Chronic Hydrocephalus

Chronic hydrocephalus is persistent abnormal CSF accumulation producing progressive ventricular enlargement over weeks, months or years.

Important forms are:

Obstructive hydrocephalus

Persistent anatomical obstruction to CSF flow.

Communicating hydrocephalus

Failure of CSF absorption despite patent ventricular pathways.

Normal pressure hydrocephalus

A chronic communicating syndrome, usually in older adults, with ventriculomegaly and characteristic gait, cognitive and urinary dysfunction.

Hydrocephalus ex vacuo

Ventricular enlargement secondary to loss of brain tissue.

This is not true CSF pressure hydrocephalus and does not benefit from shunting simply because ventricles are large.

Chronic raised pressure hydrocephalus

Symptoms can include:

Headache
Cognitive slowing
Gait dysfunction
Visual disturbance
Papilloedema
Urinary dysfunction

Normal pressure hydrocephalus

The characteristic sequence is:

Gait impairment

Usually appears first.

Typical gait:

Short stepped
Broad based
Slow
Difficulty initiating walking
Feet appear \"stuck\" to the floor

Cognitive impairment

Predominantly:

Psychomotor slowing
Reduced attention
Executive dysfunction

rather than isolated cortical amnesia.

Urinary urgency or incontinence

Usually appears later.

The complete triad is not required for diagnosis.

MRI brain: preferred.

Assess:

Ventricular enlargement
Obstructive lesion
Periventricular CSF signal
Aqueduct
Fourth ventricle
Cerebral atrophy

In suspected NPH, an Evans index greater than approximately 0.30 supports ventriculomegaly but is not diagnostic alone.

Other supportive features include disproportionately enlarged ventricles relative to cortical sulci and a narrow high convexity subarachnoid space.

CSF tap test

For suspected NPH:

Remove approximately 30 to 50 mL CSF by lumbar puncture.

Measure objective gait function before and after the procedure.

Improvement in gait after CSF removal supports likely shunt responsiveness.

A negative tap test does not completely exclude benefit.

Extended lumbar drainage over several days can improve prediction in selected equivocal patients.

Ventriculoperitoneal shunt

VP shunting is the most common definitive CSF diversion operation.

Components are:

Ventricular catheter
Valve
Distal peritoneal catheter

Programmable valves permit postoperative adjustment of opening pressure without another operation.

A practical approach is to start at a moderate pressure setting and gradually reduce it according to:

Symptoms
Ventricular response
Development of overdrainage

NPH

The symptom most likely to improve after shunting is gait dysfunction.

Urinary symptoms can also improve.

Cognitive recovery is less predictable, particularly when there is established neurodegenerative disease.

A patient with ventriculomegaly alone and no compatible clinical syndrome should not undergo a shunt.

Obstructive hydrocephalus

Treat the underlying obstruction when possible.

Options include:

Tumour removal
Colloid cyst removal
Aqueductal lesion treatment
ETV

ETV is particularly attractive for anatomically suitable obstructive hydrocephalus and avoids lifelong shunt dependence in successful cases.

Shunt malfunction

Suspect with recurrence of:

Headache
Vomiting
Drowsiness
Gait deterioration
Cognitive deterioration
Visual symptoms
Ventricular enlargement

Mechanical causes include:

Proximal catheter obstruction
Valve malfunction
Distal catheter obstruction
Disconnection
Migration

Shunt infection

Features include:

Fever
Wound erythema
Abdominal pain
Meningism
Neurological decline
Positive CSF cultures

Established shunt infection usually requires:

Remove infected shunt
Temporary external ventricular drainage where necessary
Culture directed IV antibiotics
Reimplant a new shunt only after infection control

Antibiotics alone with infected hardware left permanently in place frequently fail.

Overdrainage

Excessive CSF drainage can produce:

Orthostatic headache
Slit ventricles
Subdural hygroma
Chronic subdural haematoma

Increase programmable valve opening pressure or add anti siphon control when appropriate.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Cerebral Contusion

A cerebral contusion is traumatic bruising of brain parenchyma containing variable haemorrhage, oedema and tissue necrosis.

Common locations are:

Inferior frontal lobes
Anterior temporal lobes

because the brain impacts irregular surfaces of the skull base.

Contusions can occur at:

Coup site

Directly beneath impact.

Contrecoup site

Opposite the impact as the brain moves within the skull.

A major clinical characteristic is haemorrhagic progression, often called contusion blossoming.

A relatively small lesion on initial CT can enlarge significantly during the first hours after trauma.

Noncontrast CT: first line investigation.

The important features are:

Contusion volume
Surrounding oedema
Midline shift
Basal cistern compression
Associated subdural or subarachnoid blood

Repeat CT is warranted with:

Falling GCS
New focal deficit
New pupil abnormality
Significant initial contusion at risk of expansion

MRI can demonstrate nonhaemorrhagic components and associated axonal injury but is not required for immediate surgical decisions.

Small contusions without neurological deterioration or significant mass effect can be managed with:

Close neurological observation
ICP focused treatment when severe
Serial CT according to clinical course
Early seizure prophylaxis in significant cortical injury

Correct:

Hypoxia
Hypotension
Hypercapnia
Fever
Coagulopathy

Reverse clinically significant anticoagulation promptly when haemorrhage is expanding or surgery may be required.

Surgery

Operate when a parenchymal lesion produces:

Progressive neurological deterioration
Refractory intracranial hypertension
Significant CT mass effect

Specific operative thresholds include:

GCS 6 to 8 plus frontal or temporal contusion greater than approximately 20 cm³

with either:

Midline shift at least 5 mm

Basal cistern compression

Also operate for:

Any traumatic parenchymal mass lesion greater than approximately 50 cm³, particularly when producing significant mass effect.

Procedure

Perform craniotomy and evacuate the haemorrhagic contused tissue causing mass effect while preserving viable cortex where possible.

A large decompressive craniectomy can be added when severe swelling prevents safe bone flap replacement.

Avoid unnecessarily aggressive removal of nonexpansile contused brain simply because it appears abnormal on CT.

Refractory swelling

Persistent intracranial hypertension after focal evacuation requires:

Repeat imaging
Hyperosmolar therapy
CSF drainage where appropriate
CPP optimisation
Decompressive surgery in selected patients

Chronic Hydrocephalus

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management