Management of Intraventricular Hemorrhage

Key Points

Spontaneous intraventricular hemorrhages (IVHs) occur most commonly as extensions of parenchymal/deep hypertensive hemorrhages. Other causes can include aneurysmal rupture extension, most commonly from anterior communicating artery locations and fourth ventricular hemorrhages for posterior circulation aneurysmal rupture or arteriovenous malformations (AVMs).
IVH is an independent and important clinical problem that can influence outcome. Distended ventricular anatomy with compression of adjacent structures or obstruction of cerebrospinal fluid pathways can adversely affect intracranial pressure (ICP), which may require intervention.
Studies to clear blood from the ventricular system have been ongoing. The largest of these is the Clot Lysis: Evaluation of Accelerated Resolution (CLEAR) of IVH trials. Before performing the CLEAR procedure, vascular imaging via computed tomographic angiography (CTA) and/or magnetic resonance imaging/angiography(MRI/A) is required to rule out structural vascular lesions (aneurysm, AVM, moyamoya, arterial dissection), tumor, or hemorrhagic infarct. These etiologic studies are mandatory if the intent is to instrument the IVH or deploy thrombolysis.
The typical treatment of IVH is gauged on associated hydrocephalus, where, if present, an external ventricular drain (EVD) should be placed. In addition, intraventricular thrombolysis (IVT) using recombinant tissue plasminogen activator (rtPA) can be administered directly into the clot for accelerated resolution and to maintain patency of catheters to control ICP.
The CLEAR III trial did not show a significant benefit in functional outcome of IVH treated with thrombolytics over placebo. However, improved outcomes were accomplished in patients with large obstructive/casted IVH, and with aggressive IVH clearance (i.e., achieving >80% hematoma reduction, with multiple catheters if necessary).

Introduction

Hemorrhagic stroke involving bleed extension into the cerebral ventricles is classified as intraventricular hemorrhage (IVH). Typically, IVH is secondary to bleeding from nearby parenchymal structures from hypertension, vascular lesions, or tumors causing bleeds that extend into the ventricular system. This often occurs in 30%–50% of intracerebral hemorrhages (ICHs), mostly in association with deep, larger hematomas. Patients presenting to emergency departments (EDs) with ventricular extension of blood often come with decreased levels of consciousness and poorer prognoses. Previous studies have reported elevated rates of 30-day mortality related to IVH, with the volume of the IVH being an important factor in the overall outcome in ICH. The presence of blood in the ventricular system disturbs cerebrospinal fluid (CSF) circulation, resulting in ICP elevations and eventually compromise in cerebral perfusion pressures (CPPs). Furthermore, blood in the ventricular system may be cause mass effect on periventricular structures, causing surrounding edema and obstructive hydrocephalus. The STICH trial found that 55% of patients with IVH had hydrocephalus and only 11% of patients with hydrocephalus and IVH have a good outcome.

In this chapter we discuss primary and secondary IVH, occurring respectively in the absence, or with the extension, intraparenchymal hemorrhage. The latter may be caused by hypertension, amyloid angiopathy, vascular malformations, tumors, or other structural or vascular lesions. We discuss the natural history of IVH, its clinical features, diagnostic workup, treatment, and prognosis. The results of the Clot Lysis: Evaluation of Accelerated Resolution of Intraventricular Hemorrhage (CLEAR) program have provided a much better understanding of IVH, and a potential framework toward improving its outcome. Other causes of IVH such as germinal matrix hemorrhages in the newborn are outside the scope of this chapter.

Primary Intraventricular Hemorrhage

Spontaneous IVH without clear parenchymal hemorrhage is extremely rare and should prompt thorough diagnostic work-up. Typically, IVH without ICH is due to an occult vascular malformation that contacts the ependymal surface of the ventricular system. Rarely it has been reported that periventricular neoplasms or ruptured intraventricular aneurysms result in primary IVH. Small aneurysms arising from distal lenticulostriate or choroidal arteries have been reported as well as hemorrhages related to Moyamoya diseased vessels. Many cases of primary IVH will not yield a clear vascular etiology, and bleeding disorders or medications should also be considered as causes.

The most common brain neoplasms that bleed spontaneously are malignant astrocytomas, or metastases (melanoma, thyroid, choriocarcinoma, and renal cell tumors). Less common tumors include ependymomas, subependymomas, choroid plexus papillomas, intraventricular meningiomas, ^, pituitary tumors that erode the floor of the third ventricle, neurocytomas, granular cell tumors, and craniopharyngiomas, in addition to others reported in rare case reports.

Hypertensive Brain Hemorrhage and Intraventricular Hemorrhage

One-third to one-half of deep spontaneous ICHs extend into the ventricular system. Hypertension, which causes small vessel arteriopathy, is the major risk factor for deep ICH formation. The small penetrating arterioles present in the basal ganglia are exposed to elevated pressure. These arterioles arise at 90 degrees from major cerebral arteries and lack the support structure required to withstand variable changes in blood pressure (BP), making them prone to vascular remodeling and eventual bleeding into the parenchymal structures they supply. These vessels supply the putamen, caudate, thalamus, pons, and midbrain. The aforementioned brain structures are the most common places where deep spontaneous ICH occurs due to chronic hypertension ( Fig. 73.1 ). Higher ICH volume and its location near the ventricular system may cause IVH.

Fig. 73.1, A 58-year-old woman presents obtunded and paralyzed on the left side of her body from a deep right thalamic intracerebral hemorrhage with intraventricular hemorrhage extension. Immediate treatment should include blood pressure control and correction of any coagulopathy. External ventricular drainage should follow to control elevated intracranial pressure (ICP) from obstructive hydrocephalus and potentially to facilitate blood clearance. Initial catheter should be placed in the left (lesser casted) lateral ventricle to facilitate ICP control. After ensuring stability of bleeding and negative screening for vascular etiology, a second catheter should strongly be considered on the right (more casted) lateral ventricle for potential thrombolysis.

Hypertension is a modifiable risk factor that increases the risk of stroke twofold to fourfold. Primary prevention strategies on a population level aimed at hypertension control could decrease the incidence of ICH by a predicted 39%. Other risk factors that contribute to brain parenchymal bleeding are moderate to heavy alcohol intake and anticoagulant treatment.

Aneurysmal Intraventricular Hemorrhage

IVH can be seen in up to 45% of aneurysmal rupture cases. Blood extension from the subarachnoid space into the ventricular system is more common after the rupture of anterior communicating artery, basilar summit, and other posterior circulation aneurysms. The presence of IVH after an aneurysmal rupture and high IVH volume are associated with a poor neurologic condition and a poor outcome. ^, IVH is included in the Fisher scale, which predicts cerebral vasospasm after subarachnoid hemorrhage (SAH); however, not all analyses have found that IVH is associated with delayed cerebral ischemia or infarction. Aneurysmal IVH is associated with a higher probability (up to 50%) of requiring a ventriculoperitoneal shunt.

Up to 50% of posterior inferior cerebellar artery (PICA) aneurysm ruptures have an accompanying IVH, and case-by-case analyses have demonstrated that aneurysms located in the posterior circulation more frequently cause IVH than those in the anterior circulation. IVH extension from an SAH caused by a ruptured aneurysm in the posterior fossa may cause fourth ventricular dilation, hydrocephalus, and brainstem compression.

Vascular Malformations and Intraventricular Hemorrhage

Cerebral hemorrhage caused by arteriovenous malformations (AVMs) in contact with the ventricular wall can bleed inside the ventricles; these vascular malformations are often associated with deep venous drainage ( Fig. 73.2 ). Retrospective studies have shown that deep drainage is associated with hemorrhagic presentation and 25% of those patients present concomitantly with IVH. A prospectively analyzed AVM database showed that 16% of initial hemorrhages were primarily intraventricular and 31% were combined ICH and IVH. Periventricular cavernous angiomas and dural arteriovenous fistulas with transcerebral venous drainage are less common but can also cause IVH.

Fig. 73.2, (A and B) Ruptured basial ganglia arteriovenous malformation resulting in intraventricular hemorrhages (IVHs). In this example, the presence of an arteriovenous malformation is easily identifiable on a noninfused computed tomography. However, if parenchymal hemorrhage obscures the cardinal features, the etiology may be less obvious. Etiology screening of all IVHs should be considered, particularly if thrombolysis or other surgery for IVH is being planned. A subanalysis from the CLEAR III trial demonstrated that 11% of IVH cases screened had an underlying vascular malformation. Therefore all patients require etiology screening in the form of a CTA and/or MRI/A to properly classify lesions to dictate proper/safe intervention.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here