Practice Essentials
Posttraumatic hydrocephalus (PTH) is a frequent and serious complication that follows a traumatic brain injury (TBI). [1, 2, 3, 4] 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 one 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. [5]
PTH may present similarly to normal pressure hydrocephalus (NPH) or as a syndrome of increased intracranial pressure. [6] Because of differences in prognosis and treatment, PTH needs to be distinguished from other disease processes that can elevate intracranial pressure (ICP), such as hemorrhage, tumor, edema, venous sinus thrombus, and meningitis. Additionally, overproduction of CSF may be due to choroid plexus tumor. If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely. [7, 8, 9]
In addition to incontinence, gait deterioration, and cognitive decline, which are symptoms classically present in NPH, early symptoms of PTH may include headache, nausea, and vomiting and acute mental status changes such as confusion or lethargy. [9, 10] Arrival at a functional plateau or regression in a patient's rehabilitation course may also be a symptom of PTH.
Classification of hydrocephalus
Dandy and Blackfan introduced the classification of hydrocephalus as either noncommunicating or communicating. [11] In noncommunicating, or obstructive, hydrocephalus, normal CSF flow is blocked. As a result, CSF can accumulate in the ventricles, leading to ventriculomegaly and hemispheric displacement. The following sites are prone to the obstruction of CSF flow, which can stem from a variety of causes, including the presence of a stricture, mass, or hemorrhage [9] :
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Foramen of Monro
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Third ventricle
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Aqueduct of Sylvius
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Fourth ventricle
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Foramen of Luschka
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Foramen of Magendie
In addition, overproduction of CSF, as a result of, perhaps, a tumor of the choroid villi, may lead to relative ventriculomegaly, which could result in mass effect and, eventually, obstructive hydrocephalus.
In communicating hydrocephalus (also referred to as nonobstructive hydrocephalus), full communication between the ventricles and subarachnoid space exists. Impaired CSF absorption at the arachnoid villi, perhaps due to the presence of blood and other inflammatory mediators, may cause communicating hydrocephalus. Severe skull fractures, hemorrhage, and meningitis may predispose patients to this type of PTH. [9]
Portnoy proposed that PTH can develop as a result of increased dural sinus pressure, causing decreased CSF outflow. [12]
Normal pressure hydrocephalus (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.
Signs and symptoms of posttraumatic hydrocephalus
If PTH is acute, patients may present with coma and other focal neurologic deficits. If the condition is chronic, individuals may demonstrate a gradual decline in functional status or may show a failure to improve. [6]
Workup in posttraumatic hydrocephalus
Pertinent laboratory studies include the following:
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Urine analysis and culture - Evaluate for urinary tract infections
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Complete blood count (CBC) with differential - Evaluate for infection and anemia
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Metabolic profile - Evaluate for electrolyte abnormalities
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Thyroid-stimulating hormone (TSH), free thyroxine (free T4) - Evaluate for hypothyroidism or hyperthyroidism
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Arterial blood gas level - Assess oxygenation and acid/base balance
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Serum medication levels - Measure medication levels if toxicity suspected
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CSF analysis - Evaluate for infectious etiologies, autoimmune disease, and certain cancers
The progressive enlargement of the ventricular system shown on repeat computed tomography (CT) scans is the key to the diagnosis of PTH. [7] Magnetic resonance imaging (MRI) is useful in the evaluation of injury to structures in the posterior fossa, including cerebral aqueduct stenosis and cerebellar tonsil herniation. [12]
Another exam, the CSF tap test, is a lumbar puncture (LP) with manometry and CSF removal. Cognitive and physical functions are assessed before and after the removal of 50 mL of CSF. Improvement suggests that shunting may be beneficial.
Management of posttraumatic hydrocephalus
Shunting is the most common treatment for hydrocephalus. The outcome is typically 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 most often equipped with reservoirs that are used for transiently increasing output and for testing the patency of flow.
The resumption of rehabilitation is usually prompt after the placement of a ventriculoperitoneal (VP) shunt. [13, 14] 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. [15]
See also the following related resource in Medscape:
Resource center: Trauma
See also the following related topics in Medscape Drugs & Diseases:
Hydrocephalus [Neurology]
Hydrocephalus [Neurosurgery]
Classification and Complications of Traumatic Brain Injury
Normal Pressure Hydrocephalus [Neurology]
Normal Pressure Hydrocephalus [Radiology]
Pathophysiology
Normal anatomy and physiology
CSF is produced, primarily in the lateral ventricles by the choroid plexuses, with smaller contributions from the third and fourth ventricles, 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. [9] Primary functions of the CSF include cushioning of the brain and spinal cord and removal of neuronal metabolic waste products.
In normal adults, the following measurements have been observed [9] :
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Normal intracranial pressure (ICP) is approximately 8 mm Hg.
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The average intracranial volume is about 1700 mL.
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The average CSF volume is about 104 mL.
By volume, the intracranial contents include the following [13] :
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Brain parenchyma - About 80%
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CSF - About 10%
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Blood - About 10%
Epidemiology
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. [6, 7, 8, 14]
Mazzini and colleagues found that 50% of patients with postacute phase severe TBI had PTH but that only 11% required surgery. [8]
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. [15] 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. [7, 8]
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. [8]
