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Physiology of the Cerebrospinal Fluid and Intracranial Pressure
Chapter 10 Presentation: S. Bahram Seif, Resident of Neurosurgery Isfahan University of Medical Sciences
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Protective and Homeostatic Systems of the CNS
Skull Bones (physical protection) CSF (hydraulic shock absorption) Continuous Turnover of Extracellular Fluid (substrate supply and cellular homeostasis) BBB
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Protective Systems can Become Detrimental
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Elevated ICP Congenital lesions Neoplasms Metabolic syndromes
Infectious syndromes Infarction Hemorrhage Trauma
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HISTORICAL CONSIDERATIONS
Galen Hippocrates Early Egyptian physicians Removing Pieces Of Skull
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Monro-Kellie Doctrine
19th Century Alexander Monro George Kellie Monro-Kellie Doctrine
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Lumbar Puncture 1911 Quincke 1951 continuously ICP monitoring Lundberg
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NORMAL INTRACRANIAL PRESSURE
Upper limit of normal ICP: 15 mmHg Usual range is 5 to 10 mmHg Coughing or Sneezing: 30 to 50 mmHg
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mmHg x 1.36 = cmH2O
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ICP Evaluation Intraventricular Intraparenchymal Subdural Epidural
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CSF Pulsatility Associated with Cardiac and Respiratory activity
Changes in these pulsatile components can be one of the earliest signs
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Cardiac Component Left ventricular contraction
Peripheral arterial pulse Choroid plexus and pial arteries High-compliance venous blood vessels
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Respiratory Component
Generated by pressure changes in the thoracic and abdominal cavities
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Percussion wave (WI), the most constant, Pulsations in large intracranial arteries.
Tidal wave (W2), brain elastance. Dicrotic wave (W3), dicrotic notch in the arterial.
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ICP is synonymous with CSF Pressure
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Atmospheric pressure Hydrostatic pressure Filling pressure
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As volume is added there are two principal routes for compensation
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Distention of the spinal dura mater
Displacement of CSF and blood
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ICP depends on the total volume inside the skull
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Intracranial Space: 1500-mL
87%: the Brain 9%: CSF (ventricles, cisterns, and subarachnoid space) 4%: blood
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CSF Compartmental Extracellular space 164.5 mL
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CSF Production Choroid plexuses Ventricular ependyma
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Choroid Plexuses Invaginations of the pia mater into the ventricular cavities Roofs of the third and fourth ventricles Walls of the lateral ventricles
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Energy-dependent secretion and reabsorption processes
0.35 to 0.37 mL/min
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Higher sodium, chloride, and magnesium
Lower potassium, calcium, urea, and glucose Similar osmolality
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Peak Production Rates Late evening Early morning
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CSF pressures of less than 5 mm Hg
CSF Drainage Dural Venous System Even in CSF pressures of less than 5 mm Hg
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NPH Ventricular enlargement Absence of elevated ICP
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Gait disturbance Dementia Incontinence
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Lumbar Pressures: 6 to 24 cm H2O.
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Symptoms and Signs of Elevated Intracranial Pressure
Depends greatly on the nature and anatomic location of the underlying pathologic condition Headache, vomiting and papilledema.
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Cranial nerve palsies may arise as a result of pressure on brainstem nuclei (particularly abducens palsies)
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Papilledema Reliable Objective Good specificity
Sensitivity: observer dependent
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Vital Sign Changes Cushing response:
Arterial Hypertension and Bradycardia
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CPP = MAP - ICP
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Abnormal Respiration Cheyne-Stokes: diencephalic region
Sustained hyperventilation: midbrain and upper pons Slow respiration: Midpontine Ataxic respirations: pontomedullary lesions Rapid shallow breathing: upper medullary lesions
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Herniation Syndromes Most serious complication of raised lCP
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Central Syndrome Progressive dysfunction of structures in a rostral to caudal direction 1st Diencephalic Structures: Change in behavior or even loss of consciousness, Cheyne-Stokes respiration Pupils :small, with a poor reactivity Contralateral hemiparesis Pupils fall into a midline fixed position
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Uncal Syndrome Unilaterally dilated and poorly reactive pupil
External oculomotor ophthalmoplegia Ipsilateral hemiparesis: pressure on the contralateral cerebral peduncle on the edge of the tentorium cerebelli
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INTRACRANIAL PRESSURE MONITORING
Benefitial for Outcome
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A Waves (plateau waves)
Increases of ICP for several minutes Return spontaneously to a new baseline which is usually slightly higher
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Vasodilation: normal compensatory response to decreases in CPP, effective management involves the use of vasopressors
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B Waves Vasodilation: secondary to respiratory fluctuations in PaC02
Ventilated patients
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C Waves More rapid sinusoidal fluctuations occurring approximately every 10 seconds Fluctuations in arterial pressure.
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Intracranial Hypertension
40% to 60% of severe head injuries Major factor in the deaths of 50% of all fatalities. ICP above 20 mm Hg is highly significant in predicting outcome
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Indications GCS: 3 to 8 and an abnormal CT
If CT is normal, 2 of these shoud be present: 1)Age older than 40 years 2)Unilateral or bilateral motor posturing 3)Systolic BP below 90 mm Hg GCS>8 and significant mass lesions
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Reye's syndrom Fulminant Hepatic failure
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METHODS Gold standard: Ventriculostomy
Infection rises after 5 days (10%) Hemorrhagic Complications(2%) Parenchymal monitors: less than 1% infective complications. Parenchymal monitors: regional inaccuracy
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Device is zeroed at the level of the foramen of monro, using the external acoustic meatus as an anatomic landmark.
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There is no uniform agreement about the critical level of ICP beyond which treatment is mandatory.
15 mm Hg 20 mm Hg CPP
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MANAGEMENT OF INTRACRANIAL PRESSURE
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VCSF Temporary external drainage Ventriculosubgaleal shunt
Ventriculoperitoneal shunt
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Medications Acetazolamide, furosemide, and corticosteroids can transiently decrease CSF production. Acetazolamide also has a cerebral vasodilator effect & contraindicated in patients with closed head injury.
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VBLOOD Hyperventilation: vasoconstriction of pial vessles
Pa CO2 : 32-35 Head elevation
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VBRAIN Prevention of cerebrovascular hypertension (Inderal)
Colloid (Lund Protocol) Isotonic or hypertonic(Bollus) solutions
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Steroids(Vasogenic & Intrestitial)
Not effective in cytotoxic edema(TBI, Stroke, SAH, Meningitis, DKA)
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Barbiturates Hypothermia Osmotic agents
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Thanks
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