1.DR.THIRUMAL Moderator: Dr.A.RAJESH

2. If these premises be true, it does not then appear very conceivable how any portion of the circulating fluid can ever be withdrawn from within the cranium, without its place being simultaneously occupied by some equivalent; or how anything new or exuberant can be intruded without an equivalent displacement. - George Kellie 3. Learning objectives To discuss the physiologic mechanisms that maintain normal intracranial pressure To discuss pathological and clinical features of raised ICP To discuss the monitoring and management of raised ICP 4. HISTORICAL REVIEW 5. Understanding of the CSF circulation MAGENDIE who described a small foramen in the floor of the fourth ventricle 175 years ago. 6. ALEXANDER MONRO &GEORGE KELLIE((1823-24, Scotland) ) defined closed box concept 7. (1846) - BURROW - The concept of reciprocal volume changes between blood and CSF to account for the changes in ICP. (early 20th century) - WEED - An understanding of raised ICP encompasses an analysis of both intracranial volume and craniospinal compliance 8. 1866 Lyden measures ICP via trephine 1866 Knoll produces graphic CSF pressure trace 1870 Duret observes deleterious effects of injecting fluid in to dogs skulls 9. 1891 QUINKE introduced LP allowing CSF sampling & measurement 1900 CUSHING describes the classic Triad seen with severely elevated ICP 1960 LUNDBERG introduced long term continuous ICP monitoring via an indwelling intraventricular catheter. 10. (1972) -MARIO BROCK organised the first International Symposium on Intracranial Pressure in Hanover. (1987) - MARMAROU published his studies on intracranial compliance in the head injured and described the pressure volume index (PVI). 11. Intracranial Pressure Definition: The pressure that is exerted on to the brain tissue by external forces, such as cerebrospinal fluid (CSF) and blood. Normal ICP: adults: 10-15 mm Hg / 135-200 mm of water. children: 3-7 mm Hg infants: 1.5-6 mm Hg neonates: infratentorial) Can result in secondary hydrocephalus Compensatory mechanisms can accommodate an additional 100-120 ml in the intracranial volume 15. Monroe-Kelly doctrine: the summarized volume of the intracranial components (brain tissue, blood, CSF) is constant. Inrease of any of them is possible only at the expense of the other two, and inceases the intracranial pressure. Vintracranial vault = Vbrain + Vblood + Vcsf 16. Intracranial compensation The brain is essentially non-compressible Any increase in intracranial volume decreases CSF or CBV CSF - primarily displaced into the spinal subarachnoid space Blood - venoconstriction of CNS capacitance vessels displaces blood in jugular venous system 17. Exhaustion of compensation Once these limited homeostatic mechanisms are exhausted additional small increases in intracranial volume produce marked elevations in ICP Raised ICP may decrease CBF resulting in vicious cycle 18. ICP-Volume Curve 100 0 40 60 80 20 Volume ICP mm Hg ICP controlled due to compensation Small volume marked ICP 19. Autoregulation of cerebral blood flow Automatic alteration in diameter of cerebral blood vessels to maintain constant blood flow to brain Cerebral autoregulation is a mechanism whereby over wide range, large changes in systemic BP produce only small changes in CBF, Due to autoregulation. CPP would have to drop below 40 in a normal brain before CBF would be impaired, 20. Cerebral perfusion pressure (CPP) Pressure needed to ensure blood flow to the brain CPP = MAP ICP Normal is 70 to 100 mm Hg 20 mm Hg) is different in the various studies, thus limiting its potential use at this time 56. venous ophthalmodynamometry, which measures venous opening pressure (VOP), to calculate ICP. Drawback -requires dilation of the pupil to perform the measurement Both ONSD and VOP measurement can be performed only intermittently and therefore can be used just as a screening tool for ICP elevation rather than as a continuous monitor. 57. Tympanic membrane displacement gives an idea of Cochlear fluid pressure acts as a surrogate for ICP. But less accurate. Measuring ICP based also on changes in patterns of blood flow velocity in the intracranial arteries, which can be assessed by transcranial Doppler. Delay in visual evoked potentials. 58. Common Causes of raised ICP Increased brain volume Intracranial space occupying lesions Brain tumors Brain abscess Intracranial hematoma Intracranial vascular malformation Cerebral edema Encephalitis (viral, inflammatory) Meningitis Hypoxic ischemic encephalopathy Traumatic brain injury Hepatic encephalopathy Reyes syndrome Stroke Reyes syndrome Increase in CSF volume Hydrocephalous Choroids plexus palpilloma Increased blood volume Vascular malformations Cerebral venous thrombosis Meningitis, encephalitis 59. Intracranial hypertension secondary to traumatic brain injury Traumatically induced masses: epidural or subdural hematomas, hemorrhagic contusions, foreign body, and depressed skull fractures Cerebral edema Hyperemia owing to vasomotor paralysis or loss of autoregulation Hypoventilation that leads to hypercarbia with subsequent cerebral vasodilation 60. Goals of therapy Maintain ICP at less than 20 to 25 mm Hg. Maintain CPP at greater than 60 mm Hg by maintaining adequate MAP. Avoid factors that aggravate or precipitate elevated ICP. Indications to treat IC-HTN ICP '" 20-25 mm Hg Ropper AH :Raised ICP in neurological disesases Sem neurology 4:397-400,1984 Bullock R,Chesnut R M,Cliflon G, eral.: Guidelines for tbe management or severe head injury, The Brain Trauma Foundation (New York), The American ASliociation of Neurological Surgeons The Joint Section of Neu rotrauma and Critical Care, 1995 61. General care to minimize intracranial hypertension Optimizing cerebral venous outflow Respiratory care Fever control Blood pressure control Treatment of anemia Seizure control Sedation and analgesia 62. Optimizing cerebral venous outflow Head end elevation to 30-450 reduces the ICP 1 by Enhancing the venus outflow Promoting CSF displacement and Reducing MAP at carotids Efeect is immediate 1Neurosurgery. 2004 Mar;54(3):593-7; Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. 63. Respiratory care Avoid hypoxia (PaO2