CSF & ICP Flashcards

1
Q

How is CSF produced?

A

From arterial blood by the choroid plexus of the lateral and 4th ventricles

Combined process of diffusion, pinocytosis and active transfer

Small amount also produced by ependymal cells

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2
Q

What is CSF volume? How much is produced and at what rate?

A

Adult ~140ml with about 25ml in ventricles

Produced at rate of 0.2-0.7ml/min (600-700ml daily).

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3
Q

How is CSF circulated and absorbed?

A

Circulation aided by pulsations of choroid plexus and by motion of the cilia of ependymal cells

Absorbed across the arachnoid villi into the venous circulation. The foramina in the 4th ventricle connect to the subarachnoid space around the spinal cord

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4
Q

Name some of the functions of the CNS

9 listed in the book

A
  1. Buoyancy (brain weight reduced >95% - reduces shearing / tearing forces on neural tissue)
  2. Adjustment of intracranial volume (Monro-Kellie doctrine)
  3. Micronutrient transport (e.g. nucleosides, pyramidines, vitamin C): choroid plexus → CSF → brain cells
  4. Protein & peptide supply (macromolecules e.g. transthyretin, insulin-like growth factor, thyroxine)
  5. Buffer reservoir: if brain interstitial tissue fluid concs of H+, K+, glucose altered - ventricular fluid can buffer extracellular fluid changes
  6. Sink / drainage: Clears anion metabolites of NTs, protein products of catabolism / tissue breakdown + xenobiotic substances from CNS (active transporters in choroid plexus, or by bulk CSF drainage to venous blood / lymphatics)
  7. Immune mediation (cells adjacent to ventricles have antigen presenting capabilities - some CSF proteins drain into cervical lymphatics with potential for inducing antibody reactions)
  8. Information transfer: NT agents (e.g. amino acids, peptides) may be transported over distances to bind receptors in the parasynaptic mode)
  9. Drug delivery: some do not readily cross BBB but can be transported into CSF by endogenous proteins in choroid plexus epithelial membranes
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5
Q

What are the normal characteristics of CSF you would expect to see in clinical testing?

A

Crystal clear

Opening pressure of 80-180 mmH2O

Up to 5 mononuclear cells, 0-5 red blood cells

Glucose 60-70% of plasma values

Protein <500mg/dl and lower in ventricles

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6
Q

What can cause abnormalities in CSF pressure / volume?

A

Hydrocephalus

Idiopathic intracranial hypertension

Space occupying lesions / cerebral oedema / haemorrhage

Dural venous sinus thrombosis

CSF hypotension

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7
Q

Name six possible abnormalities in CSF constituents

A
  1. Raised white cells (meningitis, encephalitis, reactive to neoplastic involvement, autoimmune disorders, sarcoidosis)
  2. Raised red cells (traumatic tap, SAH)
  3. Low glucose (hypoglycaemia, meningitis, mumps and lymphocytic choriomeningitis infections, SAH, sarcoidosis)
  4. Raised protein (inflammatory conditions, infection, CSF block, neoplasms)
  5. Neoplastic cells (primary or metastatic, up to 3 attempts at lumbar puncture may be required to detect the abnormal cells)
  6. Oligoclonal bands (CNS myelination, not specific)
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8
Q

Name some SPECIFIC diagnostic tests that can be performed on CSF

A

TPPA (syphilis)

14-3-3 protein and S100 (sporadic or variant CJD)

Positive viral PCR (meningitis)

Positive Borrelia serology (Lyme)

Positive JC virus PCR (progressive multifocal leukoencephalopathy - PML)

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9
Q

Lumbar puncture is indicated if patients have symptoms consistent with which diseases?

A
  1. CNS infections (meningitis or encephalitis secondary to bacterial / TB, viral, fungal, protozoal and helminthic pathogens)
  2. SAH
  3. Inflammatory / Demyelinating CNS diseases: MS, sarcoidosis
  4. Inflammatory neuropathies (GBS, chronic inflammatory demyelinating polyneuropathy - CIDP)
  5. Idiopathic intracranial hypertension
  6. Unexplained pyrexia with neurological symptoms (particularly children)
  7. Malignant infiltration of meninges: leukaemia, metastatic melanoma
  8. Certain metabolic or degenerative diseases of the brain or spinal cord, inborn errors of metabolism
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10
Q

In what situations in brain imaging indicated prior to performing a lumbar puncture?

A

Symptoms (e.g. reduced consciousness) or signs (e.g. optic disc swelling) of significantly increased intracranial pressure, or focal neurological findings

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11
Q

In addition to diagnosis, what other indications are there for lumbar puncture?

A

Management of idiopathic intracranial hypertension

Administering intrathecal chemotherapeutic agents / antibiotic therapy

Measurement of pressure or lumbar infusion testing in hydrocephalus

Monitoring CSF pressure in patients with dural venous sinus thrombosis

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12
Q

When is LP contraindicated?

A

Evidence of raised intracranial pressure or focal neurological findings unless the risk of brain herniation has been excluded by cerebral imaging (note: all focal lesions do NOT automatically contraindicate lumbar pressure)

Soft tissue infection over lumbar spine area

Coagulopathy (INR >1.5) or thrombocytopenia (platelets <50,000/mm³)

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13
Q

(Info about performing lumbar puncture)

A

(Consider adding this - skip for now)

horizontal lateral decubitus position, perpendicular to be, apex of pelvic bone indentified - visualise direct to spine,

cord ends at L1-2, puncture spaces between posterior elements of 3-4 or 4-5.

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14
Q

What are the three main volumes within the skull?

A

CSF 150ml

Blood 150ml

Brain 1200ml

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15
Q

According to the Monroe-Kellie doctrine, what is compensation?

A

Brain can compensate for: expanding mass (tumour, abscess, haematoma). increased CSF (hydrocephalus), increased blood (outflow obstruction), or increased brain (oedema), by:

  • Reducing CSF volume
  • Then blood volume (initially venous then arterial)
  • To some extent brain volume (reduced ECF)
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16
Q

According to the Monroe-Kellie doctrine, what is DECOMPENSATION?

A

Eventually, further small increments in volume produce larger and larger increments in intracranial pressure

17
Q

How is cerebral blood flow calculated?

How is cerebral perfusion pressure calculated?

A

CBF = CPP (perfusion pressure) / CVR (vascular resistance)

CPP = MAP - ICP

Physiological range of CPP is 60-160mmHg

18
Q

As ICP rises, how is cerebral blood flow maintained?

A

CPP is controlled by ICP + MAP

CVR is controlled by autoregulation + chemoregulation

19
Q

How does autoregulation occur?

A

Cerebral perfusion pressure increases → arterial wall tension increases → detected by vascular smooth muscle which contracts → vessel diameter reduced → cerebral vascular resistance increases → blood flow reduced

If BP drops the opposite occurs (ensures CBF constant over physiological range of CPP - 60-160mmHg)

20
Q

How does chemoregulation occur? Why can this be problematic?

A

Mainly by pCO₂ - also pH, metabolic waste products and pO₂ (only if <50kPa i.e. periarrest)

Physiological response can lead to problems, as all are markers of hypoxia and hence increase vessel diameter with intention of increasing blood flow - however also causes increased ICP which can be detrimental

21
Q

How does chemoregulation affect clinical approach to raised ICP?

A

Clinically, can decrease pCO2 (which will reduce vessel diameter) and reduce the ICP, however this will increase CVR and therefore reduce CBF.

Ultimately: can have good ICP or good CBF - NOT both

Optimal pCO2 currently considered 4.5kPa in patient with raised ICP

22
Q

What are signs + symptoms of raised ICP?

A

Headache: mornings, lying flat, coughing, stooping

Vomiting

Papilloedema: takes time to establish and to disappear

Reduced GCS

Cushings response (↑BP ↓HR) - limited use as late sign and always already comatose!

23
Q

What are the 4 main herniation syndromes?

A
  1. SUBFALCINE: occurs early with unilateral SOLs. Rarely produces any clinical effects, although ipsilateral ACA occlusion has been recorded.
  2. LATERAL TENTORIAL (UNCAL): medial temporal lobe herniates under tentorium cerebelli (through the tentorial hiatus):
  3. CENTRAL TENTORIAL: progression from lateral tentorial herniation as ICP continues to rise. Midline lesion or diffuse swelling of hemispehres causes vertical displacement of midbrain and diencephalon through tentorial hiatus. Damage to these structures due to mechanical distortion or ischaemia secondary to stretching of perforating vessels.
  4. TONSILLAR: cerebellar tonsils through foramen magnum (caused by subtentorial expanding mass - degree of upward herniation through hiatus may also occur). Clinical effects difficult to distinguish from direct brainstem / midbrain compression.
24
Q

Which structures can be affected in a lateral tentorial (uncal) herniation?

A
  • Cerebral peduncle (against Kernohan’s notch: weakness, false localising signs)
  • Occulomotor nerve (ipsilateral fixed and dilated pupil, ptosis and impaired eye movement, but in coma)
  • PCA (homonymous hemianopia)
25
Q

Why must imaging be performed in unconscious patient before performing LP?

A

In context of raised ICP, may create pressure gradient and lead to tonsillar herniation. Therefore, CT first.

26
Q

How can raised ICP be managed clinically?

A

Removal of mass lesion (unless technically possible or prognosis dismissal)

  1. Head up: improves venous drainage and reduces ICP (30° optimal balance between venous drainage and CPP) . Ensure no neck constriction
  2. Sedation (reduces O2 consumption) - PROPOFOL initially when muscle relaxants (extreme cases - thiopentone). Hyperventilation: reduce pCO2 to 4.5kPa. Note: effect is only temporary!
  3. Mannitol: temporary effect only, for buying time until definitive treatment (surgery), start 100ml 20% mannitol (can give 1g/kg i.e. 350ml for 70kg man)
  4. Ventricular drain: reduces CSF volume + ICP
  5. Decompression: in absence of focal lesion can consider surgery in extremis - large section of skull removed, circumvents Munroe-Kellie doctrine
27
Q

Are steroids used for raised ICP?

A

Not anymore - evidence shows risks outweigh benefits

28
Q

Which structures can be affected in a central tentorial herniation?

A
  • midbrain (reduced GCS, small fixed pupils)
  • tectum (loss of upward gaze - seen in hydrocephalus)
  • pituitary stalk (SIADH)
29
Q

Which structures can be affected in a tonsillar herniation?

A

Cerebellar tonsils though foramen magnum

Brainstem - reduced GCS, reduced respiration, neck stiffness, tilt

Note: LP in setting of raised ICP may create pressure gradient and lead to tonsillar herniation - CT must be performed in unconscious patient before performing LP

30
Q

How to treat raised ICP?

A

Removal of mass lesion unless technically not possible or dismal prognosis

Head up - 30 degree optimal balance between venous drainage and CPP, ensure no constriction of neck

Sedation - reduces O2 consumption, initially propofol then muscle relaxants, in extreme cases thiopentone
Hyperventilation: reduce pCO2 to 4.5kPa, only temporary effect

Mannitol - complex actions, temporary effect, buy time until surgery - start 100ml 20% mannitol (can give 1g/kg i.e. 350ml for 70kg man)

Steroids no longer used, evidence shows risks > benefits

Ventricular drain - reduces CSF volume and ICP

Decompression: in absence of focal lesion can consider surgery in extremis, large section of skull removed, circumvents Monro-Kelly doctrine