Traumatic hydrocephalus is most often seen in patients with heavy brain injury with cerebral contusion and subarachnoid hemorrhage, and is one of the important factors causing high morbidity and mortality in comatose patients with heavy brain injury, which can be confirmed by timely cranial CT examination and can be treated with effective surgery to save the patient’s life. The literature reports that traumatic hydrocephalus in patients with subarachnoid hemorrhage can be as high as 10%-34%. There are no uniform criteria for diagnosis and treatment, and ventriculo-peritoneal shunts are effective. The classification and pathogenesis of traumatic hydrocephalus can be divided into acute and chronic forms according to the time of occurrence. Acute hydrocephalus usually refers to hydrocephalus that occurs within 2 weeks after traumatic brain injury. The possible mechanisms are: direct obstruction of the cerebral crest fluid circulation pathway by blood clots or obstruction of the arachnoid villi by red blood cells, cerebral edema, intracranial hematoma, cerebral herniation.
Brain edema, intracranial hematoma, brain herniation, brain bulge or protrusion may also compress the brain pool and subarachnoid space on the surface of the brain, affecting the circulation and absorption of cerebral crest fluid; intraventricular hemorrhage, ventricular penetrating injury
Intraventricular hemorrhage, ventricular penetrating injury, and blood accumulation can block the interventricular foramen, aqueduct, and median foramen of the fourth ventricle, preventing the return of cerebral crest fluid to the subarachnoid space; after cranial injury, increased intracranial pressure causes increased pressure in the superior sagittal sinus, resulting in decreased absorption of cerebral crest fluid. Chronic hydrocephalus, on the other hand, is mostly seen to occur within 3 weeks to 1 year after the injury. Subarachnoid hemorrhage and subdural hematoma are more common after cerebral contusion. The large amount of bloody cerebral crest fluid will produce strong irritation to the meninges, which can cause a sterile inflammatory response, adhesions between the soft meninges and the arachnoid and even blockage of the wrapped arachnoid villi, resulting in impaired circulation and absorption of cerebral crest fluid. Cerebral crest fluid circulation obstruction occurs within the ventricular system and often causes fluid accumulation in one or both ventricles. This condition is most often caused by ventricular penetrating injuries or intramedullary hematomas breaking into the ventricles, often with obstruction at the interventricular foramen, aqueduct, or exit of the four ventricles. At the beginning of chronic hydrocephalus, the patient’s intracranial pressure is higher than normal, and after the ventricles are enlarged to a certain degree, the intracranial pressure gradually decreases to the normal range because of the increased absorption surface, so it is clinically called normal cranial pressure hydrocephalus. However, because the hydrostatic pressure of the cerebral crest fluid has exceeded the pressure that the ventricular wall can withstand, the ventricles continue to expand and the brain atrophy increases, resulting in progressive dementia. The clinical manifestations of post-traumatic hydrocephalus vary depending on the urgency of onset. In addition to the clinical manifestations of the original cerebral contusion, SAH and intracranial hematoma, it also manifests as follows: 1. In acute traumatic hydrocephalus, the intracranial pressure is progressively increased and the consciousness is impaired, the degree of cerebral contusion is more serious, the coma persists after the injury or once improves and then deteriorates again, and the recovery of consciousness is still poor despite active treatment such as dehydration, removal of hematoma and decompression surgery of the bone flap and hormone. The patient’s intracranial pressure continues to rise, the decompression window is inflated, the protein content of cerebral crest fluid increases, and there is no intracranial residual or late hematoma, so it is easy to be misdiagnosed as prolonged coma or vegetative survival. 2, chronic traumatic hydrocephalus is mostly manifested as normal cranial pressure hydrocephalus, from the injury to the appearance of hydrocephalus symptoms for an average of 4 to 18 months, generally less than 1 year. The main manifestations are psychiatric symptoms, motor (gait) disorders and urinary incontinence. Apathy, emotional instability, dementia, unsteady gait, ataxia, lower limb stiffness, tremulous paralysis, and occasionally fecal and urinary incontinence, epilepsy, and impaired emotional self-control may be present. The disease progresses slowly, and symptoms fluctuate from time to time. The lumbar puncture or intracerebroventricular pressure was mostly normal on manometry, and the brain crest fluid protein level was elevated. Funduscopic examination was also free of optic disc edema and other phenomena. Diagnosis The exact diagnosis should be a combination of clinical manifestations, imaging changes and a dynamic treatment process. All patients with heavy craniocerebral injury, after timely and reasonable treatment
When the condition has been stabilized but the recovery of consciousness is poor or new signs of neurological damage appear, imaging should be performed promptly to determine the presence or absence of acute hydrocephalus. In addition, those with prolonged dementia, impaired mobility, urinary incontinence after traumatic brain injury, or progressive expansion of the decompression window after craniotomy should undergo CT or MRI examination, and if enlargement of the ventricular system is found, lumbar puncture is normal pressure
Radionuclide brain crest imaging is also valuable in the diagnosis of hydrocephalus, and the duration of retention of the nuclide in the ventricles can help to estimate the severity of hydrocephalus. Especially, patients with normal intracranial pressure and progressive compensatory enlargement of the ventricles should be given high priority. Treatment principles of traumatic hydrocephalus: The treatment of traumatic hydrocephalus is mainly based on surgery. Among them, cerebral crest fluid shunt is the only recognized safe and effective treatment method. For acute hydrocephalus, mannitol should be given to lower the cranial pressure while emergency extraventricular drainage is performed to relieve intracranial hypertension and save life. Because the traumatic hydrocephalus cerebral crest fluid is definitely different from normal people, there is bloody fluid or impurities in the cerebral crest fluid, and the content of cerebral crest fluid protein, white blood cells and red blood cells is higher than normal, so we cannot directly perform cerebral crest fluid shunt at this time, and we should perform cerebral crest fluid shunt after the cerebral crest fluid is completely purified, and after three consecutive cerebral crest fluid cultures and routine biochemistry are normal (note: the method of retaining cerebral crest fluid at this time is never lumbar puncture to retain cerebral crest fluid, because cerebral (Note: the method of retaining cerebral crest fluid at this time is never lumbar puncture, because cerebral crest fluid is produced from the ventricles, and the cerebral crest fluid retained by lumbar puncture is like the water in a stream at the foot of a high mountain, which does not really reflect the water in a high mountain), then consider performing cerebral crest fluid shunt. This procedure is indicated for obstructive hydrocephalus, communicating hydrocephalus, and normal cranial pressure hydrocephalus.