+

HYDROCEPHALUS

Vitya Chandika 2013-061-060

Priscila Stevanni 2013-061-066

Pricilia Nicholas 2013-061-070

+Definition

Abnormal accumulation

of CSF due to disturbance

of flow, formation or

absorption.

+Function of CSF

As a brain cushion, a shock absorber for brain and spinal cord.

Circulates nutrients.

Removes waste product.

Maintain ionic hemostasis

Production rate: 0.2 – 0.35 ml/min

Total volume: 120ml

+ Lateral Ventricle

Foramina Monro

3rd ventricle

Aquaductus Sylvii

4th Ventricle

Foramina Luschka & Magendie

Cisterns system

+EPIDEMIOLOGY

Estimated prevalence: 1-1.5%

Incidence of congenital hydrocephalus is 0.9-

1.8/1000 births

+ETIOLOGY

Congenital

Chiari Type 2 malformation and/or myelomeningocele (MM)

Chiari Type 1 malformation: HCP may occur wituh 4th

ventricle outlet obstruction

Primary aqueductal stenosis

Secondary aqueductal gliosis

Dandy Walker malformation: atresia of foramina of Luschka

& Magendie

X-linked inherited disorder

+ETIOLOGY

Acquired Infectious

Post meningitis

Cysticercosis

Post hemorrhagic

Post SAH

Post IVH (intraventricular hemorrhage)

Secondary to masses

Non-neoplastic: e.g. vascular malformation

Neoplastic

Post-op

Neurosarcoidosis

“Constitutional ventriculomegaly”: asymptomatic. Needs no treatment

Associated with spinal tumors

+CLASSIFICATION

Obstructive Block proximal to the arachnoid

granulation (AG). On CT/MRI: Enlargement of

ventricles proximal to block

Tumors

Blood clots

Congenital malformation

Arachnoiditis

Stenosis

+CLASSIFICATION

Communicating CSF circulation

block at level of AG

Intraventricular hemorrhage

Subarachnoid hemorrhage

Meningitis

+SPECIAL FORMS

Pseudohydrocephalus Hydrocephalus ex vacuo

Otitic hydrocephalus

External hydrocephalus

Hydranencephaly

Normal pressure hydrocephalus

Entrapped fourth ventricle

Arrested hydrocephalus

+Pathophysiology

+Aqueductal stenosisThe most common cause of congenital hydrocephalus(43%)-Aqueduct develops about the 6th week of gestation -M:F = 2:1 -Prognosis: 11-30% mortality

+Pathophysiology

Dilated temporal & frontal horn, often

asymetry, results:

-Elevation of corpus callosum

-Stretching / perforation of septum pellucidum

-Thinning of cerebral mantle

-Enlargement of third ventricle downward into

fossa pituitary

+CLINICAL MANIFESTATION

In young children Increasing head circumference Full fontanel Sutural diastasis Irritable hyperactive reflexes Vomit Setting sun appearance Thin scalp with dilated veins Macewen’s sign: cracked pot sound on percussing

over dilated ventricles

+

+CLINICAL MANIFESTATION

In older children/adults Papilledema Hypertension Nausea / vomiting Gait changes Upgaze and/or abducens palsy Incontinence Bradycardia Apnea Dementia

+CT scan / MRI

Criteria:

Size of both temporal horns (TH) ≥ 2 mm in width(in the absence of HCP, the temporal horns should be

barely visible)

and

The sylvian & interhemispheric fissures and cerebral sulci are not visible

OR

Both TH are ≥ 2 mm

and the ratio

+CT scan / MRI

Suggestive of hydrocephalus:

1. “Mickey Mouse” ventricles

2. Sagital MRI may show thinning and/or upward bowing of the corpus callosum

3. Ratio

4. Evans index:

+ CT scan

+Treatment

Diuretics

For premature infants

-Acetazolamide (carbonic anhydrase inhibitor)

~25mg/kg/day PO divided TID,

increase 25mg/kg/day each day until 100mg/kg/day is

reached

-Simultaneously start furosemide: 1mg/kg/day PO divided

TID

+Treatment

Lumbal puncture / Spinal taps

only for communicating Hydrocephalus,

Normal Pressure Hydrocephalus

+Surgical

choroid plexectomy

eliminating the obstruction

third ventriculostomy

Shunting (VP/VA)

+

+

THANKYOU