Epidemiology

ICH, like ischemic stroke, has a clear age-dependent incidence rate, occurring slightly earlier in life than ischemic attacks. Most population-based registries report an incidence of 10–15 per 100 000 per year, and variations exist towards higher rates in some populations. A decrease of rates has been reported over time from several regions of the world. The incidence of ICH is influenced by racial factors and was found to be higher in Blacks, Hispanics, and Asians compared with the white population. While the exact reasons for this decline are not known, it is reasonable to assume that a decline in rates as well as severity of arterial hypertension has significantly contributed to the declining rate of ICH [2–4].

Classification

The classification of ICH is confusing and difficult, due to the mostly unknown pathophysiology. Intracerebral hemorrhages can be distinguished by etiology and localization. Concerning localization we differentiate between lobar bleeding and ICH in deep brain structures, such as basal ganglia and thalamic bleedings. This determination is almost due to etiological factors, because deep ICH are often associated with hypertension, although hypertension is not the reason for ICH, but induces the causative arteriosclerotic microangiopathy. For this reason, deep ICH in combination with hypertension are also termed “typical” ICH. More than 50% of ICH are associated with hypertension. Other typical hypertensive bleedings are located in the cerebellum and the brainstem. The term “spontaneous ICH” (SICH) emphasizes that, apart from hypertension, no reason for the bleeding has been found.

Lobar bleedings are often associated with structural lesions, such as cerebral amyloid angiopathy (CAA), neoplasmas, and arteriovenous malformations (AVM), and are often seen in elderly patients. Lobar bleedings are often termed “atypical” ICH [5, 6]. About 40% of all ICH occur in the basal ganglia, 30% in the thalamus, 20% lobar, and about 10% occuring in the cerebellum and pons (Table 12.1). The striatum (caudate nucleus and putamen) is the most common site of “spontaneous” ICH [7, 8].

The commonly used classification into primary (due to hypertension and/or cerebral amyloid angiopathy) and secondary ICH is obsolete and should be avoided, because it mixes the etiology and risk factors of ICH. Secondary ICH may be caused by arterial disease (e.g. CAA, small-vessel disease, intracranial aneurysms, vasculitis, and Moyamoya), venous disease (e.g. sinus venous thrombosis), vascular malformations, hemostatic disorders (e.g. hematologic disease or iatrogenic disorders with e.g. VKA), or ICH in the context of other disease (e.g. trauma, neoplasms, and substance abuse). Table 12.2 indicates an overview of classification of underlying ICH etiology (Figure 12.1).

Figure 12.1 A: MRI with blood-sensitive gradient echo sequence (GRE) showing a left temporo-occipital ICH.

B: T1 after Gadolinium reveals a false aneurysm extending into ICH.

C: DSA lateral view with 4 cm nidus fed by multiple temporal feeders coming from P3 segment and superficial/deep venous drainage (Spetzler-Martin grade 4).

D: During transarterial embolization of false aneurysm and parts of the nidus (arrow marks the rupture point).

E: Lateral view with Onyx cast after complete embolization. (Courtesy of Dr. med. Markus Möhlenbruch, Neuroradiology, Klinikum Frankfurt Höchst/Heidelberg University Hospital.)

Mortality and Prognostic Factors

Although mortality could be reduced during the last 10 years it is still about 20–30% (approaching 50%) within 3 months with severe disability in the majority of survivors [1]. Half of the deaths occur within the acute phase, especially in the first 2 days. Early mortality, which is mostly reported as 30-day mortality, is higher than in ischemic stroke and largely depends on bleeding volume. In the cerebral hemispheres, a volume of over 60 ml carries an unfavorable prognosis and is seen for deep hemorrhage (93%), and slightly less often for lobar bleeding (71%). Smaller bleedings show better prognosis and less early mortality [9–11].

One multivariate analysis showed that independent prognostic factors of 30-day mortality are ICH volume, Glasgow Coma Score on admission, age over 80 years, infratentorial origin of ICH, and presence of intraventricular blood [12]. An intraventricular bleeding increases mortality 4-fold [13]. The parenchymal volume of the hemorrhage is the most decisive prognostic component. Total volumes of more than 60 ml cannot be compensated by intracranial compartmental reserve capacity. Decompensation will lead to herniation of the medial temporal lobe and downward shift with compression of the brainstem. It is also well known that hemorrhages into the thalamic region tend to rupture into the ventricles after some hours or days, and this is manifested as a dramatic clinical event with sudden deterioration [14].

It is worth noting that in one study a decreased mortality rate was seen when such patients were cared for in a setting of a neurological/neurosurgical intensive care unit compared to treatment in general intensive care units (NICUs) [15]. Also a treatment in a stroke unit compared with treatment on a general medical ward showed a reduced 30-day mortality (39% vs. 63%) [16]. It is generally believed that ICH survivors have better neurological and functional prognoses than the survivors of ischemic stroke [17].

Also hematoma growth was shown to be a crucial and independent predictor of early neurological deterioration and is associated with increased mortality and poor functional outcome [18]. A pooled individual patient meta-analysis showed that for each 10% increase in ICH growth, there was a 5% increased hazard of death, a 16% greater likelihood of worsening by 1 point on the mRS (modified Ranking Scale), or 18% of moving from independence to assisted independence or from assisted independence to poor outcome on the Barthel Index [19]. These findings indicate that early extension of the initial hematoma boundaries has substantial clinical implications.

Genetics of Spontaneous ICH

Monogenic disorders associated with spontaneously occurring ICH are not known. No genetic markers exist to date. But some disorders convey an increased risk of ICH, and have more frequent microscopic bleeding, such as hereditary CAA, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), and collagen type IV A1-associated vasculopathy. Morbus Fabry, ApoE є2є2 and є4 genotype are associated specifically with lobar ICH [20]. Genetic screening and counseling might be reasonable for pedigrees of patients with some very rare and selected cases. Defining the more complex genetics of SICH, however, will probably require defining multiple common genetic variants with weaker effects. While investigations of genetic risk factors for SICH have thus far been limited to candidate gene polymorphisms, whole-genome association studies are being undertaken in spontaneous ICH. They are likely to generate novel insights into cerebral bleeding risks and strategies for prevention [21].

Hypertension, Smoking, Alcohol, Cholesterol, and Other Risk Factors

Hypertension is the most common risk factor for SICH and the frequency has been estimated to be between 70% and 80%. The pathophysiological role of hypertension is supported by the high frequency of left ventricular hypertrophy in autopsy of patients with ICH. The role of hypertension and the beneficial effect of anti-hypertensive treatment with regard to risk of ICH were verified in several large clinical trials. In the PROGRESS trial the relative risk of ICH was reduced by 76% in comparison with the placebo-treated group after 4 years of follow-up [22].

Other risk factors for ICH in addition to old age, hypertension, and ethnicity include cigarette smoking and excessive alcohol consumption. Both the Physicians’ Health Study and the Women’s Health Study confirmed the role of smoking as a risk factor for ICH. For men smoking 20 cigarettes or more, the relative risk of ICH was 2.06 (95% confidence interval [CI] 1.08–3.96), and for women smoking 15 cigarettes or more, the relative risk was 2.67 (95% CI 1.04–6.90) [23, 24].

Several studies document an increased risk of ICH in relation to regular alcohol consumption and that spontaneous ICH can also be triggered by binge drinking [25]. It has been shown that alcohol abuse is associated with the occurrence of ICH in young age. In the study heavy drinkers (defined as alcohol consumption of more than 300g ethanol/week) had their ICH at a median age of 60 years, 14 years before the non-heavy drinkers. An empiric relation between heavy alcohol intake and arterial hypertension has been discussed. However, the underlying vasculopathy remains unexplored in these patients, although small-vessel disease was suggested [26].

While elevated cholesterol levels play a less significant role in ICH than in ischemia, statin use and/or very low levels of cholesterol have been questionable factors in increasing the risk of ICH. For example, the SPARCL study showed a small increase in risk of ICH in ischemic stroke patients treated with atorvastatin [27]. Inferences made from observational data show that statin use prior to ICH does not influence mortality or functional outcome and statin use following ICH is not associated with an increased risk of ICH recurrence [28]. Westover et al. used a mathematical decision analysis and revealed a small amplification of the risk of recurrent ICH in survivors of prior hemorrhagic stroke by the use of statins. Therefore, the authors recommend avoiding statins after an ICH, particularly in survivors of lobar ICH who are at highest risk of ICH recurrence. In case of deep ICH the analysis showed a closer balance between the risks and benefits of statins, so that statin therapy may be considered after deep ICH. Still, it remains unclear by which mechanism statins might amplify the risk of hemorrhagic stroke. So far anti-thrombotic and fibrinolytic effects have been discussed [29].

A variety of illicit drugs, such as amphetamine and cocaine, are known to cause ICH and this possibility should be kept in mind in young patients in whom other causes such as arteriovenous malformation or trauma have been excluded [30].

Oral Anti-Coagulation as a Risk Factor for ICH

The use of oral anti-coagulants such as warfarin, phenprocoumon, and acenocoumarol increases the risk of ICH 8–11 times compared to patients of similar age who are not on anti-coagulation [31, 32]. Previous medications, such as thrombolytics, also increase the risk of ICH. Anti-coagulation, also a contributing rather than a causative factor, does not only lead to a higher incidence of ICH, but also to hematoma expansion (HE) in 27–54% of the cases, and well beyond the 24-hour time window where most of HE occurs in SICH [33]. This might at least partially explain a substantial increase in mortality of up to 70%. Underlying causes of SICH and oral anti-coagulant therapy (OAT)-associated ICH might be the same, with OAT being only a precipitating factor [32, 34, 35].

Another issue arising from clinical practice comes from the increasing incidence of anti-coagulation-associated ICH in elderly people with atrial fibrillation and other cardiac diseases. While in many cases it is often not evident whether anti-coagulation (especially when within the therapeutic range) is the cause of ICH and thus can be rated as a “complication” of therapy, it might equally often be considered a failure of anti-coagulation therapy resulting from insufficient protection of the brain. Then, an ischemic infarct turning into a secondary hemorrhage is visible upon first imaging. Due to the primary ischemic lesions rapidly turning hemorrhagic, the true incidence of secondary hemorrhagic infarcts is probably higher than was previously thought.

Small-Vessel Disease

It was CM Fisher who concluded from the detailed study of two brains that hypertensive ICH most likely results from rupture of lipohyalinoic arteries followed by secondary arterial ruptures at the periphery of the enlarging hematoma in a cascade or avalanche fashion [31]. This observation of mechanical disruption and tearing of smaller vessels might account for the gradual development of ICH and can probably be considered the most relevant neuropathological correlate for the “growing” properties of hemorrhages (like a rolling snowball). The main histological findings in vessels of ICH patients include lipohyalinosis and media hypertrophy, as well as elongation of the deep penetrating arterioles of the brain. The lenticulostriate, thalamo-perforating, and basilar artery rami ad pontem are affected most often. In the cerebellum the arterioles supplying the area of the dentate nucleus are often involved, also the rami of the superior and posterior inferior cerebellar arteries. This demonstrates that the underlying cause of a hypertensive ICH is the arteriosclerotic microangiopathy and the hypertension only being a risk factor and not the bleeding cause, which can be ascertained by microbleeds in the basal ganglia in MRI.

Cerebral Amyloid Angiopathy (CAA)

CAA refers to the deposition of amyloid proteins into the cerebral vessel walls with degenerative changes. Hereditary forms of CAA are known, but CAA is most commonly sporadic and related to amyloid β (Aβ) peptide deposition. This deposition is seen in the walls of small arteries and arterioles of the leptomeninges, cerebral and cerebellar cortices, and less often in capillaries and veins. Overlaps with Alzheimer’s disease are known and therefore old age and positive ApoE є4 allele are major risk factors for both conditions. Although the metabolism and pathological triggers for CAA production and deposition are not well understood, CAA is now recognized as a major cause of non-hypertensive lobar cerebral hemorrhage in the elderly. The overlaps of CAA and dementia are recognized, although also less well understood.

CAA is a frequent finding particularly over the age of 70 years, differing only in amount and distribution. In elderly persons over the age of 90 years it is present in 50% of individuals and in Alzheimer’s disease patients it is present in over 80% of all neuropathological cases.

The biological and neuropathological interaction between Aβ deposition in primary degenerative diseases of the brain as well as in elderly patients with a high risk of parenchymal bleeding is a major focus of research. In one rare hereditary form with excessive CAA deposits, cognitive decline was independent of other Alzheimer-related pathological criteria, such as neurofibrillary tangles. Mounting evidence shows that drugs able to inhibit amyloid deposition seem to be an avenue for clinical therapy options for amyloid-associated progressive cognitive decline [36, 37].

CAA-associated hemorrhages account for the second largest group of hemorrhages after hypertension-associated bleedings and their rate depends on the case mix of elderly people at one stroke unit. Gradient echo MRI can be useful to detect silent hemorrhages in typical (cortical) areas and thus help to determine the diagnosis of CAA.

General Recommendations

At many centers non-contrast CT is the imaging modality of choice for the assessment of ICH, owing to its widespread availability and rapid acquisition time. MRI has not been favored due to its higher costs and due to the fact that conventional T1-weighted and T2-weighted MRI pulse sequences are not sensitive to blood in the hyperacute stage. However, some studies have impressively shown that blood-sensitive gradient echo (GRE) sequences are as accurate as CT for the detection of parenchymal hemorrhage and far superior to CT for the detection of chronic hemorrhage [38, 39]. Table 12.3 outlines the MRI signals in T1-, T2-, and GRE-weighted sequences relative to the different stages of the ICH. New MRI techniques, including magnetic resonance spectroscopy and diffusion tensor imaging, might have importance in the understanding of hemorrhagic injury and provide insights into the time course and pathophysiology of ICH [40].

Table 12.3 MRI signal relative to brain in different ICH stages

Source: Osborn et al. [100].

In case of lobar bleedings with an underlying arteriovenous malformation, characteristic flow voids can be seen in the brain parenchyma on MRI. CT angiography or MR angiography might reveal the underlying vascular lesion; however, in some cases, catheter angiography is required and might need to be repeated if the results were initially negative owing to the mass effect of the hematoma. Findings from imaging such as pathological calcifications, presence of subarachnoid blood, vessel abnormalities, or an unusual location of hemorrhage can be considered to support an indication for direct catheter angiography. Cavernous malformation can usually be reliably diagnosed by means of GRE MRI, where one or more hypointense rings show due to hemosiderin from a previous bleeding.

Silent hemorrhages seen on blood-sensitive gradient echo sequences have also been found quite frequently and their clinical significance as risk factors has not been fully determined. They might be relevant markers of vascular risk factors or in patients already having suffered an ICH, and might signal an increased risk of further hemorrhage. This risk might also be increased in anti-coagulation patients, but this has not yet been confirmed in controlled studies.

Spot Sign

Contrast extravasation on admission CT angiography (the so-called “spot sign”) and a contrast extravasation in a post-contrast CT scan as a predictor of HE were found in retrospective and prospective studies, extended to a proposed “spot sign score,” which is used to grade the number of spot signs (SpS) and their maximum dimension and attenuation [41–43]. The PREDICT trial, a prospective multicenter observational study (including 228 patients for primary analysis) showed that the CTA spot sign is highly predictive of HE for intraparenchymal and intraventricular hemorrhage growth, and it is associated with larger hemorrhage and a poor prognosis. The usefulness of the CTA SpS was tested in proof-of-concept trials of hemostatic drugs in patients with ICH [44] (see below). Further systematical and comparable validation of predictors of HE is warranted as this might prevent delay of appropriate therapy, but also influence estimates on prognosis or decisions to withdraw therapy (Figure 12.2).

Figure 12.2 Spot sign.

A: CCT native scan showing an acute hypertension-related ICH in the basal ganglia 90 minutes after symptom onset (ICH volume 56 ml).

B and C: CT angiography (source images) showing two spot signs indicating extravasation of contrast medium.

D: CCT 12 hours later showing a hematoma expansion (ICH volume 90 ml).

Microbleeds

MRI visualizes acute and chronic hematomas, but also old, clinically non-apparent cerebral microbleeds that are not detected on CT. Microbleeds have a hypointense appearance on MRI and are usually smaller than 5–10 mm. Pathological studies have shown that microbleeds seen with GRE MRI usually correspond to hemosiderin-laden macrophages adjacent to small vessels and are indicative of previous extravasation of blood [45]. Microbleeds were seen in 83% of ICH cases with recurrent ICH [46].

Hypertension, CAA, getting older, and, less commonly, CADASIL have been identified as important risk factors for microbleeds [47–49]. Microbleeds have been suggested as markers of a bleeding-prone angiopathy [50, 51]. The results of several case reports and small series suggest that patients with microbleeds might be at increased risk of hemorrhage when on anti-thrombotic or thrombolytic therapy. By contrast, the results of two large studies did not show an increased risk of hemorrhage in patients with microbleeds who were treated with intravenous tissue plasminogen activator [52, 53].

Although there are still many studies ongoing, microbleeds are considered to bear prognostic significance for any future bleeding event and have been confirmed as a common finding in patients with cerebral amyloid angiopathy. There they are most commonly found in lobar brain regions [36]. By contrast, in patients with intracerebral hemorrhage due to hypertensive disease, microbleeds are most commonly found in deep and infratentorial regions, although hypertension can also contribute to lobar microbleeds. A particularly noteworthy finding is that the total number of microbleeds predicts the risk of future symptomatic intracerebral hemorrhage in patients with lobar hemorrhage and probable cerebral amyloid angiopathy (Figure 12.3) [54].

Figure 12.3 Microbleeds. MRI with blood-sensitive gradient echo (GRE) sequences. Lobar microbleeds are typical for CAA, whereas the microbleeds seen in deep regions refer to hypertension.

Hematoma Expansion

An increase in the bleeding volume is an early complication of ICH. For a long time it was erroneously believed that the volume of a cerebral hematoma was usually maximal at onset. Frequently observed deterioration during the first day was attributed to developing cerebral edema and mass effect surrounding the hemorrhage. However, serial CT scans showed that clinical deterioration is often attributed to hematoma expansion and this is also a reason for high mortality [56].

The pathophysiology behind early HE is not well understood, also the frequency of increased bleeding is high. It is not clear whether it reflects leakage or rebleeding, or both. Several mechanisms of brain injury after ICH have been investigated, but most of these evolve too late to account for early HE [57]. A role for disturbed autoregulation and uncontrolled perfusion pressure in hypertension as a driving force for further bleeding is conceivable, but data on this are controversial. Brott et al. showed that “growth,” defined as a 33% increase of hematoma volume on CT, occurred in 26% of 103 patients within 4 hours after the first symptoms. Another 12% had growth within the following 20 hours. Hemorrhage growth was significantly associated with clinical deterioration [58]. Enlargement of ICH is also seen when observation periods are extended up to 48 hours, although the frequency diminishes with time from onset of symptoms. Predictors of HE include initial hematoma volume, early presentation, irregular shape, liver disease, hypertension, hyperglycemia, alcohol use, and hypofibrinogenemia (Figure 12.4) [11].

Figure 12.4 A 64-year-old man with acute left-sided hemiparesis and dysarthria; NIHSS score 9; prior ASS use, hypertension not treated.

A: CCT shows a spontaneous ICH with intraventricular hemorrhage (hematoma volume 44 ml) 1 hour after onset.

B: 2 hours later the patient developed a clinical deterioration (NIHSS score 18) with systolic blood pressure >180 mmHg despite treatment with i.v. drugs. CCT shows a hematoma expansion (hematoma volume 95 ml).

Intraventricular Hemorrhage (IVH)

Between 36% and 50% of patients with spontaneous ICH suffer additional IVH, especially ICH in the basal ganglia, and the 30-day mortality rate was reported as 43% for patients with ICH and IVH compared with 9% in patients suffering ICH alone without IVH. Tuhrim et al. found that location of parenchymal origin of ICH, distribution of ventricular blood, and total volumes are predictors of outcome in patients with spontaneous ICH and intraventricular extension. Furthermore, hydrocephalus was found to be an independent predictor of mortality [13].

Edema

Edema after ICH is observed in the acute and subacute phases and may increase up to 14 days [59]. Shrinking of the hematoma due to clot retraction leads to an accumulation of serum in the early phase [57]. Thrombin and several serum proteins were found to be involved in the inflammatory reaction of the perihematomal zone [60, 61]. Factors released from activated platelets at the site of bleeding, such as vascular endothelial growth factor, may interact with thrombin to increase vascular permeability and contribute to the development of edema [62]. Several studies in SICH suggest that the role of perihematomal ischemia is small and has no great clinical importance [63].

Surgical Approach

Insufficient evidence exists with regard to the efficacy of surgical treatment for SICH, and whether or not surgical approaches are beneficial remains controversial. Surgical procedures with varying amounts of supportive evidence include conventional craniotomy, minimally invasive surgery (MIS), and decompressive craniectomy. The diverse methods of MIS include stereotactic guidance with aspiration and thrombolysis with alteplase (rtPA) or urokinase and image-guided stereotactic endoscopic aspiration. The Surgical Trial in IntraCerebral Hemorrhage (STICH), still the largest prospective trial on surgery in SICH, failed to show an outcome benefit over conservative treatment [64]. A subgroup analysis showed that patients with superficial hematomas and without intraventricular hemorrhage (IVH) presented a more encouraging picture of surgery. The STICH II trial investigated the suggestion that patients with superficial lobar hematomas and no IVH might benefit from early hematoma evacuation (<12 hours after randomization) [65]. The trial did not show a positive clinical effect of surgical hematoma evacuation within at least 50 hours after ictus at 6 months. A meta-analysis of 2 186 cases concluded that in particular early surgery (<8 hours of ictus) might be beneficial [66]. It has been shown that patients with smaller bleeds have a better clinical outcome and a lower mortality, which led to the hypothesis that methods of removing ICH in stable patients could result in lowered risk of mortality and improved outcome [67].

For intraventricular bleedings recommendations are difficult due to lack of evidence. During the hyperacute phase of IVH and acute hydrocephalus, as a common complication, the insertion of an external ventricular drainage (EVD) may represent a life-saving procedure by reducing elevated intracerebral pressure. However, EVD is frequently obstructed by blood resulting in insufficient drainage of cerebrospinal fluid (CSF) with no or only little effect on ventricular blood clearance and ventricular size [68]. In patients with supratentorial ICH and IVH the CLEAR III trial investigated the benefit of an intraventricular fibrinolysis. This placebo-controlled RCT of 500 subjects tested whether scheduled intraventricular boluses of rtPA (alteplase), given through clinically indicated ventriculostomy catheters, could improve functional outcomes in patients with IVH from ICH by accelerating resolution of the intraventricular clot [69]. Unfortunately the results were neutral; the proportion of patients who achieved a good functional outcome at 6 months was similar in both groups, although mortality was 11% lower in the rtPA group than in the saline group (control group). Furthermore, the trial showed that the approach is safe. Due to different reasons only 30% of patients given rtPA reached the goal of 80% clot reduction, which might be one of the reasons that the treatment was not effective in improving functional outcomes, and indicates that the pathophysiological premise of the trial was correct: that effective clearance of IVH could improve functional outcomes and mortality.

Furthermore, intraventricular fibrinolysis reduced permanent shunt dependency, probably by decreasing inflammation of CSF-absorbing Pacchioni granulations. In patients with communicating hydrocephalus, lumbar drainage may represent a simple and less invasive alternative for extracorporal CSF drainage with a lower complication profile compared with EVD. The recent randomized, controlled LUCAS-IVH trial investigated efficacy and safety of a combined strategy (intraventricular fibrinolysis followed by a lumbar drainage versus fibrinolysis alone) on shunt dependency in patients with ICH and severe IVH and provided evidence that the combined approach is feasible, safe, and significantly reduces rates of permanent shunt dependency for aresorptive hydrocephalus post-ICH [70].

The combination of stereotactic minimal invasive aspiration and clot lysis with rtPA has been proposed, especially with regard to deep hematomas. Whether this approach is safe and can indeed lead to a better outcome was investigated in the MISTIE trial, combining stereotactic clot aspiration (starting 6 hours after clot stabilization) with different doses of rtPA within the first 72 hours from onset. The specific objective of MISTIE (96 subjects) was to test the efficacy and safety of this intervention and assess its ability to remove blood clot from brain tissue. The trial showed that MIS plus rtPA seems to be safe and shows greater clot resolution than does conventional medical treatment. Asymptomatic hemorrhages were more common in the intervention group than in the standard medical care group; all other safety outcomes (as mortality or symptomatic bleeding) did not differ [71]. The ongoing MISTIE III trial investigates if the intervention improves clinical outcome (NCT 01827046). These results, if replicable, could lead to the addition of surgical management as a therapeutic strategy for intracerebral hemorrhage.

The strategy of decompressive craniectomy is beneficial in patients with malignant middle cerebral artery infarction. Based on the common pathophysiological mechanisms of these two conditions, this procedure is also frequently performed in patients with ICH. The ongoing randomized controlled SWITCH trial (Decompressive Hemicraniectomy in Intracerebral Hemorrhage) aims to determine whether decompressive surgery and best medical treatment in patients with SICH will improve outcome and reduce mortality compared to best medical treatment only (NCT 02258919).

The treatment of spontaneous supratentorial ICH will remain controversial until a definitive prospective randomized controlled trial shows evidence in favor of a particular treatment. At present, the recommendations for or against surgery are based on conflicting evidence.

Currently available data for infratentorial ICH data are even worse – no prospective randomized trial of surgery for cerebellar ICH analogous to STICH has been conducted. Small, retrospective, observational studies suggest that initial neurological condition, level of consciousness, evidence of brainstem compression, and a tight posterior fossa on imaging are associated with outcome and might influence the decision to evacuate infratentorial ICH [72]. The 2015 AHA/ASA ICH management guidelines recommend surgical removal of the hematoma as soon as possible in patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction.

Related posts:

Chapter 4 – Imaging for Prediction of Functional Outcome and for Assessment of Recovery Chapter 8 – Cardiac Diseases Relevant to Stroke Chapter 16 – Stroke and Dementia Chapter 19 – Acute Therapies for Stroke Chapter 22 – Management of Acute Ischemic Stroke and its Late Complications Chapter 21 – Intensive Care of Stroke

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