It can be divided into primary or secondary, primary hemorrhage being far less common than secondary:
- primary: blood in the ventricles with little (if any) parenchymal blood
- secondary: a large extraventricular component is present (e.g. parenchymal or subarachnoid) with secondary extension into the ventricles
In adults, secondary intraventricular hemorrhage is usually the result of an intracerebral hemorrhage (typically basal ganglia hypertensive hemorrhage) or subarachnoid hemorrhage with ventricular reflux.
Intraventricular hemorrhage is a distinct entity in pediatrics and considered separately; see intraventricular hemorrhage of the newborn.
There are numerous causes of intraventricular hemorrhage and as such no single demographic can be identified; rather each underlying etiology contributes its own patient population. Having said that, secondary hemorrhage is far more common and as such the dominant demographic is that of patients with intraparenchymal or subarachnoid hemorrhage: older individuals are thus most commonly affected.
Clinical presentation of intraventricular hemorrhage (regardless of cause) is similar to that of subarachnoid hemorrhage. Patients experience sudden onset of severe headache 2. Signs of meningism are also present (i.e. photophobia, nausea and vomiting and neck stiffness). Larger hemorrhages can result in loss of consciousness, seizures, and brainstem compression with cardiorespiratory compromise.
Secondary intraventricular hemorrhage is much more common than primary IVH 5.
Some of the more common causes of primary intraventricular hemorrhage in adults include 2,5:
- vascular malformations
- anticoagulation therapy / coagulopathy
- intraventricular tumors
Secondary causes of intraventricular hemorrhage include:
- extension from other intracerebral hemorrhages
- subarachnoid hemorrhage
Non contrast CT of the brain is the mainstay of acute evaluation of patients presenting to with sudden onset headache or stroke-like symptoms. Blood in the ventricles appears as hyperdense material, heavier than CSF and thus tends to pool dependently, best seen in the occipital horns. Acutely, if the volume is significant blood can fill the ventricle, and clot forming a 'cast'.
There is often obstructive hydrocephalus, and care must be taken in distinguishing this from ex vacuo dilatation of the ventricles.
MRI is more sensitive than CT to very small amounts of blood, especially in the posterior fossa, where CT remains marred by artifact.
Both FLAIR and more recently SWI (especially at 3T) are sensitive to small amounts of blood. Especially the latter will demonstrate tiny amounts of blood pooling in the occipital horns, and resulting in susceptibility induced signal drop out 3,4.
On FLAIR the signal intensity will vary depending on the timing of the scan. Within 48 hours blood will appear as hyperintense to the attenuated adjacent CSF 4. Later the signal is more variable and can be difficult to distinguish from flow related artifact (particularly in the third and fourth ventricles) unless other sequences are also used.
Treatment and prognosis
The main treatment approaches of intraventricular hemorrhage can be divided into two:
- treatment of the underlying cause of hemorrhage (e.g. aneurysm, AVM)
- treatment of obstructive hydrocephalus
The latter may merely require careful monitoring of clinical state and serial CTs to assess for ventricular size, or may require ventricular drain placement. A number of patients will go on to require permanent CSF diversion (VP shunt).
- 1. Giray S, Sen O, Sarica FB et-al. Spontaneous primary intraventricular hemorrhage in adults: clinical data, etiology and outcome. Turk Neurosurg. 2009;19 (4): 338-44. Turk Neurosurg (link) - Pubmed citation
- 2. Bogousslavsky J, Caplan LR. Stroke Syndromes. Cambridge University Press. (2001) ISBN:0521771420. Read it at Google Books - Find it at Amazon
- 3. Sohn CH, Baik SK, Lee HJ et-al. MR imaging of hyperacute subarachnoid and intraventricular hemorrhage at 3T: a preliminary report of gradient echo T2*-weighted sequences. AJNR Am J Neuroradiol. 2005;26 (3): 662-5. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 4. Bakshi R, Kamran S, Kinkel PR et-al. Fluid-attenuated inversion-recovery MR imaging in acute and subacute cerebral intraventricular hemorrhage. AJNR Am J Neuroradiol. 1999;20 (4): 629-36. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 5. Arboix A, García-Eroles L, Vicens A, Oliveres M, Massons J. Spontaneous primary intraventricular hemorrhage: clinical features and early outcome. ISRN neurology. 2012: 498303. doi:10.5402/2012/498303 - Pubmed