Congenital hydrocephalus is present at birth and can be caused by events during fetal development or genetic abnormalities. It is characterized by an abnormally large head size. Acquired hydrocephalus develops after birth from injuries or diseases. It is divided into communicating hydrocephalus, caused by blocked CSF absorption, and obstructive hydrocephalus, caused by blocked ventricular flow. Normal pressure hydrocephalus occurs when hydrocephalus reaches an equilibrium state, causing gait, urinary, and cognitive issues without enlarged head size or elevated pressure.

1. HYDROCEPHAL
US

2. INTRODUCTION
• The term hydrocephalus is derived from the
Greek word “hydro” meaning water and
“cephalus” meaning head .
• As the name implies ,it is a condition in which
the primary characteristic is excessive
accumulation of fluid in the brain .
• Although hydrocephalus was once known as
“water in the brain “ the water is actually
cerebrospinal fluid (CSF)-a clear fluid that
surrounds brain and spinal cord.

5. DEFINITION
• Hydrocephalus is a condition caused by a
imbalance in the production and absorption of
CSF in the ventricular system .when production
exceeds absorption ,CSF accumulates ,usually
under pressure ,producing dilation of the
ventricles.
OR
Hydrocephalus is a condition of
ventricular enlargement as a result of an
obstruction to the normal flow of CSF.

6. EPIDEMIOLOGY
• The incidence of congenital hydrocephalus was
highest in Africa ,south east Asia ,Latin America and
lowest in united states Canada.
• Incidence was higher in low and middle income
countries than in higher income countries.
• In India ;
*Congenital hydrocephalus 0.2-0.5/1000 birth.
*Hydrocephalus can follow 10-15 % of patients
suffering from subarachnoid hemorrhage.

7. • The majority of hydrocephalus is seen by 2 years
of age .
• After 2 years of age , incidence decreases with
increasing age.
• The is no geographic distribution in worldwide
distribution of hydrocephalus.

8. ANATOMY AND PHYSIOLOGY
• The brain , spinal cord and their protective
covering;
 The brain and spinal cord form the central
nervous system.
 Surrounded and protected by the bones of
the skull and the vertebral column .
 The bones of the skull are called cranium
and places where bones meet and grow are called
sutures.
 The brains major component are the
cerebrum ,cerebellum and the brainstem.

12. The spinal cord extends from the brainstem ,through
a very large opening (foramen of magnum ) in the
base of the skull and down the spine.
Lying between the brain and the skull are 3
protective coverings;
#Dura mater
#Arachnoid mater
#Pia mater
 These are the meninges which completely surround
the brain and spinal cord.

14. Cerebrospinal fluid
• Cerebrospinal fluid is the clear ,colorless and
transparent fluid that circulates through the
ventricles of the brain , subarachnoid space
and central canal of spinal cord .it is the part of
extracellular fluid.
PROPERTIES
Volume:104ml (mean);70-160ml(range)
Rate of reaction:0.3ml per min
Specific gravity :1.005
Reaction :alkaline

15. lymphocytes :6/cu mm.
Average rate of formation :21 to 22ml/L
(500mlday).
COMPOSITION
CSF contains more amount of sodium than
potassium .
Some lymphocytes .
Lymphocytes are added when CSF flows in
spinal cord .

17. FUNCTIONS OF CSF
Water jacket for the spinal cord and brain,
protecting from injuries.
Provide brain with buoyancy .
Brain and spinal cord have no lymphatic
channels, the CSF through its “sink action",
serves to remove waste products of cerebral
metabolism ,the main ones being co2, lactate
and hydrogen ions.
Provide a stable chemical environment for
neurons ,astrocytes and myelinated fibres.

18. FORMATION OF CEREBROSPINAL
FLUID
The choroid plexus located in the floor of the
lateral , third and fourth ventricles are the main
sites of CSF formation .some of the CSF is also
formed by the meninges even after the choroid
plexus are removed.
The thin walled cells of the plexus allow passive
diffusion of substances from the blood plasma
into the extracellular space surrounding choroid
cells.
The choroid epithelial cells ,contain organelles
that carry out active transport.

19. The blood vessels in the subependymal regions and
pia also contribute to CSF and some substances enter
the CSF as readily from the meninges as from the
choroid plexus .
The transport of sodium ,the main cation of CSF ,is
accomplished by the action of a sodium –potassium
ion exchange pump at the apical surface of choroid
plexus cells ,the energy for which is supplied by ATP.
Penetration of certain drugs and metabolites into
CSF is directly related to the lipid solubility .
Largest amount of CSF is formed in the lateral
ventricle.
Normally about 500ml of CSF is formed every day
and an equal amount is absorbed.

20. CIRCULATION OF CSF
Harvey Cushing aptly termed the CSF
“third circulation “,comparable to that of
blood and lymph.

22. ABSORPTION OF CSF
Absorption of CSF is mainly through the
arachnoid villi. These are microscopic
excrescences of arachnoid membranes that
penetrate the Dura mater and protrude into
the superior sagittal sinus and other venous
structures (spinal veins).
The arachnoid villi ,most numerous on
both sides of the superior sagittal sinus, also
present at the base of the brain and around
the spinal cord roots and act as functional
valves that permit unidirectional “bulk flow”
of CSF into the vascular lumen.

24. CLASSIFICATION OF HYDROCEPHALUS
1)According to age affected;
a]Congenital
b]Acquired  Communicating
 Noncommunicating
2)According to blockade of CSF flow [In
1914 , Dandy and Blackfan introduced the
terms ]Functional classification;
a]Communicating hydrocephalus
b]NoncommunicatingObstructive.

25. 3)That affects adults are;
a]Hydrocephalus ex- vacuo/colpocephaly.
b]Normal pressure hydrocephalus

26. ETIOLOGY
A) Congenital hydrocephalus
Aqueductal stenosis.
Due to Arnold chiari 1 and 2 malformation.
Post infections (Toxoplasmosis, cytomegalic
inclusion disease,rubella,syphilis).
Obstruction of foramen of luschka and
foramen of magendie.
Dandy Walker malformation.
Myelomeningocele.
Intracranial and intraventricular bleed.

27. B)Acquired hydrocephalus
1]Communicating hydrocephalus
Subarachnoid hemorrhage
Bacterial meningitis
Malignant meningitis
Increased venous pressure
Head injury
Extra ventricular obstruction by
infection (TB).

28. 2]Noncommunicating Obstructive
hydrocephalus
Intraventricular obstruction
tumor(posterior fossa tumor ,brain stem
glioma ,tumor of pineal body, choroid plexus).
Papilloma, ependymoma ,colloid cyst.
infections (cerebral abcess,ventriculitis).
hemorrhage.

29. C) Seen in adults
1]Hydrocephalus ex-vacuo.
Stroke
Traumatic injury
Degenerative diseases like Alzheimer's
diseases.
Dementias

30. 2)Normal pressure hydrocephalus
Subarachnoid hemorrhage.
Head trauma
Infection
Tumor
Complications on surgery
Sometimes idiopathic

31. CONGENITAL HYDROCEPHALUS
• Congenital hydrocephalus is present at
birth and may be caused by either events
or influences that occur during fetal
development or genetic abnormalities .
• In Dandy- walker syndrome posterior fossa
cyst continues with 4th ventricle.
• Aqueduct stenosis accounts for 33% of
hydrocephalus .In 2% of the cases this
could be familial with x linked recessive
inheritance.

32. • In Arnold - chiari syndrome the portions of
cerebellum and brainstem herniating into
cervical spinal canal ,blocking the flow of CSF to
the posterior fossa.

33. ACQUIRED HYDROCEPHALUS
• Acquired hydrocephalus develops at the time of
birth or at some point afterward.
• This type of hydrocephalus can affect individuals
of all ages and are caused by injury or disease.
• Mostly seen after 6 months of age.
1)Communicating hydrocephalus
• Communicating hydrocephalus is a condition
that results when the arachnoid villi are unable
to adequately reabsorb CSF.

34. • It occurs when the flow of CSF is blocked after it
exit the ventricles .
• Block is at the level of the arachnoid
granulations.
• This form is called communicating because the
CSF can still flow between the ventricles ,which
remain open.
2) Noncommunicating hydrocephalus
• Also known as obstructive hydrocephalus .
• It is a condition that results when the ventricular
system does not communicate with the
arachnoid villi due to some obstruction in the
normal pathway of CSF flow.

35. • Obstruction to the flow of CSF occurs
within the ventricles

36. HYDROCEPHALUS EX-VACUO
• Occurs when stroke or traumatic injury causes
damage to the brain.
• In this case brain tissue actually shrink ,i.e.
cerebral atrophy .
• Accelerated by Alzheimer's disease
,Creutzfeldt-Jakob, alcoholism etc.
• Colpocephaly is the ventricular enlargement
because of failure of development of brain.

37. NORMAL PRESSURE HYDROCEPHALUS
• In , meningeal and ependymal diseases,
hydrocephalus may develop and reach a stable
state .
• It is said to be compensated –formation of CSF
equilibrates with absorption .
• Once equilibrium is attained ICP gradually falls,
though it still maintain a gradient from ventricle to
basal cistern to cerebral subarachnoid space .
• At this stage CSF pressure reaches high normal
level(150-200mmH20) but the patient manifests

38. the cerebral effects of hypothalamic state.
• Adams ,Fisher and Hakim named it as
normal pressure hydrocephalus.
• The triad of clinical finding seen in NPH are
slowly progressive gait disorder,
impairment of mental function and later
sphincter incontinence .
• Grasp reflex in feet and falling attacks may
occur but there are no Babinski signs .
• Headache are infrequently a complaint
and there is no papilledema.

39. RISK FACTORS
•Newborns
Abnormal development of CNS.
Bleeding within the ventricles ,complication
of premature birth.
Infection in the uterus during pregnancy, such
as rubella or syphilis , cause inflammation in fetal
brain tissue.
Maternal medication or alcohol use during

40. Life style modifiable maternal
pathologies such as obesity ,diabetes or
hypertension.
Lack of prenatal care and low
socioeconomic status.
Any age group
Lesions or tumors of the brain or spinal
cord.
Central nervous system infections
(bacterial meningitis or mumps).
Bleeding in the brain from a stroke or
injury or other traumatic injury.

41. PATHOGENESIS OF HYDROCEPHALUS

44. (1)One foramen of monro may be blocked by a
tumor or horizontal displacement of central brain
structures forms large cerebral mass
expansion of lateral ventricle or portion of it.
(2)Tumors [colloid cyst ] in 3rd ventricle blocks
flow of CSF from both foramina of monro
dilation of both lateral ventricle .
(3)Development or acquired lesion in aqueduct of
sylviusdilation of both lateral ventricle and third
ventricle.
(4)Obstruction in 4th ventricle  dilation of both
lateral ventricle ,3rd ventricle and aqueduct of
sylvius.

45. (5)Obstruction in foramina of magendie and
luschka[congenital failure of opening of
foramina ,Dandy-Walker
syndrome]obstruction to lateral ,3rd and
4th ventricle.
(6)Blockade of CSF flow in subarachnoid
space enlargement of entire ventricular
system.
(7)Meningeal obstruction at arachnoid villi
or blockade of the venous sinuses into
which CSF is absorbed Hydrocephalus

46. NOTE :-
According to Ayer, the ventricle closest
to the obstruction enlarges the most.
Causes for overproduction of CSF
Papilloma's of the choroid plexus.
ventricular obstruction.
pilocarpine ,extract of pituitary gland.
injection of isotonic saline.
injection of hypotonic saline .

47. Causes for decreased absorption of CSF
Congenital aplasia of the arachnoid villi.
Damage of arachnoid villi in case of
meningitis.
Thrombosis of superior sagittal sinus.

48. CLINICAL MANIFESTATIONS
•Infants
changes in head
An unusually large head.
rapid increase in the size of head.
fontanel (bulging or tense soft spot) on
top of head.

49. Physical signs and symptoms
vomiting
sleepiness
poor feeding
seizures
irritability
eyes fixed downward (sun setting sign)
poor growth
deficits in muscle tone and strength
poor responsiveness to touch

51. •Toddlers and older children
head ache
blurred or double vision(diplopia)
sun setting sign
abnormal enlargement of toddlers head
sleepiness or lethargy
poor coordination
poor appetite
seizures
urinary incontinence

53. nausea and vomiting
unstable balance
irritability
change in personality
decline in school performance
delays or problems with previously acquired
skill, such as walking or talking.
•Young and middle-aged adults
headache and lethargy
loss of coordination or balance
loss of bladder control or a frequent urge to
urinate

54. impaired vision
decline in memory, concentration and thinking skills .
•Older adults
loss of bladder control or frequent urge to urinate.
memory loss
poor coordination or balance
shuffling gait or feeling of being stuck
diplopia
loss of thinking and reasoning
vertigo and seizures

57. Book picture
• Headache
• Lethargy
• Loss of bladder control
or frequent urge to
urinate.
• Memory loss.
• Loss of coordination or
balance.
• Impaired vision.
• Loss of thinking and
reasoning .
• Vertigo and seizures.
Patient picture
• Headache
• Difficulty in walking with
Left sided weakness and
deviation while walking.
• Difficulty in focusing with
eyes.
• vertigo

58. SYNDROMES OF HYDROCEPHALUS
• Hydrocephalus give rise to various syndromes
depending on the age of patient and rapidity of
evolution.
1)Early in life ,before fusion of cranial sutures
and cause enlargement of head.
2)Later ,if the cranial sutures have fused ,the
head remains normal in size and ventricular
enlargement remain asymptomatic or cause gait,
urinary and cognitive difficulties ,called arrested
or compensated hydrocephalus  NPH

59. Congenital or infantile hydrocephalus
•Causes
fetal and neonatal infections.
intraventricular matric hemorrhage in
premature infants.
type 2 chiari malformation.
aqueductal stenosis and Dandy- Walker
syndrome.

60. •Manifestations
frontal bones are bossed and skull tends
to be brachiocephalic except in Dandy –
Walker syndrome(dolichocephalic).
distended veins in face due to
enlargement of skull.
fretful, feeds poorly and vomit frequently.
languid , uninterested in daily activities.
setting sun sign ???

61. OCCULT CHILDHOOD HYDROCEPHALUS
• The ventricular enlargement becomes evident
only after the sutures have closed.
• It may give rise to normal pressure
hydrocephalus.
•Causes
cerebellar or frontal stroke
minor cranial trauma.
•Manifestations


62. plantar reflexes are sometimes extensor.
urinary urgency leading to sphincteric
incontinence.

63. ACUTE HYDROCEPHALUS
•Causes
subarachnoid hemorrhage from a ruptured
aneurysm.
bleeding from an arteriovenous malformation.
deep intracerebral hemorrhage.
•Manifestations
bilateral Babinski signs –coma ,increased
tone in the lower limbs and extensor
posturing.

64. pupils become mitotic and limitation of
upward gaze .
????
•Treatment
drainage of CSF by a ventricular catheter.
If untreated ;
???

65. DIAGNOSTIC EVALUATION
• History and physical examination
• Typical cracked –pot sound (Macewen’s
sign) of the skull bone.
• MRI
• CT Scan
• Cranial ultrasonography
• X-ray skull
• ICP Monitoring – Lumbar puncture.

66. Physical examination
• On physical examination
Unsteady gait
Visual disturbances
Decreased muscle strength

67. • MRI(Magnetic resonance imaging)
MRI Brain shows post op changes for
anterior cerebral artery aneurysm with hyper
dense clip is seen in inferior hemisphere
fissure. Gliosis and encephalomalacia is seen in
right basal frontal lobe.
• CT Scan
CT Brain shows ventriculomegaly due to
accumulation of CSF suggesting the evidence
for hydrocephalus(communicating) and need
for VP Shunt.

69. •Cranial ultrasonography
Is usually done to diagnose
congenital hydrocephalus .Cranial
ultrasound is a technique for scanning the
brain using high frequency sound waves .it
is used almost exclusively in babies because
their fontanelle (the soft spot on the skull)
provides an “acoustic window”.
•Skull x-ray
Examine the bones of the
skull, including the facial bones , the
nose and sinuses.It is used to diagnose

70. • Separation of sutures
• Erosion of sutures
• Increased convolutional markings (silver
beaten appearance.
• Lumbar puncture(ICP monitoring)
Procedure ;
Position the patient in lateral recumbent position.
Apply topical anesthetic 30 to 45 min prior to
procedure.

71. Spinal cord ends at L1-L2 ,so sites for puncture
are located at L3-L4 or L4-L5.
Clean the area with povidone iodine from
puncture site radially out to 10cm and allows to
dry.
Anesthetize with lignocaine if topical not
used,intradermally raising a wheal at needle
insertion site.
Advance needle through wheal to desired
interspace .
Careful not to inject into a blood vessel or spinal
canal.
Insert spinal needle with stylet with bevel up to,

72. keeping cutting edge parallel with nerve
and ligament fibers.
Hold needle firmly.
Decrease in resistance indicates that
ligament flavum and Dura are punctured .
Remove stylet and check for flow of spinal
fluid .
When CSF flows, attach manometer to
obtain opening pressure if desired.

75. Indications ;
Laboratory analysis.
Measure pressure of CSF.
To diagnose
meningitis
meningoencephalitis
subarachnoid hemorrhage
malignancy
Contraindications;
 Unstable patient (Reduced GCS)with
cardiovascular or respiratory instability.
Unstable bleeding disorder .

76. Complications;
 Headache
Nerve trauma
Apnea
Ocular muscle palsy
Subarachnoid epidermal cyst.

77. PATIENT PICTURE:
• LFT Normal
• Hematological examination
neutrophils increased (84.7%)
lymphocytes increased (41%)
• Serological testing
HIV 1 &2
HBsAg Nonreactive
HCV
• ECG sinus rhythm

78. Book picture
• Physical examination and
history.
• Ophthalmoscopy.
• MRI
• CT scan
• Cranial ultrasonography.
• Skull x-ray.
• ICP monitoring (lumbar
puncture0
Patient picture
• History and physical
examination.
• MRI
• CT Scan
• Lumbar puncture.
• ECG.

79. MANAGEMENT
relief of hydrocephalus
treatment of complications
management of problems caused by pathology

80. Medical management
• Diuretics :- acetazolamide and furosemide
treat post hemorrhagic hydrocephalus in
patients ;decrease secretion of CSF at the
level of the choroid plexus .
• Anticonvulsants :-interfere with impulse
transmission of cerebral cortex and
prevent seizures.
• Antibiotics :-for shunt infections such as
septicemia ,ventriculitis ,meningitis or
given as a prophylactic treatment.

81. • To counteract acidosis give alkasol.
• Oral glycerol-reduce CSF production.

82. Surgical management
Shunt
A Shunt is made up of radio plastic and has
ventricular catheter ,pressure valve ,pumping
chamber and distal catheter that directs the flow
of CSF from the ventricles to other areas of the
body from where it is absorbed.

83. 1)Ventriculoperitoneal shunt

84. 2)Ventriculoatrial shunt

85. 3)Lumboperitoneal shunt

86. 4)Ventriculopleural shunts

87. •Complications of shunt
1)Malfunction
2)Shunt infection
3)Subdural hematoma
4)Others
???
•Signs of shunt infection
1)Fever (> 0r=to 100.4)
2)Redness or swelling
3)Pain

88. Endoscopic third ventriculostomy

89. Book picture
• Pharmacological therapy
diuretics
anticonvulsants
antibiotics
alkasol
oral glycerol
Patient picture
antibiotics
inj.monocef
inj.amikacin
anticonvulsant
inj.eptoin
antiemetic
inj.emeset
analgesic
inj.PCM
inj.Tramadol
PPIs
inj.pantop
hypnotic and sedative
tab .zolpidem

90. Book picture
• Shunts
ventriculoperitoneal
shunt.
ventriculoatrial shunt.
lumboperitoneal shunt.
ventriculopleural shunt.
• Endoscopic third
ventriculostomy.
Patient picture
• Ventriculoperitoneal
shunt.

91. Nursing management
A) Teach the family about the management
required.
Treatment is surgical by direct removal of an
obstruction and insertion of shunt to provide
primary drainage of the CSF to an extra cranial
compartment, usually peritoneum
(ventriculoperitoneal).
Complications of shunt.
A third ventriculostomy is a new nonshunting
procedure used to treat children with
hydrocephalus.

92. B)Provide preoperative nursing care.
understanding of the neurological disease and
its systemic presentation.
monitor vital signs of the pt.
obtain accurate neurological status of the pt.
provide psychological support to the pt.
provide preoperative medications to the pt.
monitor increase in intracranial pressure –
observe ,report and document all signs of
increased ICP.

93. C)Provide postoperative nursing care
access for signs of increased ICP and check for
the following ,weakness, unsteady gait ,seizures
,visual disturbances ,fullness and behavior.
administer prescribed medications which may
include antibiotics to prevent infection and
analgesics for pain.
if there is increased ICP elevate the head of the
bed or allow the patient to sit up to enhance
gravity flow through shunt.
observe the patient for abdominal distention (in
case of vp shunt.

94. maintain intake output chart .
provide shunt care.
* monitor for shunt infection.
*monitor for shunt over drainage.
*slit ventricle syndrome.
D)Teach home care
encourage the patient to participate in age
appropriate activities as tolerated .encourage
family members to provide a normal lifestyle as
possible.
explain how to recognize signs and symptoms of
increased ICP.???
Frequent screening and follow ups.

95. Nursing diagnosis
•Pre operative
1)Anxiety related to abnormal condition
and surgical intervention.
2)Acute Pain related to disease condition.
3)Risk for injury due to difficulty in walking
with left sided deviation during walk.

96. Anxiety related to abnormal
condition and surgery
•Goal
Reduce anxiety of the patient.

97. • Explain to the patient as well as family
the condition and the surgical procedure
in terms they can understand.
• Answer the queries of the patient as well
as the family members.
• Ask the family members to give
psychological support to yhe

98. Risk for injury due to difficulty
in walking, shuffling gait…
•Goal
To prevent injury due to shuffling gait
,difficulty in walking and left sided deviation
during walking.

99. • Assess the patient for falls /injury
and give supporting aids such as
walker.
• Keep ward/ room clear from
obstacles and things that may
cause injury.
• Monitor neurological status of the
patient.

100. •Post operative
1)Risk for infection related to presence of a shunt.
2)Deficient knowledge related to family members
understanding of the patients condition and home
care.
3)Risk for impaired skin integrity due to pressure
from physical immobility.

101. Risk for impaired skin integrity
related to pressure from physical
immobility
•Goal
Maintain skin integrity

102. • After stunting procedure ,keep the
patients head turned away from the
operative site .
• Reposition the patient every 2 hours.
• Inspect the dressing over the shunt
procedure every 4 hourly.

103. Risk for infection related to
presence of shunt
•Goal
Prevent infection due to the
presence of shunt.

104. • Observe for and promptly report
any signs of infection.
• Perform wound care thoroughly as
ordered.
• Administer antibiotics as ordered .
• Record vital signs 2 hourly

105. Prognosis
•Day 1
The patient was having difficulty in walking
and was unable to walk without support .He had
also the complaint of left sided deviation during
walk. The patient undergone CT brain, MRI ,CBC,
ESR,ECG and other serological testing.
•Day 2
The patient planned for VP shunt. Pre
operative orders checked and vitals taken.Pre
operative medications given as ordered.

106. •Day 3
The patient received from ICU .Post
operative vitals taken .post operative medications
provided as ordered. Ensure proper dressing at
procedure site.
•Day 4
Proper dressing of procedure site and assess
the shunt for any infection. Monitor vitals 2
hourly.

107. Health education
There is no known way to prevent
normal pressure hydrocephalus. A healthy
lifestyle ,including no smoking ,maintaining a
healthy weight and regular exercise may help
avoid conditions such as high blood pressure
,heat disease ,diabetes and stroke that might
contribute to normal pressure hydrocephalus.
Wearing a seat belt and safety helmet when
indicated can help avoid head injury ,another
cause of normal pressure hydrocephalus.

108. THANKYOU