Traumatic hydrocephalus is most commonly seen in patients with heavy brain injury with cerebral contusion and SAH, and is one of the important factors causing high morbidity and mortality in comatose patients with heavy brain injury. Causes Subarachnoid hemorrhage is common after cerebral contusion. The large amount of bloody cerebrospinal fluid will produce strong stimulation to the meninges, which can cause a sterile inflammatory response, and therefore, adhesions can occur between the soft membranes and the arachnoid, and even block the arachnoid villi, thus causing impaired circulation and absorption of cerebrospinal fluid. This is similar to hydrocephalus caused by subarachnoid obstruction due to septic meningitis, i.e., although cerebrospinal fluid produced by the choroid plexus can flow out of the ventricles, it is obstructed in the subarachnoid space and prevents cerebrospinal fluid from circulating through the cerebral convexity to the arachnoid granules for absorption in the basal pool, cricoid pool, and lateral fissure pool. As a result, patients often present with symptoms of increased intracranial pressure and an enlarged ventricular system, and their condition will worsen if they do not receive timely and reasonable treatment. Occasionally, cerebrospinal fluid circulation obstruction occurs within the ventricular system, causing fluid accumulation in one or both ventricles. This is usually due to ventricular penetrating injury or intramedullary hematoma breaking into the ventricles, often with obstruction at the interventricular foramen, aqueduct, or exit of the four ventricles. Occasionally, hydrocephalus can be caused by herniation of the cerebellar curtain, occlusion of the cricoid pool due to brainstem displacement, or compression of the aqueduct; or hydrocephalus can also occur due to inappropriate decompression of the greater trochanter and severe brain bulging and displacement, resulting in obstruction of cerebrospinal fluid circulation. Acute hydrocephalus refers to hydrocephalus that occurs within 2 weeks after injury. The possible mechanisms are: 1. Direct blockage of cerebrospinal fluid circulation by blood clots or blockage of arachnoid villi by red blood cells, which affects cerebrospinal fluid absorption. 2. 2. Cerebral edema, intracranial hematoma, brain herniation, brain bulge or protrusion may also compress the cerebral pool and the subarachnoid space on the brain surface, affecting the circulation and absorption of cerebrospinal fluid. 3, intraventricular hemorrhage, ventricular penetrating injury, blood accumulation can block the interventricular foramen, aqueduct and median foramen of the fourth ventricle, so that the cerebrospinal fluid cannot flow back to the subarachnoid space. The ventricular system is enlarged, especially in the anterior horn of the lateral ventricle; there are obvious interstitial edema bands around the lateral ventricle, especially in the frontal horn; the enlargement of the ventricle is more than the enlargement of the brain pool; there is no atrophy in the brain gyrus and the brain sulcus is not widened. However, it needs to be differentiated from cerebral atrophy, because cerebral atrophy caused by severe brain contusion, axonal injury, cerebral ischemia, hypoxia and necrosis also has CT images of ventricular enlargement. The latter is characterized by generalized enlargement of the lateral ventricles, widening of the sulci, and absence of a translucent edema zone around the ventricles. In contrast, in patients with cerebral atrophy, this angle is often greater than 140°; furthermore, in the sagittal plane, the third ventricle can be seen to be spherically enlarged, and the optic fossa and funnel fossa become shallow and blunt, whereas in patients with cerebral atrophy, the anterior and posterior walls of the third ventricle, the funnel fossa, and the optic fossa are not significantly deformed, and maintain their original contours despite enlargement. 2.Radionuclide brain pool imaging There may be reflux from the brain pool to the ventricles, most commonly from the median foramen of the fourth ventricle back to the ventricles, and the ventricular system is visualized but the subarachnoid space is not, indicating that the circulation and absorption of cerebrospinal fluid are impaired. Clinical diagnosis Post-traumatic hydrocephalus has different clinical manifestations depending on the acute and slow onset. In addition to the clinical manifestations of cerebral contusion, SAH, intracranial hematoma, etc., there are: 1. Acute traumatic hydrocephalus presents with increased intracranial pressure, more serious cerebral contusion, persistent coma after injury or once improved and then worsened, and poor recovery of consciousness despite multiple treatments such as dehydration, hematoma removal, decompression surgery and hormones. The patient’s intracranial pressure continues to rise, the decompression window brain bulge, cerebrospinal fluid protein content increases, and there is no other residual or late hematoma in the cranium, so it is easy to be misdiagnosed as a prolonged coma or vegetative. 2, chronic traumatic hydrocephalus Chronic traumatic hydrocephalus mostly manifests as normal cranial pressure hydrocephalus, the average of 4.18 months since the injury to the appearance of hydrocephalus symptoms, generally less than 1 year. Patients mainly present with psychiatric symptoms, motor (gait) disorders and urinary incontinence. Clinical manifestations such as apathy, emotional instability, dementia, unsteady gait, ataxia, lower limb rigidity, tremor palsy, and occasionally fecal and urinary incontinence, epilepsy, and impaired emotional self-control may occur. The disease progresses slowly, and symptoms fluctuate from time to time. The lumbar puncture or intracerebroventricular pressure was mostly normal on manometry, and the cerebrospinal fluid protein level was elevated. There is no optic disc edema on fundus examination. In most patients with severe traumatic brain injury, after timely and reasonable management, if the condition has stabilized but the recovery of consciousness is poor or new signs of neurological damage appear, imaging should be performed promptly to determine the presence of acute hydrocephalus. In addition, CT or MRI examination should be performed if dementia, mobility disorders, or urinary incontinence occur for a long time after traumatic brain injury. If enlargement of the ventricular system is found, lumbar puncture with normal pressure and radionuclide cerebrospinal fluid imaging are also valuable for the diagnosis of hydrocephalus, and the retention time of the nuclide in the ventricles can help to estimate the severity of hydrocephalus. Treatment of traumatic hydrocephalus, either intracranial hypertensive hydrocephalus or normal pressure hydrocephalus, should be treated by shunting with a one-way valve shunt. However, it is sometimes possible to reduce the incidence of later hydrocephalus in patients with acute hydrocephalus if intracranial pressure monitoring is performed early after head trauma and blood cerebrospinal fluid is drained promptly (Kollusi et al., 1984). In any case, when traumatic hydrocephalus is suspected, early imaging should be performed to clarify the diagnosis and shunt surgery should be performed as soon as possible to relieve progressive brain tissue atrophy caused by hydrocephalus. There are two types of shunts: ventriculo-peritoneal and ventriculo-atrial, as the latter is not suitable for shunting patients with cerebrospinal fluid containing air, contaminated tissue, or blood clots and/or with newly performed extraventricular drainage. Therefore, ventriculo-ventricular shunts are more commonly used for post-traumatic hydrocephalus. This procedure is indicated for obstructive hydrocephalus, communicating hydrocephalus, and normal cranial pressure hydrocephalus. The purpose is to place the end of the shunt into the pelvic cavity to prevent closure of the greater omentum. The pressure of the patient’s cerebrospinal fluid should also be measured, and a medium-pressure shunt device (55-85 mmH20) should be used for those above 140 mmH2O; a low-pressure shunt device should be used for those below 140 mmH2O (McQuarrie et al., 1984). Chhabra et al. (1993) also developed a “Z” flow shunt device to avoid excessive drainage due to posture. The procedure is performed under local or general anesthesia with the patient lying supine with the head to the left and the right shoulder slightly elevated to allow lateral extension of the neck. The cranial hole is first drilled in the right posterior temporal part (4 cm behind and above the external auditory canal), and the ventricular triangle is reached by vertical puncture with a cerebral needle 3-4 cm deep, which confirms that there is cerebrospinal fluid outflow without excessive discharge, and then the ventricular end of the shunt is inserted into the ventricle in the direction and depth of the cerebral needle, and then the one-way valve is fixed slightly below the bone hole. Then a tunnel is made through the subcapsular tendon layer of the scalp from behind the ear to the subcutaneous side of the neck, and the ventral end of the shunt is introduced to meet the valve outlet, and the scalp incision is then sutured. The distal end of the shunt was continued subcutaneously through the neck and chest to the right lower abdomen. Then an appendicitis maix incision is made, and the end of the shunt is carefully fed into the recto-vesical crypt or utero-rectal crypt along the right side of the pelvic wall with a ring forceps after cutting the peritoneum. After surgery, the abdominal wall incision and segmental skin incision were closed as usual without drainage. Postoperatively, antibiotics were administered to prevent infection, and the valve was pressed 2 to 3 times daily to avoid obstruction of the one-way valve shunt device. Ventriculoperitoneal shunt is one of the methods of treating hydrocephalus, and there are many ways to perform the procedure. As far as the puncture points of the ventricles are concerned, there are frontal horn punctures; occipital horn punctures; and lateral ventricular triangle punctures. In terms of the abdominal drainage machine, there are those that place the drainage tube onto the liver; those that place it into the pelvis; and those that place it into the ureter. I believe that the best method is to puncture the posterior horn of the ventricle, and the best method is to place the abdominal tube onto the liver. The specific method is as follows. The participants are divided into two groups: one for the head, which performs the ventricular puncture and places the ventricular drainage tube; and one for the abdomen, which performs the subcutaneous tunnel to the neck. The specific method is illustrated by the occipital angle puncture and suprahepatic drainage. 1, fixed point: take the righteous point 6CM on the occipital tuberosity, 3CM from the midline as the center, cut the scalp longitudinally about 3CM, use the mastoid retractor, pull open the incision, on that can effectively stop the bleeding, but also can make the surgical field clear. The outer plate is exposed, drilled, and if there is bleeding, the bleeding is stopped with bone wax. The meninges are electrocoagulated, and the dura is cut crosswise at the center of the drilled hole to accommodate a puncture needle size. The flushed ventricular drainage tube is inserted into a matching needle inserted parallel to the sagittal surface in the direction of the midpoint of the brow arch, and the needle inserted 4-5 cm and withdrawn, and the cerebrospinal fluid is withdrawn backward until the cerebrospinal fluid no longer flows, and then sent forward 2 cm. This can prevent the drainage tube from forming an angle and making the drainage poor, and can also fix the drainage tube so that it cannot move freely. 2. Meanwhile, the abdominal team makes a 5 CM long incision in the subxiphoid median line, only to the anterior sheath, and makes a subcutaneous tunnel along the skin with a through strip toward the neck, preferably on the surface of the deep fascia. A small incision is made on the clavicle, the through strip is led out and tied to the tip with a thick thread, the thread is led to the incision in the abdomen, and the upper end of the abdomen is tied to the thread and led to the incision in the neck. 3. The head group is arced outward along the upper end of the head incision so that the flap of the head is in an approximate 1/4 circle. At this 1/4 exposure, the regulator, the core component of the ventriculoperitoneal drainage tube, is placed, and the tunnel is made at the outermost end of the incision to the cervical incision, to which the ventriculoperitoneal drainage tube is led, and the regulator is used to connect the ventriculoperitoneal tube to the ventral tube, to debug the drainage device to see if it is patent, and to find the cause if it is not patent, and to reposition the tube. If not, find the cause and reposition the tube until it is clear. The ventricular tube will be taken down. Medical education network 4, after the commissioning, the abdominal group cut open the abdominal cavity, find the hepatic ligament, the distal end of the laparotomy tube placed on the liver about 15CM fixed in the hepatic ligament, so that it can not move to the liver for the purpose. 5, then connect the laparotomy tube with the regulator to debug whether it is smooth, at this time, because the distal end of the laparotomy tube can not be seen, as long as the regulator pump can be pressed down to show that it is smooth. At this time, you can also see through the pump whether there is bleeding in the cerebrospinal fluid, 6, two groups can be simultaneously sutured incision.