This document defines and classifies hydrocephalus, describing its causes, symptoms, diagnosis, and treatment. Hydrocephalus is caused by an imbalance between cerebrospinal fluid production and absorption, leading to buildup in the brain ventricles. It can be communicating or non-communicating, and congenital or acquired from conditions like brain defects, hemorrhage, or infection. Symptoms depend on whether it develops acutely or chronically. Diagnosis involves imaging tests and clinical assessment. Treatment is usually surgical placement of a shunt to drain fluid from the brain ventricles.

1. HYDROCEPHALUS
PREPARRED BY LUCIANA CHOMBA

2. Definition
• Hydrocephalus of the central nervous system is due to an imbalance
between spinal fluid production and absorption leading to a build-up
of cerebrospinal fluid (CSF).

3. Classification
Based on its underlying mechanisms,
hydrocephalus can be classified into
communicating and non-communicating
(obstructive).
Both forms can be either congenital or acquired.
Congenital is due to an obstruction of the cerebral
aqueduct (aqueductal stenosis).
Acquired hydrocephalus may result from spina
bifida, intraventricular hemorrhage, meningitis,
head trauma, tumors, and cysts.

4. Communicating
Communicating hydrocephalus, also known as
non-obstructive hydrocephalus, is caused by
impaired cerebrospinal fluid reabsorption in the
absence of any CSF-flow obstruction between the
ventricles and subarachnoid space.
It has been theorized that this is due to
functional impairment of the arachnoid
granulations (Villi), which are located along the
superior sagittal sinus and is the site of
cerebrospinal fluid reabsorption back into the
venous system.

5. Non-communicating
Non-communicating hydrocephalus, or
obstructive hydrocephalus, is caused by a CSF-
flow obstruction ultimately preventing CSF from
flowing into the subarachnoid space (either due
to external compression or intraventricular mass
lesions).
Foramen of Monro obstruction may lead to
dilation of one or both lateral ventricles.
The aqueduct of Sylvius, normally narrow to
begin with, may be obstructed by a number of
genetically or acquired lesions (e.g., atresia,
ependymitis, hemorrhage, tumor) and lead to
dilation of both lateral ventricles as well as the
third ventricle.

6. Fourth ventricle obstruction will lead to dilatation of the aqueduct as
well as the lateral and third ventricles.
The foramina of Luschka and foramen of Magendie may be
obstructed due to congenital failure of opening.

7. Hydrocephalus has a variety of causes
including:
Congenital brain defects
Hemorrhage, either into the ventricles or the subarachnoid space
Infection of the central nervous system like syphilis, herpes,
meningitis, encephalitis, or mumps.
Tumuor

8. Incidence
Hydrocephalus is believed to occur in approximately one to two of
every 1,000 live births.
The incidence of adult onset hydrocephalus is not known.
There is no known way to prevent hydrocephalus

9. Normal physiology and pathophysiology of
hydrocephalus
Cerebrospinal fluid (CSF) normally surrounds the
brain and spinal cord, serving to cushion the
nervous tissue as well as wash away metabolic
byproducts.
CSF is made within the brain by a specialized tissue
known as choroid plexus.
This specialized modified cuboidal epithelium
secretes CSF at a constant rate of .37 cc/minute, or
roughly 500 ccs per day.

10. Normal physiology and pathophysiology of
hydrocephalus cont
The CSF production rate is energy dependent and constant.
The composition of this fluid is similar to an ultrafiltrate of plasma.
Choroid plexus in found within the 4 ventricles of the brain, the two
lateral ventricles, the midline third ventricle and the fourth ventricle
of the posterior fossa.

11. Normal physiology and pathophysiology of
hydrocephalus cont
The CSF normally circulates through these
ventricles by way of communication pathways.
The two lateral ventricles join the third ventricle by
way of the Foramena of Monro.
The third ventricle joins the fourth ventricle by way
of the Aqueduct of Sylvius, and CSF exits the fourth
ventricle by way of the midline foramen of
Magendie and the lateral Foramina of Luschka.

12. Normal physiology and pathophysiology of
hydrocephalus cont
CSF then circulates up over the convexity of the
cerebral hemispheres where it is absorbed by
another specialized tissue, the arachnoid
granulations or arachnoid villi.
The arachnoid granulations are a single cell layer
of cuboidal epithelium which allow CSF to cross
into the venous system in an energy passive
process by forcing fluid across the membrane,
utilizing the pressure differential between the
intracranial pressure (ICP) and the pressure
within the venous sinuses.

13. Normal physiology and pathophysiology of
hydrocephalus cont
Normally, the arachnoid granulations (villi)can
absorb several times more than that which is
produced.
however, if the arachnoid granulations become
scarred because of trauma or infection, or if they
become obstructed by blood products from a
hemorrhage, then CSF can no longer be absorbed
well and begins to build up in the subarachnoid
spaces, putting pressure on the brain.

14. Normal physiology and pathophysiology of
hydrocephalus cont
If CSF flow is blocked at this level, this is termed
"communicating hydrocephalus".
If the CSF pathways are blocked elsewhere, such as
at the level of the aqueduct of Silvius, then this is
termed obstructive hydrocephalus or
noncommunicating hydrocephalus.
As the intracranial pressure begins to rise in
response to a build up of CSF, the patient becomes
symptomatic.

15. Symptoms of Acute hydrocephalus
If the blockage of CSF flow happens rapidly, such as
following a sudden hemorrhage, the brain has little
time to compensate and the intracranial pressure
rises rapidly and to a sufficient degree to cause
rapid deterioration into coma.
Patients will experience:
Headache due to increased intacranial pressure
nausea and vomiting, due to increased intacranial
pressure

16. confusion, due to increased intacranial pressure
agitation and then somnolence due to increased intacranial pressure
If acute hydrocephalus is not treated emergently, the patient’s
intracranial pressure will reach the point at which cerebral perfusion
is compromised and the patient will deteriorate from coma to death.

17. Symptoms of Chronic hydrocephalus
If there is partial obstruction or partial blockage to CSF absorption
such that CSF pressure builds gradually, then the brain
accommodates to this change at first, and the onset of symptoms is
more insidious.
This is typically seen in patients with slow growing tumors.

18. s/s
They typically present with the following:
 headaches
nausea at night or upon awakening in the morning, with
improvement in their symptoms as they get up and walk around.
In infants with open sutures, chronic hydrocephalus manifests by
increased head growth due to increased ICP

19. Signs of a cute hydrocephalus
In the young child with an open fontanelle, an
infant will develop:
 Bulging fontanelle
Separation of the cranial sutures.
Rapid head growth is noted in premature and
newborn infants.
Intermittent episodes of bradycardia and apnea.
They may develop crossing of the eyes in
response to stretching of the abducens nerves or
may develop a conjugate downgaze, termed the
"setting sun" sign.

20. Signs of a cute hydrocephalus
In the young infant, irritability and somnolence is a
late occurrence.
Papilledema occurs over hours to days and may not
be seen in the acute state.
Severe headache,
 vomiting and alteration of mental status are
followed by somnolence as cortical perfusion
becomes further compromised.

21. Signs of chronic hydrocephalus
Chronic hydrocephalus beyond infancy often manifests
similarly to the syndrome of Normal Pressure
Hydrocephalus in which the patient presents with an
ataxic gait,
urinary incontinence, and
Either dementia or a decline in short-term memory.
Patients may describe intermittent headaches which
are typically worse upon arising first thing in the
morning or which awaken them from sleep at night.
They may have chronic papilledema or optic atrophy
with constriction of their visual fields.

22. Diagnosis
Skull x-ray: Skull radiographs can demonstrate findings
of raised intracranial pressure. Separation of the cranial
sutures may be shown.
Ultrasound: In the newborn infant with an open
fontanelle, sonography at the bedside can demonstrate
the ventricular size and large subdural collections.
Computerized tomography: It will give sufficient detail
to rule out most tumors which might obstruct the
ventricular system.
Magnetic resonance imaging: MRI gives the highest
resolution image of the brain.May show aqueductal
stenosis.
Clinical picture will show bulging of the fontanels and
enlargement of the head

23. Treatment
Hydrocephalus treatment is surgical. It involves the placement of a
ventricular catheter into the cerebral ventricles to bypass the flow
obstruction/malfunctioning arachnoidal granulations and drain the
excess fluid into other body cavities, from where it can be resorbed.
Common shunts include:

24. Peritoneal cavity (ventriculo-peritoneal shunt),
Right atrium (ventriculo-atrial shunt),
Pleural cavity (ventriculo-pleural shunt), and gallbladder.
A shunt system can also be placed in the lumbar space of the spine
and have the CSF redirected to the peritoneal cavity (Lumbar-
peritoneal shunt).

25. Treatment
An alternative treatment for obstructive hydrocephalus in
selected patients is the endoscopic third ventriculostomy
(ETV), whereby a surgically created opening in the floor of
the third ventricle allows the CSF to flow directly to the
basal cisterns, thereby shortcutting any obstruction, as in
aqueductal stenosis.
 Examples of possible complications include:
 shunt malfunction,
shunt failure, and
shunt infection

26. THE END
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