I. Overview
Post-traumatic hydrocephalus 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) intracranial subarachnoid space, making it partially or completely abnormally enlarged.
The reported incidence of PTH varies widely and increases significantly with the increase in the success rate of rescue of patients with heavy craniocerebral trauma. Li Xuejun, Department of Neurosurgery, Xiangya Hospital, Central South University
II. 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.
1.Acute: within ≤3d after injury.
2.Subacute: 4-13d after injury.
3, chronic: ≥14d after injury.
(b) Classification according to pressure.
According to the measured pressure (lumbar puncture), it is classified into 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.
2, extraventricular hydrocephalus: cerebrospinal fluid accumulates in the cavity outside the ventricles, which may be accompanied (or not) by ventricular enlargement.
Among the latter there are two types of accumulation with 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.
(1) Obstructive: obstruction of any part of the ventricular system including the interventricular foramen, the third ventricle, the middle cerebral aqueduct, and the fourth ventricle may lead to obstructive PTH.
(2) 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 leading to 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 ventricle and fourth ventricle 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. New septum of the ventricular system after TBI can also lead to PTH.
(2) 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 impaired cerebrospinal fluid reabsorption, and the tissue debris generated during surgical treatment of patients with TBI can aggravate postoperative tissue adhesions and mechanical obstruction of the arachnoid granules, and reoperative patients are at greater risk of mechanical 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) Brain tissue displacement and altered cerebrospinal fluid dynamics theory: There is a correlation between the development of PTH and subdural fluid accumulation between the cerebral hemispheres in patients with heavy TBI treated 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, which can develop into PTH on this basis.
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
The main factors that may be associated with the occurrence of PTH include.
(i) Subarachnoid hemorrhage and intraventricular hemorrhage: most scholars believe that intraventricular hemorrhage affects the cerebrospinal fluid circulation pathways within the brain, 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.
(ii) 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: 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: some studies suggest that the upper border of the decompression window is too close to the midline (<25 mm) during desmoid decompression is an independent risk factor for the development of PTH; and those with postoperative interhemispheric subdural effusion have an increased risk of 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 the injury.
IV. Diagnosis and differential diagnosis
(I) Diagnostic criteria
According to the history of craniocerebral trauma, typical clinical manifestations and imaging signs, the following diagnostic criteria of PTH in China are formulated.
1.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.
③Patients with TBI who have improved clinical status after injury or early postoperative period, and then show increased consciousness impairment or worsening neurological status, or the postoperative decompression window is gradually expanded due to PTH, or the patient’s neurological status continues to be in a low-scoring state.
3. Imaging: cranial CT scan and MRI examination are the most common 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 examination: MRI cerebrospinal fluid dynamics assessment should be used in units where available to help establish the diagnosis.
(4) Lumbar puncture: 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 mechanisms and factors associated with the development of PTH, preventive measures should focus on reducing and minimizing risk factors in terms of.
Avoiding excessive dehydration and diuresis; timely removal of factors that obstruct the ventricular system (e.g., intracranial hemorrhage, cerebral edema, and cerebral infarction); intraoperative removal and flushing of hemorrhage from the operative field as much as possible, early postoperative drainage of bloody cerebrospinal fluid to reduce adhesions caused by hemorrhage and blockage of CSF return pathways; intraoperative emphasis on aseptic operation and use of dural hypotonic sutures as much as possible to avoid postoperative incisional CSF leakage and intracranial infection to reduce the 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 can show a quiescent state or even gradually resolve on their own. However, for patients with PTH who have clinically aggravated impairment of consciousness or neurological status once improved and then worsened, gradually aggravated outside the decompression window, and have typical signs on imaging and progressive aggravation, timely treatment should be given.
1. Temporary treatment methods.
①Pharmacological therapy: the use of drugs that inhibit cerebrospinal fluid secretion and osmotic dehydrating agents and diuretics that reduce 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 shunting. (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 catheterization, hyaline septal fistula, and neonatal septal fistula within the ventricular system.
(ii) Technical aspects of permanent treatment
1. Contraindications to cerebrospinal fluid bypass: Regardless of the type of bypass used, intracranial infections that are not effectively controlled, the presence of foci of infection on the bypass 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 2.5~3cm next to the midline, 2cm in front of the hairline or coronal suture; the occipital horn puncture point is usually 3cm next to the midline and 6~7cm above the occipital ridge. the placement depth is 2cm within the ventricle. the incidence of shunt adhesion and blockage is lowest when the ventricular end of the shunt is placed in the frontal horn of the lateral ventricle.
3, abdominal incision and shunt ventral end treatment: according to the principle of easy operation, small surgical trauma, the most familiar access and the individual state of the patient. 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 pelvic cavity. The length of the ventral end of the shunt, the distal end of the shunt can be in the pelvic cavity is appropriate.
4, the choice of shunt tube: shunt tube including fixed pressure tube and adjustable pressure shunt tube two categories. 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 to 14 days postoperatively. Long-term follow-up is usually done 1 month to 1 year or more after surgery.
The indicators of efficacy assessment after PTH include two main aspects: clinical performance and imaging performance. The assessment of clinical performance, which is the most important and reliable assessment index, mainly includes consciousness status, neurological status, tension of decompression window, cognitive function, urinary function, and daily living ability.
The imaging assessment 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.; conservative or surgical treatment should be taken according to the site of bleeding, the amount of bleeding and the presence or absence of corresponding clinical manifestations.
2, infectious complications: including intracranial infection, incisional infection, abdominal infection and puncture tract infection, etc.; 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: including shunt blockage (most common at the ventricular end, shunt pump, and abdominal end), fracture, exposure (skin ulceration on the surface of the channel), and ectopic (ectopic at the abdominal end into the intestinal cavity, bladder, vagina, chest cavity, pericardium, stomach, and prolapse into the abdominal cavity under the skin, etc.). 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: including excessive shunt and insufficient shunt. 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 by early cranial repair if the patient’s condition permits.
5. Other complications: including epilepsy. Manage according to clinical epilepsy standardization.