Hydrocephalus Treatment & Management

  • Author: Alberto J Espay, MD; Chief Editor: Michael Hoffmann, MBBCh, MD, FCP(SA), FAAN, FAHA   more...
 
Updated: Apr 27, 2010
 

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:
    • Decreasing CSF secretion by the choroid plexus - Acetazolamide and furosemide
    • Increasing CSF reabsorption - Isosorbide (effectiveness is questionable)
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Surgical Care

  • Surgical treatment is the preferred therapeutic option.[13]
  • 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:
    • Choroid plexectomy or choroid plexus coagulation may be effective.
    • 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.
    • In these cases, tumor removal cures the hydrocephalus in 80%.
    • 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.
  • 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.
    • 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.
    • 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.
    • A lumboperitoneal shunt is used only for communicating hydrocephalus, CSF fistula, or pseudotumor cerebri.
    • A Torkildsen shunt is used rarely. It shunts the ventricle to cisternal space and is effective only in acquired obstructive hydrocephalus.
    • 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:
    • Ventricular tap in infants
    • Open ventricular drainage in children and adults
    • LP in posthemorrhagic and postmeningitic hydrocephalus
    • VP or VA shunt
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Consultations

  • Neurosurgeon
  • Neurologist
  • Neurorehabilitation specialist
  • Ophthalmologist
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Diet

  • Regular, as tolerated
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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 risk of subdural hematoma.
  • In treatment of normal pressure hydrocephalus (NPH), gradual postoperative mobilization is recommended.
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Contributor Information and Disclosures
Author

Alberto J Espay, MD  Assistant Professor, Department of Neurology, Gardner Family Center for Parkinson's Disease and Movement Disorders, Director of Clinical Research, University of Cincinnati

Alberto J Espay, MD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society

Disclosure: Boehringer-Ingelheim Consulting fee Board membership; Medtronic Grant/research funds Other; Novartis Honoraria Speaking and teaching; Solvay Consulting fee Board membership; NIH Grant/research funds KL2 Research Scholars mentored career development award

Specialty Editor Board

Anthony M Murro, MD  Professor, Laboratory Director, Department of Neurology, Medical College of Georgia

Anthony M Murro, MD is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard J Caselli, MD  Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale

Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Michael Hoffmann, MBBCh, MD, FCP(SA), FAAN, FAHA  Professor of Neurology, University of Central Florida College of Medicine; Director of Cognitive Neurology, Director of Stroke Program, James A Haley Veterans Affairs Hospital

Michael Hoffmann, MBBCh, MD, FCP(SA), FAAN, FAHA is a member of the following medical societies: American Academy of Neurology, American Headache Society, American Heart Association, and American Society of Neuroimaging

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Eugenia-Daniela Hord, MD, to the original writing and development of this article.

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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.
Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates dilatation of the lateral ventricles.
Noncommunicating obstructive hydrocephalus caused by obstruction of foramina of Luschka and Magendie. This MRI axial image demonstrates fourth ventricle dilatation.
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).
 
 
 
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