1. Raised Intracranial Pressure
03/05/12
Jeremy Kam
Intern
Royal Melbourne Hospital

2. Overview and Objectives
Basic Principles
Review Basic Anatomy of Skull and Spinal Cord
Review Basic Physiology of CSF production and flow
Monro Kellie Doctrine and concepts of CBF and CPP
Conceptualising ICP
Spectrum of Intracranial Pressure
Causes of Raised ICP
Assessment of Raised ICP
Symptoms
Signs and basic examination techniques
Investigating ICP
Management
Monitoring
Treatment

3. Contents of the Skull and the Monro Kellie Doctrine
1. Skull is a rigid box: The volume inside the cranium is a fixed volume (nearly). 2. The cranial contents incompressible (nearly) 3. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another

4. FIXED BOX: SKULL/SPACE

5. 1. BRAIN

6. 2. CSF

7. 3. BLOOD

8. Intracranial Volume

9. Intracranial pressure
“Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF).”
Constantly changing: exercise, coughing, straining, respiratory cycle
ICP normal values
Age Group
Normal Range (mmHg)
Adults and older children
< 10-15
Young Children
3-7
Term Infants
1.5-6
Standing

10. INTRACRANIAL PRESSURE VS INTRACRANIAL VOLUME

12. INTRACRANIAL PRESSURE VS INTRACRANIAL VOLUME

13. CEREBRAL PERFUSION PRESSURE
CPP = MAP – ICP
CEREBRAL PERFUSION PRESSURE = MEAN ARTERIAL PRESSURE – INTRACRANIAL PRESSURE
Why do we care?
Brain survival depends on cerebral blood flow meeting cerebral metabolic requirements
Cerebral blood flow depends on Cerebral Perfusion Pressure
CPP depends upon ICP
Normal CPP > 50 mmHg

14. Cerebral Blood Flow

15. INTRACRANIAL HYPERTENSION (finally)
What happens if ICP is too high?
CPP = MAP – ICP
As ICP increases. Where MAP is constant. CPP will decrease.
Ideally CPP > 70-80mmHg
This is bad.
IC-HTN = ICP >20mmHg for >10 minutes
Increased ICP  Decreased CPP  Decreased CBF
MAP will compensate for awhile.
CBF = CPP/CVR

16. Intracranial Hypertension
Why do we care?
Raised ICP may CAUSE problems itself e.g herniation, decrease in cerebral perfusion ischemia  edema
Raised ICP may be a SIGN of problems being caused e.g mass effect; tumour, haemorrhage

17. CAUSES OF RAISED ICP

18. SPECTRUM OF Raised ICP ACUTE VS CHRONIC SEVERE VS MILD
SYMPTOMS AND SIGNS from raised ICP
SYMPTOMS AND SIGNS from CAUSE of raised ICP
E.g:
Acute Traumatic Intracranial Haemhorrhage  Mass Effect Vs
Neoplasm causing Mass effect

19. CAUSES OF RAISED ICP

20. Intracranial Haemhorrages
Subdural Hematoma
Epidural Hematoma
Intracerebral Haemorrhage
Subarachnoid Haemorrhage
Cerebral Contusion

21. Space occupying Lesion
Brain Abscess:
Develop as a result of a localized bacterial cerebritis followed by necrosis and encapsulation
Mechanisms:
– Haematogenous
– Extension from neighbouring structures
– Penetrating injuries
Symptoms of infection may be absent in 50% of cases
Treatment: Excision drainage

22. Hydrocephalus
1 Obstructive hydrocephalus – obstruction from lesion along ventricle system. E.g tumor, colloid cyst, primary stenosis. 2 Communicating hydrocephalus - (a) obstruction to flow of CSF through the basal cisterns or (b) failure of absorption of CSF through the arachnoid granulations over the cerebral hemispheres. The most common causes of communicating hydrocephalus are infection (especially bacterial and tuberculous) and subarachnoid haemorrhage (either spontaneous, traumatic or postoperative). Treatment: Ventriculoperitoneal Shunt, 3rd Ventriculostomy

23. Traumatic Brain Injury

24. Cerebral Oedema
Middle cerebral artery occlusion causing extensive infarction with mass effect. The appearances after decompressive craniotomy are shown in the third panel.

25. SYMPTOMS and Signs 1. Decreased LEVEL OF CONSCIOUSNESS - DROWSINESS
MOST IMPORTANT
never put down to simple sleepiness – measure Glasgow Coma Scale
Requires serial assessment  Progressive decrease in GCS = worsening ICP state
2. Altered MENTAL STATUS
Confusion, restlessness, lethargy, difficulty thinking,
3. HEADACHE
Frontal, worse after lying down, Relieved by vomiting, Severe, Worse with coughing and straining
4. NAUSEA and VOMITING
Persistent
5. VISUAL CHANGES
Pupillary Dysfunction
Changes in Vision
VI nerve Palsy – false localising sign
Papilloedema - requires more than 24 hours

26. Glasgow Coma Scale

27. Abducens Palsy

28. Papilloedema Venous engorgement (usually the first signs)
loss of venous pulsation
hemorrhages over and / or adjacent to the optic disc
blurring of optic margins
elevation of optic disc
Paton's lines = radial retinal lines cascading from the optic disc

29. PROGRESSION OF SIGNS
Continuous DECREASE in GCS  stuporous comatose  difficulty to arouse
VISUAL CHANGES
Pupils become unilaterally enlarged progressing to fixed and dilated – eventually bilaterally fixed and dilated
Papilloedema
NEUROLOGICAL FUNCTION
Decorticate or Decerebrate Posturing
Loss of corneal and gag reflexes
Hemiplegia –that progresses
VITAL SIGNS
Bradycardia
Increasing Hypertension – with widening pulse pressure
Irregular Respiration – neurogenic Hyperventilation
Respiratory arrest
Cushing's Triad
Hyperthermia
SIGNS OF BRAIN HERNIATION

31. Cushing’s TRIAD HYPERTENSION (Widening Pulse Pressure) BRADYCARDIA
seen in 33% of IC-HTN
HYPERTENSION (Widening Pulse Pressure)
BRADYCARDIA
RESPIRATORY IRREGULARITY
INDICATES IMPENDING HERNIATION

32. BRAIN HERNIATION Syndromes
Transtentorial:
Foramen Magnum
Subfalcine

33. Severity and indications
Indications for Treatment:
ICP ≥ mmHg as the upper limit. Initiate Treatment for ICP > 20 mmHg – in combination with clinical exam and brain CT findings.
Herniation can still occur at ICP < 20
Higher mortality and worse outcomes among patients with ICP persistently >20 compared to < 20.
CPP Targets:
Avoid CPP < 50mmHg
Initiate treatment when CPP falls below 60mmHg

34. LUMBAR PUNCTURE IS CONTRAINDICATED
INVESTIGATIONS
LUMBAR PUNCTURE IS CONTRAINDICATED
CT Brain
MRI Brain
Biopsy
Angiography
Transcranial Doppler Flow Velocity

35. MANAGEMENT - MONITORING
Indications for ICP Monitoring:
CT CRITERIA:
For salvageable patients with severe traumatic brain injury – GCS ≤ 8 after cardiopulmonary resuscitation
Abnormal admitting brain CT (60% risk of IC-HTN) or
Normal brain CT but with ≥2 risk factors (=60% risk of IC –HTN vs 13% r.f -ve):
Age >40 years
SBP < 90 mmHg
Decerebrate or decorticate posturing on motor exam – unilateral or bilateral
Neurological criteria – where GCS ≥ 9 – low risk for IC-HTN – serial neurological exam
Multiple system injury – where ICP likely to be effected by interventions e.g large volume IV fluids, PEEP
Traumatic IC Mass – EDH, SDH, depressed skull fracture
Post Op – may elect
Non-traumatic
Contraindications to ICP monitoring: “awake” patient, coagulopathy

36. INVASIVE ICP Monitoring
Intraventricular Catheter – IVC
Most accurate, allows therapeutic CSF drainage
May be difficult to insert into compressed or displaced ventricles, may obstruct
Intraparenchymal monitor
Subarachnoid Screw (bolt)

37. MANAGEMENT 1. MAINTAIN CEREBRAL PERFUSION PRESSURE by LOWERING ICP
Reduce size of brain VOLUME by decreasing cerebral volume, CSF fluid volume, or blood volume while maintaining cerebral perfusion
Make more SPACE – e.g surgical decompression
GOAL ICP <20 mmHg and CPP > 50mmHg
2.DECREASE METABOLIC DEMANDS
3. PREVENT COMPLICATIONS
GI risk of developing Cushing stress ulcers and GI bleeding. Give PPIs and H2 antag.
Fluid and electrolytes – diabetes inspidus - desmopressin. Close monitoring of electrolytes.
Hematological – DIC can occur after severe head injury. Coagulopathies aggressively treated FFP and Vit K 10mg a daily.
Nutrition
4. IDENTIFY CAUSE – TREAT
e.g remove space occupying lesions, insert VP shunt

38. BLOOD VOLUME ↓ ICP via ↑ Venous Outflow
Elevation of Head of Bed degrees
optimised trade off between promoting Venous Outflow vs Reducing MAP
Keep Neck Straight Midline, avoid tight trach tape
Maintain CPP with Normotension
Avoid Hypotension (SBP < 90 mm Hg) Achieved via normalising intravascular volume. Use of pressors if needed.
Control hypertension if present, Nitroprusside if nil tachy vs beta blocker if tachy
Hyperventilation
May be necessary for brief periods when acute neurologic deterioration. Do not use prophylactically. Short term.
Ventilate to NORMOcarbia PaCO2 = 35-40mmHg)
Avoid Hypoxia (PaO2 < 60mmHg or sat 90%) – maintain airway and oxygenation ↓O2 = bad

39. BRAIN VOLUME OSMOTIC AGENTS EUVOLEMIA CORTICOSTEROIDS
Mannitol - Effects occur within 20 minutes; does not cross intact blood-brain barrier; observe for rebound ICP; gm/kg IV over 24h
Frusemide 10-20mg IV q6 hours. PRN ICP > 20.
Hypertonic Saline - When refractory to mannitol – 3% saline infusion or bolus – if serum osmolarity greater than 320 – hold no more benefit
EUVOLEMIA
CORTICOSTEROIDS
Decreases cerebral edema in brain tumors
Reduce CSF production, stabilize blood-brain barrier and cell membranes -> overall improvement of neuronal function
Dexamethasone

40. CSF VOLUME
Drain CSF
Ventriculostomy – Pliable catheter inserted into lateral ventricle on nondominant side
Can remove CSF intermittently or continuously
Removal of even small amount will dramatically decrease ICP
Shunts

41. DECREASING METABOLIC DEMAND
TEMPERATURE CONTROL
Antipyretic medications, cooling blanket
SEIZURE CONTROL
Phenytoin: mg/kg; not to exceed 50 mg/min
Diazepam: 5-10 mg bolus at 2 mg/min
Barbiturates (Pentobarbital & thiopental) when not responsive to conventional therapy
SEDATION
Paralyzing agents; CV monitoring; endotracheal intubation; mechanical ventilation; ICP monitoring; arterial pressure monitoring
Reduce sympathetic tone
ENVIRONMENT
dark room – free from noise minimise stimulus.

42. SURGICAL MANAGEMENT Decompressive Craniectomy
Considered for IC-HTN refractory to medical treatment.
Surgical Mx of subdural, epidural or intraparenchymal hematoma.