Fig. 2.1
Intracranial hemorrhage in cerebral amyloid angiopathy. Axial and coronal T2- and axial T1-weighted images (a–c) demonstrate a large right intracranial hemorrhage with perilesional edema. Axial T2*-weighted gradient-echo images, (d, e), reveal multiple and bilateral microhemorrhages mostly located in the cortex
CT is the most used technique in ICH diagnosis since it is generally more readily available and rapidly carried out.
MRI is equivalent to CT for the evaluation of acute ICH. The gradient-echo imaging technique with T2 weighting is the best option to detect ICH in the acute phase. Furthermore, MR angiography might provide both secondary causes of ICH and information about the intracranial vasculature (arterial and venous).
Since up to 15 % of subjects with ICH carry vascular abnormalities as a potential cause of ICH, CT angiography (CTA) is more often utilized in acute settings in order to clarify the etiology of ICH. CTA may detect the so-called spot sign (i.e., contrast extravasation [>1–1.5 mm]), which could be interpreted as a marker of ongoing bleeding, risk for hematoma expansion, and poor outcome.
2.1.4 Therapy
Acute Management
Airway: prompt intubation is the preferred approach in non-conscious patients.
Blood pressure: guidelines recommending blood pressure treatment are available by the American heart Association/American Stroke Association (AHA/ASA) [10] and the European Stroke Initiative (EUSI) [11].
Hemostatic therapy: ongoing bleeding might be prevented by an early correction of an underlying coagulopathy.
Intracranial pressure (ICP): ICP monitoring and treatment are advised if Glasgow Coma scale score ≤8, transtentorial herniation, significant IVH, or hydrocephalus.
Hyperglycemia: a careful glycemic control in the early phase is mandatory [10].
Temperature: fever control would lower mortality and improve outcome.
Seizures: antiepileptic drugs should not be used routinely (AHA/ASA recommendation). Indications are, indeed, the presence of clinical or electroencephalographic seizures in patients with a deterioration of mental status [10].
2.1.5 Prognosis
ICH carries the worst prognosis of all acute cerebrovascular diseases [1]. Half the deaths occur in the acute phase, mostly in the first 48 h [1, 12]. The 30-day mortality for ICH has been reported up to 35 % and 50 % in “developed and developing countries,” respectively [2]. Full functional recovery at 6 months is expected in only 20 % of survivors [1]. An early and effective treatment is crucial in order to avoid the occurrence of ICH complications, which are the major predictors of early mortality and poor outcome.
ICH complications include hematoma expansion (HE), perihematomal edema (PHE), intraventricular hemorrhage (IVH) with hydrocephalus, venous thromboembolic events, seizures, hyperglycemia, hypertension, infections, and fever [13] (Table 2.1).
Table 2.1
ICH complications
Definition and characteristics | Risk factors | Outcome | |
|---|---|---|---|
Hematoma expansion (HE) | Increase in volume (33–50 %) Absolute change in hematoma volume (1.5–20 mL) on repeat CT scan | “Spot sign” Large hematoma volume at presentation Early presentation (≤3 h) Heterogeneity of hematoma density on CT scan Warfarin use | Every 10 % increase in ICH growth (by CT scans within 24 h): 5 % increased risk of death 16 % increased risk of worsening outcome 18 % increased risk of poor outcome evaluated on the Barthel index or poor functional independency |
Perihematomal edema (PHE) | Increase in volume by 75 % in the first 24 h Strong increase during the first week and maximum during the second week after bleeding | Hyperglycemia Disorder of the coagulation factors Statins Increase of systolic blood pressure | Unclear correlation with clinical outcome and mortality |
Intraventricular hemorrhage (IVH) | Common after ICH (30–50 % of patients) | Mean arterial pressure >120 mmHg at baseline Large ICH at baseline | Poor functional outcome and high overall mortality (50–75 %), mostly at presentation 30-day mortality rate: 43 % in ICH with IVH vs. 9 % in ICH without IVH IVH growth increases risk of death or severe disability at 90 days Patients with ICH + IVH total volume >40 mL have ~40 times more probability to have a poor prognosis Patients with ICH + IVH total volume >50 mL have 100 % unfavorable outcome |
IVH and hydrocephalus | Extension of ICH into the ventricles with direct mass effect of ventricular blood, up to acute obstructive hydrocephalus (AOH) 50 % of IVH due to ICH develop AOH by obstruction of the third and fourth ventricle | AOH more commonly related to: Large IVH Thalamic hemorrhages | AOH in IVH reduces the chance of positive outcome (from 15.1 to 11.5 %) |
Seizures | 50–70 % occur within the first 24 h 90 % in the first 3 days Overall 30 day risk: 8 % Early seizures: occurred <2 weeks Late seizures: occurred >2 weeks | Increased midline shift on 48–72 h follow-up CT scan is independently associated with seizures | Early seizures are predictive of epilepsy |
Venous thromboembolic events (VTE) | Rate of symptomatic VTE: 3–7 % Risk of pulmonary embolism 1–2 %; deep vein thrombosis (DVT) 1–4 % Subclinical DVT up to 17 % | Severe stroke Advanced age Lengthy immobilization Increased prothrombotic activity | Worse incidence of DVT in black patients Women at greater risk of VTE VTE is associated with a 30-day mortality rate of 35–52 % |
Fever | Direct consequence of accompanying infections or brain damage Observed in up to 40 % of ICH patients | Early rise in body temperature is a great risk factor for adverse outcome | Poor outcome (relative risk increased by 2.2 times) worsened by a longer duration of fever Increased mortality (by a factor of 1.8 for each 1 °C increase in baseline body temperature) |
Hyperglycemia | A response to stress and severity of ICH About 60 % of ICH patients may develop hyperglycemia | Hyperglycemia associated with larger hematoma size | Predictor of early mortality and worse functional outcome in non-diabetic patients with ICH Predictor of 30-day mortality in diabetic and non-diabetic patients with ICH |
Increased blood pressure (BP) | BP ≥140/90 mmHg occurred in >70 % of ICH patients Unknown mechanism for BP increase, most likely a multifactorial process | Associated with HE, PHE, rebleeding | Worse outcome Increased mortality, but similar poor outcome for systolic BP <120 and >220 mmHg |
Adverse outcome with increased early mortality during the hyperacute phase is often related to HE, IVH with hydrocephalus, and hyperglycemia [13].
Poor outcome with early neurological deterioration is similarly associated with HE, hydrocephalus, and PHE.
“ICH score” [14] is a simple, reliable grading scale developed to predict the 30-day mortality, using features as the Glasgow Coma scale, intracerebral hematoma volume, IVH, infratentorial location, and age. The higher the score, the greater the mortality (Table 2.2).
Table 2.2
ICH score (The higher the score, the greater the mortality)
Parameter | Points | |
|---|---|---|
Glasgow Coma scale 3–4, 5–12, 13–15 | 2, 1, 0 | |
Hematoma volume (≥30 cm3) | 1 | |
Intraventricular hemorrhage | 1 | |
Infratentorial localization | 1 | |
Age ≥80 years old | 1 | |
Thirty-day mortality (points; % of mortality) | 1 (13 %), 2 (26 %), 3 (72 %), 4 (97 %), 5 (100 %) | |
Moreover, the ICH score is a useful grading scale for long-term functional outcome after acute ICH. The score stratifies subjects with regard to 12-month functional outcome as assessed by modified Rankin scale [15].
Additionally, a suitable score (i.e., the “functional outcome risk stratification [FUNC] score”) is assessed in order to perform a prediction model for ICH functional outcome [16]. Rather than mortality, the FUNC score predicts the functional independence at 90 days by using similar features of ICH score (Table 2.3). The higher the FUNC score, the greater the possibility for a functional independence.
Table 2.3
FUNC score [16] (The higher the score, the greater the possibility for a functional independence)
Component | Points |
|---|---|
ICH volume (cm 3 ) | |
<30 | 4 |
30–60 | 2 |
60 | 0 |
Age (years) | |
<70 | 2 |
70–79 | 1 |
≥80 | 0 |
ICH location | |
Lobar | 2 |
Deep | 1 |
Infratentorial | 0 |
Glasgow Coma scale score | |
≥9 | 2 |
≤8 | 0 |
Total FUNC score (points; % of patients with functional independence at 90 days) | 0–4 (0 %), 5–7 (13 %), 8 (42 %), 9–10 (66 %), 11 (82 %) |
2.2 Primary Cerebellar Hemorrhage
Primary cerebellar hemorrhages (PCHs) are spontaneous hemorrhages in the cerebellar parenchyma, caused neither by tumor, vascular malformation, or aneurysm nor by a trauma. PCHs are roughly 10 % of all ICH and about 15 % of cerebellar strokes. The clinical features regard the anatomy of the posterior fossa. Conditions related to the blockage of the fourth ventricle thus creating an obstructive hydrocephalus and/or compression of the brainstem might determine a decision of a rapid life-saving surgical treatment.
The most relevant complications are brainstem compression, hydrocephalus, and brain herniation.
A recent comprehensive review evaluated all studies and case reports with PCH from 1927 to 2011 [17]. Since many data were not actually comparable because of group heterogeneity, the authors provided only studies of mortality with data on treatment regimens. The overall mortality rate was 30.9 %, distinguishing 33.3 % for the medical, and 29.1 % for the surgical group. However, the clinical outcome in survivors of PCH was slightly in favor of a conservative treatment. This might be related to the fact that the patients who underwent surgery were treated for life-threatening complications, and were, therefore, already at a higher risk of death compared to those treated conservatively.
2.3 Intracranial Hemorrhage Due To Vascular Malformations
Key Facts
Terminology and definitions – Intracranial hemorrhage due to arteriovenous malformations (AVM), aneurisms, cavernous malformation (CM), intracranial dural arteriovenous fistulas (DAVFs), Moyamoya disease (MMD).
Epidemiology – Prevalence 15–18/100,000 adults (AVM); 9–20/100,000 persons/year (SAH); 0.4–0.6 % (CMs); 10–15 % of all intracranial vascular abnormalities (DAVFs); 0.35–0.54 per 100,000 (MMD).
Clinical features – Acute or chronic focal neurological deficit due to intraparenchymal hematoma or mass effect (AVM, CM, DAVFs, MMD) or to ischemic-hemorrhagic lesion (MMD); sudden onset of a severe headache (i.e., “thunderclap headache: the worst headache of my life,” neck pain, and rigor) (SAH).
Diagnostic markers
CSF – Red blood cells (SAH).
Genetics – Hereditary CMs: 50 % of patients with onset of bleeding before 15 years carry CCM3 mutations. Early bleeding occurs in 26 % and 39 % of patients with CCM1 and CCM2 mutations, respectively.
Imaging – Acute bleeding: urgent CT scan; lumbar puncture (in SAH when unclear CT), and/or CT angiography of the brain; MRI – MR angiography; digital subtraction angiography.
Prognosis
Principles of treatment – Surgery (CMs, MMD), stereotactic radiosurgery, embolization (AVM, SAH); surgery (DAVFs).Related posts:
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