The cerebrospinal fluid (CSF) is produced in the choroid plexus of the lateral ventricle; circulated throughout a system with critical passages at the foramen of Monro, third ventricle, and aqueduct of Sylvius; and absorbed through arachnoid villi. Any impingement at these sites causes increased hydrostatic pressure in a matter of hours (Box 11.1). Enlargement of the ventricular system may be acutely created by a mass obstructing CSF outflow or by sudden stretching and ballooning out from introduction of a jet of arterial blood. Only ventriculostomy results in adequate diversion of flow and, in fact, may be lifesaving.
There is an urgency when patients present with acute hydrocephalus in the emergency department. This chapter describes clinical presentation, causes, and shunt placement. Definitive management, carefully planned later, could imply resection or debulking of the tumor or permanent placement of a ventriculoperitoneal shunt.
Patients with acute obstructive hydrocephalus have diminished alertness at presentation. Often in retrospect, episodes of headache are said to have been common and frequently intense. Earlier periods of blurred vision and obscuration (sudden grayouts or blackouts lasting seconds) associated with papilledema (due to pressure-induced relative ischemia of the optic nerve) are reported.2 Papilledema may occur, implying longstanding increased CSF pressure, but remains an uncommon clinical finding in most intraventricular, pineal, or choroid plexus tumors. Unfortunately, the diagnosis in some patients is made only after symptoms and signs referable to brain stem compression or brain stem shift have occurred.
Decreased consciousness from ventricular enlargement may have several mechanisms. First, hydrocephalus may impair the ascending reticular activating system (ARAS) at the level of the periaqueduct, which pushes against relay nuclei and fibers of the ARAS when it expands. Second, displacement of the upper brain stem by a massively enlarged third ventricle may tilt it backward and kink its structure. Third, when intracranial pressure from increased ventricular pressure rises above the cerebral perfusion pressure, and certainly when the increase in pressure occurs rapidly, global ischemic damage to both hemispheres or herniation of brain tissue bilaterally through the tentorium or foramen magnum produces an advanced stage of coma. Fourth, and by an indirect mechanism, decreased arousal may also be caused by tumor infiltration into paramedian thalamic nuclei or the mesencephalon, which at the same time obstructs normal CSF flow (see Chapter 8). Finally, tumors that obstruct the ventricles may produce clinical signs from compression by the mass effect itself to the brain stem (e.g., pinealoma). These signs may combine to form Parinaud's syndrome, consisting of upward gaze palsy and impaired convergence, with a so-called light-near dissociation of the pupillary light reflex (pupil constriction to accommodation and not to light).2The lesion for the classic finding of Parinaud's syndrome is in the dorsal midbrain (pretectum) and interrupts the supranuclear mechanisms for upward gaze. However, the dorsal midbrain can also be distorted by enlargement of the posterior third ventricle and periaqueductal structures.
Box 11.1. Pathophysiology of Acute Hydrocephalus
Acute hydrocephalus occurs when normal physiologic equilibrium is disturbed. CSF (an ultrafiltrate from capillaries) is produced in the choroid plexus and may increase in the plexus papilloma. The circulation of CSF depends on several variables, such as rate of production (400–600 mL/day), choroid plexus pulsations (filling of choroid plexus with each arterial pulse generates a pumping force), resistance (series of conduits, including foramina, aqueduct of Sylvius, and arachnoid villi), and sagittal sinus pressure (CSF pressure is greater, and flow depends on this pressure gradient). Absorption is linearly related to CSF pressure. Some of the CSF is merely recycled.1 Reduction in CSF volume therefore may be achieved by decreasing CSF production (carbonic anhydrate inhibitors; acetazolamide, which takes hours to achieve the effect), removing obstructing tumor, and improving absorption (e.g., corticosteroids to reduce inflammatory response in arachnoid villi). Enlargement of the ventricles is incremental, with elevation of the corpus callosum after dilation of the lateral ventricles and eventually reduction of the convexity gray matter.
Pineal gland tumors may directly compress the midbrain, and compression may persist despite CSF diversion methods. Colloid cysts are incidentally found, but they obstruct the foramen of Monro only after reaching a critical size. Intermittent headaches may precede acute deterioration, which can lead to sudden brain death.
Specific Disorders Associated with Acute Hydrocephalus
In a large proportion of patients, the cause of acute hydrocephalus in adults seen in the emergency department is ventricular dilatation associated with subarachnoid hemorrhage, lobar hematoma, primary intraventricular hemorrhage, or, less commonly, malfunctioning ventriculolumbar or peritoneal shunts for previous hydrocephalus. The causes of acute hydrocephalus associated with masses in adults are shown in Table 11.1.3,4,5,6,7,8,9,10,11,12,13,14
Primary intraventricular hemorrhage commonly causes acute hydrocephalus, although a more delayed course has been noted. Usually, the hemorrhage is massive (Fig. 11.1A, see also Chapter 14). Intraventricular introduction of a thalamic, caudate, or large lobar hematoma produces acute ventricular enlargement. Acute hemorrhage in the cerebellum, particularly when it extends to the vermis, may rapidly block the fourth ventricle, leading to obstructive hydrocephalus (Fig. 11.1B).
Hydrocephalus in intracerebral hematoma is an independent predictor of poor outcome.15,16,17 In addition, one study seriously questioned the use of ventriculostomy in parenchymal supratentorial hemorrhage.18 Ventricular drainage controlled intracranial pressure but did not consistently improve level of consciousness, suggesting direct irreversible tissue damage from hydrocephalus. Moreover, hemorrhagic dilatation of the fourth ventricle has been identified as an important indicator of poor outcome, confirming the impression that sudden massive enlargement causes damage to the periaqueductal area.19
Acute hydrocephalus in pontine hemorrhage is merely a consequence of its destructive hemorrhage, and ventriculostomy will not reverse coma. Extension to the mesencephalon and occasionally bilaterally to the thalamus precludes awakening. (After several unsuccessful attempts in our patients, we generally have abandoned ventriculostomy in this condition.)
Cerebellar hematoma and acute hydrocephalus can be treated by ventriculostomy when the fourth ventricle is blocked and no brain stem compression is evident on computed tomographic (CT) scans. Only in this particular clinical situation can ventriculostomy be beneficial; in all other instances, decompression of the pons by suboccipital craniotomy is more logical.
Table 11.1. Masses Causing Acute Obstructive Hydrocephalus
Aneurysmal Subarachnoid Hemorrhage
CT scan evidence of acute hydrocephalus is common in aneurysmal subarachnoid hemorrhage (Fig. 11.2). Acute hydrocephalus may be caused by obstruction of CSF outflow at the level of the ambient cisterns, by clogging of the arachnoid space with subarachnoid blood, or occasionally from the mass effect of a giant aneurysm obstructing the third ventricle.20 Commonly, the temporal horns are dilated early, typically before identifiable dilatation of the third and lateral ventricles. Ventriculostomy is certainly justified when clinical worsening in level of consciousness is clearly documented, when serial CT scans unmistakably demonstrate further enlargement, or when the third ventricle has changed into a balloon-shaped structure. One may argue that early ventriculostomy is a safeguard against re-bleeding in the first hours; but conversely, it may be argued that reducing the CSF pressure may reduce the sealing pressures of the aneurysm and thus increase the risk of bleeding. However, early ventriculostomy did not increase rebleeding in our study with patients before they underwent early repair of the aneurysm.21
Figure 11.1 A: Acute hydrocephalus in intraventricular hemorrhage due to sudden arterial jet of blood (arrows). B: Acute hydrocephalus (note enlarged temporal horns) associated with cerebellar hematoma effacing the fourth ventricle (arrows).
Figure 11.2 Acute hydrocephalus in subarachnoid hemorrhage with intraventricular blood (third ventricle and posterior horns, arrows) from ruptured anterior cerebral aneurysm.
Obstruction of the ventricular communication with the subarachnoid space by inflammatory exudate is the most likely mechanism of bacterial meningitis. Acute obstructive hydrocephalus can occur several weeks after bacterial meningitis begins and typically appears insidiously. The ventricular system, however, can be enlarged soon after the illness but usually to a minor degree and transiently (Fig. 11.3). Rarely is there a need to place a ventriculostomy tube early when hydrocephalus occurs within the first days, but late-onset hydrocephalus (10% in adult bacterial meningitis) may require placement of a drain.
Pineal Region Tumors
Pineal region tumors predominate in young adults (and children). Compression of the quadrigeminal plate depends on the size of the tumor, and Compression of the cerebral quad or tumor growth into the posterior third ventricle produces obstructive hydrocephalus.
Pineal parenchymal neoplasms can be divided into pineoblastoma (with histologic characteristics nearly identical to those of medulloblastoma) and pineocytoma (characteristic rosette formation).
Figure 11.3 A: Acute hydrocephalus in pneumococcal meningitis (arrows). B: Resolution (particularly temporal horns) of the enlargement but also reappearance of sulci 4 days after antibiotic therapy.
The outcome of pineoblastoma is poor, with survival rarely extending beyond 2 years.6 Pineocytoma with neuronal differentiation, such as large rosette formation or ganglion cells, has a much better long-term outcome, up to three decades after diagnosis, resection, and radiotherapy. Radiosurgery may be useful as adjuvant therapy.22 Germinomas may arise from this location, as may other germ cell tumors, such as teratomas, embryonal carcinoma, endodermal sinus tumor, and choriocarcinoma.
Germinomas are very radiosensitive, and long-term survival or cure is expected after resection. CSF should be sampled at the time of ventricular shunting. Choriocarcinoma and pineal germinoma secrete human chorionic gonadotropin. Alpha-fetoprotein is increased in endodermal sinus tumors, infiltrating teratoma, embryonal carcinoma, and choriocarcinoma.23 CSF markers may help in differentiation. High-dose methotrexate has been suggested in patients with distant metastasis (bone and meninges).24
Colloid Cyst of the Third Ventricle
The incidence of colloid cyst of the third ventricle is about 0.5%–2% of all intracranial tumors. This developmental abnormality is filled with homogeneous viscous material containing cellular debris. Its location in the third ventricle causes intermittent marked enlargement of the ventricles or ventricular diverticula, and death may ensue if recurrent headaches are not sufficiently investigated.5,25,26 Colloid cysts are a cause of sudden death in pediatric patients.27,28 Deterioration was observed in 32% of symptomatic patients, emphasizing its not so benign presence.29
In the Karolinska Hospital-based series of 37 consecutive patients, five patients were admitted to the emergency department and two died despite emergency ventriculostomy.30,31
Full resection should be planned. Unfavorable long-term results were associated with aspiration and subtotal resection.30 However, transcallosal microsurgery produced excellent results.30,31,32,33
Neoplastic growth of the epithelial lining on the ventricular surface is most commonly supratentorial in adults and more commonly intratentorial in children.7,34 Seeding throughout the CSF occurs in some instances. These malignant tumors grow slowly, and outcome is determined by grade, with 5-year survival of 80% in patients with low-grade tumors. Anaplastic or poorly differentiated ependymoma with typical histologic features of high mitotic activity, vascular proliferation, and necrosis reduces survival to 50%.
Tumors of the choroid plexus often are papillary and highly vascularized. Intratumoral hemorrhage is frequent. Localization is commonly in the fourth ventricle in adults.35,36 These tumors do not invade and are comparatively easy to resect.
Epidermoid cysts are ectodermal elements displaced during embryogenesis that become symptomatic in adults.37 Rupture of the cyst may cause aseptic ventriculitis. Predilection is for the fourth ventricle; and because of compression of the brain stem, cranial nerve palsy, ataxia, and hemiparesis may occur. Because of its slow growth and pliable nature, however, it may produce only intermittent headaches.
Neuroimaging in Acute Hydrocephalus
Different sites of obstruction in acute hydrocephalus are shown in Figure 11.4. CT scanning clearly delineates the degree of hydrocephalus and in many instances the obstructing tumor. Usually, the largest parts of the ventricular system (the anterior horns of the lateral ventricles) enlarge first, the temporal horns next, and then the third and fourth ventricles. When hydrocephalus has developed over weeks, subependymal effusions are clear evidence of increased CSF pressure. These periventricular hypodensities may occur in up to 40% of patients with acute obstructing hydrocephalus, but this capping surrounding the ventricle may also be evident in elderly patients with long-standing hypertension and diabetes but no hydrocephalus.38
The degree of hydrocephalus can be carefully assessed by several measuring systems. These simple linear measurements not only determine the degree of hydrocephalus but also can be used to monitor change. The ventricular size index measures the bifrontal diameter (transverse inner diameter) and divides it by the frontal horn diameter. The bicaudate index might be more reliable because consistent normal values have been established. This index is determined by the width of the frontal horns at the level of the caudate nuclei divided by the maximum width of the brain at the same level (Fig. 11.5). Alternatively, ventricular volume can be measured on CT or magnetic resonance imaging (MRI), outlining each slice and multiplying the area of outline by slice thickness. The total volume is the sum of these volumes including the calculated interslice gaps. In adults, there is little experience in acute neurologic disorders with this technique.39
Figure 11.4 Examples of different sites of obstruction (arrows). A–C: Arteriovenous malformation with giant vein of Galen. D,E: Colloid cyst in third ventricle (note absence of third ventricle). Examples of different sites of obstruction (arrows). F: Neurocytoma in third ventricle. G: Low-grade glioma in pineal region. H: Central nervous system lymphoma compressing fourth ventricle.
The temporal horns remain sensitive indicators for hydrocephalus on CT scans. Temporal horns, usually barely visible, become large, boomerang-shaped ventricles in acute hydrocephalus. This configuration often clearly differentiates obstruction from cortical cerebral atrophy. Other features compatible with atrophy rather than hydrocephalus are widening sylvian and interhemispheric fissures, leaving marked hypodense fluid-filled spaces and prominent dilated cortical sulci.
It is important to identify tumors that may obstruct the ventricular system, particularly those located in the intraventricular compartment, which may be isodense to the brain tissue. Characteristically, colloid cysts of the third ventricle are very subtle and difficult to detect because they blend in with brain tissue. A mass should be strongly considered if the third ventricle cannot be identified or the septum pellucidum is widened, separating the posterior medial aspects of the frontal horns. It is important to scrutinize the posterior fossa for a mass lesion that may be evident only from distortion of the fourth ventricle.
However, MRI should disclose any obstructive mass lesion.40 MRI also is particularly important to demonstrate meningeal enhancement (e.g., in sarcoidosis or carcinomatous meningitis)41,42 and lesions typically not well recognized on CT scanning (e.g., smaller pineal region cysts).
Figure 11.5 Measurement on computed tomographic scan of the ventricular system in acute hydrocephalus. Numbers indicate normal values. The ventricular size index (VSI) is not corrected for age. BCI, bicaudate index.
Untreated obstructive hydrocephalus leads to altered arousal, coma, and in some cases brain death and, thus, needs urgent neurosurgical intervention irrespective of its cause. Unfortunately, the rarity and rapid progression of acute obstructive hydrocephalus often delay diagnosis and limit the ability to treat. The emphasis in the emergency department is therefore on early intervention with ventriculostomy and identification of the trigger. Acute CSF diversion with placement of a ventriculostomy drain into the largest ventricle has priority and, if feasible, should be performed in the emergency department suite. The ventriculostomy tube is connected to a manometric CSF drainage system draining at 10–15 cm H2O. If the CSF is bloody, drainage at 0 cm H2O or lower should be considered, to reduce clotting in the catheter (Box 11.2). Alternative techniques, such as fenestration of the septum pellucidum or third ventriculostomy, are highly experimental.43,44 Placement of a ventriculostomy drain in patients with aneurysmal subarachnoid hemorrhage has been linked to rebleeding when the aneurysm is not secured with a clip or coil. We and others have found no such relationship21,45 and believe its placement is indicated in patients with persistent stupor, vertical downgaze, pinpoint pupils, and documented enlarging size in CT. Some endovascular radiologists prefer a ventriculostomy drain in place to safeguard (see Chapter 13) the effects of rebleeding associated with placement of coils. (Its presence will allow release of ventricular blood that otherwise would massively enlarge the ventricular system.)
Ventricular clearing of blood with ventriculostomy is not optimal and may lead to obstruction of the catheter; use of intraventricular thrombolytic agents is currently under investigation. Hemoventricle with hydrocephalus from primary intraventricular hemorrhage has been treated with additional instillation of urokinase.46 One study of 22 patients treated with intraventricular urokinase found a trend toward better outcome than that in a nearly similar control group. Clearance of the third ventricle predicted better outcome, suggesting that the focus of monitoring of these patients should perhaps be clearance of third ventricle clot.47
Box 11.2. Ventriculostomy
A ventricular catheter is inserted in the right (or, better, nondominant) frontal region. The patient is fully supine. In many instances, the bur hole is placed 1–2 cm anterior to the coronal suture in the midpupillary line (Fig. 11.6). The catheter is directed to the middle of the nose. The ventricular system (particularly when dilated) is reached at 5–7 cm below the skin. After insertion, the tube is subcutaneously tunneled and secured. Many neurosurgeons administer antibiotics. Complications are rare. They include ventriculitis (probably reduced with antibiotic prophylaxis and subcutaneous tunneling); epidural, subdural, or intraparenchymal hematoma (mostly in patients with severe coagulopathy); malfunctioning through blood clot obstruction; migration against the ventricular wall; and, rarely, creation of a dural arteriovenous fistula. All are reasons to replace the catheter.
Figure 11.6 Technique of ventriculostomy showing landmarks and approach.
Definitive treatment of the obstructing mass warrants endoscopic removal in most cases, and some patients need permanent ventriculoperitoneal shunts or fenestration of the third ventricle, accomplished by endoscopic techniques.48,49,50 The lamina terminalis, septum pellucidum, and floor of the third ventricle can all be punctured and then dilated with catheters to divert CSF. Cerebrospinal shunts usually employ valve systems draining at CSF pressures of more than 10 mm Hg. Overdrainage may lead to subdural effusions or subdural hematomas.51
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