Medical Care
Medical treatment in hydrocephalus is used to delay surgical intervention. It may be tried in premature infants with posthemorrhagic hydrocephalus (in the absence of acute hydrocephalus). Normal CSF absorption may resume spontaneously during this interim period.
Medical treatment is not effective in long-term treatment of chronic hydrocephalus. It may induce metabolic consequences and thus should be used only as a temporizing measure.
Medications affect CSF dynamics by the following mechanisms:
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Decreasing CSF secretion by the choroid plexus - Acetazolamide and furosemide
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Increasing CSF reabsorption - Isosorbide (effectiveness is questionable)
Surgical Care
Surgical treatment is the preferred therapeutic option. [4]
Repeat lumbar punctures (LPs) can be performed for cases of hydrocephalus after intraventricular hemorrhage, since this condition can resolve spontaneously. If reabsorption does not resume when the protein content of cerebrospinal fluid (CSF) is less than 100 mg/dL, spontaneous resorption is unlikely to occur. LPs can be performed only in cases of communicating hydrocephalus.
Alternatives to shunting include the following:
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Choroid plexectomy or choroid plexus coagulation may be effective in cases of CSF over-production.
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Opening of a stenosed aqueduct has a higher morbidity rate and a lower success rate than shunting, except in the case of tumors. However, lately cerebral aqueductoplasty has gained popularity as an effective treatment for membranous and short-segment stenoses of the sylvian aqueduct. It can be performed through a coronal approach or endoscopically through suboccipital foramen magnum trans-fourth ventricle approach.
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In cases where a tumor is the cause, removal cures the hydrocephalus in 80%.
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Endoscopic fenestration of the floor of the third ventricle establishes an alternative route for CSF toward the subarachnoid space. It is contraindicated in communicating hydrocephalus, but can be used especially with aqueductal stenosis.
Shunts eventually are performed in most patients. Only about 25% of patients with hydrocephalus are treated successfully without shunt placement. The principle of shunting is to establish a communication between the CSF (ventricular or lumbar) and a drainage cavity (peritoneum, right atrium, pleura). Remember that shunts are not perfect and that all alternatives to shunting should be considered first.
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A ventriculoperitoneal (VP) shunt is used most commonly. The lateral ventricle is the usual proximal location. The advantage of this shunt is that the need to lengthen the catheter with growth may be obviated by using a long peritoneal catheter.
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A ventriculoatrial (VA) shunt also is called a "vascular shunt." It shunts the cerebral ventricles through the jugular vein and superior vena cava into the right cardiac atrium. It is used when the patient has abdominal abnormalities (eg, peritonitis, morbid obesity, or after extensive abdominal surgery). This shunt requires repeated lengthening in a growing child.
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A lumboperitoneal shunt is used only for communicating hydrocephalus, CSF fistula, or pseudotumor cerebri.
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A Torkildsen shunt is used rarely. It shunts the ventricle to the cisternal space and is effective only in acquired obstructive hydrocephalus.
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A ventriculopleural shunt is considered second line. It is used if other shunt types are contraindicated.
Rapid-onset hydrocephalus with increased intracranial pressure (ICP) is an emergency. The following can be done, depending on each specific case:
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Ventricular tap in infants
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Open ventricular drainage in children and adults
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LP in posthemorrhagic and postmeningitic hydrocephalus
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VP or VA shunt
Consultations
Consultation with the following may prove helpful:
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Neurosurgeon
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Neurologist
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Neurorehabilitation specialist
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Ophthalmologist
Activity
Most surgeons agree that, with the use of antisiphon devices, no special positioning is required after shunting. However, some surgeons used to leave patients in whom a standard shunt had been placed in a recumbent position for 1-2 days after surgery to minimize the risk of subdural hematoma.
In treatment of normal pressure hydrocephalus (NPH), gradual postoperative mobilization is recommended.
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Noncommunicating obstructive hydrocephalus caused by obstruction of the foramina of Luschka and Magendie. This MRI sagittal image demonstrates dilatation of lateral ventricles with stretching of corpus callosum and dilatation of the fourth ventricle.
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Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.
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Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.
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Communicating hydrocephalus with surrounding "atrophy" and increased periventricular and deep white matter signal on fluid-attenuated inversion recovery (FLAIR) sequences. Note that apical cuts (lower row) do not show enlargement of the sulci, as is expected in generalized atrophy. Pathological evaluation of this brain demonstrated hydrocephalus with no microvascular pathology corresponding with the signal abnormality (which likely reflects transependymal exudate) and normal brain weight (indicating that the sulci enlargement was due to increased subarachnoid cerebrospinal fluid [CSF] conveying a pseudoatrophic brain pattern).
