CEREBROSPINAL FLUID(CSF) circulation, causes of increased ICP, Monitoring assesment and management of raised ICP

1. CEREBROSPINAL
FLUID
(CSF) circulation,
causes of increased
ICP, Monitoring
assesment and
management of raised
ICP
Dr Smita Joshi
Dr Guneet Chadha
Dr Sneha S, Dr S.N Maiti.

2. Introduction
• CSF – Clear fluid present in the
ventricles of the brain, the central canal
of the spinal cord, and the subarachnoid
space.
• CSF is produced in the brain by
modified ependymal cells in the choroid
plexus (approx. 50-70%), and the
remainder is formed around blood
vessels and along ventricular walls.

3. Functions of CSF
• Protects, lubricates the brain.
• Provides nutrients, removes waste.
Volume :- 90-150 ml adult
:- 10-60 ml in newborn
• Modulates pressure changes
(Buoyancy)
• Chemical buffer to maintain constant
ionic environment.
• Transport medium for nutrients and
metabolites, endocrine substances
and even neurotransmitter.

4. Macroscopic CSF spaces
• Two lateral ventricles
• Third ventricle
• The aqeduct of sylvius
• Fourth ventricle
• Central canal of the Spinal
cord
• Subarachnoid space
• Continuous with extracellular fluid of brain
parenchyma

5. CSF composition
• 20 ml of fluid produced every hour in
choroids plexus and reabsorbed by
arachnoid villi

6. Formation of CSF
• Choroid plexuses of lateral, third and
fourth ventricles
• Ependymal lining of ventricular system
• Pia-glial membrane
• Blood vessels
• Cells are believed to actively secrete
Na+ into the ventricular system in
exchange for K+. Sodium ions
electrically attract Cl- and osmotically
draw water from the blood vascular
system to constitute the CSF.

7. Blood-Brain Barrier (BBB)
• Physiological barrier to flow of
substances from blood to brain tissue
• The BBB functions to preserve a stable
environment for neurons of the CNS

8. Blood-Brain Barrier (BBB)

9. Brain capillary
• Tight junctions
• Surrounded by astrocytes
• Carrier mediated transport of glucose and amino
acids

10. Blood-Brain Barrier
• Lipid soluble molecules will cross easily.
• High CO2/low O2 produce vasodilation
and decrease resistance of BBB
• Injury or inflammation
decreases the resistance of BBB
(allows some antibiotics to be used for
treatment)

11. Blood CSF barrier

12. Circulation of CSF
Lateral ventricles
Interventricular foramen of Monroe
third ventricle
(aqueduct of Sylvius)
fourth ventricle
spinal cord central canal;
also, out the lateral apertures to the subarachnoid space to the venous system

14. Absorption of CSF
1. Through the arachnoid villi into the
central venous sinus and other
sinuses
2. Absorption by veins and capillaries
of CNS
3. Also along the cranial nerves into the
lymphatic channels. substantial role
in neonates as arachnoid granulations
are sparse.

15. Arachnoid granulation

16. ICP,causes of
increased
ICP,monitoring
assessment and
management of raised
ICP

17. INTRACRANIAL PRESSURE
• The cranium contains neural
tissue,blood and CSF enclosed in
duramater and bone.The pressure
within this space is reffered as
INTRACRANIAL PRESSURE.
• Normal intracranial pressure: 5-
15mmHg/ 5-20cm H2O.

18. Physiology: Monro-Kellie
Hypothesis
• The cranial vault is a rigid sturcture with a
fixed total volume,consisting of brain (80%) ,
blood (12%) and CSF fluid(8%).
• Any increase in one component must be
offset by an equivalent decrease in another to
prevent a rise in intracranial pressure.This is
Monro Kellie Hypothesis
• CPP = MAP - ICP(or CVP whichever is
greater)

19. Intracranial Compensation

20. Effects of trauma
• Increase in volume of any or all of the
intracranial components.
• Loss of autoregulation which can lead to
excessive CBF.
• Increased CSF production in response
to cerebral hyperemia

21. Effects of trauma
• Hypercapnia or hypoxia, which may
cause vasodilation and increase CBF.
• Combination of these leads to an
increase in ICP and subsequent
herniation or ischemia (focal or global).

22. • Accumulation of blood,CSF or tumour
within brain increases ICP
• Brain volume increases in head
injury,SOL,haemorrhage,severe
hypoxia.
• CBF increases whenever there is loss
of autoregulation , hypoxia, hypercarbia,
drugs(halothane)

23. • CSF increases in increased
production,decreased absorption like in
infection,absent congenital villi etc.

24. Causes of Increases ICP
• Physiological causes-coughing , sneezing,
straining during stool
• Pathological causes-
• Intracranial hemorrhage
– Traumatic brain injury
– Ruptured aneurysm
– Arteriovenous malformation
– Other vascular anomalies

25. Causes continued
• Central nervous system infections
• Neoplasm
• Vasculitis
• Ischemic infarcts
• Hydrocephalus
• Pseudotumor cerebri

26. Herniation Syndromes
Herniation results when there is a
pressure difference between the
intracranial compartments, and can occur
in four areas of the cranial cavity
– Subfalcian (1)
– Transtentorial (2)
– Foramen magnum (3)
– Retroalar

27. Symptoms
• Global symptoms of elevated ICP
–Headache
–Decreased level of consciousness
–Vomiting
• Focal symptoms-May be caused by local
effects in patients with mass lesions or
herniation syndromes
• Medullary coning

28. Symptoms
• Additional features of traumatic head injury
– Decreased level of consciousness.
– Visual changes
• Infants may present with less specific
symptoms
– Irritability
– Bulging fontanel
– Lethargy
– Poor feeding

29. Symptoms
• Nontraumatic
–Headache
• Nocturnal awakening
• Recurrent and localized
–Nuchal rigidity(kernigs and brudzinki
sign)
–Focal neurologic deficit
–Persistent vomiting.
–Lethargy

30. Presentation: Signs
• Level of consciousness
–Can range from irritability to
obtundation or coma
• Hemiparesis, hyperreflexia, and
hypertonia
• Cushing triad
–Systemic hypertension, bradycardia,
and respiratory depression

31. Presentation: Visual Signs
• Papilledema-If present
can confirm the
diagnosis.
• Retinal hemorrhages-
should raise the
suspicion of
nonaccidental head
trauma

32. Presentation:Signs
• Infants may develop
– Macrocephaly
– Split sutures
– Bulging fontanel
• Hydrocephalus
– “Sun set"
appearance of the
eyes may appear

33. Presentation: Signs
• Dilated pupil
–Usually on the
side of the
lesion
• Cranial nerve
palsies of the
third, fourth, and
sixth cranial
nerves can occur.

35. Monitoring of ICP
Lundberg first described:
• A – Plateau waves:
acute elevations 5-20min, rapid fall
amplitude 50-100mmHg
correlate with neurologic
deterioration.
• B – rhythmic variation along with
periodic breathing; freq: 0.5-2/min.
• C – rhythmic variations associated with
waves of the systemic blood pressure

36. A waves
B waves

37. Monitoring of ICP
1. Intraventricular catheter
2. Subarachnoid bolt
3. Subdural / epidural
Catheter
4. Intraparenchymal
insertion of fiberoptic
transducer.

38. Modalities for reduction of
ICP
• Hyperventilation
• Head elevation
• Osmotic agents(Mannitol)
• Fluid management
• Diuretics
• Corticosteroids
• Barbiturates
• Hypothermia
• Surgical.

39. Initial Stabilization
• The treatment of intracranial
hypertension depends upon the
condition of the patient and the etiology
• Maintenance of adequate ventilation
and blood pressure is important.

40. Initial Stabilization: Airway
• A definitive airway must be established
• Indications for endotracheal intubation
elevated ICP include:
– Refractory hypoxia
– Hypoventilation
– Glasgow coma score of 8
– Loss of airway protective reflexes
– Acute herniation requiring controlled
hyperventilation

41. Initial Stabilization: Breathing
• Ventilation should be provided as
necessary to maintain a PaCO2 in the
low- to mid-30s
–Mild hyperventilation Hypocapnia
cerebral vasoconstriction reduced
CBF decrease in CBV
decreases ICP

42. Management: Mannitol
• Establishes an osmotic gradient between
plasma and parenchymal tissue, resulting in a
net reduction in brain water content.
• Dosage - 0.25 to 0.5g/kg IV.
Disadvantages:
• Congestive cardiac failure
• Hypokalemia and hypernatremia
• Hyperosmolar state
• Renal failure due to hypoperfusion
• Exacerbation of cerebral edema

43. Loop diuretics
Furosemide
Used in conjunction with mannitol to
treat raised ICP.
Dosage:1mg/kg every 6hourly
Mechanism of action
• removing free water
• decreases CSF production
• decreases edema.
• appropriate in patients with fluid overload

44. Hypertonic saline
Mechanism of action:
• Membrane stabilising effect preserves BBB.
• Reduction of blood viscosity due to
enhancement of the intravascular volume
• Rapid absorption of cerebrospinal fluid
Complications
• Coma, seizures,CCF, Hypokalemic
acidosis,Renal failure
Dosage-Dosage of 3% saline 1-2ml/kg every
12hourly over 5 min

45. Steroids
• Dexamethasone is the most widely used
• . Mechanism of action:
1. reduction in CSF production
2. membrane stabilisation & restoration of
BBB
3. improves CSF bulk outflow at arachnoid villi
Dosage:
Dexamehtasone 10mg loading dose
followed by 4mg every 6hourly

46. Management: Barbiturates
• Pentobarbital most commonly used.
• Works by decreasing the cerebral
metabolic rate reduction in CBF
decreases ICP

47. Management: Hypothermia
• Controlled hypothermia(32-35deg C)
has been shown to help reduce ICP in
some patients with refractory
intracranial hypertension and may
improve outcome

48. Management: Glycemic Control
• Both hyperglycemia and hypoglycemia
have been associated with poor
outcomes
• Hyperglycemia is treated with insulin and
avoidance of excessive use of dextrose-
containing intravenous fluids
• Hypoglycemia can adversely affect
infants and children who have smaller
glycogen stores

49. Management: CSF Drainage
• In cases of uncontrolled intracranial
hypertension, an intracranial drain can
be placed to remove CSF and monitor
ICP
• External drainage(ventriculostomy)
• Internal Drainage
-ventriculoperitoneal shunt
-ventriculoatrial shunt

50. Operative decompression
• Internal decompression:
Usually temporal or sometimes frontal
lobectomy.
• External decompression:
Decompressive craniotomy and
duroplasty

51. Suspected raised ICP
GCS <8
Sedate, paralyse, intubate, hyperventilate
Elevate head end 300
CT scanSurgery
if operable lesion
Nonoperative lesion
ICP Monitor
Ventricular CSF drainage
Osmotherapy
Barbiturate
Surgical options:
Decompressive craniectomy
Lobectomy

52. THANK YOU