Disturbances of Intra-Cranial Pressure (ICP) and Hydrocephalus

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

2. 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

3. 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

4. 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

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

7. Papilloedema

8. 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

9. 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

11. 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

12. 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

15. 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

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

19. Detail of lateral tentorial herniation

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

24. Symmetrical tentorial herniation

29. 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

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

31. 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

32. 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

33. 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 • congenital

35. 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

36. Modern Management of Hydrocephalus SHUNTS ‘ COST

37. 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

38. 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

40. Long term shunt survival Sigma Standard Delta 1.0 .8 Cumulative shunt survival .6 .4 p=.04 .2 0 1 2 3 4 5 6 Time (years) C. Sainte Rose

42. ETV’s may also fail

43. 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

44. Intracranial haemorrhages

45. 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

46. Presentation of SAH • 5 ways

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

48. Diagnosis of SAH • 2 steps

49. 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

50. Same patient, GCS 12