Advances in the diagnosis and treatment of hydrocephalus after aneurysmal subarachnoid hemorrhage

  Subarachnoid hemorrhage (SAH) accounts for approximately 5-10% of all strokes, and its most common cause is ruptured intracranial aneurysm. Hydrocephalus is a common complication of aneurysmal subarachnoid hemorrhage and was first reported by Bagely in 1928. Hydrocephalus can lead to significant neurological impairment in patients with SAH, accelerating progression and even leading to death. Understanding the clinical features of hydrocephalus after SAH can improve the diagnosis and treatment of hydrocephalus after aneurysmal SAH and improve the prognosis of patients by providing early diagnosis and treatment.  Epidemiology The incidence of hydrocephalus after SAH is about 20-70%, and the difference in incidence may be related to the timing, number of imaging examinations and case selection after the onset of the disease. Some asymptomatic hydrocephalus may resolve early on its own and be missed. According to the time of hydrocephalus occurrence, there are two types of hydrocephalus: acute hydrocephalus occurs within 2 weeks after SAH and chronic hydrocephalus occurs after 2 weeks. The incidence of acute hydrocephalus is about 20-30%, and the incidence of chronic hydrocephalus varies from 6-67%.  Pathogenesis Aneurysm rupture leads to SAH, and acute or chronic hydrocephalus can occur under the action of various factors. The main cause of acute hydrocephalus is considered to be the rupture of aneurysm with a large number of clots collecting, compressing, blocking the four ventricles, the aqueduct and the opening of the aqueduct and interventricular foramen, or blood covering and blocking the arachnoid granules, which together affect the cerebrospinal fluid circulation. Acute hydrocephalus does not always develop into chronic hydrocephalus, and about 30% of acute hydrocephalus develops into chronic hydrocephalus. The pathogenesis of chronic hydrocephalus has not been completely clarified, and it is currently believed that the stimulation of erythrocyte breakdown products (especially iron-containing hemoglobin and bilirubin) after subarachnoid hemorrhage together with arachnoid fibrosis and adhesions leading to impaired absorption of cerebrospinal fluid by arachnoid granules is the main formation mechanism of chronic hydrocephalus after SAH.  There are many debates about the risk factors for hydrocephalus after SAH, but the following factors have a more precise effect on the formation of hydrocephalus after SAH, and it is important to understand the risk factors for hydrocephalus after SAH for early diagnosis, early intervention and prognosis improvement.  The main factors affecting hydrocephalus after SAH include: age, hypertension, Hunt-Hess classification and Fisher classification, number of SAH, intracerebroventricular and pool blood accumulation, and site of aneurysm. Graff et al. showed that the history of hypertension and preoperative and postoperative hypertension had a significant correlation with the occurrence of hydrocephalus after SAH; Hunt-Hess classification and the incidence of hydrocephalus were basically parallel, with the incidence of I-II grade being 9.2% and III-II grade 9.2%. Fisher’s classification directly reflects the amount and distribution of SAH, and the wider the distribution, the higher the incidence of hydrocephalus, but intracerebral hemorrhage does not increase the incidence of hydrocephalus in grade IV patients; repeated SAH can lead to more serious cerebrospinal fluid circulation obstruction and chronic subarachnoid fibrosis. The incidence of hydrocephalus increases with the number of hemorrhages; intracerebroventricular hemorrhage and pool hemorrhage often block the opening of the middle cerebral aqueduct, the exit of the four ventricles and the basal pool, affecting the normal circulation of the CSF, and therefore are recognized as the main factors leading to the formation of early acute hydrocephalus; hydrocephalus has the highest incidence in posterior circulation aneurysm SAH, followed by anterior communication aneurysm. The incidence of hydrocephalus is highest in posterior circulation aneurysm SAH, followed by anterior communicating aneurysm, both of which bleed heavily and are not easily cleared after hemorrhage, and are also responsible for higher Fisher classification due to the ease of breaking into the three ventricles and lateral ventricles.  The clinical manifestations of acute hydrocephalus are mostly seen in patients with Hunt-Hess grade III or above or multiple hemorrhages. The clinical manifestations are non-specific and include symptoms of acute intracranial pressure increase and disorders of consciousness, including severe headache, vomiting, signs of meningeal irritation, disorders of consciousness and oculomotor disorders. The most significant is the impairment of consciousness, especially for those who gradually develop coma, narrow pupils, loss of light reflexes and relatively intact brainstem reflexes in 1-2 days. Thus, it is difficult to differentiate symptoms between acute hydrocephalus and SAH, and imaging data has important diagnostic value.  The clinical manifestations of chronic hydrocephalus after SAH are no improvement or short-term improvement followed by re-deterioration or the typical triad of normal pressure hydrocephalus: mental retardation, gait instability and urinary incontinence. Extrapyramidal symptoms such as horizontal nystagmus and frontal lobe symptoms such as strong grip reflex and suck reflex may also be present.  Diagnosis The diagnosis of hydrocephalus after aneurysmal SAH is based on imaging in addition to clinical symptoms. Dilation of the ventricles after hydrocephalus occurs first in the frontal horn, where there is less white matter around the ventricles, and finally in the lateral ventricular body and occipital horn. When this dilation tears the epithelium of the ventricular canal, cerebrospinal fluid enters the subventricular extracellular tissue, causing periventricular edema. Diagnosis of hydrocephalus imaging measurement criteria: bilateral lateral ventricular frontal horn tip distance >45mm, or bilateral caudate nucleus inner margin distance >25mm, or third ventricular width >6mm, or fourth ventricular width >20mm, the above criteria should first exclude primary brain atrophy. The Hensson ventricular index, commonly used abroad to measure the severity of hydrocephalus, is the distance between the anterior horn of the ventricles at the level of the caudate nucleus and the inner plate of the skull at the level of unity, and its normal upper limit varies with age.  Treatment The treatment of hydrocephalus after aneurysmal SAH can be divided into two types of methods: non-surgical treatment and surgical treatment.  Non-surgical treatment: Hydrocephalus occurs in 20% of patients within 72 hours of SAH onset by CT examination, but 1/3 of them have no hydrocephalus symptoms, and about 50% of patients with acute hydrocephalus resolve spontaneously within 24 hours of onset. Therefore, for patients with acute hydrocephalus without consciousness change after SAH is detected, close observation is needed, and drugs to inhibit cerebrospinal fluid secretion such as acetazolamide should be applied appropriately, while dehydrating drugs such as mannitol and tachyphylaxis should be applied to lower intracranial pressure and improve cerebral edema. Conservative treatment is only suitable for mild hydrocephalus or as part of the preoperative preparation.  Surgical treatment: Surgical treatment includes extraventricular drainage, lumbar pool placement drainage and intraoperative endplate fistula in the acute phase, and V-P shunt in patients with chronic hydrocephalus.  The use of extraventricular drainage in acute hydrocephalus is the most effective method, which can improve the patient’s condition rapidly within a short period of time, but improper application of this treatment can lead to infection and rebleeding in the ventricular system. Some scholars have shown that extraventricular drainage can improve 78% of patients’ consciousness within 24 hours, but the incidence of ventriculitis is 50% and the rate of aneurysm rebleeding is 42%. As a necessary emergency resuscitation measure, extraventricular drainage should be strictly controlled and measures to prevent complications should be strengthened. (1) For patients with combined hydrocephalus, early clamping or embolization of the aneurysm should be performed to reduce the risk of rebleeding; 2) Appropriate elevation of the ventricular extracorporeal drainage height to control the intracranial pressure at 15 mmHg to reduce the chance of aneurysm rebleeding; 3) Drainage tube subcutaneously for several centimeters to prevent cerebrospinal fluid leakage; 4) Avoid unnecessary irrigation of the drainage tube and keep the drainage device airtight; 5) Prophylactic application of antibiotics; 6) Try to control the drainage time in 7-10 days. Lumbar puncture and lumbar pool puncture placement with continuous drainage can reduce the incidence of chronic hydrocephalus by draining bloody cerebrospinal fluid in patients without obstruction in the third and fourth ventricles, which can release the breakdown products of red blood cell rupture and reduce the degree of arachnoid adhesions and fibrosis. It should be used with caution in patients with high intracranial pressure, as it is likely to induce brain herniation, so this treatment is chosen for preoperative application of mannitol or slow release of cerebrospinal fluid intraoperatively.  Endplate fistula is mainly used to reduce the incidence of chronic hydrocephalus. It is mainly indicated for: (1) patients with imaging suggestive of significant supratentorial ventricular enlargement, triventricular round-like enlargement and significant paraventricular edema; (2) patients with hemorrhage into the ventricles; (3) patients with significant increase in intracranial pressure before surgery; (4) patients with significant intraoperative bulging of the endplate membrane. The incidence of distant hydrocephalus is only 4.2%, which is lower than the average of 20%. The end-plate fistula during open aneurysm clamping has some clinical application.  Intracerebrospinal fluid shunt (V-P shunt) is one of the most commonly used and effective treatments, but there is disagreement about the indications and timing of shunts for this disease. Early shunts should be performed when the cerebrospinal fluid contains a lot of blood and high protein, which can easily block the shunt tube. Considering that it takes at least 10 days for the normalization of bloody cerebrospinal fluid and fibrosis of the arachnoid after SAH, shunts for chronic hydrocephalus should therefore be performed at least 2 weeks after SAH when the cerebrospinal fluid is normal. The typical normal pressure hydrocephalus has been recognized by neurosurgeons with the triad of hydrocephalus, and the efficacy of V-P shunts in patients with CT-confirmed hydrocephalus has been confirmed. The triad of unstable walking preceded by mental retardation has a more positive outcome, and shunting is less effective in those who present with mental retardation alone.  Prognosis The mortality rate of aneurysmal hydrocephalus is about 20%. Early diagnosis, early selection of the right conservative treatment measures and CSF external or internal drainage methods are important factors in improving the patient’s prognosis.

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