Intraventricular hemorrhage

INTRODUCTION — Intraventricular hemorrhage (IVH) confined to the ventricular system within the brain is uncommon, accounting for only about 3 percent of all spontaneous intracranial hemorrhage [1]. IVH more commonly occurs in the setting of intracerebral hemorrhage or subarachnoid hemorrhage.

The assessment of the patient with IVH focuses on identifying the underlying cause of the hemorrhage, which may have significant treatment implications. Common to patients with IVH, regardless of etiology, is a risk for sudden and potentially fatal obstructive hydrocephalus, requiring acute clinical decision-making regarding the use of external ventricular drainage and other interventions.

This topic discusses the causes, clinical presentation, diagnosis, and treatment of IVH. Intracerebral, subarachnoid, subdural, and epidural hemorrhage are discussed separately:

●(See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)

●(See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)

●(See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

●(See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis".)

●(See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)

●(See "Subdural hematoma in adults: Management and prognosis".)

●(See "Intracranial epidural hematoma in adults".)

IVH in the newborn is also discussed separately. (See "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Risk factors, clinical features, screening, and diagnosis" and "Germinal matrix and intraventricular hemorrhage (GMH-IVH) in the newborn: Management and outcome".)

EPIDEMIOLOGY AND DEFINITIONS — Primary IVH refers to bleeding confined to the ventricular system within the brain. Primary IVH is uncommon, accounting for only about 3 percent of all spontaneous intracerebral hemorrhage [1]. The following demographic characteristics were reported in a 2008 review of published cases series of primary IVH [2]:

●The median age is 55 years (range 9 to 91 years).

●Males and females are equally represented.

●Half of patients have a history of hypertension.

Secondary IVH refers to the more common occurrence of IVH in the setting of intracerebral hemorrhage or subarachnoid hemorrhage. The epidemiology of intracerebral hemorrhage and subarachnoid hemorrhage is discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

ETIOLOGY — IVH most commonly occurs as a secondary phenomenon when parenchymal or intracerebral hemorrhage (ICH) ruptures into the ventricular space or when subarachnoid hemorrhage (SAH) extends into the ventricles. IVH is estimated to complicate 40 to 60 percent of ICH and 10 percent of SAH cases [3-5]. In one retrospective review, warfarin therapy was associated with IVH risk, volume at presentation, and subsequent expansion in patients with deep or lobar ICH [6]. The underlying causes of ICH and SAH are discussed separately. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Nonaneurysmal subarachnoid hemorrhage".)

IVH can also complicate closed head injury. Usually, this is in the setting of other traumatic brain injury, including contusion and traumatic SAH; isolated IVH is a relatively rare complication of head trauma [7-9].

Primary IVH is uncommon; in consequence, studies estimating the frequency of various etiologies have been limited. Retrospective case series derived from tertiary referral centers are subject to ascertainment bias. Further, definitions of primary IVH have varied among different authors and studies. While most limit their use of the term to hemorrhages entirely localized within the ventricle, others have included hemorrhages that originate within 15 mm of the ependymal surface [10]. The latter criteria invariably classify thalamic, caudate, and medial putaminal bleeds (usually secondary to chronic hypertension) associated with IVH as primary IVH.

Among series that more strictly limit the definition of IVH, vascular malformations are the most frequently identified cause of primary IVH. In small case series, vascular malformations have been identified in 14 to 58 percent of patients with primary IVH [2,10-15]. Reported causes of primary IVH include:

●Vascular malformations (usually arteriovenous malformations or arteriovenous fistulas) [1,2,10-19]. (See "Brain arteriovenous malformations".)

●Intraventricular tumors (papilloma, neurocytoma, meningioma, metastases, astrocytoma, ependymoma) [11,20-26]. (See "Overview of the clinical features and diagnosis of brain tumors in adults".)

●Intraventricular aneurysms developing within the distal lenticulostriate or choroidal arteries (occasionally reported in association with Moyamoya disease) [10,16,22,27]. Occasionally aneurysms of the anterior communicating artery, posterior inferior cerebellar artery, or basilar tip rupture into the ventricles without other overt subarachnoid blood [2,10,14]. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

●Moyamoya disease [1,2,16,22,28-31]. (See "Moyamoya disease and moyamoya syndrome: Etiology, clinical features, and diagnosis".)

●Coagulopathies, acquired or inherited [2,10,12,29,32-34]. (See "Thrombotic and hemorrhagic disorders due to abnormal fibrinolysis".)

●Pituitary apoplexy [35]. (See "Causes, presentation, and evaluation of sellar masses", section on 'Causes'.)

●Vasculitis [36]. (See "Primary angiitis of the central nervous system in adults".)

●Fibromuscular dysplasia [10]. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia".)

●Sympathomimetic agents [37,38]. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication", section on 'Central and peripheral nervous system'.)

In approximately 20 to 50 percent of cases (depending in part on the intensity of the investigation), no cause is identified [11,12,16,33]. About half of these patients have chronic hypertension; this is believed, but not known, to cause primary IVH in the same way it is understood to cause ICH. It is speculated that some patients with IVH may have had a small hypertensive intraparenchymal hemorrhage, too small to see on computed tomography (CT) or magnetic resonance imaging (MRI), which arises in proximity to the ventricular system and produces IVH as its primary manifestation. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Pathogenesis and etiologies'.)

CLINICAL FEATURES

Clinical presentation — Patients with secondary IVH present with clinical features typical of intracerebral hemorrhage or subarachnoid hemorrhage. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

Patients with primary IVH typically present with abrupt headache, often associated with nausea, vomiting, and impaired consciousness (confusion, disorientation) [2,11,33,39]. A minority of patients have frank loss of consciousness at the onset [12]. Symptoms are usually sudden in onset; however, nearly a quarter of patients are reported to have progressive or fluctuating symptoms [11,12]. The degree of neurologic impairment, often measured as the Glasgow Coma Scale (table 1) is an important prognostic indicator. (See 'Prognosis' below.)

Focal neurologic findings are relatively uncommon with primary IVH and most typically involve cranial nerve abnormalities [10]. Such cranial nerve palsies are generally of the "false localizing" type due to stretching across the basilar skull surface and include dysfunction of the sixth and third nerves. Seizures are not common but can occur [1,10,11,17]. Most patients are hypertensive on presentation, and some will have an elevated body temperature or suffer cardiac arrhythmias [12]. Nuchal rigidity is inconsistently present.

The clinical symptoms and signs of IVH reflect a sudden increase in intracranial pressure that results from sudden introduction of blood volume into the intracranial space [40]. In addition to pressure effects, it is speculated that blood products in the cerebrospinal fluid space may affect brain function.

Complications — Patients with primary or secondary IVH are at risk for sudden neurologic deterioration, which may result from obstructive hydrocephalus, recurrent hemorrhage, or other complications [12]:

●Hydrocephalus – Acute obstructive hydrocephalus can result when cerebrospinal fluid circulation is obstructed by blood clots. Patients with blood in the third or fourth ventricle are at most risk of this complication [12]. One-half to two-thirds of patients with IVH have some degree of hydrocephalus on the initial computed tomography (CT) scan of the head [2,11,12,15,41]. This can be rapidly fatal and usually requires urgent intervention with insertion of an external ventricular drain [8,40]. (See 'External ventricular drain' below.)

Patients may also develop communicating hydrocephalus as a delayed complication of IVH; this usually presents more gradually. (See 'Prognosis' below.)

●Hemorrhage extension – Recurrent hemorrhage or hemorrhage extension occurs in up to 20 to 25 percent of patients with IVH [12,40,42,43]. The highest risk of this is in those with an underlying etiology of vascular malformation or aneurysm or in the setting of a coagulopathy. The presence of a coexisting intraparenchymal hemorrhage is also associated with an elevated risk of IVH expansion, especially those that have expanded on follow-up imaging or are located in the thalamus [42].

●Cerebral vasospasm – Cerebral ischemia due to arterial vasospasm is unusual in cases of primary IVH, but this complication has been described in isolated cases [19,44-46]. In contrast, vasospasm is a common complication of aneurysmal subarachnoid hemorrhage. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis".)

●Other medical complications – Neurologic deterioration due to medical complications is common in the setting of IVH. These include pulmonary embolism, pneumonia and other infections, and electrolyte imbalance. Other medical complications of IVH include cardiovascular instability, deep venous thrombosis, and gastrointestinal bleeding.

DIFFERENTIAL DIAGNOSIS — The presentation of primary IVH overlaps with those of aneurysmal subarachnoid hemorrhage and other forms of stroke. Urgent diagnostic evaluation, including head CT, is required to identify these alternative conditions to reduce risk of morbidity and initiate time-sensitive therapeutic interventions. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Approach to reperfusion therapy for acute ischemic stroke" and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis" and "Cerebral venous thrombosis: Treatment and prognosis".)

Other conditions that may present with a headache with sudden onset also include reversible cerebral vasoconstriction syndrome, cervical artery dissection, and posterior reversible leukoencephalopathy syndrome, among others (table 2). A noncontrast head CT can distinguish IVH from these other entities. (See "Overview of thunderclap headache", section on 'Diagnostic evaluation'.)

DIAGNOSTIC EVALUATION

Imaging diagnosis — Noncontrast head CT is the test of choice to diagnose IVH. CT rapidly and reliably identifies blood within the ventricular system, helps to identify parenchymal intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH) associated with the IVH, and also identifies concurrent hydrocephalus.

IVH may be identified infrequently by brain MRI or other neuroimaging studies, typically when these studies are performed to evaluate other conditions.

Evaluation for underlying causes and monitoring — Neuroimaging studies are typically required to define the etiology of a primary IVH. In the absence of an obvious precipitant such as trauma or coagulopathy, we recommend patients with primary IVH undergo neuroimaging to assess for underlying causes.

Computed tomography — Close examination of the initial head CT should be performed to identify secondary IVH due to ICH or aneurysmal SAH. Hemorrhagic findings in the brain regions surrounding the ventricles (caudate and thalamus, in particular) may identify ICH (image 1). Similarly, the presence of subarachnoid blood in the basal cisterns or cortical sulci should raise concern for aneurysmal SAH with secondary IVH. If ICH or SAH is present, diagnostic evaluation should be pursued. (See "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis", section on 'Evaluation and diagnosis' and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Identifying the source of bleeding'.)

The extent of IVH can be graded by head CT. The Graeb score and other scoring systems have been proposed [47-49], but none are widely implemented in clinical practice.

The CT scan should be repeated emergently for any neurologic deterioration to identify recurrent hemorrhage or obstructive hydrocephalus. Acute imaging findings associated with an elevated risk of IVH growth include irregular hemorrhage shape, intralesional hypodensity, and coexisting intraparenchymal hemorrhage [42,43]. CT scans are also used to monitor hydrocephalus, particularly during attempts to clamp or remove a drain. Transcranial ultrasonography has been suggested as a possible alternative to serial CT to monitor ventricular size, but the reliability and reproducibility of this technique has yet to be independently validated [50].

Other neuroimaging studies — For most patients with IVH, we typically start with MRI and magnetic resonance angiography (MRA) or CT angiography to investigate for underlying causes (image 2). If the MRI/MRA or CT angiography is unrevealing, we recommend digital subtraction angiography, in agreement with guidelines from the American Heart Association/American Stroke Association [51].

In a prospective observational study of patients with IVH who underwent catheter angiography, vascular lesions were found in 11 of 17 (65 percent), including 10 patients with arteriovenous malformations, and one with aneurysm [14]. A retrospective review of published case series similarly estimated the yield of angiography at 56 percent, additionally identifying cases of Moyamoya and dural arteriovenous fistula [2]. If the cause of the IVH remains undetermined, it is reasonable in some cases to consider repeat contrast MRI and possibly catheter angiography one to two months following the initial studies after reabsorption of blood products has occurred.

Other tests — Other tests that are important to include are blood clotting studies (prothrombin time, partial thromboplastin time, and platelet count). A toxicology screen should also be considered.

Because electrolyte imbalances can complicate IVH, these should be measured at baseline and followed regularly.

MANAGEMENT

General measures — The treatment of IVH focuses on cessation of bleeding, relieving hydrocephalus, and controlling intracranial pressure (ICP).

Specific therapy aimed at treating the underlying cause should be undertaken (aneurysm or arteriovenous malformation obliteration). (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Vascular malformations of the central nervous system".)

Patients who have a moderate to severe IVH (impaired alertness and/or extensive intraventricular blood on imaging) should be followed in an intensive care setting. Medical complications are common (eg, pneumonia, deep venous thrombosis, gastrointestinal bleeding, cardiovascular instability, supraventricular tachycardia, hypo- and hypernatremia) and require appropriate monitoring and treatment [1,11]. The head of the bed should be placed at 30 degrees or greater to decrease ICP and reduce the risk of aspiration. Euvolemia should be maintained using isotonic crystalloid solutions, and any elevations in body temperature should be treated aggressively.

For prevention of deep venous thrombosis, mechanical thromboprophylaxis using intermittent pneumatic compression stockings is recommended until a bleeding source has been identified and secured. At that time, antithrombotic therapy can be used. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)

Because seizures are an infrequent complication of IVH, prophylactic antiseizure medications are not generally used but should be initiated immediately should seizures occur.

Management of antithrombotic medications

Reversing anticoagulation — For most patients with IVH, we discontinue anticoagulant medications and give agents to reverse their effects. However, for some patients with small acute IVH and no signs of hydrocephalus who are receiving anticoagulation for a compelling indication such as a mechanical heart valve, the risk-benefit calculation may favor continued anticoagulation with close observation of neurologic status. In such circumstances, we generally use intravenous heparin during the acute period given the ability to rapidly reverse its anticoagulant effect. (See "Anticoagulation for prosthetic heart valves: Management of bleeding and invasive procedures", section on 'Management of bleeding'.)

If reversal of anticoagulation is indicated, the appropriate intervention depends upon the anticoagulant the patient is taking, the time since last dose, and the urgency with which reversal is needed. Some patients prescribed anticoagulant medications may not require reversal agents if laboratory testing or the time interval since last dose indicates they are effectively not anticoagulated.

The strategies used to reverse anticoagulation in patients with IVH are the same as those used for patients with intracerebral hemorrhage. These strategies are discussed separately. (See "Reversal of anticoagulation in intracranial hemorrhage", section on 'Reversal strategy for specific anticoagulants'.)

Patients on antiplatelets — Antiplatelet medications are typically stopped at the time of diagnosis for most patients with acute IVH. However, we balance the thrombotic risks of discontinuation with the hemorrhagic risks of continuing antiplatelets at an individual level. We may continue antiplatelet medications during acute monitoring for selected patients at high risk of thrombosis such as those with established atherosclerotic disease or who have undergone intravascular stent placement and who have small IVH. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk" and "Antithrombotic therapy for elective percutaneous coronary intervention: General use" and "Overview of carotid artery stenting" and "Endovascular techniques for lower extremity revascularization", section on 'Antiplatelet therapy'.)

We reserve platelet transfusions for those with specific indications, including those with a thrombocytopenia (<100,000/microL) or a known platelet defect. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Platelet function disorders'.)

Blood pressure management — The optimal blood pressure management in patients with IVH remains undefined. Aggressive blood pressure lowering may minimize the risk of further hemorrhage but must be weighed against the risk of decreased cerebral perfusion in patients with increased ICP.

It seems reasonable to gradually lower elevated blood pressure in patients with normal ICP. Intravenous antihypertensives such as labetalol or nicardipine are typically used, although other agents are acceptable [52]. In the absence of better data specific to IVH, the guidelines outlined for blood pressure management in the setting of ICH seem reasonable [51]. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Blood pressure management'.)

External ventricular drain — An external ventricular drain (EVD) is a small catheter inserted through the skull usually into the lateral ventricle, which is typically connected to a closed collecting device to allow for drainage of cerebrospinal fluid (figure 1). The EVD can also be connected to a transducer that records ICP.

We recommend an EVD for patients with IVH with hydrocephalus and neurologic decline [51]. Rarely, bilateral EVDs may be needed if hemorrhage obstructs the foramen of Monro [53].

The major complications associated with EVD are catheter occlusion due to clotted blood at the intraventricular orifice and infection. The former may be relieved by irrigation or catheter replacement. Symptoms suggestive of infection should prompt cerebrospinal fluid analysis for cell count and culture along with antibiotic therapy as appropriate. Staphylococci are the most common pathogens. Higher rates of bacterial ventriculitis/meningitis occur with longer duration of EVD placement [54]. Prophylactic catheter change does not reduce the risk of infection. The management and prevention of infections in patients with an EVD are discussed in greater detail separately. (See "Infections of cerebrospinal fluid shunts".)

Additional management options — In addition to EVD placement, adjunctive approaches have also been used for selected patients with IVH for the prevention and treatment of hydrocephalus.

Intraventricular thrombolysis — The utility of intraventricular thrombolysis (IVT) for patients with IVH and an EVD is uncertain. IVT use involves shared decision-making and includes discussing individual risks and benefits. Instillation of thrombolytic agents into the ventricles may improve mortality by hastening clot resolution, thereby avoiding the morbidity associated with EVD occlusion and shortening the duration of EVD use. It is also possible, although unproven, that more rapid resolution of IVH may decrease the long-term incidence of communicating hydrocephalus. However, IVT use may increase the risk of bleeding and severe disability.

Evidence supporting the use of IVT for EVD has been reported in case series, observational studies, and pooled analyses. These studies have suggested a benefit for IVT, showing increased clot resolution and, in some cases, decreased mortality [3,39,55-66]. The results of randomized clinical trials, on the other hand, have not shown clear benefit:

●The Clot Lysis: Evaluating Accelerated Resolution of Intraventricular Hemorrhage (CLEAR III) trial included 500 patients with IVH and compared treatment with 1 mg alteplase (tPA) or placebo injected through an EVD every eight hours until clot reduction or a clinical endpoint occurred, or 12 doses were given [67]. At 180 days, the primary efficacy outcome of a modified Rankin scale (mRS) score of 3 or less was similar in each group (48 versus 45 percent comparing alteplase to placebo; risk ratio [RR] 1.06, 95% CI 0.88-1.28). Patients who received IVT had a lower mortality (18 versus 29 percent; RR 0.60, 95% CI 0.41-0.86), but a higher rate of severe disability indicated by an mRS score of 5 (17 versus 9 percent; RR 1.99, 95% CI 1.22-3.26). Bleeding complication rates were similar (2 percent) in both groups. One criticism of the CLEAR-III trial is that only a minority of patients experienced substantial IVT removal, suggesting the possibility of benefit with more effective methods for clot removal.

●The Intraventricular Hemorrhage Thrombolysis Trial, a multicenter randomized controlled study, enrolled 48 patients and compared IVT (3 mg tPA) to control (normal saline); each treatment was injected through an EVD every 12 hours until clot reduction or a clinical endpoint occurred (median duration of dosing was 7.5 days for IVT) [68]. The rate of clot resolution was faster for IVT than placebo (18 versus 8 percent per day). Rates of death and ventriculitis were lower than expected and did not differ significantly between treatment groups. Symptomatic bleeding complications were more frequent in the tPA group (23 versus 5 percent), but this did not reach statistical significance. The dose used in this study was higher than that used in the CLEAR III trial.

Bleeding complications are a concern with IVT; recurrent IVH and/or ICH expansion is reported in 8 to 20 percent of patients after IVT [16,40,57,58,68,69]. Typically, patients with known aneurysm or vascular malformation were excluded from early studies of IVT. However, IVT has been used without complication in a few reported cases after the vascular malformation or aneurysm was surgically treated [16,70-72], and even before surgery, in few patients with these lesions [17,73]. Systemic bleeding complications are unlikely to be significantly increased with IVT; in CLEAR IVH, systemic coagulation parameters were similar after administration of tPA and placebo [74].

It is also possible that the risk of bacterial meningitis/ventriculitis may be increased with IVT therapy, but this has not been demonstrated so far [40,57,67,68]. IVT has not been associated with systemic complications [75].

IVT is reserved for selected patients with acute IVH and an EVD at centers experienced with this approach.

Lumbar drainage — The use of lumbar drainage combined with IVT was studied in an open-label trial that was stopped early after 30 patients were enrolled; patients with severe IVH with tamponade of the third and fourth ventricles requiring EVD were treated with IVT (control group) or IVT combined with lumbar drainage [76]. The primary endpoint (need for permanent shunt placement of prolonged requirement for cerebrospinal fluid drainage) occurred more frequently in the control versus combined treatment groups (7 out of 16 versus 0 out of 14). In a meta-analysis that included patients in this study as well as an additional 67 patients treated outside of the clinical trial, the combined intervention was associated with a significant reduction (OR 0.24; 95% CI 0.01-0.36) for shunt dependency. This analysis found no significant differences in functional outcomes or cerebrospinal fluid infection rates at 90 days; bleeding complications were less frequent in the combined treatment group (odds ratio 0.4, 95% CI 0.30-0.53).

PROGNOSIS — The reported in-hospital mortality of IVH varies from 20 to 50 percent [1,2,4,10-12,33,57]. Secondary IVH carries a higher risk of death than primary IVH [15,33,75]. Advanced age, underlying coagulopathy, Glasgow Coma Scale score of 8 or less, and hydrocephalus at presentation are also associated with a higher risk of death [2,12,33,41,75]. While some studies have found that the extent of IVH correlates with prognosis [2,12,41,48], others have not [10,11,15]. The results of one study found that the volume of blood in the third ventricle was a strong and independent predictor of poor outcomes, while the volume of blood in the lateral ventricles, fourth ventricle, or entire ventricular system did not correlate significantly with prognosis [77]. The authors speculated that blood in the third ventricle may affect critical contiguous structures in the midbrain.

Other long-term complications of IVH include:

●Neurocognitive sequelae – Patients with significant IVH are often confused, agitated, and disoriented [1]. These symptoms are often slow to recover and a significant proportion (about half of survivors) are left with disabling cognitive deficits [1,11,16].

●Noncommunicating hydrocephalus – IVH along with a secondary inflammatory/fibrotic response may lead to impaired absorption of cerebrospinal fluid at the arachnoid granulations. This may be manifest by a more subacute decline in cognition, gait, and urinary continence that can occur weeks or later after the initial IVH or as a failure to wean off EVD. Such patients may require permanent ventriculoperitoneal shunt [40]. Approximately 30 to 50 percent of patients with IVH require a shunt placement [16,57,64,71,78-81]. (See "Normal pressure hydrocephalus".)

●Late recurrence of intracerebral hemorrhage or IVH – Recurrent hemorrhage is uncommonly reported after IVH. In one series, 2 of 14 survivors had a subsequent intracerebral hemorrhage [12], while in another series there was no recurrent bleeding in a group of 13 patients after 67 months [11]. The risk of this complication is likely highest in those with an unrecognized and/or unsecured vascular lesion (eg, Moyamoya) [27,82].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)

SUMMARY AND RECOMMENDATIONS

●Terminology and etiologies – Intraventricular hemorrhage (IVH) can complicate intracerebral hemorrhage or subarachnoid hemorrhage (secondary IVH). Less commonly, IVH occurs in isolation (primary IVH). The most commonly identified cause of primary IVH is a vascular malformation. Up to half of patients with primary IVH do not have a cause (other than hypertension) identified. (See 'Epidemiology and definitions' above and 'Etiology' above.)

●Clinical features – Patients with IVH usually present with sudden headache, nausea and vomiting, and impaired alertness. (See 'Clinical features' above.)

●Diagnostic evaluation – Patients with a clinical presentation of IVH should undergo immediate noncontrast head computed tomography (CT). The primary purpose is to exclude subarachnoid hemorrhage and to identify the IVH and evaluate its severity and potential for obstructive hydrocephalus. (See 'Computed tomography' above.)

Individuals with primary IVH should have magnetic resonance imaging with magnetic resonance angiography and/or conventional angiography to identify the underlying etiology, particularly a vascular malformation or aneurysm that may require surgical intervention. (See 'Other neuroimaging studies' above.)

●Management

•Monitoring – Because acute obstructive hydrocephalus often complicates IVH that involves the third and fourth ventricles, such patients should be closely monitored. When neurologic deterioration occurs, emergent CT scan should be done to exclude the development of obstructive hydrocephalus or recurrent hemorrhage. (See 'General measures' above and 'Computed tomography' above.)

•Blood pressure – The optimal blood pressure management in patients with IVH is uncertain. For patients with IVH and elevated blood pressure, intravenous antihypertensives such as labetalol or nicardipine may be used to lower blood pressure gradually while maintaining adequate cerebral perfusion. Aggressive blood pressure lowering may minimize the risk of further hemorrhage but must be weighed against the risk of decreased cerebral perfusion in patients with increased ICP. (See 'Blood pressure management' above.)

•External ventricular drain – We recommend external ventricular drainage (EVD) for patients with neurologic deterioration that occurs with ventricular enlargement over conservative management (Grade 1B). An EVD can reduce clot burden, treat hydrocephalus, and facilitate ICP monitoring. (See 'External ventricular drain' above.)

•Additional management options – The use of intraventricular thrombolysis involves shared decision-making and after assessing individual risks and benefits and is reserved for patients at experienced centers with established protocols. (See 'Intraventricular thrombolysis' above and 'Lumbar drainage' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges James Pacelli Jr, MD, who contributed to earlier versions of this topic review.