A case of chronic subdural hematoma after endoscopic third ventriculostomy

Endoscopic third ventriculostomy (ETV), as the most commonly used surgical method for obstructive hydrocephalus, has been widely accepted and used
because of its safety and effectiveness.
As a postoperative complication, chronic subdural hematoma (CSDH) is rare in ETV and has been reported and discussed
.
The author reported one case of postoperative CSDH of ETV, and discussed
its mechanism, clinical characteristics, and prevention measures in combination with the literature.

The patient, a 27-year-old male, was admitted to Li Huili Hospital
of Ningbo Medical Center on December 19, 2014 due to "headache with unresponsiveness and memory loss for half a year".

Anamnesis: 1 occasionally convulsions of limbs 1 year ago, which resolved
on their own.
Nothing special
.
Physical examination: clear, accurate orientation, cranial nerve (-), neck softness, limb muscle strength grade V, bilateral lower limb muscle tone slightly higher, bilateral Pap sign negative
.
MRI of the head is enhanced: the lateral and third ventricles are significantly enlarged, the midbrain aqueduct is narrowed, and the empty sella is (Figure 1).

Fig.
1 Preoperative MRI scan with enhanced scan

Clinical diagnosis: primary midbrain aqueduct stenosis with obstructive hydrocephalus, empty sella
.
On December 24, 2014, the ETV
was lowered under general anesthesia.
During the operation, the right frontal cortex was punctured, and a 6 mm rigid endoscope was used to continuously lavage (10~20 mL/min)
with Wönlinger's solution at 37 °C.
The procedure went smoothly and without bleeding
.
The intraoperative ostomy is 8 mm in diameter and the Liliequist membrane
is opened.
After the ostomy is completed, the puncture channel is filled with an absorbable gelatin sponge, and drugs such as epilepsy prevention are given after surgery
.
The patient's postoperative process went smoothly and his headache improved
.
Postoperative 5-day MRI cerebrospinal fluid velocity measurement showed patency, slightly shrinking of the ventricular system, and a small subdural effusion (Figure 2).

Fig.
2 Postoperative 5-d MRI scan and cerebrospinal fluid flow measurement results

The patient was discharged 9 days after the operation
.
CT of the head 4 weeks after surgery showed extensive isodense subdural hematoma in the right frontotemporoparietal occipital with slightly compression of the ipsilateral ventricle (Figure 3).

The patient had no symptoms of discomfort and ordered outpatient follow-up observation
.
Head MRI 5 weeks postoperatively: hematoma evolves to CSDH (Figure 4).

The patient remains asymptomatic
.
In view of the obvious mass effect of CSDH, drilling and drainage under local anesthesia was performed
.
The operation and postoperative process went smoothly, the patient recovered well, and there was no recurrence
of subdural hematoma or hydrocephalus for more than 1 year of follow-up.

Fig.
3 Head CT examination 4 weeks after surgery showed extensive isodense subdural hematoma and ipsilateral ventricle compression of the right frontotemporoparietal occipital

Fig.
4 MRI scan of the head 5 weeks after surgery showed chronic subdural hematoma in the right frontotemporoparietal occipital region

discuss

ETV has fewer
surgical complications than ventriculoperitoneal shunt (VPS).
Subdural hematomas and effusions are more common after VPS, associated with excessive shunting, and have a lower
incidence after ETV in adults.
The Bouras and Sgouros searches reviewed 2985 ETV procedures with subdural hematomas and effusions occurring in 0.
3% and 0.
27%,
respectively.
CSDH secondary to ETV is rare, with only a small number of individual cases reported
.

The mechanism of CSDH after ETV surgery is not clear, and it is currently thought to be closely
related to the occurrence of subdural effusion/hemorrhage.
There are several hypothetical explanations in the literature:

(1) Intraoperative cortical vascular injury or scalp vascular bleeding leads to the accumulation
of blood in the subdural space.

(2) A variety of factors cause brain tissue collapse, subdural space enlargement, subdural effusion or blood accumulation
.
Massive cerebrospinal fluid loss during ETV surgery can displace the ventricular collapse cortex, resulting in enlargement
of the subdural space.
In most patients, due to long-term obstructive hydrocephalus, the ventricular wall is compressed and dilated, and the cerebral cortex is thinned
.
These patients have reduced brain tissue elasticity and poor recruitment ability, and it is difficult to adapt to the pressure changes
after ETV surgery.
Even a slight decrease in pressure during and after surgery may lead to narrowing of the ventricles, collapse of brain tissue, and subsequent subdural effusion or bridging tears
.

(3) Cerebrospinal fluid leaks from the unclosed corticostomy to the subdural space to form effusion
.
For example, Schroeder et al.
pointed out that a large ventricle and a large corticostomy mouth are more likely to cause the accumulation
of subdural cerebrospinal fluid.
This cerebrospinal fluid effusion can come from the ventricles, or from a perforated subarachnoid space in
the cortex.
ETV causes the direct flow of cerebrospinal fluid from the third ventricle to the basal cistern and subarachnoid space, resulting in a rapid increase in
subarachnoid CSF volume.
If the cortical subarachnoid fluid absorption capacity does not adapt to this change, or if there is a congenital defect in cerebroident fluid absorption, it may increase the pressure in the subarachnoid space, and the cerebrospinal fluid can flow to the subdural space
through the arachnoid rupture at the ostomy site.

(4) Another reason may be caused by
excessive drainage of cerebrospinal fluid.

The general perception is that excessive drainage of ETV rarely occurs, but if the absorption capacity of subarachnoid cerebrospinal fluid in the cortex is normal, it may form a "breakthrough" in absorption in a short period of time, resulting in the effect
of "excessive shunting".
In addition, the diameter of the ostomy and whether the Liliequist membrane is further opened are also important factors
affecting the patency of the stoma and the flow rate of cerebrospinal fluid.
The surgery generally requires the diameter of the ostomy to reach 5~10 mm, and the Liliequist membrane of the foot pool is opened to facilitate drainage
.
However, whether the size of the ostomy is related to excessive drainage is inconclusive, and the discussion is rare, and only one literature mentions the ostomy diameter as 10 mm
.

The opening of the Liliequist membrane facilitates the flow
of cerebrospinal fluid to the interfoot cistern.
Freudenstein et al.
reduced hydrocephalus after opening the Liliequist membrane from aneurysm surgery, but increased the incidence of subdural effusion, speculating that opening the Liliequist membrane during ETV surgery may also be a contributing factor
to the occurrence of subdural effusion 。 In addition, Beni-Adani et al.
reported a case of CSDH after ETV surgery, and the patient experienced a series of intracranial pressure changes such as symptomatic hydrocephalus - low intracranial pressure caused by VPS - removal of shunt to reproduce hydrocephalus - reduction of pressure after ETV, speculating that this repeated and sharp intraventricular pressure fluctuation in the short term will interfere with the circulatory regulation ability of cerebrospinal fluid, and then promote the formation of
subdural effusion.

However, not all subdural effusions develop into CSDH, and most subdural effusions are absorbed
.
If a subdural effusion forms and the capacity to absorb the CSDF is not adjusted to absorb it, it may further evolve into CSDH.

Studies on the mechanism of CSDH formation suggest that subdural effusion (especially cerebrospinal fluid with red blood cells and hematogenous inflammatory factors) lasting for several weeks can induce the migration and proliferation of inflammatory cells in the dural-arachnoid boundary cell layer, resulting in infiltration of fibroblasts in the dural side boundary cell layer, the formation of a large number of new blood vessels, and the formation of the CSDH epimembrane
that is prone to bleeding.
Thus, delayed absorption of subdural effusions may lead to CSDH formation and progression
due to epimata formation, slow oozing, or bridging tears.

To summarize the characteristics of the cases reported in the existing literature:

The age of the patients ranged from 16~69 years old; The causes of hydrocephalus were all aqueduct stenosis, among which 2 patients underwent VPS and ventricular drainage due to severe symptoms before ETV surgery, CSDH occurred in 3 cases on the same side of ETV surgery, 2 cases on the opposite side, and 2 cases appeared on both sides, which shows that its occurrence is not absolutely related to corticostomy.
5 patients had symptoms such as headache, and the other 2 were asymptomatic; All patients required borehole drainage due
to the large amount of hematoma.
These patients are characterized by years of hydrocephalus, decreased cortical thickness, significant intraventricular pressure changes before and after surgery, and CSDH occurring
weeks after surgery.
This patient also has the above similar characteristics and processes
.
The formation process of CSDH should be the result of a combination of factors, and the above characteristics may also be the factors of
CSDH.

The key to preventing the occurrence of postoperative CSDH is to prevent the occurrence
of subdural effusion as much as possible.
The following measures can help achieve this:

(1) Pay attention to try to avoid a large loss
of cerebrospinal fluid during surgery.
When using a thin diameter endoscopic instrument, the corticopuncture channel should not be too large, so that the instrument can be close in and out; Continuous irrigation of Ringer's fluid (10~20 mL/min) during surgery helps to maintain intraventricular pressure balance; Closure of the corticopuncture channel when removing endoscopic instruments helps reduce cerebrospinal fluid loss and subdural effusion
.

(2) Considering that it is difficult for the ventricular drainage tube to achieve the purpose of maintaining intraventricular pressure balance by controlling the drainage flow, and may lead to ventricular collapse after surgery, indwelling
should be avoided as much as possible.
Early postoperative lumbar puncture may help reduce the occurrence
of subdural effusions.

(3) If necessary, replenish Ringer's fluid in the ventricle at the end of surgery to maintain ventricular morphology
.

If CSDH occurs after ETV surgery and the mass effect is obvious, surgical management is required, and the effect of drilling and drainage is better
.
Some patients have adapted to long-term intracranial hypertension, and even if CSDH occurs, symptoms such as obvious headache may not occur, which may cause omission or delay, so regular imaging review
should be emphasized after ETV surgery.