Hydrocephalus Indian scenario – A review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3208920/?

report=printable

J Pediatr Neurosci. 2011 Oct; 6(Suppl1): S11–S22. PMCID: PMC3208920

doi: 10.4103/1817-1745.85704

Hydrocephalus Indian scenario – A review

N. K. Venkataramana

Department of Neurosurgery, Advanced Neuroscience Institute, BGS Global Hospital, Bangalore, India
Address for Correspondence: Dr. N. K. Venkataramana, BGS Health and Education City, No. 67, Uttarahalli Road, Kengeri, Bangalore -
560 060, India. E-mail: drnkvr@gmail.com

Copyright : © Journal of Pediatric Neurosciences

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract
Hydrocephalus is a common clinical problem seen in pediatric neurosurgical practice. Hydrocephalus
involves dilatation of the cerebral ventricular system with corresponding, compressive effects on the
parenchyma. It can be communicative or obstructive types. Congenital, acquired, infective, and secondary
hydrocephalus have different clinical features with different modality of treatments. Ventriculoperitoneal
shunt is the gold standard of treatment. Endoscopic 3rd ventriculostomy is rapidly gaining prominence as
an alternative. Various kinds of hydrocephalus, their pathophysiology, treatment and complications are
reviewed.

Keywords: Complications, hydrocephalus, outcome, shunts

Introduction
Hydrocephalus is a condition wherein excess of cerebrospinal fluid (CSF) accumulates within the
ventricular system and cisterns of the brain leading to increased intracranial pressure (ICP) and related
consequences. This can apparently result from various causes that can affect a fetus, infant, child or adult
(Rekate). Numerous definitions of hydrocephalus have been proposed. Summarily, it can be described as an
imbalance between production and absorption of CSF.[1] Over production of CSF can also be a cause of
hydrocephalus due to choroid plexus tumors, but these are rare (tumors) in clinical practice.

History
Hydrocephalus has been recognized for centuries. Accumulation of fluid in various intracranial
compartments was recognized by Hippocrates (BC 460–377) and Claudies Galen (130–200 AD). The
studies of Thomas Willis (1621–1675) facilitated the understanding of ventricular system and CSF
pathways. Franciscus Sylvius (1614–1672), Alexander Monroe (1733–1817) and Francois Magendie
(1783–1855) have made important anatomical contributions for the CSF pathway. Finally, Key and Retzeus
(1876) established the modern concept of CSF circulation. At that stage, the diagnosis and management
was not clear, resulting in high mortality. Dandy and Blackfan (1913) further contributed by creating
experimental models of hydrocephalus which led to the classification and differentiation between the
non-communicating (obstructive) and communicating forms with distinct possible treatment strategies. The
treatment options were extirpation of choroid plexus, removing obstructive pathologies or creation of
conduits to drain CSF from the intracranial compartment. The history of the treatment of hydrocephalus has

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been described in detail by John Scarff in 1963. Walter Dandy proposed 3rd ventriculostomy in 1922 for
obstructive variety. Other surgical procedures include Torkildson′s procedure which involves draining the
lateral ventricle into the cisterna magna, and ventriculocisternostomy in case of aqueductal obstruction. A
flood of operative techniques for the diversion of CSF have come into vogue since 1939. In the 1950s,
synthetic, biologically tolerant polymers, particularly silicone elastomers, became available and thus
heralded an era of shunts. Meanwhile, advances in optics and endoscopes repopularized the endoscopic 3rd
ventriculostomy as originally described by Mixter.

Indian scenario

Large heads were generally ignored in the past. Proving the fact that excessive fluid inside the head was the
cause of hydrocephalus and its effects used to be a challenge. Though plain X-rays were indicative, they
were not necessarily confirmatory. Air and contrast ventriculography was the key diagnostic investigation.
The introduction of computed tomography (CT) in 1980s has rapidly advanced the detection and treatment.
The number of ventriculoperitoneal (VP) shunts has risen in many centers across the country. Indian
economy had put several restraints in the usage of western shunts, hence surgeons resorted to valve less
infant feeding tubes as shunts. However, they were found to be useful particularly in post-infective
hydrocephalus. They were not only economical but also effective in situations where CSF protein was high.
Regional research and development and industrial association paved the way to the development of
economical Indian shunts which have now became popular even outside India. Though etiological factors
have changed over the years, the incidence of hydrocephalus has remained more or less similar across the
country. Both neurosurgeons and pediatric surgeons were treating hydrocephalus. In the last decade,
endoscopic third ventriculostomy (ETV) has become a popular surgical procedure for hydrocephalus and
the technique is being practiced all over the country. An Indian study group of neuroendoscopy was
founded creating a platform for scientific discussion and sharing the experience. Over the years,
improvement in social status, awareness, better nutrition and better perinatal care have resulted in reduction
in major anomalies and associated hydrocephalus. Prenatal diagnosis has become a reality in most centers.
The post-infective hydrocephalus has seen a decline. However, recently, there has been a resurgence of
tuberculosis leading to increase in the incidence of TB meningitis with hydrocephalus. Programmable
shunts are now available but sparingly used.

Embryology

Ventricular system develops from the corresponding vesicles of the developing neural tube. The cavity of
each telencephalic vesicle becomes the lateral ventricle and that of the diencephalic becomes the 3rd
ventricle. The cavity of rhombencephalon forms the 4th ventricle. Its continuation into the spinal cord is the
central canal. During development, each lateral ventricle is a spherical space within the telencephalic
vesicle. With the forward and backward growth, the ventricle gets elongated anteroposteriorly. The
posterior end of the telencephalic vesicle now grows downward and forward to form the temporal horns,
making the ventricles “C” shaped. Finally, the occipital horns grow backward. The approximation of the
two growing telencephalic vesicles makes the medial walls of the lateral ventricles appose each other
forming a septum. The floor of this becomes the roof of 3rd ventricle and its lateral invagination forms the
choroidal fissure. A fold of piameter extends into this fissure, forming the tela choroidea. A bunch of
capillaries develops within this fold, leading to the formation of choroid plexus.[2–4]

Cerebrospinal fluid production and absorption

Majority of the CSF production is by the choroid plexus which contributes 70 – 80% of the total daily
volume. A small proportion of CSF may be produced from ventricular ependyma and brain parenchyma.
CSF production occurs by a combination of filtration across the endothelium and active transport of sodium

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by the choroidal epithelia. Cerebral perfusion pressure and ICP appear to have only minimal effect on CSF
production under physiological conditions. CSF, which is largely formed in the lateral ventricles, passes
through foramen of Monroe to the 3rd ventricle and reaches 4th ventricle through the aqueduct of Sylvius.
Then, it presumably exits through median foramen of Magendi and lateral foramen of Luschka. The CSF
dissects into intercellular space of meninx primitive to form the subarachnoid space. From the
subarachnoid space, the CSF reaches the parasaggital arachnoid granulations.[5]

CSF is produced at a rate of 0.33 ml/min, which is approximately 500 ml/day. The total volume of CSF
varies with age and in the adults is 100–150 ml of which 15–25 ml is contained within the ventricles. The
mechanisms of absorptions of CSF have been extensively investigated. Direct absorption from the brain
parenchyma, choroid plexus or by the lymphatic channels in the region of the cribriform plate has been
postulated. The arachnoidal villi and granulations contribute to the maximum absorption. The villi are the
herniations of arachnoidal tissue into the dural venous sinuses. Two mechanisms have been proposed. The
“closed” mechanism is where the villi are a blind diverticulation and absorption occurs by a process of
seepage across the endothelial covering. The open mechanism indicates the presence of channels across the
villi, opening and closing in a valve-like manner and permitting unidirectional flow of CSF. Tripathi and
Tripathi have proposed transmembrane transport mechanism consisting of vacuoles carrying CSF across
the endothelial layer. Recently, the role of CNS microcirculation in the absorption of CSF has contributed
to the understanding of the pathogenesis of hydrocephalus. As these mechanisms are not still clear, we are
forced to follow our understanding and classification based on traditional concepts of CSF circulation.[6]

Etiology and pathophysiology of hydrocephalus

The incidence of congenital hydrocephalus is about 0.2–0.5/1000 live births. A higher incidence has been
reported in elderly primiparous mothers. It can be associated with a variety of physiological and
pathological conditions.[7,8] Obstruction at any point along the CSF pathway may result in hydrocephalus.
Traditionally, the obstruction may be within the ventricular system, resulting in non-communicating
hydrocephalus or the impairment of circulation is through the subarachnoid space or defective absorption in
the venous system, resulting in communicating hydrocephalus. Whatever be the etiology, hydrocephalus is
further divided into congenital and acquired forms. The etiology of congenital hydrocephalus remains
obscure. An inheritable form of aqueductal stenosis has been described in males (X-linked hydrocephalus).
The other mechanism of hydrocephalus is over production of CSF, seen in choroid plexus papillomas.[9]

Rekate has classified hydrocephalus based on the CSF flow obstruction. Impaired absorption is another
mechanism wherein venous sinus occlusions, vein of Galen malformations and developmental anomalies
like craniostenosis with malformation of the skull base can lead to formation of hydrocephalus. Diseases of
the arachnoidal villi can also result in hydrocephalus due to impaired absorption.[10]

Classification

Based on the results of their neutral phenosulfonaphthalein tests, Dandy and Blackfan subdivided
hydrocephalus into two groups.[11] If the chemical injected into the lateral ventricle was recovered within
20 min from the spinal subarachnoid space, the hydrocephalus was termed “communicating,” implying a
patent communication between the ventricles and the subarachnoid space. If no recovery was possible, the
hydrocephalus was termed “non-communicating” or obstructive. With the present CT and magnetic
resonance imaging (MRI) techniques, it is possible to localize with accuracy the exact site of blockage of
flow to CSF. Hence, a more helpful classification is as follows: The hydrocephalus may be due to 1)
overproduction of CSF (a rare entity); 2) obstructive, wherein the obstruction to the flow of CSF in the a)
lateral ventricles, b) foramen of Monroe, c) 3rd ventricle, d) aqueduct of Sylvius, e) 4th ventricle or f)
subarachnoid spaces; or 3) absorption defect. Based on the site of blockage to the CSF flow, the

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hydrocephalus may be 1) monoventricular or unilateral, 2) biventricular (both lateral ventricles), 3)

triventricular (3rd and both lateral ventricles), or 4) pan ventricular (4th, 3rd and both lateral ventricles).
Depending on the exact etiology, a secondary classification could be added under the following headings:
1) congenital, 2) traumatic, 3) inflammatory, 4) neoplastic, and 5) degenerative.[12]

Clinical features

The presentation of hydrocephalus differs in the case of the neonate and infant compared with the older
child or adult. Prior to closure of the cranial sutures and obliteration of the fontanella, hydrocephalus results
in disproportionate head growth. Thus, over the first 2–3 years of life, measurement of the occipito-frontal
circumference and plotting this on a centile chart provides a simple and sensitive test. Wherever possible,
sequential measurements (corrected for gestational age) should be obtained in order that the trend of head
growth in relation to the centile lines can be demonstrated. Clinical symptoms are often subtle and include
general irritability, poor feeding and slow attainment of milestones. In addition to head size, clinical signs
include bulging of the fontanellae, wide separation of the cranial sutures, prominence of scalp veins, and
“setting sun” of the eyes [Figure 1]. This later clinical sign is attributed to pressure on the mid-brain tectum
by CSF in the suprapineal recess. Papilledema can be difficult to diagnose in an infant and indeed is
commonly absent in infantile hydrocephalus and so is an unreliable sign.

In older children and adults, the classical symptom complex consisting of raised ICP, headache, vomiting
and drowsiness is more likely to herald an underlying diagnosis of hydrocephalus. When hydrocephalus
has developed insidiously, cognitive impairment, poor concentration and behavioral changes occur. Visual
obscurations and papilledema are more common in adults than in the younger age group. In both groups of
patients, the presence of bradycardia, hypertension and irregularities in breathing pattern implies critical
elevation of ICP and should be treated promptly.

Investigations

In the neonate, the supratentorial ventricular system can be reliably evaluated using ultrasound. This is the
imaging modality of choice in the investigation and monitoring of the infant with an open fontanella.
Hematomas or other ventricular masses responsible for hydrocephalus can also be identified. Ultrasound
provides a non-invasive and readily available tool for both diagnostic purposes and for measuring
ventricular size in serial studies.

CT and MRI

In order to fully evaluate the entire ventricular system and investigate the underlying etiology of
hydrocephalus, CT or MRI imaging is required. There is a range for normal ventricular size, but ventricular
size changes with age, rendering absolute measurements of ventricular dimensions of little use. No single
radiological parameter can be relied upon to distinguish hydrocephalus from the other causes of ventricular
enlargement mentioned above. Some features, however, are strongly suggestive, particularly if present in
combination. Enlargement of the temporal horns of the lateral ventricles and enlargement of the 3rd
ventricle, commensurate with the enlargement of the rest of the ventricular system, are in favor of
hydrocephalus. Obliteration of the basal cisterns and effacement of the cortical sulci further support a
diagnosis of hydrocephalus with increased ICP. When the ventricles are under pressure, there may be
transependymal flux of CSF into the periventricular parenchyma, particularly at the tips of the frontal,
occipital and temporal horns. This appears as low density on CT scan or a rim of high signal intensity on
the T2-weighted MRI scans.

Plain X-rays of skull give an indication about large size skull with different shapes of vault, sutural
separation, cranio lacunae, flat anterior cranial fossa, thinning of vault bones, sellar changes and “beaten

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silver” appearance may be seen as a sign of raised ICP. Small posterior fossa is often associated aqueductal
stenosis [Figure 2]. On the contrary, a large one might suggest Dandy walker cyst. Multiple calcifications
may be an indication of infectious etiology. Ventriculography, which was the “gold standard” during the
yesteryears, can demonstrate the large size of the ventricles and also the site of the obstruction. It is still
valuable in evaluating CSF dynamics. Cerebral angiography is not a usual investigation except in vein of
Galen malformations and in assessing major venous anomalies. However, hyperplasia, occlusion and
elongation of cerebral arteries are usually seen. Venous angle during the venous phase is an indicator of
degree of hydrocephalus.[13,14]

Electrophysiology

EEG and evoked potentials, though not of diagnostic value, have been found to be useful in evaluating
clinical outcomes in hydrocephalus. The electrical activity has been correlated to the functional integrity of
the cortical mantle. The EEG abnormalities could be focal or diffuse, and useful in detecting seizure
discharges. The incidence of seizures in hydrocephalus can vary from 18.2 to 65%. The other abnormalities
include focal slowing, focal attenuation, and multifocal paroxysmal discharges and generalized discharges.
[15,16] Because of the close anatomical relationship of posterior visual pathway, enlarged ventricles might
contribute to visual evoked potential (VEP) abnormalities. Similar abnormalities were reported in
brainstem auditory evoked response (BAER). These could be due to increased ICP, decreased cerebral flow,
herniation of upper brainstem or congenital anomalies affecting the auditory or visual system and
technically due to alteration of the median through the electrical signals called volume conduction.[17,18]
Brainstem auditory evoked potentials, when serially performed, help in identifying the structural
abnormalities of brainstem and can also be an earlier indicator of shunt malfunction [Tables 1 and 2
].[19–21]

Natural history

Laurence suggested that outlook in hydrocephalus was not without hope and survival to adult life was
between 20% and 30%. Among the survivors, 73% were educable.[22,23]

Treatment

Treatment of hydrocephalus is indicated wherever the hydrocephalus is progressive and associated with
increased ICP. A variety of treatments have been tried for hydrocephalus.

Medical management Medical measures may be appropriate under certain circumstances. Osmotic
diuretics and acetazolamide (inhibitor of carbonic anhydrase) have been used. Carbonic anhydrase is an
enzyme present in the choroid plexus and is necessary for the formation of CSF. However, the effects are
not sustained. Hence, it is useful in only as a temporary measure in post-hemorrhagic hydrocephalus.
Historically, compression bandage of the head had been advocated in neonatal hydrocephalus.

Bypassing the site of obstruction to CSF flow by diverting the CSF from ventricular cavity to a site where
it is readily absorbed is the basic principle underlying the treatment of hydrocephalus.[24] Based on this,
shunt procedures have become the mainstay of surgical treatment even in severe hydrocephalus. Shunts can
alter the process dramatically in infantile hydrocephalus. Endoscopic 3rd ventriculostomy is an important
alternative in select situations beyond 1 year. Numerous shunt systems have been devised and marketed

The shunt assembly comprises a proximal catheter located in the cerebral ventricles and a distal catheter
draining into selected site of CSF absorption, connected by a valve and reservoir incorporated into the
shunt system. Numerous shunt systems are available in the market, though all of them have their
shortcomings and are prone to similar complications. The proximal catheter has blind-ended tube with
multiple side holes to facilitate CSF drainage. A number of devices which are available, such as stylet,

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endoscope, and neuronavigation, assist to facilitate the placement of the catheter into the ventricle. The
valve designs are based on differential pressures, and may be fixed or programmable. Four types of
differential pressure valves are commonly encountered: Slit valves, miter valves, ball and spring, and
diaphragm valves. The fixed valves have low-, medium- or high-pressure alternatives. The setting defines
the opening or more commonly the closing pressure of the valve. In order to overcome the limitations of
the fixed-resistance valves, programmable valves were developed whose operating pressure can be varied
by an externally applied magnetic field. They alter the position of an internal rotor, and thus vary the
pressure setting. The pressure gradient across the valve is the difference between the intraventricular
pressure and the intra-abdominal pressure in the supine position. In addition, posture gravity and the added
hydrostatic pressure can alter the differential pressures. Anti-siphon device is a siphon-controlled device
that can be incorporated with the valves. This device houses a mobile membrane which moves in response
to the pressure change. When the intrashunt pressure falls, the membrane will occlude the shunt lumen,
thereby preventing overdrainage.[25] The alternative sites for placing the distal end include the right
atrium, pleural cavity and the gall bladder. Peritoneal cavity is the commonest site of placement of distal
catheter.[26] In communicating hydrocephalus, lumboperitoneal shunt is another good option.[27]

Indian shunt systems

The cost of most internationally available shunt systems is relatively high for people in most developing
countries. To make matters worse, periodic revisions of shunt systems and associated infections add to the
cost. To overcome this problem, many innovative shunt systems have been designed in India. These include
Upadhyaya Shunt System, Chhabra Shunt System, and Sri Chitra Shunt System.[28] Among these,
Chhabra Shunt systems have become more versatile and popular. Several studies have confirmed their
efficacy and functionality on a par with the standard shunt systems.[29] They have “Slit N Spring”, “Z”
flow, low-pressure, medium-pressure, and high-pressure valves. These valves were evaluated and
compared with the western systems and found to be equally effective.[30] Low cost of these shunts is of
major advantage. These shunt systems are becoming popular now in countries outside India. These shunts
are economical and effective.

Endoscopic treatment

With the improvement in the optics and advent of modern neuroendoscopes, a variety of treatments are
now possible through endoscopic techniques. Popular among them is the endoscopic 3rd ventriculostomy
for aqueductal stenosis. In addition, septostomy, extirpation of choroid plexus, removal of parasitic cysts,
removal of migrated shunts and arachnoid cysts can be treated effectively through neuroendoscopy.

Endoscopic 3rd ventriculostomy is effective in most obstructive hydrocephalic children. The efficacy in
infective hydrocephalus is debatable. Recently, there have been several publications indicating that ETV is
effective in some children suggesting that ETV can be attempted as a primary procedure before a VP shunt.
Similarly, the effectiveness of ETV in children under the age of 1 year is variable.[31,32]

Intellectual outcome

The determinants of intelligence levels and the pattern of intelligence in hydrocephalic children are not
fully established.[33] Many studies have been published concerning the intelligence in both treated and
untreated groups. But the criteria like diagnostic studies, time of intervention and IQ assessment
methodologies are different. Hagberg and Sgogrin defined an IQ of 90 as normal. But Lorbar and Zachary
used IQ greater than 70 as normal.[34] Foltz and Shurtlef described the children who have an IQ more than
75 as “functional”. Age at which the shunt is placed, type of hydrocephalus, status of shunt function,
associated anomalies and consequent complications, have all been incriminated as the responsible factors.
In addition, genetic, social, educational and economic backgrounds also seem to influence the issue.

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However, reviews suggest there is a decline in mortality and achievement of 50–70% incidence of normal
IQ with an effective functional shunt. Nelson and Rekate correlated IQ with the width of frontal cortical
mantle and concluded that IQ was found to be normal with cortex of more than 3 cm.[35–37] Type of
hydrocephalus, degree of ventricular dilatation and number of revisions do not seem to affect IQ, as was
suggested by Dennis and Raimondi. Children with myelomeningocele pose additional problems due to
added physical disability. Untreated children have a mortality of over 80%. Gilllian, Soare and Raimondi
reported an IQ of above 80 in 63% of their children with meningomyelocele with hydrocephalus. IQ seems
to have an inverse relationship with location of the sac and sensory level, as reported by Lorbar. The
perceptual motor deficit in children with myelomeningocele could be part of the disease entity or related to
decreased stimulation due to disability or due to a combination.[38,39] Upadhyaya in his Indian series did
not find any correlation between age at operation and nature of hydrocephalus. But severity of
hydrocephalus seems to correlate with decline in the IQ. The prognostic factors reported are a) clinica –
etiology, degree of motor and sensory deficits, level of meningocele, severity of hydrocephalus, seizures,
ventriculitis and sex of the child; b) radiologica – nature of the hydrocephalus, degree of ventricular
dilatation and topography of cerebral vasculature; c) perioperativ – age of surgery, continuing shunt
function and complications. Venkataraman et al., conducted a prospective study on neuropsychological
development of 40 children with hydrocephalus. Fifteen of them had associated myelomeningocele and
only six of them had age – appropriate neuropsychological development before surgery. Following shunt
surgery, improvement in neuropsychological function was observed in all children. However, the extent of
improvement in relation to mental age was significantly higher when CSF diversion was done prior to 6
months of age. Recovery of neuropsychological function seems to have a particular pattern and suggested
some form of hemispheric functional lateralization in their series.[40] The children with head
circumference more than 50 cm and shunt intervention done beyond the age of 18 months had developed
higher incidence of subdural hematomas and their intellectual outcomes were uniformly poor, suggesting
that beyond a stage, cortical mantle loses its ability to reconstitute, thereby leading to poorer outcomes as
well as complications.[41–44]

Complications of shunts

Extensive range of complications has been reported in the literature. They could be classified as
mechanical, like shunt blockage, disconnection, migration and relative shortening of length. The
flow-related complications are CSF overdrainage leading to subdural hematoma, subdural collections,
low-pressure headaches, secondary craniostenosis, cranial deformity, and asymmetrical drainage can lead
to trapping or isolation of a part of a ventricular system. The slit ventricular syndrome is a complication
related to absorption. Besides, ascites, loculations, hydrocele, perforation of the stomach, large and small
bowel, gall bladder and vagina are also described.[45–48]

Shunt infection is the common complication accounting for significant morbidity and mortality. Reported
series have shown the incidence ranging from 5 to 15%. Some centers have reported an incidence as low as
1%. Although many factors appear to contribute to shunt infection, it is likely that the contamination of the
shunt system at the time of surgery is the primary cause. Approximately 70% of shunt infections present
within 2 months and the remaining by 6 months of the surgical procedure.[49,50] A high index of suspicion
is maintained for symptoms and signs such as pyrexia, meningismus, irritability and even a general lack of
well-being. CSF examination is needed to confirm the diagnosis and may be obtained by the aspiration of
reservoir or from the ventricle. Appropriate antimicrobial therapy and management of the shunt system is
necessary for a good outcome. The commonest organism is coagulase-negative staphylococci, but
Staphylococcus epidermidis and Staphylococcus aureus are also often recognized. Enterococci, micrococci
and coryneforms also account for a significant proportion.[3] Controversy exists as to the retaining or
immediate removal of shunt system. The most common strategy is removal of the shunt with placement of

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an external drain with appropriate antibiotics. A fresh shunt may be placed once the CSF is sterile. There
are several reports indicating that antibiotics given at the time of surgery reduce the incidence of infection.
The role of prophylactic antibiotic, its type, duration and route of administration are still controversial. The
more recent technique of antibiotic delivery has been to incorporate antibiotics into the silicon tubing
which gradually leaches out and provides protection in the early postoperative period. Antibiotic-
impregnated shunts are now available; however, the long-term results need to be evaluated.[51–56]

Miscellaneous – Seizures, metastasis, hemorrhage related to catheters and silicone allergy.[57–60]

Special types of hydrocephalus

Post-hemorrhagic During the embryonic development, germinal matrix is the site of intense cellular
perforation. The germinal matrix is a large structure, which begins to involute by the end of 2nd trimester
and completes by 34 weeks. The blood vessels of the germinal matrix have immature connective tissue and
lack autoregulatory capacity. Due to these factors, premature infants born before 34 weeks have a high
incidence of hemorrhage. Hemorrhage is detected in 40–45% of immature infants whose birth weight is
less than 500 g, and 20% of infants who suffer intraventricular hemorrhage will develop hydrocephalus
requiring a shunt. Majority occurs within the first few days of birth. Clinical symptoms can be misleading
due to prematurely. Serial ultrasound examinations are helpful especially the head circumference is
increasing. Ventricular catheter with a subcutaneous reservoir is much safer in avoiding repeated cerebral
punctures. Recently, intraventricular fibrinolytic therapy instituted soon after the hemorrhage has been
shown to prevent chemical arachnoiditis and reduce a shunt dependency.[61–65]

Meningomyelocele Hydrocephalus complicates open spina bifida in 85–90% of patients. It may manifest
after closure of the meningomyelocele as the sac acts as a CSF sump. This is usually associated with Chiari
malformation; it is preferable to treat hydrocephalus simultaneously to facilitate wound healing after the
repair of myelomeningocele.[66]

Aqueductal stenosis The growth of the tectum and tegmentum makes the lumen of the neural tube narrow
in the region of mesencephalon, leading to narrowing of aqueduct of Sylvius. Aqueductal stenosis occurs in
approximately 10% of children. Several theories exist regarding primary versus secondary forms of
aqueductal stenosis. External pressure on mesencephalon has been proposed to obliterate aqueduct
secondarily. Scarring and gliosis following infection or hemorrhage can cause acquired aqueductal stenosis.
Tumors from the surrounding structures have potential chance to block the aqueduct. Imaging is
confirmatory in such situations.[67]

Dandy Walker syndrome This anomaly comprises agenesis of the cerebellar vermis with cystic dilation of
the 4th ventricle, enlargement of the posterior fossa and hydrocephalus. The hydrocephalus manifests in the
postnatal period. Additional brain malformations leading to neural developmental delay are reported in
70% of cases. Treatment with placement of proximal catheter in the lateral ventricle, 4th ventricle and both
the ventricles with a wide connecter has been described. Ideal situation is to treat 4th ventricular
hydrocephalus and subsequently supratentorial hydrocephalus by shunt or endoscopic method.

Post-meningitic Hydrocephalus can occur following a range of infectious or inflammatory diseases.

Organization of the inflammatory exudates, along with scarring or gliosis can produce obstruction to CSF
flow both in the ventricular system and in the subarachnoid spaces, leading to either obstructive or
communicating hydrocephalus. Bacterial, parasitic and granulomatous infections like tuberculosis and
fungal infections can also lead to hydrocephalus [Tables 3 and 4]. Hydatidosis and toxocara and viral
infections are rare causes. Hydrocephalus in the presence of infection poses several management
challenges. Hydrocephalus can be acute causing a large increase in the ICP and rapid deterioration of
clinical condition. The goals of treatment are early diagnosis, effective relief of raised ICP, CSF diversion

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and treatment of primary infection. Clinical evaluation, radiological imaging and CSF examination
including culture are essential in establishing the diagnosis. In granulomatous infections, at times it is very
difficult to differentiate the type of infection warranting tissue diagnosis or stereotactic biopsy. The
outcome depends on effective management of infection, hydrocephalus and the associated complications.
External ventricular drainage may be used as a temporary measure till the infection is resolved before
implanting a shunt or 3rd ventriculostomy. The incidence of shunt infections and malfunction is very high,
needing multiple revisions.[66] Endoscopic 3rd ventriculostomy is gaining popularity with 50–60% success
rates in select cases.[32,68,69]

Subarachnoid hemorrhage Hydrocephalus can follow 10–15% of patients suffering from subarachnoid
hemorrhage. The incidence increases with the presence of intraventricular hemorrhage. The mechanism is
impaired absorption due to blockade at multiple sites.

Normal pressure hydrocephalus Usually seen in adulthood, this is classically characterized by gait
deterioration, dementia and urinary incontinence. Imaging usually shows enlarged ventricles. In some
cases, there may be an attributable cause like infection or hemorrhage. The ICP related symptoms may not
be evident. A number of investigations have been advocated in selection of patient for shunt therapy, like
isotope cisternography, infusion tests to detect increased CSF resistance in flow, ICP monitoring and
therapeutic lumbar drainage. CSF diversion in carefully selected patients gives favorable clinical
outcomes.[70]

Hydrocephalus and venous hypertension The role of raised venous pressure as a cause of hydrocephalus
has been described long ago as otitic hydrocephalus. Similar clinical situations have been described in
achondroplasia and syndromiccranio stenosis. The deformed skull base resulting in narrowing of the
jugular foramen leading to impaired intracranial venous drainage has been described. The raised pressure
within the cranial venous sinuses reduces the pressure gradient across the arachnoid villi, resulting in
impaired absorption. Hydrocephalus also accompanies vein of Galen aneurysms.[71]

Arrested hydrocephalus Hydrocephalus may evolve into a chronic state in which persistent ventricular
enlargement with normal CSF pressure exists. Though it is controversial, this entity appears more of a
compensated ventriculomegaly. Treatment strategies should be weighed between the benefits versus risks
in individual situations. The exact criteria on which hydrocephalus is labeled as arrested are not clear.
Many do not believe in such a concept. However, they need to be monitored clinically and by intellectual
development. Disproportionate head growth or progression of ventricular size or an intellectual decline is
an indication for intervention.

Multiloculated hydrocephalus Multiloculated hydrocephalus is still a challenge to treat. It usually occurs

after an initial episode of neonatal meningitis or a germinal matrix hemorrhage. CT scan or MRI is usually
diagnostic. CT ventriculography has been advocated to know the communication between the cysts. This
condition needs to be differentiated from the cysts associated with hydrocephalus, including dorsal cyst
malformations. Among the various treatment options available, placement of multiple shunts, single shunt
with multiple fenestrations of all the loculations or craniotomy with lysis of intraventricular septations,
stereotactic cyst aspiration, or endoscopic cyst fenestrations with shunt insertion have also been described.
The endoscopic option appears the most ideal and can be performed through a single burr hole with the aid
of a steerable endoscope. Large fenestrations are usually recommended to prevent a recurrent cyst
formation. Identifying the loculated cysts is usually a problem as most often the differentiation between a
normal parenchyma and the septum is difficult, as well as it is easier to get disoriented during the scopy.
Intraoperative ultrasound or navigational systems can be of considerable help. After the perforations are
made, the multiple cavities are communicated with each other and a single shunt can be placed into one of
the major cavities. Repeat procedures are also advised in case the initial one fails to relieve the symptoms.
However, the intellectual outcome in these children has been poor. Only 20% of them can reach normal

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expected levels of IQ with the best possible treatment. The number, extent of loculations, degree of
parenchymal damage, etiology and effectiveness of treatment seem to influence the ultimate outcome. If
the loculations are unilateral, they can be communicated to the opposite ventricle through a septum
pellucidotomy.

Hydrocephalus ex vacuo This condition generally indicates enlargement of ventricles, secondary to

cerebral parenchymal damage. The ex vacuo of cerebral atrophy can be associated with aging, head trauma,
severe infection, hypoxia or ischemic insults. Of late, ventriculomegaly following radiotherapy and
chemotherapy has been noted. They are usually associated with white matter loss, concomitant enlargement
of the cortical subarachnoid spaces and basal cisterns. The periventricular lucency is absent. A number of
structural abnormalities of the brain such as calpocephali, holoprocencephali and agenesis of the corpus
callosum may also be associated with ventricular enlargement and do not necessarily require any
intervention.

Footnotes
Source of Support: Nil.

Conflict of Interest: None declared.

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Figures and Tables

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Figure 1

Setting sun sign

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Figure 2

Aqueductal stenosis

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Figure 3

Asymmetrical ventricles

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Figure 4

CT ventriculography

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Figure 5

Dandy Walker malformation

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Figure 6

Pre-op. Arachnoid cyst with hydrocephalus

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Figure 7

Post-op. Following endoscopic ventriculocystocisternostomy

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Figure 8

Bilateral SDH following shunt

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Figure 9

Shunt complication extradural and subdural hematoma

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Figure 10

Slit ventricle

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Figure 11

Meningitis with hydrocephalus

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Figure 12

Meningitis with ventriculitis

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Figure 13

Hydatid cyst with hydrocephalus

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Figure 14

Multiloculated hydrocephalus

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Table 1

Pre-operative BAER in congenital Hydrocephalus

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Table 2

Post-operative BAER after shunt

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Table 3

Imaging characteristics in infections

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Table 4

Special sequences in infections

Articles from Journal of Pediatric Neurosciences are provided here courtesy of Medknow Publications

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