Hydrocephalus is a common and potentially devastating complication of aneurysmal subarachnoid hemorrhage (SAH). Its incidence is approximately 20% to 30%, and its onset can be acute, within 48 hours after SAH, or rarely chronic, occurring in a delayed fashion weeks and even months after the hemorrhage. Early recognition of its signs and symptoms and accurate interpretation of computed tomography (CT) studies are important for the management of patients with SAH. Clinically, a poor neurologic grade has the highest correlation with an increased incidence of hydrocephalus. Radiographically, the bicaudate index on CT studies has emerged as the best marker of this condition. Although further studies are needed to understand the complex pathophysiology of this condition, hydrocephalus after SAH can be treated effectively using current technology.
Hydrocephalus often complicates the initial injurious effects of subarachnoid hemorrhage (SAH) ( Fig. 1 ). In 1928, Bagley was the first to suggest that ventricular dilatation could be a consequence of SAH. Most studies report an overall 20% to 30% incidence of hydrocephalus after SAH. Although debate still exists over its pathophysiology, this condition typically presents acutely but can also occur in a delayed fashion, rarely even months after the initial hemorrhage. Its clinical sequelae can be devastating and lead to further neurologic deterioration and longer hospital stays. Early recognition and treatment, however, can lead to improved patient outcomes. Several strategies have been developed to minimize the need for placement of either temporary intraventricular catheters (IVCs) or permanent shunts. Intraoperative techniques used to reestablish normal cerebrospinal fluid (CSF) flow and resorption include fenestration of the lamina terminalis and thorough irrigation of blood out of the arachnoid cisterns. Postoperative techniques used to encourage CSF reabsorption in patients with IVCs or lumbar drains involve a steady, daily increase in the pop-off pressures, which is guided by recorded intracranial or thecal pressures, CSF output volume, and the patient’s neurologic status. In patients without IVCs or lumbar drains but with persistent symptoms, serial lumbar punctures are necessary. Endovascular treatment of aneurysms may be associated with a higher rate of shunt-dependent hydrocephalus. In some institutions permanent shunting rates have been reduced to approximately 7%.
Etiology
The exact mechanism by which hydrocephalus develops after SAH remains poorly understood, although altered CSF dynamics in the acute and chronic states have been extensively studied. Although it is generally accepted that hydrocephalus after SAH is of the “communicating” type, it is likely that this condition has communicating and noncommunicating components. Decreased absorption of CSF at the arachnoid granulations is defined as communicating hydrocephalus and an anatomic obstruction, as noncommunicating. Traditionally, if all 4 ventricles are equally dilated on CT scan, then hydrocephalus is presumed to be of the communicating type. This interpretation does not take into account that if the obstruction occurs at the foramina of Luschka and Magendie (ie, the outflow of the fourth ventricle), a noncommunicating or obstructive type of hydrocephalus may be misinterpreted radiologically as being communicating, given that all the ventricles are dilated. It is generally assumed that fibrosis of the leptomeninges and arachnoid granulations from blood product deposition causes impaired CSF flow and decreased absorption.
There is increasing evidence, however, that hydrocephalus after SAH may be caused primarily by fibrosis and partial obstruction of the fourth ventricular outflow and secondarily by impaired CSF absorption. Based on this understanding, creation of an anterior third ventriculostomy has been proposed to facilitate CSF fluid dynamics with increased blood clearance, decreased leptomeningeal fibrosis, and better balance between CSF production and resorption. In the authors’ experience, the overall shunt rate in patients undergoing fenestration of the lamina terminalis can be reduced to 2.3%, whenever possible. The efficacy of lamina terminalis fenestration, however, has yielded conflicting results in other series, and a multi-center, randomized, controlled trial will most likely be necessary to determine the overall effectiveness of this technique.
The type of hydrocephalus may be a function of the site of hemorrhage and not of the temporal breakdown of blood in the subarachnoid space. This hypothesis may explain why ruptured posterior circulation aneurysms are associated with higher rates of hydrocephalus as compared with ruptured anterior circulation aneurysms. Posterior circulation aneurysmal rupture may be more likely to cause impaired CSF egress from the fourth ventricle and an obstructive pattern of hydrocephalus. Alternatively, anterior circulation aneurysmal rupture may cause hydrocephalus primarily by fibrosis of the leptomeninges and arachnoid granulations and result in a communicating pattern in the acute and delayed states. It is evident that the pathophysiology of chronic hydrocephalus remains poorly understood and that several hypotheses exist regarding its cause.
Diagnosis
Acute hydrocephalus, which develops 48 to 72 hours after SAH, occurs in approximately 20% of patients. Most patients with aneurysmal SAH present with headache, nausea, and vomiting, which are symptoms attributable to the presence of acute blood in the subarachnoid space but are also compounded by hydrocephalus. Subacute hydrocephalus, which develops 3 to 7 days after the hemorrhage, is rare and has a frequency of 2% to 3%. Because the clinical diagnosis of hydrocephalus after SAH is difficult, its recognition is based primarily on radiographic findings, specifically CT scans.
Although several ventricular measurements based on CT studies have been used to establish the diagnosis of hydrocephalus, currently, the preferred marker for this condition is the bicaudate index. Historically, there has been an evolution of radiological markers for hydrocephalus. In 1979, Vassilouthis and Richardson measured the ratio between the width of the lateral ventricles at the foramen of Monro and the inner diameter of the skull at the same level. A ratio less than 1:6.4 was considered normal and a ratio more than 1:4 represented marked ventricular dilatation, suggestive of hydrocephalus. In 1970, Galera and Greitz compared the maximum width of the frontal horns to that of the skull at the same axial level. Other studies have focused on volumetric measurements, suggesting that linear measurements are less accurate. Zatz and colleagues reported that the best correlation between ventricular volume and linear measurements existed with the width of the third ventricle. However, they concluded that the empiric radiographic evaluation by a radiologist is more accurate than any linear ratio in diagnosing hydrocephalus. Currently, the preferred system for the objective diagnosis of hydrocephalus is based on the bicaudate index ( Fig. 2 ).
Using data from 2 separate control groups showing the distribution of bicaudate values in patients without neurologic disease, Gijn and colleagues proposed that hydrocephalus should be diagnosed when the bicaudate index was more than the age-corrected 95th percentile ( Table 1 ).
| Age (Years) | Upper 95% Confidence Value |
|---|---|
| <30 | 0.16 |
| <50 | 0.18 |
| <60 | 0.19 |
| <80 | 0.21 |
| <100 | 0.25 |
In this manner, atrophic changes that result in ventriculomegaly and are not the result of increased ventricular CSF pressures are taken into account. They then prospectively studied 174 consecutive patients with SAH and found that 20% (34 of 174) had bicaudate indices greater than the 95th percentile for their age. Using similar criteria, Hasan and colleagues reported a consecutive series of 473 patients with SAH and found an incidence of acute hydrocephalus in 19% of patients (91 of 473). Several large retrospective series have confirmed these findings.
Chronic hydrocephalus (presenting later than one week after SAH) develops in an additional 10% to 20% of patients. Although the cause may be different, this diagnosis must be entertained in the setting of progressive neurologic decline. As a general rule, SAH patients who regress clinically weeks to months after discharge should have a follow-up CT scan and clinical evaluation to rule out delayed hydrocephalus.
Diagnosis
Acute hydrocephalus, which develops 48 to 72 hours after SAH, occurs in approximately 20% of patients. Most patients with aneurysmal SAH present with headache, nausea, and vomiting, which are symptoms attributable to the presence of acute blood in the subarachnoid space but are also compounded by hydrocephalus. Subacute hydrocephalus, which develops 3 to 7 days after the hemorrhage, is rare and has a frequency of 2% to 3%. Because the clinical diagnosis of hydrocephalus after SAH is difficult, its recognition is based primarily on radiographic findings, specifically CT scans.
Although several ventricular measurements based on CT studies have been used to establish the diagnosis of hydrocephalus, currently, the preferred marker for this condition is the bicaudate index. Historically, there has been an evolution of radiological markers for hydrocephalus. In 1979, Vassilouthis and Richardson measured the ratio between the width of the lateral ventricles at the foramen of Monro and the inner diameter of the skull at the same level. A ratio less than 1:6.4 was considered normal and a ratio more than 1:4 represented marked ventricular dilatation, suggestive of hydrocephalus. In 1970, Galera and Greitz compared the maximum width of the frontal horns to that of the skull at the same axial level. Other studies have focused on volumetric measurements, suggesting that linear measurements are less accurate. Zatz and colleagues reported that the best correlation between ventricular volume and linear measurements existed with the width of the third ventricle. However, they concluded that the empiric radiographic evaluation by a radiologist is more accurate than any linear ratio in diagnosing hydrocephalus. Currently, the preferred system for the objective diagnosis of hydrocephalus is based on the bicaudate index ( Fig. 2 ).
Using data from 2 separate control groups showing the distribution of bicaudate values in patients without neurologic disease, Gijn and colleagues proposed that hydrocephalus should be diagnosed when the bicaudate index was more than the age-corrected 95th percentile ( Table 1 ).
| Age (Years) | Upper 95% Confidence Value |
|---|---|
| <30 | 0.16 |
| <50 | 0.18 |
| <60 | 0.19 |
| <80 | 0.21 |
| <100 | 0.25 |
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