Disturbances of Intra-Cranial Pressure (ICP) and Hydrocephalus Andrew Danks Chairman of Neurosurgery, MMC

Significance of raised ICP depends clinical context Fast vs Slow tempo slow rise allows compensation brain shift / moulding/atrophy CSF shifts even bone moulding / atrophy Young child splitting of sutures, head growth can often allow compensation

Normal ICP Normally 10-15 cm water in supine position lower in young children -5 to 0 cm water in standing position at foramen of Munro (mid temple) CSF actively secreted at 20 ml/hr or so CSF resorbed at arachnoid villi in pressure-dependant mechanism CSF pressure is the driver for head growth

Benign Intracranial Hypertension Chronic raised ICP up to 40 - 60 cm water no hydrocephalus / brain distortion normal brain function may get headaches, papilloedema, and visual loss due to raised venous or CSF pressure

Clinical Features of Chronically Raised ICP Symptoms : headache vomiting impaired mentation, conscious state Signs : papilloedema : vision at risk poor upgaze, 6th nerve palsy

Papilloedema

Common causes of acute ICP Severe head injury Intracranial haematoma Tumour / abscess Infection - meningitis, encephalitis Metabolic Post operative swelling Ischaemic strokes Hydrocephalus Sub-arachnoid haemorrhage

ICP Reflects : Volume of contents / volume of cranium contents = brain blood CSF pathology : tumour, haematoma, etc oedema : intracellular / extracellular normal ICP = 5 - 15 cm water, postural

CT and MRI show shapes of tissues, not pressure Pressure can often be inferred However, significant traps exist in “acutely blocked shunt”, ventricles often are not dilated some pts have slit ventricles when controlled some pts do not dilate ventricles due to stiff walls, but pressure increased

More important than ICP : Cerebral perfusion pressure CPP = Arterial pressure - ICP accepted goal in ICU setting = 60 mmHg Herniation brain tissue forced between compartments damage to this brain further increased ICP

Consequences of herniation Local damage in herniated tissue infarction vessel compression / traction further oedema due to above nerve damage due to pressure 3rd nerve CSF entrapment - more pressure

Acute trans-tentorial herniation unilateral Medial temporal lobe forced into tentorial hiatus Third nerve palsy, pupil first mid-brain compression ipsilateral contralateral vs. opposite tentorial edge

Detail of lateral tentorial herniation

Acute trans-tentorial herniation symmetrical Diencephalon symmetrically forced into tentorial hiatus does NOT catch third nerve symmetrical decline of conscious state with posturing etc. pupils small not dilated

Symmetrical tentorial herniation

Treatment of Acutely Raised ICP Diagnose and treat concurrently ETT, hyperventilate and paralyse Mannitol (1gm/kg) CT call neurosurgeon : specific treatments : drain CSF in hydrocephalus evacuate haematoma dexamethasone for tumour oedema

Complicating factors in emergency neurosurgery B C D dilutional : low sodium E epilepsy F fever : increases ICP, metabolism

Hydrocephalus Acute vs. chronic adult vs.infant head size non-communicating vs. communicating former may be prone to rapid decline LP dangerous in former, helpful in latter

Clinical Hydrocephalic Syndromes acute hydrocephalus headache, vomiting, drowsiness, declining consciousness, papilloedema chronic hydrocephalus in child big head, headache, papilloedema, false localizing signs “normal Pressure” hydrocephalus triad of gait apraxia, incontinence, dementia may be sequel to SAH, meningitis,etc compensated hydrocephalus chronic ventriculomegaly, stabilized, asymptomatic differential includes cerebral atrophy

Causes of hydrocephalus Non-communicating : tumour esp. in posterior fossa aqueduct stenosis/blockage Arnold - Chiari malformation Communicating : congenital sludge in SA space : SAH, meningitis blocked arachnoid villi

These T1 MRI show the cyst displacing the fornices anteriorly and the subsequent hydrocephalus from the colloid cyst pushing superiorly against the foramen of Monro from within the third ventricle.

Obs. ZI…. Thomas ( 13 - 01 1992 ) At 6 yrs : headaches, drowsiness, rapid visual deterioration 24-08-1998 : OD = 4/10 OG = 2/10 CT and MRI : Craniopharyngioma Hydrocephalus 30-08-1998 : OD = 1/20 OG = 1/10 VP Shunt 02-09-1998 : OD = 3/10 OG = 2/10 03-09-1998 : Total resection of C. 18-02-1999 : OD = 1/30 OG = 0 9

Modern Management of Hydrocephalus SHUNTS ‘ COST

Treatment of hydrocephalus Treat cause if possible eg remove tumour, treat meningitis External ventricular drain if acute / infected Lumbar puncture, IF COMMUNICATING Ventriculo-peritoneal shunt - with valve Other shunts : V-Atrial, V-pleural, Lumbo- p Endoscopic 3rd ventriculostomy treatment of choice in aqueduct stenosis, 4th ventricle obstruction

Common problems with V-P shunts Blockage - early or late Infection - acute or delayed up to 6 months Over-drainage subdural hygroma/haematoma slit ventricles, small head to due to chronic effects on head growth headaches

Long term shunt survival Sigma Standard Delta 1.0 .8 Cumulative shunt survival .6 .4 p=.04 .2 1 2 3 4 5 6 Time (years) C. Sainte Rose

ETV’s may also fail

Has this person got a blocked shunt ? Headache, drowsiness, N&V GCS, eye movements, fundi Does the valve pump and refill ? Scan and compare Very closely, slice by slice The trap is interval decrease in vents after shunting, which may take 1 year, then later increase due to blockage Catheter position, disconnection (XR series) N/S Registrar

Intracranial haemorrhages Traumatic Spontaneous Extradural Y Rare Subdural Y acute/chronic Sometimes Subarachnoid Intracerebral Intraventricular

Intracerebral haemorrhage Presentation – Acute stroke, declining consciousness, seizure Cause – Aneurysm, AVM, trauma, hypertension Surgical evacuation in minority Young patients, larger lobar haematomas Cerebellar haematomas Not elderly, basal ganglia

Presentation of SAH 5 ways

Presentation of SAH sudden death sudden LOC, recovering or persisting. SUDDEN severe headache meningeal signs / symptoms lumbago, several days later

Diagnosis of SAH 2 steps

Diagnosis of SAH CT : acute blood is white LP - if and only if CT is normal best after 12 hours to allow xanthochromia experienced operator - traumatic tap problematic

Same patient, GCS 12

2 different patients

WHO Grading of SAH patients 1 : normal neurologically 2 : GCS 13-14 3 : GCS 13-14, focal cerebral signs 4 : GCS 9-12 5 : GCS < 9

Early management of SAH acute resusc, ETT and ICU if GCS < 8 Otherwise, monitor closely Immediate transfer to neurosurgery CTA, DSA, control aneurysm CONTROL BP TO PREVENT RE-BLEED Start nimodipine, control pain with small doses of narcotics Hydrallazine, clonidine Early deterioration : rebleed, hydrocephalus