CSF ANALYSIS

1. CSF

4. FORMATION
• Cerebrospinal fluid (CSF)
• produced by the choroid plexus in the lateral, third, and fourth ventricles
• by both filtration and active transport
• 50–70% of the CSF
• the remainder is formed around blood vessels and along the ventricular walls
• approximately 20 mL per hour
• 550 mL/d.
• circulates through the subarachnoid space between the arachnoid mater and
the pia mater
• The CSF is propelled along the neuroaxis by a cranio-caudal pulsatile wave
induced by flow in the cerebral arteries and by the associated expansions of
the vascular compartment in the cranial vault

5. • CSF turns over about 3.7 times
a day

8. • At a pressure of 112 mm H2O,
• which is the average normal CSF pressure, formation and absorption are
equal
• external hydrocephalus, communicating hydrocephalus.
• Below a pressure of approximately 68 mm H 2 O, absorption stops.
Large amounts of fluid accumulate when the capacity for CSF reabsorption
is decreased

9. internal hydrocephalus, non communicating
hydrocephalus
• Fluid also accumulates proximal to the block and distends the
ventricles when the foramens of Luschka and Magendie are blocked
or there is obstruction within the ventricular system

11. Reabsorption of CSF
• CSF is reabsorbed in the arachnoid villi, located along the superior
sagittal and intracranial venous sinuses and around the spinal nerve
roots.
• Each arachnoid villus functions as a one-way valve permitting
unidirectional flow of CSF into the blood. Arachnoid villi and venous
sinuses are separated by endothelial cells connected by tight
junctions .
• Arachnoid villi normally allow the passage of particles less than 7.5
micron in diameter from the CSF into the blood.

12. The villi consist of projections of the fused arachnoid
membrane and endothelium of the sinuses into low
pressure venous sinuses. Similar, smaller villi project
into veins around spinal nerve routes. These
projections may contribute to the outflow of CSF into
venous blood by a process known as bulk
flow, which is unidirectional

13. • Arachnoid villi normally allow the passage of particles less than 7.5
micron in diameter from the CSF into the blood.
• Movement of CSF and cellular components across arachnoid villi
occurs via transport within giant vesicles. These vesicles may become
obstructed by bacteria or cells as a result of an inflammatory process
or by red blood cells during subarachnoid haemorrhage

14. • Lipid-soluble molecules or drugs readily diffuse across the vascular
endothelium and epithelium of the choroid plexus into the interstitial
fluid and CSF.
• In contrast, ionically charged molecules generally require active
transport for entry into the CSF.

15. CSF PRESSURE
• Cerebrospinal fluid (CSF) secretion and reabsorption remain in
balance in most healthy individuals
• The normal CSF pressure as measured with a manometer in a patient
lying flat in the lateral decubitus position with the legs extended is
between 60 and 250 mm H20
• ICP is normally ≤15 mmHg in adults, and pathologic intracranial
hypertension (ICH) is present at pressures ≥20 mmHg

17. Causes of intracranial hypertension
• Central nervous system infections (eg, encephalitis, meningitis, abscess)
• Ischemic stroke
• Neoplasm
• Vasculitis
• Hydrocephalus
• Hypertensive encephalopathy
• Idiopathic intracranial hypertension (pseudotumor cerebri)
• Traumatic brain injury/intracranial hemorrhage
• Subdural, epidural, or intraparenchymal hemorrhage
• Ruptured aneurysm
• Diffuse axonal injury
• Arteriovenous malformation or other vascular anomalies

19. monro kellie doctrine

20. • Because brain tissue and spinal fluid are essentially
incompressible, the volume of blood, spinal fluid, and brain in the
cranium at any time must be relatively constant (Monro-Kellie
doctrine).
• More importantly, the cerebral vessels are compressed whenever
the intracranial pressure rises. Any change in venous pressure
promptly causes a similar change in intracranial pressure. Thus, a rise
in venous pressure decreases cerebral blood flow both by
decreasing the effective perfusion pressure and by compressing
the cerebral vessels. This relationship helps compensate for
changes in arterial blood pressure at the level of the head

21. The relationship between intracranial volume
and pressure is nonlinear
initial increase in volume results in a small increase in
pressure because of intracranial compensation (blue
line). Once intracranial compensation is exhausted,
additional increases in intracranial volume result in a
dramatic rise in intracranial pressure (red line).

22. Cerebral blood flow
• The average cerebral blood flow in young adults is 54 mL/100
g/min

24. • CBF = (CAP - JVP) ÷ CVR
• where CAP is carotid arterial pressure, JVP is jugular venous pressure, and
CVR is cerebrovascular resistance.

25. Cerebral blood flow (CBF) determines the
volume of blood in the intracranial space. CBF
increases with hypercapnia and hypoxia.

26. In both groups, initial increases or decreases in mean
arterial pressure are associated with maintenance of
cerebral blood flow due to appropriate changes in
arteriolar resistance. More marked changes in pressure
are eventually associated with loss of autoregulation,
leading to a reduction (with hypotension) or an elevation
(with marked hypertension) in cerebral blood flow. These
changes occur at higher pressures in patients with
hypertension, presumably due to arteriolar thickening.
Thus, aggressive antihypertensive therapy will produce
cerebral ischemia at a higher mean arterial pressure in
patients with underlying hypertension.

27. Cerebral perfusion pressure (CPP)
• Cerebral perfusion pressure (CPP) is a clinical surrogate for the
adequacy of cerebral perfusion. CPP is defined as mean arterial
pressure (MAP) minus ICP.
• CPP = MAP - ICP

28. • Conditions associated with elevated ICP, including mass lesions and
hydrocephalus, can be associated with a reduction in CPP. This can
result in devastating focal or global ischemia.
• On the other hand, excessive elevation of CPP can lead to
hypertensive encephalopathy and cerebral edema due to the
eventual breakdown of autoregulation, particularly if the CPP is >120
mmHg
• A higher level of CPP is tolerated in patients with chronic hypertension
because the autoregulatory curve has shifted to the right

32. CF
HEADACHE probably mediated via the pain fibers of cranial nerve
(CN) V in the dura and blood vessels
IMPAIRED GLOBAL CONSCIOUSNESS due to either the local effect of mass lesions or
pressure on the midbrain reticular formation, and
vomiting
Signs include CN VI palsies, papilledema secondary to impaired axonal transport and
congestion
Triad of bradycardia, respiratory depression, and
hypertension
(Cushing triad, sometimes called Cushing reflex or
Cushing response)
Focal symptoms of elevated ICP • ocal effects in patients with mass lesions or by
herniation syndromes

33. Papilledema, characterized by blurring of the optic
disc margins, loss of physiologic cupping,
hyperemia, and fullness of the veins

34. • Herniation results when pressure gradients develop between two
regions of the cranial vault.
• The most common anatomic locations affected by herniation
syndromes include subfalcine, central transtentorial, uncal
transtentorial, upward cerebellar, cerebellar tonsillar/foramen
magnum, and transcalvarial

35. Downward and backward shifting of the
cerebrum and brainstem may occur when
intracranial hypertension develops, resulting
in either respiratory depression and/or death
due to herniation of the cingulate gyrus, the
uncus of the temporal lobe, or the cerebellar
tonsils.

36. Indications FOR RX OF raised ict
• history that suggests elevated ICP (eg, head trauma, sudden severe
headache typical of subarachnoid hemorrhage)
• suggests elevated ICP (unilateral or bilaterally fixed and dilated
pupil[s], decorticate or decerebrate posturing, bradycardia,
hypertension and/or respiratory depression)
• Glasgow Coma Scale (GCS) ≤8

37. • standard resuscitation techniques should be instituted as soon as
possible
• Head elevation
• Maintain euvolemia
• Avoid hypovolemia and hypotension
• Hyperventilation to a PCO2 of 26 to 30 mmHg
• Osmotic therapy and diuresis
• Intravenous mannitol (1 to 1.5 g/kg)
• AVOID HYPOVOLEMIA
• HYPOVOLEMIA AGGRAVATE ISCHEMIC BRAIN INJURY
• Furosemide, 0.5 to 1.0 mg/kg intravenously, may be given with mannitol to potentiate
its effect
• Decompressive craniectomy

38. • Isotonic saline
• Best solution
• Slightly hypertonic 308mOsm/L with respect to plasma 285 mOsm/L
• Does not calcium

39. AVOID HYPOTTONIC FLUID &
HYPOOSMOLALITY
• HYPOOSMOLALITY  INDUCE OR AGGRAVATE CEREBRAL EDEMA
AVOID
5% DEXTROSE • Hypoosmalaity
• Ability to cause hyperglycemia
RL • Hypotonic
• Contains ca2+ reperfusion injury

42. Hyperventilation

43. Fluid management
• Patients should be kept euvolemic and normo- to hyperosmolar
• achieved by avoiding all free water (including D5W, 0.45 percent [half
normal] saline, and enteral free water) and employing only isotonic
fluids (such as 0.9 percent [normal] saline).
• Serum osmolality should be kept >280 mOsm/L, and often is kept in the 295
to 305 mOsm/L range.
• Hyponatremia is common in the setting of elevated ICP, particularly in
conjunction with subarachnoid hemorrhage

44. Avoid hyperglycemia
• Hyperglycemia in the immediate period after stroke (in patients with
nonlacunar stroke a/w increased morbidity & mortality
• ENHANCES BRAIN INJURY
• DISRUPTS BBB
• INCREASED CEREBRAL EDEMA
• CAUSE HAEMORRHAGIC TRANSFORMATION OF INFARCT
• AVOID HYPERGLYCEMIA
• FIRST 24 HRS FOR ANT CIRCULATION STROKE
• FIRST 72 HRS IN POST CIRCULATION STROKE
EVOLUTION OF STROKE
OCCURS DURING THIS
PERIOD

45. HYPERGLYCEMIA
AT TIME OF
STROKE 
DTERMINE
SEVERITY
IMMEDIATE POST STROKE PERIOD
DETERMINES EXTENSION OF
STROKE

46. • there are actually two barriers:
• blood-brain barrier and
• blood-CSF barrier.
• Both barriers separate the central nervous system (CNS) from
systemic immune responses and affect the composition of the brain
interstitial fluid and CSF.

47. Blood brain barrier
• The blood-brain barrier controls the content of
brain interstitial fluid. It has a 5000-fold greater
surface area than the blood-CSF barrier . The
anatomic basis for the blood-brain barrier is a
series of high-resistance, tight junctions
between endothelial cells as well as astrocytes
with processes that terminate in overlapping
fashion on capillary walls.
• Lipid-soluble small molecules with a molecular
mass less than 400 to 600 Da are transported
readily through the blood-brain barrier. In
contrast, many drugs and other small molecules
cannot cross this barrier system

48. Blood-CSF barrier
• The blood-CSF barrier controls the composition of the CSF, which, as
noted above, is primarily dependent upon secretion in the choroid
plexus. The blood-CSF barrier is formed by tight junctions between
choroid epithelial cells.

50. LUMBAR PUNCTURE

51. INDICATIONS
DIAGNOSTIC THERAPEUTIC
Urgent ●Suspected CNS infection (with the
exception of brain abscess or a
parameningeal process).
●Suspected SAH in a patient with a
negative CT scan
• Spinal anesthesia
• Intrathecal administration of chemotherapy
• Intrathecal administration of antibiotics
• Injection of contrast media for myelography or for
cisternography
Nonurgent ●Idiopathic intracranial hypertension
(pseudotumor cerebri)
●Carcinomatous meningitis
●Tuberculous meningitis
●Normal pressure hydrocephalus
●CNS syphilis
●CNS vasculitis

52. CONTRAINDICATIONS
• Possible raised intracranial pressure (ICP) with risk for cerebral
herniation
• Thrombocytopenia or other bleeding diathesis, including ongoing
anticoagulant therapy
• Suspected spinal epidural abscess

53. COMPLICATIONS
• Post-LP headache
• Infection
• Bleeding
• Cerebral herniation
• Minor neurologic symptoms such as radicular pain or numbness
• Late onset of epidermoid tumors of the thecal sac
• Back pain

54. COMPOSITION OF THE CSF

55. Total volume: 150 ml
Opening pressure: 70-180 mm of water
Appearance: Clear and colorless with no clots
(viscosity similar to water)
Cells Adults: 0-5 cells/cmm
Glucose 45-80 mg/dl. (Normally CSF glucose is 60%
or 2/3rds of blood glucose)
Proteins: 15-45 mg/dl. (Normally CSF proteins are
1% of plasma proteins)
Oligoclonal bands: Negative
Chloride: 120-130 mEq/L (20 mEq/L more than
serum level)
BILIRUBIN ABSENT

57. Turbid CSF
• – Leukocytes >200 cells/cmm
• – Red cells >400 cells/cmm
• – Microorganisms like bacteria, fungi, or amebae
• – Radiographic contrast media
• – Aspiration of epidural fat during LP
• – Raised proteins.

58. Blood-mixed CSF
• CSF will appear grossly bloody if ≥6000 RBCs/microL are present

59. XANTHOCHROMIA
• increased CSF concentrations of
protein (≥150 mg/dL) or
• systemic hyperbilirubinemia (serum
bilirubin >10 to 15 mg/dL)
• SAH AFTER 12 HOURS OF BLEEDING
• FROINS SYNDROME

60. Froin's syndrome
• Froin's syndrome is a combination
of xanthochromia, excess
proteins in CSF, and spontaneous
formation of a coagulum in CSF
on standing. It results from
complete block of subarachnoid
space.

61. • Distal to the block stagnation of CSF occurs leading to higher protein
transudation, and resulting xanthochromia (due to bilirubin binding
to albumin) and hypercoagulability (due to high fibrinogen level)

62. OTHER COLOURS OF CSF
PINK Red cell lysis and hemoglobin breakdown
ORANGE CAROTENINEMIA
BROWN Meningeal metastatic melanoma

63. CELLS IN CSF
• Presence of blood in CSF due to traumatic tap or subarachnoid
hemorrhage artefactually raises theleucocyte count by 1 WBC
per 1000 red cells. This correction factor should be used if patient's
hemogram is normal.
• If significant anemia or leukocytosis is present,then leukocyte count
in CSF should be corrected as follows:

64. • The CSF is normally acellular, although up to 5 white blood cells
(WBCs) and 5 red blood cells (RBCs) are considered normal in adults
when the CSF is sampled by lumbar puncture (LP)

66. PROTEIN
• Normal CSF protein level in adults is 15-45 mg/dl
• CSF protein can also be elevated by a subarachnoid hemorrhage or a
traumatic LP. The presence of CSF bleeding results in approximately
1 mg of protein/dL per 1000 RBCs/microL.
• When assessing the potential effect of CSF bleeding on an elevated
CSF protein concentration, the CSF protein concentration and RBC
count should be performed on the same tube of CSF

67. Immunoglobulins and oligoclonal bands
• Immunoglobulins are almost totally excluded from the CSF in healthy
individuals. The blood to CSF ratio of IgG is normally 500:1 or more.
• Elevations in oligoclonally expanded immunoglobulin concentrations
in the CSF, termed oligoclonal bands, may occur in any disorder that
disrupts the blood-brain barrier.
• Oligoclonal bands may also be caused by intrathecal production of
IgG, and the presence of such bands is a diagnostic criterion for
multiple sclerosis. Examples of other diseases that can cause
oligoclonal bands in the CSF include infections (eg, nervous system
Lyme disease), autoimmune diseases, brain tumors, and
lymphoproliferative diseases.

70. • CSF glucose
• measured by glucose oxidase method.
• Normal range is 45-80 mg/dl.
• CSF glucose <40 mg/dl is abnormal
• Decreased CSF glucose occurs in following conditions:
• • Acute bacterial meningitis
• • Tuberculous meningitis
• • Fungal meningitis
• • Meningeal involvement by malignant tumor(meningeal carcinomatosis)
• • Hypoglycemia
• CSF glucose is normal in viral meningitis.

71. DECREASED CSF GLUCOSE
hypoglycorrhachia
INFECTIOUS NON INFECTIOUS (because of cellular or
inflammatory infiltrates that disrupt the active
transport of glucose into the CSF)
• mycobacterial,
• mycoplasmal (M. pneumoniae),
• treponemal,
• fungal CNS infections
• leptomeningeal carcinomatosis,
• leukemia,
• CNS lymphoma,
• severe subarachnoid hemorrhages,
• neurosarcoidosis

73. • bacterial meningitis, the classic findings are
• A CSF WBC count above 1000/microL, usually with a neutrophilic
predominance
• A CSF protein concentration above 250 mg/dL
• A CSF glucose concentration below 45 mg/dL (2.5 mmol/L)