AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Posttraumatic hydrocephalus (PTH) is a frequent and serious complication that follows a traumatic brain injury (TBI).^{1, 2, 3} Its incidence varies greatly from study to study, largely based on different criteria for its diagnosis.  However, PTH could greatly impact morbidity following a TBI and could result in increased mortality if it is not recognized and treated.

PTH may result from 1 or a combination of pathophysiologic factors. It can be caused by the overproduction of cerebrospinal fluid (CSF), the blockage of normal CSF flow, or insufficient absorption that results in excessive accumulation of CSF around the brain. Ultimately, PTH is caused by an imbalance that occurs between CSF production and absorption.⁴

PTH may present as normal pressure hydrocephalus (NPH) or as a syndrome of increased intracranial pressure.⁵ Because of differences in prognosis and treatment, PTH needs to be distinguished from cerebral atrophy (ie, hydrocephalus ex vacuo) and ventricular enlargement caused by a failure of brain development. If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely.^{6, 7}

Classification

Dandy and Blackfan introduced the classification of hydrocephalus as either noncommunicating or communicating.⁸ In noncommunicating hydrocephalus (also called obstructive hydrocephalus), CSF accumulates in the ventricles because of CSF flow blockage. As a result, the ventricles enlarge and the hemispheres expand. The following sites are prone to the obstruction of CSF flow⁹:

• Foramen of Monro
• Third ventricle
• Aqueduct of Sylvius
• Fourth ventricle
• Foramen of Luschka
• Foramen of Magendie

Conversely, in communicating hydrocephalus (also referred to as nonobstructive hydrocephalus), full communication between the ventricles and the subarachnoid space exists. Impaired CSF absorption may cause communicating hydrocephalus. The apparent mechanism is partial occlusion of the arachnoid villi, perhaps by blood and inflammatory mediators. Severe skull fractures, hemorrhage, and meningitis may predispose patients to this variant of PTH.⁹ Portnoy proposed that PTH develops as a result of increased dural sinus pressure, causing decreased CSF outflow.¹⁰

NPH, a form of communicating hydrocephalus, may result from subarachnoid hemorrhage caused by an aneurysm rupture or a TBI, encephalopathy, or Alzheimer disease. NPH often presents as the classic triad of a progressive gait disorder, impairment of mental function, and urinary incontinence.⁹ In NPH, ventricles enlarge despite normal or even slightly reduced intracranial pressure, and they continue to press against brain parenchyma.

See also the following related topic in Medscape:
Resource Center Trauma

See also the following related topics in eMedicine:
Hydrocephalus [Neurology]
Hydrocephalus [Neurosurgery]
Management and Staging of Traumatic Brain Injury
Normal Pressure Hydrocephalus [Neurology]
Normal Pressure Hydrocephalus [Radiology]

Pathophysiology

Normal anatomy and physiology:

In adults, the following features are encountered in posttraumatic hydrocephalus⁹:

• Normal intracranial pressure (ICP) is approximately 8 mm Hg.
• The average intracranial volume is about 1700 mL.
• The average CSF volume is about 104 mL.

By volume, the intracranial contents include the following¹¹:

• Brain parenchyma - About 80%
• CSF - About 10%
• Blood - About 10%

CSF is primarily produced in the lateral ventricles by the choroids plexus at a rate of 500 mL/d. The CSF flows down toward the third ventricle through the foramen of Monro and into the fourth ventricle through the cerebral aqueducts. The CSF then exits the ventricular system through the foramen of Magendie (medially) and the foramen of Luschka (laterally) and flows into the perimedullary and perispinal subarachnoid spaces. The CSF continues around the brainstem to the basal and ambient cisterns. It then flows to the lateral and superior surfaces of the cerebral hemispheres, where it is largely absorbed through the arachnoid villi.

The total volume of CSF is replaced several times daily.

Frequency

United States

The onset of PTH may vary from 2 weeks to years after TBI. Studies cite a wide range of incidence (0.7-50%); part of this variation results from underdiagnosis and atypical presentation, as well as from the fact that different sets of clinical criteria are used to diagnose PTH.^{5, 6, 7, 12}

Mazzini and colleagues found that 50% of patients with postacute phase severe TBI had PTH but that only 11% required surgery.⁷ 

International

In a multi-year study, Kim and colleagues followed 789 patients who had suffered a TBI, diagnosing PTH in 129 (16.3%) of them.¹³ Sixty-four patients with PTH required shunting.

Mortality/Morbidity

If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely.^{6, 7}

Race

Race does not appear to be a factor in the development of PTH.

Sex

Sex does not appear to be a risk factor in the development of PTH.

Age

Increased age appears to increase the risk of developing PTH.⁷

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Posttraumatic hydrocephalus (PTH) often has an atypical presentation and therefore may be easily missed. A high level of clinical suspicion is important for diagnosis.^{14, 15}

• If acute, patients may present with coma and other focal neurologic deficits.
• If chronic, patients may demonstrate a gradual decline in functional status or may show a failure to improve.⁵ The decline in performance or functioning may be initially observed by therapists.

The cognitive decline of NPH may present similarly to dementias in elderly patients.¹⁶ However, Alzheimer disease more commonly presents insidiously over a period of years, with progressive memory impairment, anomia, apraxia, agnosia, and a decline in executive function.¹⁷ Dementia in NPH usually presents with subcortical features.

Physical

• PTH may present as a syndrome of increased intracranial pressure with symptoms of papilledema, focal neurologic deficits, or coma.⁵
• Most commonly, PTH presents as noncommunicating hydrocephalus with the following findings⁴:
• • Papilledema resulting from increased intracranial pressure and transmission through the subarachnoid space
  • Cognitive changes, including decreased memory, decreased attention, and irritability
• Headaches (common)
• NPH often presents as a classic triad of the following symptoms⁹:
• • Progressive gait disorder
  • Impairment of mental function
  • Urinary incontinence
• In NPH, headaches are not common and papilledema is not usually seen on funduscopic examination; patients may present with frontal release signs.⁴

Causes

Obstructive hydrocephalus may be caused by tumors, infection, abscesses, cysts, or trauma. NPH may result from a subarachnoid hemorrhage caused by an aneurysm rupture, a TBI, or encephalopathy.¹⁸

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to Be Considered

Intracranial bleeding
Electrolyte imbalance
Adverse effects of medications
Hypoxia
Infection
Tumors
Stroke
Seizures
Uremia
Encephalopathy
Dementia

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Urine analysis and culture - Evaluate for urinary tract infections.
• Complete blood count (CBC) with differential - Evaluate for infection and anemia.
• Metabolic profile - Evaluate for electrolyte abnormalities, including syndrome of inappropriate secretion of antidiuretic hormone (SIADH), cerebral salt wasting, calcium deficiency, hypoglycemia, hyperglycemia, and encephalopathy (uremic or hepatic).
• Thyroid-stimulating hormone (TSH), free T4 - Evaluate for hypothyroidism or hyperthyroidism.
• Arterial blood gas level - Assess oxygenation and acid/base balance.
• Serum medication levels - Measure medication levels if toxicity suspected.

Imaging Studies

• Noncontrast CT scan of the brain is one of the most commonly used diagnostic modalities.
• • The progressive enlargement of the ventricular system shown on repeat computed tomography (CT) scans is the key to the diagnosis of PTH.⁶
  • CT scans may show enlarged lateral ventricles, effaced cerebral sulci, and dilation on ventricles proximal to an obstruction.⁴
  • Periventricular edema may occur in white matter, particularly around the frontal horns.⁴
  • Sulcal enlargement with ventricular enlargement suggests atrophy and hydrocephalus ex vacuo rather than hydrocephalus.⁴
  • Large cisterns and focal regions of encephalomalacia suggest atrophy.⁵
• Magnetic resonance imaging (MRI) is another method of diagnostic evaluation.¹⁹
•     MRI is more useful in the evaluation of injury to structures in the posterior fossa, including cerebral aqueduct stenosis and cerebellar tonsil herniation.²⁰
•     It is the neuroimaging study of choice in patients with NPH.²⁰
•     MRI may be more useful than CT scanning in the identification of other neurologic disorders, especially cerebrovascular disease.¹⁷

Mazzini studied another imaging technique, single-photon emission CT (SPECT).⁷ Mazzini found that SPECT had higher sensitivity than MRI or CT scanning in the demonstration of temporal lobe abnormality secondary to PTH.

Other Tests

• Radionuclide cisternography:⁴
• • Radioiodinated serum albumin (RISA) injected into the subarachnoid space by way of lumbar puncture (LP) can normally be detected in the cisterna magna, basal cisterns, and subtentorial subarachnoid space within 6 hours, with little accumulation in the ventricular system. In NPH, RISA accumulates in the ventricular system with delayed pericerebral diffusion.
  • Cisternography is usually normal in hydrocephalus ex vacuo.
• Although debate exists, cisternography may be a useful adjunct to CT scanning of the brain.

Procedures

• CSF tap test
• • This test is an LP with manometry and CSF removal.
  • Imaging of the brain should be performed before initiating the LP. The risk of cerebral herniation associated with the LP is increased in patients with greatly elevated ICP.
  • The CSF tap test may be a useful predictor of the potential benefits of shunting.  Kim (2005) found that symtomatic improvement after lumbar drainage has a significant role in predicting the result of shunting.
  • CSF pressure is normally 110 mm water. Shunting may help if the pressure is 135-275 mm water, and it does help if the pressure is greater than 275 mm water.
  • Cognitive and physical functions are assessed before and after the removal of 50 mL of CSF. Improvement suggests that shunting may be beneficial.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Rehabilitation Program

Physical Therapy

The resumption of rehabilitation is usually prompt after the placement of a ventriculoperitoneal (VP) shunt.²¹ Patients are typically observed for 2-3 days postoperatively. They then return to rehabilitation services to complete their brain-injury rehabilitation program. Successful shunting is usually related to more obvious and rapid improvements during rehabilitation efforts.²²

Occupational Therapy

See Physical Therapy.

Speech Therapy

See Physical Therapy.

Recreational Therapy

See Physical Therapy.

Surgical Intervention

• Before treatment, conditions such as infection, anemia, hypoxia, seizure disorder, uremia, and encephalopathy must be ruled out or addressed. If PTH is suspected, prompt neurosurgical evaluation is highly recommended.
• Shunting is the most common treatment for hydrocephalus. The outcome is usually favorable.
• A shunt is usually placed from the right ventricle to the peritoneal space. The right side is normally used to avoid injury to the language centers on the left side of the brain. Shunts are usually equipped with reservoirs that are used for transiently increasing output and for testing the patency of flow.
• Patients with acute presentations and clear signs of high-pressure hydrocephalus benefit from a shunting procedure. Patients with chronic presentations can be observed with frequent CT scanning of the brain to monitor for progression of hydrocephalus.⁵
• In a study by Tribl and Oder, 52% of patients with PTH had significant improvement within 3 months of shunting.²³
• Patients with NPH also may benefit from a shunting procedure. In patients with a TBI and communicating hydrocephalus, Groswasser found that shunting promoted a recovery of consciousness and motor capacity but not a return of neurobehavioral function.⁶
• Complications and shunt malfunctions are common.^{23, 21} Complications of shunts include the following:
• • Infection - Wound infection or contamination during placement
  • Shunt failure - Displacement and leakage
  • Occlusion - Kinking and tube clotting
  • Overshunting - More fluid is shunted than necessary
  • Placement errors
• Assessing the efficacy of surgical intervention can be problematic because of the heterogeneity of TBI severity, TBI location, nonuniform diagnostic criteria used across studies, variants of PTH, the severity of PTH, and the length of time between the occurrence of a TBI and the development of PTH. Further research is needed to control for confounding factors, elucidate criteria for surgical intervention, and assess the outcome of surgery.¹⁵

Consultations

When hydrocephalus is confirmed, consultation with a neurosurgeon should be expedited.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The management of hydrocephalus centers on the reduction of intracranial pressure and on the correction of factors that lead to increased ICP. Elevation of the head may help to reduce pressure, as well as to maintain normotensive blood pressure. Medications with osmotic effects (such as mannitol) or that reduce CSF production (such as acetazolamide) may have limited value. Hence, medications likely do not play a major role in the treatment of PTH. The condition is treated surgically. 

The discontinuation of medications that may contribute to the impairment of cognitive or physical functioning should be considered.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients typically make rapid gains in the first 1-2 weeks following shunt placement for PTH; therefore, rehabilitation may be beneficial as PTH resolves.
• Because shunts may malfunction, physicians should monitor patients for the signs and symptoms of PTH.

Further Outpatient Care

• Patients or caregivers should seek immediate medical evaluation and attention if the signs and symptoms of PTH return.

Complications

• The possible complications of PTH include the following:
• • Cerebral herniation
  • Risk of aspiration as a result of dysphagia
  • Increased risk of falls
  • Inability to benefit from rehabilitation

Prognosis

• Groswasser found that in patients who developed communicating hydrocephalus following a TBI, the duration of coma was longer and the incidence and severity of behavioral problems was greater.⁶ Furthermore, in patients with a TBI and communicating hydrocephalus, the rate at which these individuals returned to their previous occupation was lower than it was in patients with a TBI but no PTH.
• Patients typically do well after the placement of a shunt for PTH. Tribl and Oder's study indicated that the best predictor of outcome following shunting is the patient's pre-operative status. The authors' results also indicated that age at time of injury does not influence outcome.²³
• Similarly, Kim and colleagues found evidence that symptomatic improvement after pre-operative lumbar drainage provides a strong indication of the results of shunt placement and that age and sex seems to have no impact on outcome.¹³
• Shunts may malfunction and require revision or replacement; therefore, careful monitoring for the signs and symptoms of functional decline is important for the physiatrist and for caretakers.

Patient Education

• Patients and caregivers need to be educated about symptoms that might suggest shunt failure and should be instructed as to when medical evaluation should be sought.
• For excellent patient education resources, visit eMedicine's Dementia Center. Also, see eMedicine's patient education article Normal Pressure Hydrocephalus.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• The main medicolegal risks are a failure to recognize the problem and to arrange for a neurosurgical assessment.
• An awareness that hydrocephalus occurs in patients with a TBI and that it occurs with signs and symptoms that are common to numerous other TBI complications should result in a low threshold for performing CT scanning when hydrocephalus is suspected.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Bontke CF. Medical complications related to traumatic brain injury. Phys Med Rehabil: State Art Rev. 1989;3:43-58.
2. Narayan RJ, Gokaslan ZL, Bontke CF. Neurologic sequelae of head injury. In: Rosenthal M, ed. Rehabilitation of the Adult and Child With Traumatic Brain Injury. 2^nd ed. Philadelphia, Pa: Davis; 1990:94-106.
3. Stein S, Schrader P. Neurologic sequelae. Phys Med Rehabil: State Art Rev. 1990;4:543-57.
4. Katz RT, Brander V, Sahgal V. Updates on the diagnosis and management of posttraumatic hydrocephalus. Am J Phys Med Rehabil. Apr 1989;68(2):91-6. [Medline].
5. Guyot LL, Michael DB. Post-traumatic hydrocephalus. Neurol Res. Jan 2000;22(1):25-8. [Medline].
6. Groswasser Z, Cohen M, Reider-Groswasser I, et al. Incidence, CT findings and rehabilitation outcome of patients with communicative hydrocephalus following severe head injury. Brain Inj. Oct-Dec 1988;2(4):267-72. [Medline].
7. Mazzini L, Campini R, Angelino E, et al. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil. Nov 2003;84(11):1637-41. [Medline].
8. Dandy WE, Blackfan KD. Internal hydrocephalus: an experimental, clinical, and pathological study. Am J Dis Child. 1914;8:406.
9. Adams RD, Victor M. Disturbances of cerebrospinal fluid and its circulation, including hydrocephalus and meningeal reactions. In: Principles of Neurology. 4^th ed. New York, NY: McGraw-Hill Information Services Co; 1989:623-35.
10. Portnoy HD, Chopp M, Branch C, et al. Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. J Neurosurg. May 1982;56(5):666-78. [Medline].
11. Kaye AH, Laws ER, eds. Brain Tumors: An Encyclopedic Approach. 2^nd ed. New York, NY: Churchill Livingstone; 2001:205.
12. Mori K, Shimada J, Kurisaka M, et al. Classification of hydrocephalus and outcome of treatment. Brain Dev. Sep-Oct 1995;17(5):338-48. [Medline].
13. Kim SW, Lee SM, Shin H. Clinical Analysis of Post-Traumatic Hydrocephalus. J Korean Neursurg Soc. 2005;38:211-214.
14. Long DF. Diagnosis and management of intracranial complications in traumatic brain injury rehabilitation. In: Horn LJ, Zasler ND, eds. Medical Rehabilitation of Traumatic Brain Injury. Philadelphia, Pa: Hanley & Belfus; 1996:333-62.
15. Paoletti P, Pezzotta S, Spanu G. Diagnosis and treatment of post-traumatic hydrocephalus. J Neurosurg Sci. Jul-Sep 1983;27(3):171-5. [Medline].
16. Wostyn P, Audenaert K, De Deyn PP. Alzheimer's disease-related changes in diseases characterized by elevation of intracranial or intraocular pressure. Clin Neurol Neurosurg. Feb 2008;110(2):101-9. [Medline].
17. Factora R, Luciano M. Normal pressure hydrocephalus: diagnosis and new approaches to treatment. Clin Geriatr Med. Aug 2006;22(3):645-57. [Medline].
18. Tian HL, Xu T, Hu J, et al. Risk factors related to hydrocephalus after traumatic subarachnoid hemorrhage. Surg Neurol. Aug 16 2007;[Medline].
19. Nasel C, Gentzsch S, Heimberger K. Diffusion-weighted magnetic resonance imaging of cerebrospinal fluid in patients with and without communicating hydrocephalus. Acta Radiol. Sep 2007;48(7):768-73. [Medline].
20. Graff-Radford NR. Normal pressure hydrocephalus. Neurol Clin. Aug 2007;25(3):809-32, vii-viii. [Medline].
21. Wu Y, Green NL, Wrensch MR, et al. Ventriculoperitoneal shunt complications in California: 1990 to 2000. Neurosurgery. Sep 2007;61(3):557-62; discussion 562-3. [Medline].
22. Bontke CF, Zasler ND, Boake C. Rehabilitation of the head-injured patient. In: Narayan RK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York, NY: McGraw-Hill; 1996:841-58.
23. Tribl G, Oder W. Outcome after shunt implantation in severe head injury with post-traumatic hydrocephalus. Brain Inj. Apr 2000;14(4):345-54. [Medline].

Article Last Updated: Feb 12, 2008