Intraventricular hemorrhage in adults

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Abstract
Intraventricular hemorrhage (IVH) in adults usually occurs in the setting of aneurysmal subarachnoid hemorrhage or hypertension-related intracerebral hemorrhage. Thus, the underlying cause of IVH is apparent from history and radiographic findings. If the underlying cause of IVH is not apparent, additional studies, including cerebral angiography, magnetic resonance imaging, and toxicology screening, should be performed to identify etiologic agents that may alter management of IVH. Management of IVH is thus done amidst (and must be tempered by) the multiple pharmacologic, surgical, and critical care interventions directed toward the diagnosis and treatment of the underlying cause of IVH. The most immediate threat to life posed by IVH is the development of acute obstructive hydrocephalus. If the hydrocephalus is contributing to a neurologic decline, it must be treated emergently with external ventricular drainage (EVD) through an intraventricular catheter (IVC). The patient with IVH should be evaluated and treated for deficient clotting function before an IVC is inserted. For this purpose, clotting function can be adequately assessed by prothrombin and partial thromboplastin times. Insertion of an IVC may significantly lower intracranial pressure, increasing the transmural pressure difference across the wall of a ruptured cerebral aneurysm and precipitating rerupture of the aneurysm. Therefore, with IVH secondary to a ruptured cerebral aneurysm, it is advisable to delay treatment of hydrocephalus that is not contributing to a neurologic decline until the aneurysm is repaired. Hydrocephalus contributing to significant neurologic decline in the setting of a ruptured aneurysm must be treated immediately despite the unprotected status of the aneurysm. Extreme diligence must be used to allow for the slow, controlled release of cerebrospinal fluid after IVC insertion. This will mitigate the effects of increasing the transmural pressure gradient across the wall of the ruptured aneurysm. In the patient with a neurologic deficit who has IVH-related hydrocephalus and an associated intracerebral hemorrhage, it is best to assume that the hydrocephalus is a significant contributor to the deficit and that it should be treated with EVD. An IVH that is not causing hydrocephalus but is apparently occluding one or both foramina of Monro or the third ventricle should be treated with EVD because obstructive hydrocephalus may develop precipitously and, if unrecognized, may cause irreversible brain damage or death. An IVH that is not likely to cause hydrocephalus because of small volume relative to its location can be followed expectantly. Intraventricular injections of thrombolytic agents through an IVC is a treatment option that may be considered in all patients with IVH that is causing or threatening to cause obstructive hydrocephalus. Unrepaired cerebral aneurysms, untreated cerebral arteriovenous malformations, and clotting disorders are contraindications for this intervention. The surgical evacuation of IVH has a role only in very rare cases in which the IVH is causing a significant mass effect independent of hydrocephalus and associated intraparenchymal brain hemorrhage. Intraventricular hemorrhage (IVH) in adults usually occurs in the setting of aneurysmal subarachnoid hemorrhage or hypertension-related intracerebral hemorrhage. Thus, the underlying cause of IVH is apparent from history and radiographic findings. If the underlying cause of IVH is not apparent, additional studies, including cerebral angiography, magnetic resonance imaging, and toxicology screening, should be performed to identify etiologic agents that may alter management of IVH. Management of IVH is thus done amidst (and must be tempered by) the multiple pharmacologic, surgical, and critical care interventions directed toward the diagnosis and treatment of the underlying cause of IVH. The most immediate threat to life posed by IVH is the development of acute obstructive hydrocephalus. If the hydrocephalus is contributing to a neurologic decline, it must be treated emergently with external ventricular drainage (EVD) through an intraventricular catheter (IVC). The patient with IVH should be evaluated and treated for deficient clotting function before an IVC is inserted. For this purpose, clotting function can be adequately assessed by prothrombin and partial thromboplastin times. Insertion of an IVC may significantly lower intracranial pressure, increasing the transmural pressure difference across the wall of a ruptured cerebral aneurysm and precipitating rerupture of the aneurysm. Therefore, with IVH secondary to a ruptured cerebral aneurysm, it is advisable to delay treatment of hydrocephalus that is not contributing to a neurologic decline until the aneurysm is repaired. Hydrocephalus contributing to significant neurologic decline in the setting of a ruptured aneurysm must be treated immediately despite the unprotected status of the aneurysm. Extreme diligence must be used to allow for the slow, controlled release of cerebrospinal fluid after IVC insertion. This will mitigate the effects of increasing the transmural pressure gradient across the wall of the ruptured aneurysm. In the patient with a neurologic deficit who has IVH-related hydrocephalus and an associated intracerebral hemorrhage, it is best to assume that the hydrocephalus is a significant contributor to the deficit and that it should be treated with EVD. An IVH that is not causing hydrocephalus but is apparently occluding one or both foramina of Monro or the third ventricle should be treated with EVD because obstructive hydrocephalus may develop precipitously and, if unrecognized, may cause irreversible brain damage or death. An IVH that is not likely to cause hydrocephalus because of small volume relative to its location can be followed expectantly. Intraventricular injections of thrombolytic agents through an IVC is a treatment option that may be considered in all...