Hydrocephalus Follow-up

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

Further Inpatient Care

  • Patients with shunt-dependent hydrocephalus should be admitted for consideration of shunt revision if shunt malfunction or infection is suspected.
  • In children, shunt revisions are scheduled according to growth rate.
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Further Outpatient Care

  • Patients on acetazolamide (ACZ) or furosemide (FUR) should be followed for possible electrolyte imbalance and metabolic acidosis. Clinical signs that should prompt attention are lethargy, tachypnea, or diarrhea.
  • Patients with shunts should be reevaluated periodically, including assessment of distal shunt length in growing children. The first follow-up examination usually is scheduled 3 months after surgery, and CT scan or MRI of the head should be done at that time. Follow-up is performed every 6-12 months in the first 2 years of life. In children aged 2 years and older, follow-up is performed every 2 years.
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Inpatient & Outpatient Medications

  • Medications include acetazolamide and furosemide. These are helpful for temporizing the hydrocephalus until compensation occurs. If compensation does not occur, then shunting is indicated.
  • Medications should not be used in patients with functional shunts.
  • Medication is not effective in long-term treatment of chronic hydrocephalus, and it may induce metabolic consequences.
  • If seizures occur, antiepileptic drugs are recommended.
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Transfer

  • In cases of acute hydrocephalus or shunt complications, immediately transfer the patient to a center with a neurosurgery service.
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Deterrence/Prevention

  • Avoid trauma: The valve and tubing system are located superficially under the skin and can be damaged easily by trauma.
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Complications

  • Related to progression of hydrocephalus
    • Visual changes
      • Occlusion of posterior cerebral arteries secondary to downward transtentorial herniation
      • Chronic papilledema injuring the optic disc
      • Dilatation of the third ventricle with compression of optic chiasm
    • Cognitive dysfunction
    • Incontinence
    • Gait changes
  • Related to medical treatment
  • Related to surgical treatment
    • Signs and symptoms of increased intracranial pressure (ICP) can be a consequence of undershunting or shunt obstruction or disconnection.
    • Subdural hematoma or hygroma is secondary to overshunting. Headache and focal neurological signs are common.
    • Treat seizures with antiepileptic drugs.
    • Shunt infection occasionally can be asymptomatic. In neonates, it manifests as alteration of feeding, irritability, vomiting, fever, lethargy, somnolence, and a bulging fontanelle. Older children and adults present with headache, fever, vomiting, and meningismus. With ventriculoperitoneal (VP) shunts, abdominal pain may occur.
    • Shunts can act as a conduit for extraneural metastases of certain tumors (eg, medulloblastoma).
    • Hardware erosion through the skin occurs in premature infants with enlarged heads and thin skin who lie on 1 side of the head.
    • VP shunt complications include peritonitis, inguinal hernia, perforation of abdominal organs, intestinal obstruction, volvulus, and CSF ascites.
    • Ventriculoatrial (VA) shunt complications include septicemia, shunt embolus, endocarditis, and pulmonary hypertension.
    • Lumboperitoneal shunt complications include radiculopathy and arachnoiditis.
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Prognosis

  • Long-term outcome is related directly to the cause of hydrocephalus.
  • Up to 50% of patients with large intraventricular hemorrhage develop permanent hydrocephalus requiring shunt.
  • Following removal of a posterior fossa tumor in children, 20% develop permanent hydrocephalus requiring a shunt. The overall prognosis is related to type, location, and extent of surgical resection of the tumor.
  • Satisfactory control was reported for medical treatment in 50% of hydrocephalic patients younger than 1 year who had stable vital signs, normal renal function, and no symptoms of elevated ICP.
  • Criteria exist for predicting improvement with shunting in NPH, but they are controversial.
    • If gait disturbance precedes mental deterioration, the chance of improvement is 77%. Patients with dementia and no gait disturbance rarely respond to shunting.
    • Focal impingement of corpus callosum on MRI indicates unstable ICP and is associated with a good response to shunting.
    • Initial OP of CSF greater than 100 mm H2 O predicts better response.
    • Response to a single LP or to controlled CSF drainage via lumbar subarachnoid catheter (ELD) has some value in predicting outcome.
    • Cerebral blood flow of 32 mL/100 g per minute or greater predicts clinical improvement after shunt.
    • CSF pressure of 180 mm H2 O with frequent Lundberg B waves on continuous CSF pressure monitoring is associated with good prognosis after shunting. Lundberg B waves represent an accentuation of physiological phenomena, reflecting arterial waves. They represent fluctuating ICP waves of 4-8 per minute frequency and 20-30 mm Hg (260-400 mm H2 O) amplitude. Occasionally they can occur in normal sleep.
    • Large ventricles with flattened or invaginated sulci (entrapped sulci) suggest that hydrocephalus is not due to atrophy alone. These patients have good prognosis with shunting.
    • If isotopic cisternography shows persistent ventricular activity on a late scan (42-72 h), the probability of improving with shunting is 75%.
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Patient Education

  • Knowledge of the signs and symptoms of shunt malfunction or infection and the necessity for emergent medical evaluation in these instances is mandatory in patients, family members, and caregivers.
  • The patient, family, and caregivers should know that periodic re-evaluation is necessary.
  • Pumping the shunt is contraindicated in most cases.
  • Patients with vascular shunts, and some patients with other types of shunts, should receive prophylactic antibiotics before dental procedures or instrumentation of the bladder.
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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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