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Hydrocephalus Follow-up

  • Author: Stephen L Nelson, Jr, MD, PhD, FAAP; Chief Editor: Jasvinder Chawla, MD, MBA  more...
Updated: Apr 13, 2016

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.


Further Inpatient Care

Patients with shunt-dependent hydrocephalus should be admitted for consideration of shunt revision if shunt malfunction or infection is suspected.[17]

In children, shunt revisions are scheduled according to growth rate.


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.



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



See the list below:

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


See the list below:

  • 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.


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%.

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.

Contributor Information and Disclosures

Stephen L Nelson, Jr, MD, PhD, FAAP Section Head of Pediatric Neurology, Associate Professor of Pediatrics, Neurology, and Psychiatry, Tulane University School of Medicine

Stephen L Nelson, Jr, MD, PhD, FAAP is a member of the following medical societies: Academic Pediatric Association, American Academy of Neurology, American Academy of Pediatrics, American Medical Association, Association of Military Surgeons of the US, Child Neurology Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

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

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

Disclosure: Nothing to disclose.


Alberto J Espay, MD, MSc Associate Professor, Director of Clinical Research, Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati College of Medicine

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

Disclosure: Abbott Consulting fee Consulting; Chelsea therapeutics Consulting fee Consulting; Novartis Honoraria Speaking and teaching; TEVA Consulting fee Consulting; NIH Grant/research funds K23 Career Development Award; Eli Lilly Consulting fee Consulting; Great Lakes Neurotechnologies Other; Michael J Fox Foundation Grant/research funds Other; Lippincott Williams & Wilkins Royalty Book; American Academy of Neurology Honoraria Speaking and teaching

Eugenia-Daniela Hord, MD Instructor, Departments of Anesthesia and Neurology, Massachusetts General Hospital Pain Center, Harvard Medical School

Eugenia-Daniela Hord, MD is a member of the following medical societies: American Academy of Neurology and American Pain Society

Disclosure: Nothing to disclose.

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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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