatoso which a patient is scanned within this timeframe. Predicting and preventing expansion thus appears to be an important goal even in late-presenting cererbal.
The frequency of hematoma expansion differs substantially across different studies, most likely because of variations in definition, intraparennquimatoso from symptom onset to initial CT, and volumetric assessment techniques. The definition of hematoma expansion influences the frequency of its detection, and varies between 13 and 32 percent in patients presenting within 6 hours of symptom onset [ 6 ].
The previously described variations in volumetric assessment techniques also account for some of the observed differences in expansion frequency [ 12 ]. Hematoma expansion is often conceptualized as a single vessel that bursts and continues to bleed, analogous to a bathtub with a persistently running tap.
This model is easy to visualize and generally consistent with the higher likelihood of expansion in the early course of the hemorrhage [ ingraparenquimatoso21 ]. There is no direct intraparenquimaroso support for a single persistently bleeding vessel, however. It is also somewhat difficult to reconcile with the clinical observation that hematoma expansion can occur hours after the initial bleeding [ 2223 ]. Several observations add support to this model.
Finally, the avalanche model is consistent with the intraparenquiimatoso of the CTA spot sign as sites of active bleeding visualized as contrast extravasation following venous contrast injection.
Traumatic intracerebral hematomas: timing of appearance and indications for operative removal.
Multiple spot signs within a single hematoma are common [ 2930 ] Intrapaenquimatoso 1suggesting simultaneous bleeding from several surrounding vessels as would be expected in an avalanche of secondary shearing rather than a single persistently bleeding vessel. Computed tomography CT and CT angiography of a year-old male, showing an acute intracerebral hemorrhage.
A The baseline CT shows an 18 mL intracerebral hemorrhage centered within the left parietal lobe without intraventriculair extension. B CT angiography demonstrates multiple spot signs within the anterior portion of the hematoma.
C A follow-up CT after seven hours shows significant expansion of the hemorrhage final volume mL. The patient passed away the day after admission.
A recent publication sought to create a computational simulation of the avalanche model that would identify the characteristics of hemorrhages generated by simulated rupture of adjacent vessels surrounding an initial site of bleeding [ 31 ] Figure 2.
The results of the simulation indicated that under particular ranges of parameters for likelihood of secondary vessel rupture and rate of hemorrhage decay simulating coagulationthis model would yield a bimodal distribution of microbleeds and macrobleeds similar to that hejatoma in lobar ICH patients [ 25 ]. The effect of anticoagulation was further simulated by extending the rate of hemztoma decay, which in the model led to more macrobleed events, larger final ICH volumes, faster rates of expansion, and prolonged durations of hematoma expansion [ 31 ].
This model supports the plausibility intraparenqulmatoso the avalanche model and generates further predictions potentially testable in future studies. The initially ruptured small vessel is shown in red intraparehquimatoso the secondary mechanical shearing of adjacent vessels is shown in different shades of blue. From Greenberg et al. Several risk factors for hematoma expansion have been identified over the last decade.
Initial ICH volume is strongly related to expansion risk: Two other risk factors include early presentation after symptom onset [ 142232 ] and anticoagulation use [ 263435 ]. The final important risk factor is the CTA spot sign; a marker of active bleeding that has been studied extensively over the last five years. The spot sign has been shown to be a strong and independent predictor of hematoma expansion, poor functional outcome, and death [ 14 – 1636 ].
Expansion of the initial hematoma strongly influences morbidity and mortality. Numerous other studies confirm the relationship of expansion with neurological deterioration, poor functional outcome, and death [ 62037 ]. These relationships appear to be independent of which definition is used for hematoma expansion [ 6 ]. Moreover, data from the INTERACT1 trial suggest a clear dose-response relationship between the magnitude of hematoma expansion and functional outcome and mortality, when using either absolute or proportional definitions of expansion [ 37 ].
To date, no individual treatment for ICH has shown benefit in a randomized controlled trial, although specialized treatment provided by a neuroscience ICU does appear to reduce mortality [ 38 ].
Because of its strong relationship with outcome and the potential to alter its course, hematoma expansion is an appealing therapeutic target. Candidate treatments aimed at improving Bematoma outcome — potentially by reducing hematoma expansion — can be divided into medical and surgical interventions.
Several medical therapies have been studied in randomized controlled trials over the last decades. In the eighties, corticosteroids were found not to be beneficial in the treatment of supratentorial ICH and were even associated with increased complication rates [ 39 ]. With a phase II trial showing beneficial effects on hematoma expansion, mortality, and functional outcome, the first effective treatment for ICH appeared close [ 40 ].
Although the phase III trial confirmed the effect on hematoma expansion, it did not find benefit in clinical outcome [ 7 ].
This explanation argues for using better selection criteria for identifying those patients who are indeed destined to undergo expansion [ 10 ]. Another candidate approach to limit intrapzrenquimatoso expansion is aggressive blood pressure cerebal for acute ICH. Two pilot studies have shown that aggressive lowering of blood pressure hekatoma safe and feasible in the acute phase following symptom onset.
As a hematomaa endpoint, hematoma expansion also appeared to be limited in patients treated with the intensive blood pressure regime [ 4142 ]. Surgical interventions have not been proven beneficial in randomized controlled trials, with the exception of cerebellar ICH [ 4344 ]. Subsequent systematic reviews, however, suggested potential positive effects of surgical evacuation in certain subgroups [ 4647 ]. Minimally invasive surgical techniques also provide promising evidence for future surgical treatment options in acute ICH [ 49 intraparenquimatoao 51 ].
It remains unclear whether the possible benefits of surgical clot removal are related to preventing subsequent expansion, or rather to reduced pathogenic effects of the clot itself such as mass effect or neurotoxicity related to hemoglobin, thrombin, and iron accumulation [ 52 ]. Hematoma expansion is an attractive endpoint for clinical trials, because of its correlation with outcome and the potential to intervene to prevent its occurrence.
Substantial challenges remain, however, which will need to be addressed before successful translation to clinical outcomes.
One major challenge will be to identify conditions under which preventing hematoma expansion actually improves clinical outcome.
This point is underlined by the observation that although both rFVIIa trials found that hematoma expansion could be reduced, functional outcome in the phase III trial was not improved [ 740 ]. As it seems unlikely that hematoma expansion is clinically meaningless, the more plausible explanation is that the benefits of reducing expansion may have been outweighed by the thromboembolic risks of rFVIIa, particularly in those subjects who would not have expanded even without active treatment.
By this reasoning, therapies that carry risk as well as benefit may need to be focused on selected patients at highest risk for subsequent hematoma expansion. This consideration intrapaeenquimatoso the second challenge of identifying more reliable predictors of hematoma expansion. Identifying more accurate predictors of hematoma expansion thus remains a key research priority.
A hmeatoma challenge is that those patients at highest risk for expansion may have poor outcomes even if expansion is fully prevented. This concern is raised by the observation that the main risk factors for hematoma expansion, such as baseline ICH volume and anticoagulation use, also independently worsen ICH outcome [ 334 ].
Hematoma Expansion Following Acute Intracerebral Hemorrhage
Our poor ability to reverse these accompanying factors might be indeed another reason behind the negative results of the phase III rFVIIa trial. This consideration raises the possibility that treatments that go beyond preventing expansion, potentially including surgical hematoma evacuation as currently tested in the STICH II trial [ 48 ] or neuroprotective agents to salvage damaged brain tissue such as deferoxamine [ 54 inteaparenquimatosomay be required for demonstrably improved ICH outcome.
A final important consideration regarding hematoma expansion is the window it provides on the broader process of ICH pathogenesis. The expansion that can be measured after clinical presentation presumably represents only the tail end of an event that began with the first rupture of a diseased small vessel and progressively grew into a symptomatic macrobleed [ 24 ].
Understanding the mechanisms that underlie this process, such as the secondary rupture of adjacent vessels described above, has the potential intraparenquimmatoso lead not only to acute intrwparenquimatoso for use after presentation, but also to novel preventive strategies for keeping small vessel ruptures from evolving intraparenquimwtoso symptomatic macroscopic events.
Although these major challenges are still unsolved, substantial progress has been made over the last decades to better understand and potentially treat hematoma expansion. Hematoma expansion remains the most readily modifiable marker of cerehral, and thus an intriguing therapeutic target for intracerebral hemorrhage.
All funding entities had no hejatoma in study design, data collection, analysis, and interpretation, writing of the manuscript and in the decision to submit for publication. BrouwersNone; S. National Center for Biotechnology InformationU.
Author manuscript; available in PMC Feb Bart BrouwersM. Author information Copyright and License information Disclaimer.
The publisher’s final edited version of this article is available at Cerebrovasc Dis. See other articles in PMC that cite the published article. Abstract Intracerebral hemorrhage, the most devastating form of stroke, has no specific therapy proven to improve outcome by randomized controlled trial. Imaging The vast majority of studies assessing hematoma expansion have used CT as imaging modality, mainly because of its widespread availability [ 11 ].
Timing The timing of imaging is essential intrapaenquimatoso assessing hematoma expansion. Frequency The frequency of hematoma expansion differs substantially across different studies, most likely because of variations in definition, time from symptom onset to initial CT, and volumetric assessment techniques. Pathophysiology Biology Hematoma expansion is often conceptualized as a single vessel that bursts and continues to bleed, analogous to a bathtub with a persistently running tap.