Traumatic hydrocephalus

Introduction to traumatic hydrocephalus Traumatic hydrocephalus is more common in severe brain injury with brain contusion and laceration. SAH patients are one of the important factors causing high mortality in patients with severe brain injury and coma. CT diagnosis is timely and effective surgical treatment is expected. Save the lives of patients. basic knowledge The proportion of the disease: the incidence of this disease is about 10% Susceptible people: no special people Mode of infection: non-infectious Complications: brain contusion, subarachnoid hemorrhage, multiple intracranial hematoma

Causes of traumatic hydrocephalus

(1) Causes of the disease

Subarachnoid hemorrhage is more common after brain contusion. A large amount of bloody cerebrospinal fluid will cause strong stimulation to the meninges, which can cause aseptic inflammation. Therefore, adhesion between the soft membrane and the arachnoid can occur, and even arachnoid villi can be blocked. , causing cerebrospinal fluid circulation and absorption disorders, which is similar to hydrocephalus caused by subarachnoid obstruction caused by purulent meningitis, that is, cerebrospinal fluid produced by the choroid plexus can flow out of the ventricle, but is blocked by the arachnoid The lower cavity and the brain basement pool, the ring pool and the lateral fissure pool prevent the cerebrospinal fluid from circulating through the cerebral convex surface to the arachnoid granule absorption. Therefore, the patient often has symptoms of increased intracranial pressure, and the ventricular system also expands, if not obtained. Timely and reasonable treatment, the condition will worsen. Sometimes cerebrospinal fluid circulatory obstruction occurs in the ventricular system, causing water accumulation in one or both ventricles. This condition is caused by ventricular penetrating injury or intramedullary hematoma breaking into the ventricle. In the interventricular space, the outlet tube or the outlet of the fourth ventricle is blocked, and may be blocked by the cerebellum, and the brain stem is displaced to cause the ring pool to occlude or guide the water. Oppressed can also cause hydrocephalus; or because of improper hemicraniectomy, severe brain swelling, shift, lead to obstruction of cerebrospinal fluid circulation associated with hydrocephalus also when there is discovery.

(two) pathogenesis

Traumatic hydrocephalus can be divided into acute and chronic. Acute hydrocephalus refers to hydrocephalus that occurs within 2 weeks after injury. The possible mechanisms are:

1. The blood clot directly blocks the cerebrospinal fluid circulation pathway or affects the absorption of cerebrospinal fluid due to obstruction of the arachnoid villi by red blood cells.

2. Cerebral edema, intracranial hematoma, cerebral palsy, brain swelling or protrusion can also oppress the subarachnoid space in the brain pool and brain surface, affecting the circulation and absorption of cerebrospinal fluid.

3. Intraventricular hemorrhage, ventricle penetrating injury, blood accumulation can block the interventricular pores, the water conduit, the fourth ventricle median hole, so that the cerebrospinal fluid can not return to the subarachnoid space.

Chronic hydrocephalus refers to hydrocephalus that occurs within 3 weeks to 1 year after injury. The reason may be that subarachnoid hemorrhage stimulates the meninges, causing aseptic inflammation to form adhesions, blocking the subarachnoid space and arachnoid villi. Cerebrospinal fluid absorption and reflux, mainly cerebrospinal fluid absorption disorder, pathological section can be seen arachnoid thickening fibrosis, ependymal destruction and demyelination around the ventricle, Johnston believes that the absorption of cerebrospinal fluid and subarachnoid and superior sagittal sinus The pressure difference is related to the resistance of the arachnoid villi particles. When the intracranial pressure increases after traumatic brain injury, the pressure of the superior sagittal sinus increases, and the pressure difference between the subarachnoid space and the superior sagittal sinus becomes smaller. The arachnoid villus microtubule system is compressed or even closed, which directly affects the absorption of cerebrospinal fluid. The hydrostatic pressure in the brain is increased due to the accumulation of cerebrospinal fluid, and the ventricles are progressively enlarged.

Therefore, in the early stage of chronic hydrops, the patient's intracranial pressure is higher than normal, and after the ventricle is expanded to a certain extent, the intracranial pressure is gradually reduced to the normal range due to the increased absorption surface, so it is called clinically. It is a normal intracranial pressure hydrocephalus, but because the hydrostatic pressure of the cerebrospinal fluid has exceeded the pressure that the ventricle wall can withstand, the ventricles continue to expand, and the brain atrophy is aggravated and progressive dementia is caused.

Traumatic hydrocephalus prevention

(1) Close observation of consciousness, pupillary changes, vital signs and physical activity, attention to observation of Bp, P, R and pupil changes, recorded on special records.
(2) Note that effective cooling measures should be taken to reduce the oxygen consumption and basal metabolism of brain cells above T>38.50C. Ice, ice pillows, frozen infusions, ice packs should be placed on both sides of the neck, under the eyes and groin. For patients with cooling, face color, P, R and sweating signs should be observed to prevent excessive collapse.
Complication observation
(1) Observe the symptoms of slow and incompetent P, fast and irregular, headache, vomiting, elevated Bp, and enlarged intracranial pressure on one side of the pupil.
(2) Observe the surrounding skin, if there is ulcer or cerebrospinal fluid leakage, report it to the doctor for treatment.
(3) Observe the presence or absence of abdominal pain or abdominal discomfort.

Traumatic hydrocephalus complications Complications, brain contusion, subarachnoid hemorrhage, multiple intracranial hematoma

May be complicated by brain contusion, subarachnoid hemorrhage, intracranial hematoma.

Symptoms of traumatic hydrocephalus Common symptoms Quadrilateral compression gait instability Intracranial pressure increased dementia coma paralysis hydrocephalus urinary incontinence dehydration tremor

Post-traumatic hydrocephalus due to acute and slow onset, clinical manifestations are also different, in addition to the original brain contusion, SAH, intracranial hematoma and other clinical manifestations, and:

1. Acute traumatic hydrocephalus showed increased intracranial pressure, severe brain contusion and laceration, persistent coma after injury or a degree of improvement and deterioration, although dehydration, excision of hematoma, decompression surgery and hormones Treatment, but the recovery of consciousness is not good, the patient's intracranial pressure continues to rise, the decompression window brain bulges, the protein content of cerebrospinal fluid increases, there is no residual or delayed hematoma in the skull, so it is easy to be misdiagnosed as persistent coma or vegetative.

2. Chronic traumatic hydrocephalus is often characterized by normal intracranial pressure hydrocephalus. The average symptom of hydrocephalus after injury is 4.18 months, generally less than 1 year. The patient is mainly characterized by mental symptoms and exercise. Gait) dysfunction and urinary incontinence, may appear apathy, emotional instability, dementia, gait instability, ataxia, lower limb stiffness, tremor palsy and other clinical manifestations, occasionally large, urinary incontinence, epilepsy, emotional self-control Decreased and other symptoms, the disease develops slowly, the symptoms fluctuate, the pressure on the lumbar puncture or intraventricular pressure during normal pressure measurement is normal, the protein content of cerebrospinal fluid is increased, and the fundus examination is also ignored.

Traumatic hydrocephalus examination

Lumbar puncture: acute traumatic hydrocephalus, with increased intracranial pressure, should not be worn; chronic is normal pressure, cerebrospinal fluid protein content can be increased.

1. CT, MRI examination of the expansion of the ventricular system and especially the anterior horn of the lateral ventricle. There is a significant interstitial edema around the lateral ventricle, especially in the frontal horn. The extent of ventricle enlargement is greater than the enlargement of the cerebral cistern; there is no atrophy in the cerebral gyrus, and the sulci is not widened. However, it needs to be differentiated from brain atrophy because of severe brain contusion, axonal injury, cerebral ischemia, hypoxia and necrosis, etc. The resulting brain atrophy also has CT images of enlarged ventricles. The latter features: the lateral ventricle is generally enlarged, the sulci is widened, and there is no translucent edema around the ventricle. Although the MRI examination is the same as that seen by CT, it is more clear and Clear: First, the expansion of the anterior horn of the lateral ventricle and the interstitial edema around the ventricle, which can show a distinct high signal on the T2-weighted image; secondly, the angle between the two sides of the coronal plane can be measured less than 120 °, on the contrary, in the brain atrophy patients, this angle is often greater than 140 °; in addition, in the sagittal plane, the third ventricle is spherically enlarged, and the crypt and funnel crypt become shallow and blunt, but in patients with brain atrophy, The front and rear walls of the third ventricle, the funnel crypt, the crypt is not obviously deformed, although it is enlarged, it still maintains its original contour.

2. Radionuclide cerebral angiography may have nucleus from the cerebral cistern to ventricle reflux, the most common is the nucleus from the fourth ventricle mesopores back to the ventricle, the ventricular system is developed and the subarachnoid space is not developed, indicating cerebrospinal fluid The circulation and absorption have obstacles.

Diagnosis and diagnosis of traumatic hydrocephalus

In patients with severe traumatic brain injury, after timely and reasonable treatment, although the condition is stable but the consciousness is not restored well or there are new signs of nerve damage, the imaging examination should be carried out in time to determine whether there is acute hydrocephalus. In addition, Dementia, mobility disorder, and urinary incontinence after prolonged traumatic brain injury should be performed by CT or MRI. If the ventricular system is enlarged, lumbar puncture is normal pressure, radionuclide cerebrospinal fluid imaging examination is also important for the diagnosis of hydrocephalus. According to the time that the nuclides stay in the ventricle, it is helpful to estimate the severity of hydrocephalus.

Note that with chronic subdural hematoma, cerebrovascular accident, premature or senile dementia, leukoencephalopathy and depression, imaging should be differentiated from brain atrophy, see the auxiliary examination.

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