(2014) Expert consensus on the diagnosis and treatment of hydrocephalus after craniocerebral trauma in China
I. Overview
Post-traumatic hydrocephalus (PTH) is one of the common complications after craniocerebral trauma, which is caused by abnormal changes in cerebrospinal fluid circulation dynamics due to increased secretion, or (and) impaired absorption, or (and) impaired circulation of cerebrospinal fluid, resulting in abnormal accumulation of cerebrospinal fluid in the intracerebroventricular or (and) subarachnoid space within the skull, resulting in its partial or total abnormal enlargement. The reported incidence of PTH varies greatly, and with the increase in the success rate of treatment for patients with severe craniocerebral trauma, the incidence of PTH has also increased significantly.
Classification of PTH
According to the time of occurrence, pressure site, presence or absence of obstruction in the ventricular system and clinical status, PTH has the following classifications.
(i) Classification according to the time of occurrence.
(i) Acute: within 3 d post-injury.
(ii) Subacute: 4 – 13 d after injury.
(iii) Chronic: ≥14d post-injury.
(b) Classification according to pressure.
According to the measured pressure (lumbar puncture), it is classified as high pressure (> normal range) and normal pressure (within normal range).
(c) Classification according to the site of cerebrospinal fluid accumulation.
(① intraventricular hydrocephalus: simple enlargement of the ventricular system.
(ii) Extra-ventricular hydrocephalus: accumulation of cerebrospinal fluid in the extra-ventricular space, which may be accompanied (or not) by ventricular enlargement. Among the latter, there are two types of accumulation, direct communication with the cerebrospinal fluid circulation and restricted, also called subdural effusion. Clinical hydrocephalus is usually considered to be intraventricular hydrocephalus.
(iv) Classification according to the presence or absence of obstruction in the ventricular system.
(i) Obstructive: obstruction of any part of the ventricular system including the interventricular foramen, the third ventricle, the midbrain aqueduct, and the fourth ventricle may lead to obstructive PTH.
(ii) Traffic: the ventricular system is not obstructed, but is caused by adhesions to the convex surface of the brain or (and) the arachnoid membrane at the base of the skull, or (and) obstruction of the intracranial reflux veins resulting in impaired cerebrospinal fluid reabsorption.
(E) Classification according to clinical status
(i) Progressive: patients have PTH-related clinical manifestations that are progressive in nature.
(ii) insidious: the patient has no PTH-related clinical manifestations although the ventricles are enlarged.
③Static: The patient’s abnormal accumulation of cerebrospinal fluid stops and the ventricular system no longer enlarges, and the PTH-related clinical manifestations do not progress.
III. Occurrence mechanism and risk factors
(I) Occurrence mechanism
The exact mechanism of hydrocephalus occurrence has not been elucidated. Due to the diversity and complexity of TBI, there are still several theories and hypotheses about the mechanism of PTH occurrence. The main ones include.
① Mechanical obstruction of the ventricular system.
Intraventricular hemorrhage after TBI may cause obstruction of the interventricular foramen, third and fourth ventricles causing acute PTH, while hemorrhage near the ventricles, especially posterior cranial fossa hemorrhage, can easily cause occupational effects leading to deformation and displacement of the ventricular system and obstruction. large cerebral infarction and cerebral edema in one hemisphere after TBI is also one of the mechanisms causing deformation and displacement of the ventricular system leading to PTH. post-TBI ventricular Systemic neovascularization of the septum is also known to cause PTH.
(ii) Impaired reabsorption.
Most scholars believe that one of the main reasons for the occurrence of PTH is the formation of subarachnoid adhesions and fibrosis of the arachnoid granules caused by SAH after TBI, which leads to impairment of cerebrospinal fluid reabsorption, and the tissue debris produced in TBI patients undergoing surgical treatment can aggravate postoperative tissue adhesions and mechanical obstruction of the arachnoid granules, and reoperative patients are at greater risk of mechanical blockage of the arachnoid granules The risk of mechanical blockage of arachnoid granules is greater in reoperative patients. Intracranial infection is an even more common factor that exacerbates tissue adhesions.
(iii) The theory of brain tissue displacement and altered cerebrospinal fluid dynamics.
There is a correlation between the occurrence of PTH and interhemispheric subdural fluid accumulation after treatment of heavy TBI patients with debulking decompression. The repositioning of displaced brain tissue after debridement decompression and the affected cerebrospinal fluid dynamics after cranial opening can cause subdural fluid accumulation, on which PTH can develop.
④ Fluid imbalance caused by arachnoid tears or (and) excessive dehydration and diuresis is one of the common mechanisms leading to the formation of subdural fluid.
(ii) Associated factors
(i) Subarachnoid hemorrhage and intraventricular hemorrhage.
(i) Most scholars believe that intraventricular hemorrhage affects the cerebrospinal fluid circulation pathways within the ventricles, while subarachnoid hemorrhage leads to subarachnoid adhesions and fibrosis of the arachnoid granules, both of which are major risk factors for the development of PTH.
② Primary injury.
The more severe the injury, the longer the preoperative coma, and the higher the preoperative intracranial pressure in patients with craniocerebral trauma, the higher the incidence of PTH.
(③) Age.
PTH can occur in injured patients of any age, and the incidence of PTH is high in advanced age survivors.
(iv) Intracranial infection.
(ii) Intracranial infection is one of the main factors aggravating subarachnoid adhesions, and ventriculitis is a high risk factor for PTH requiring intervention.
⑤ Desmoid decompression and postoperative interhemispheric subdural effusion.
It has been suggested that the upper border of the decompression window too close to the midline (<25 mm) during debulking decompression is an independent risk factor for the development of PTH, while those with postoperative interhemispheric subdural effusion are at increased risk for subsequent intracerebroventricular hydrocephalus. Other factors: skull base fracture is one of the risk factors for the occurrence of PTH and may be associated with the occurrence of skull base arachnoid adhesions after injury.
IV. Diagnosis and differential diagnosis
(I) Diagnostic criteria
Based on the history of craniocerebral trauma, typical clinical manifestations and imaging signs, the following diagnostic criteria for PTH in China are formulated.
1.Medical history.
A clear history of craniocerebral trauma.
2.Clinical manifestations.
① Headache, vomiting and impaired state of consciousness are often the main manifestations of acute PTH. (ii) In subacute and chronic high-pressure PTH, optic nerve papillary edema or (and) hypopthalmia may occur.
(ii) Those with normal pressure PTH may present with one or more of the classic triad of cognitive dysfunction, gait instability, and urinary incontinence.
(iii) TBI patients with post-injury or early postoperative clinical status improvement followed by worsening consciousness impairment or worsening neurological status manifestations, or postoperative decompression windows due to progressive outgrowth of PTH, or patients with persistent low scoring neurological status.
3. Imaging examinations.
Cranial CT scans and MRI examinations are the most commonly used diagnostic imaging methods for clinical screening of PTH. The imaging bases for the diagnosis of PTH are.
①required signs: progressive enlargement of the ventricular system on imaging is necessary for the diagnosis of hydrocephalus, typically manifested by enlargement of the frontal angle of the lateral ventricles, rounding of the third ventricle and enlargement of the temporal angle, and in a few patients, asymmetric enlargement of the ventricular system.
(②Auxiliary signs: some patients may show cerebrospinal fluid leakage around the enlarged ventricles with hypodensity (on CT scan) or high signal (on T2-weighted imaging of MRI), which is an auxiliary sign for the diagnosis of PTH; and the narrowing of the cerebral sulcus on the convex side of the brain is also one of the auxiliary signs for the diagnosis of normal pressure PTH.
③Supplementary tests: MRI cerebrospinal fluid dynamics assessment should be used in units where available to help establish the diagnosis.
4. Lumbar puncture examination.
This test does not determine the presence of PTH, but it helps to refine the diagnosis and aids in the decision of surgical treatment. Lumbar puncture should be included as a routine test in the diagnosis and treatment of PTH for the following purposes.
(i) Pressure measurement: to confirm whether PTH is hypertensive or normal pressure.
②Cerebrospinal fluid examination: to retain a certain amount of cerebrospinal fluid specimen for relevant examination to assess the efficacy and confirm the presence of contraindications to surgery.
(iii) Cerebrospinal fluid drainage effect test: it helps to identify PTH and simple compensatory enlargement of the ventricles, and also helps to screen whether normal pressure hydrocephalus is suitable for shunt surgery; usually 30 ml of cerebrospinal fluid is released by each lumbar puncture to compare the neurological functional status before and after the release.
(ii) Differential diagnosis
Cerebral atrophy is a common phenomenon after TBI, which can have clinical manifestations similar to PTH and compensatory enlargement of the ventricular system, and needs to be differentiated from PTH. Cerebral atrophy is commonly seen after diffuse axonal injury and cerebral hypoxia, and the typical imaging presentation is enlargement of the ventricular system accompanied by widening of the cerebral sulcus, with no manifestation of periventricular exudative hypodensity.
In contrast, those with pure subdural effusion need to be differentiated from chronic subdural hematoma with low density, which is low and high signal on T1- and T2-weighted imaging of MRI, respectively, while the latter is both high signal.
V. Prevention
Based on the premise of the mechanism of occurrence and factors associated with PTH, preventive measures should focus on reducing and minimizing risk factors in terms of.
1. avoiding excessive dehydration and diuresis.
2. timely removal of factors that obstruct the ventricular system (e.g., intracranial hemorrhage, cerebral edema, and cerebral infarction)
3. intraoperative removal and flushing of bleeding from the operative field as much as possible, early postoperative drainage of bloody cerebrospinal fluid to reduce adhesions caused by bleeding and blockage of the CSF return pathway.
4. Intraoperative emphasis on aseptic operation and use of dural reduction sutures as much as possible to avoid postoperative incisional CSF leakage and intracranial infection in order to reduce mechanical blockage caused by inflammatory adhesions that lead to PTH.
VI. Treatment
(I) Treatment strategy
For patients with clinically insignificant PTH, follow-up observation should be preferred, because some patients with hydrocephalus may show a quiescent state or even gradually resolve on their own. However, PTH patients with clinically aggravated impairment of consciousness or neurological status once improved and then worsened, gradual aggravation of expansion outside the decompression window, and progressive aggravation with typical signs on imaging should be given timely treatment.
1.Temporary treatment methods.
①Drug therapy.
Use of drugs that inhibit cerebrospinal fluid secretion and osmotic dehydrating agents and diuretics that lower intracranial pressure.
②Surgical treatment.
Release a certain amount of cerebrospinal fluid through intermittent lumbar puncture, controlled lumbar pool drainage, extraventricular drainage and subcutaneous Ommaya capsule implantation to temporarily relieve intracranial hypertension, drain bloody cerebrospinal fluid and control intracranial infection.
2. Permanent treatment methods.
① Cerebrospinal fluid body cavity shunt.
It is still the main modality of PTH treatment. Among them, lateral ventriculo-abdominal shunt takes the first place; although lateral ventriculo-atrial shunt is gradually decreasing, it is still an indispensable choice for those who have a history of abdominal surgery, or abdominal infection after shunt. (b) In some cases of traffic PTH, lumbar pool-abdominal shunts may be used.
(ii) Intracranial diversion of cerebrospinal fluid.
Endoscopic third ventriculostomy is the most commonly used, followed by endplate fistula, midbrain aqueductoplasty, hyaline septal fistula and neonatal septal fistula within the ventricular system.
(ii) Technical aspects of permanent treatment
1. Contraindications to cerebrospinal fluid body cavity shunts.
Regardless of the type of shunt used, intracranial infection not effectively controlled, the presence of foci of infection on the shunt route, the presence of infection in the abdominal cavity and abnormal cerebrospinal fluid examination after intracranial hemorrhage are listed as contraindications to surgery.
2. Ventricular puncture site and length of tube placement.
When performing lateral ventricular-abdominal shunt and lateral ventricular-atrial shunt, frontal and occipital angle punctures are most commonly used. The frontal horn puncture point is usually 2.5-3 cm next to the midline and 2 cm in front of the hairline or coronal suture; the occipital horn puncture point is usually 3 cm next to the midline and 6-7 cm above the external occipital ridge. The incidence of shunt adhesions and blockage is lowest when placed in the frontal horn of the lateral ventricle.
3. Abdominal incision and treatment of the abdominal end of the shunt.
According to the principle of easy operation, small surgical trauma, the access most familiar to the operator and the individual status of the patient, a comprehensive determination is made. Usually, a small peritoneal incision is used to place the shunt into the abdominal cavity, and intestinal peristalsis can lower the abdominal end of the shunt into the pelvis. The length of the abdominal end of the shunt, the distal end of the shunt can be in the pelvis is appropriate.
4, the choice of shunt tube.
The shunt tube includes two categories: fixed pressure tube and adjustable pressure shunt tube. Before surgery, according to the initial pressure measured by lumbar puncture, choose the type of fixed pressure tube and set the initial pressure of adjustable pressure tube. The advantage of adjustable pressure shunts is that the set pressure of the shunt pump can be adjusted according to the clinical and imaging follow-up results after surgery to reduce excessive or insufficient shunts after surgery. Antimicrobial shunts and anti-siphon devices are recommended.
5. Management of subdural fluid.
The vast majority of subdural effusions are self-absorbing; a few progress progressively and cause an occupying effect, or transform into chronic subdural hematomas. In patients with symptoms and signs, borehole drainage, subdural-peritoneal shunt or lateral ventriculo-peritoneal shunt (in those with ventricular enlargement) are options. A small amount of thick peritoneal formation requires craniotomy.
6. Intracranial diversion of cerebrospinal fluid.
Endoscopic third ventriculostomy is recognized as the treatment of choice for obstructive hydrocephalus. Endoscopic treatment is also one of the effective options for those with failed shunts and for those with the presence of neoplastic septa in the ventricles. The implementation of intracranial diversion of cerebrospinal fluid should follow the relevant standardized principles.
(iii) Efficacy assessment
Short-term postoperative efficacy assessment is usually chosen 1 – 14 days postoperatively. Long-term follow-up is usually done 1 month – 1 year or more after surgery.
The indicators of postoperative efficacy assessment after PTH include two main aspects: clinical performance and imaging performance.
Assessment of clinical manifestations.
It is the most important and reliable assessment index, mainly including consciousness status, neurological status, tension of decompression window, cognitive function, urinary function, and ability to perform daily life.
Imaging assessment.
It is mainly the follow-up observation of cranial CT or (and) MRI. Whether the preoperative enlarged ventricles are reduced on imaging is not a reliable assessment indicator. In patients with preoperative hyperbaric PTH, the enlarged ventricles may shrink postoperatively, whereas in patients with isobaric PTH, the ventricular system may shrink insignificantly or unchanged due to prolonged extensional deformation. For those with preoperative periventricular system exudate, the reduction of postoperative exudate is one of the reliable evaluation indicators.
(D) Common complications and management after shunt surgery
1.Hemorrhagic complications.
Including various types of intracranial hemorrhage, subdural hemorrhage, etc.; according to the site of hemorrhage, the amount of hemorrhage and the presence of corresponding clinical manifestations, conservative or surgical treatment is taken.
2.Infectious complications.
Including intracranial infection, incisional infection, abdominal infection and puncture tract infection; under the premise of necessary debridement and anti-infection treatment, if the infection cannot be effectively controlled, the shunt needs to be removed as early as possible, and the corresponding treatment will be performed after the infection is effectively controlled.
3. Shunt-related complications.
These include blockage of the shunt (most common at the ventricular end, shunt pump, and abdominal end), fracture, exposure (skin ulceration on the surface of the channel), and ectopic (ectopic entry of the abdominal end into the intestinal cavity, bladder, vagina, chest cavity, intrapericardium, stomach, and prolapse of the abdominal cavity into the subcutaneous area). When such complications occur, it is usually necessary to remove the shunt and determine that no infection exists before proceeding with the appropriate treatment.
4. Shunt abnormalities.
This includes excessive shunting and insufficient shunting. The former is mainly manifested as lacunar ventricular syndrome, and some patients may develop subdural fluid or hemorrhage; the latter is manifested as no improvement of clinical symptoms, no reduction of the ventricular system or aggravation of hydrocephalus signs. If a pressure-adjustable shunt is used, the set pressure can be adjusted to control the cerebrospinal fluid drainage and alleviate excessive or insufficient shunting. If a constant-pressure shunt is used, the shunt pump needs to be replaced. Those with excessive shunts may also be relieved if the patient’s condition allows for early skull repair.
5. Other complications.
Including epilepsy. Manage according to clinical epilepsy standardization.
VII. Notes
1.The Chinese Expert Consensus on the Diagnosis and Treatment of Hydrocephalus after Craniocerebral Trauma is a guiding document within the neurosurgery industry in China and does not have legal efficacy.
2. As the research related to post-craniocerebral trauma hydrocephalus progresses and the relevant evidence-based medical evidence increases, the Chinese Expert Consensus on the Diagnosis and Treatment of Post-Craniocerebral Trauma Hydrocephalus will be revised and improved accordingly.
3.The Chinese Expert Consensus on the Diagnosis and Treatment of Post-Cranial Traumatic Hydrocephalus is applicable to adult patients.