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Raised icp


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Raised icp

  1. 1. DR.THIRUMAL Moderator: Dr.A.RAJESH
  2. 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these premises be true, it does not then appear very conceivable how any portion of the circulating fluid can ever be withdrawn from within the cranium, without its place being simultaneously occupied by some equivalent; or how anything new or exuberant can be intruded without an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. 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
  5. 5. Understanding of the CSF circulation — MAGENDIE who described a small foramen in the floor of the fourth ventricle 175 years ago.
  6. 6. ALEXANDER MONRO &GEORGE KELLIE((1823-24, Scotland) ) defined closed box concept
  7. 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. 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. 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. 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. 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: <-2 mm Hg
  12. 12. Intracranial Pressure  Skull has three essential components  Brain tissue 78% (1400ml)  Blood 12% (75-100ml)  CSF 10% (75-100ml)
  13. 13.  Principle buffers in the brain: CSF & to a lesser extent, venous blood volume as they are connected to low pressure outlets.  CSF: spinal subarachnoid space [through foramen magnum].  Venous blood: Jugular veins, Emissary veins.
  14. 14.  Brain can distort in a plastic fashion allows some compensation (supratentorial >infratentorial) Can result in secondary hydrocephalus  Compensatory mechanisms can accommodate an additional 100-120 ml in the intracranial volume
  15. 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. 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. 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. 18. ICP-Volume Curve 100 0 40 60 80 20 Volume ICP mm Hg ICP controlled due to compensation Small volume marked ICP
  19. 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. 20.  Cerebral perfusion pressure (CPP)  Pressure needed to ensure blood flow to the brain  CPP = MAP – ICP  Normal is 70 to 100 mm Hg  <50 mm Hg is associated with ischemia and neuronal death  The critical parameter for brain function and survival is not actually ICP, rather it is adequate cerebral blood flow (CBF) to meet CMR02 demands Cerebral Blood Flow
  21. 21. Cerebral edema  Net increase in water content of both intracellular & extracellular compartment of cerebral tissue  Classification :  Vasogenic edema : neoplasms, hematomas, abscesses  Cytotoxic edema : hypoxia/ischemia  Interstitial edema : obstructive hydrocephalus—.
  22. 22. Definition of herniation Herniation of brain tissue from one compartment (separated by calvarial and /or dural boudaries) to another.
  23. 23. SEVEN MAJOR PATTERNS OF BRAIN SHIFT (PLUM AND POSNER ‘S CLASSIFICATION)  falcine herniation,  lateral displacement of the Diencephalon  uncal herniation  central transtentorial herniation  rostrocaudal brainstem deterioration  tonsillar herniation  Upward brainstem herniation
  24. 24. falcine herniation occurs when an expanding lesion presses the cerebral hemisphere medially against the falx. Ipsilateral anterior cerebral artery (ACA) infarction as ACA is entrapped under the falx  Headache  Contralateral leg weakness
  25. 25. LATERAL DISPLACEMENT OF THE DIENCEPHALON  Occurs when an expanding mass lesion pushes the diencephalon laterally.  Monitored by displacement of the calcified pineal gland  This lateral displacement is roughly correlated with the degree of impairment of consciousness
  26. 26. Uncal herniation  ipsilateral fixed and dilated pupil  impaired level of consciousness  Hemiparesis  Visual disturbances  PCA infarcts
  27. 27. Central transtentorial  Coma due to impairment of the ascending arousal system at the diencephalic level  Pituitary stalk may become partially avulsed, causing diabetes insipidus  Midbrain involvement- perinaud syndrome
  28. 28. Rostrocaudal brainstem deterioration  Downward displacement of the midbrain or pons  Stretches the medial perforating branches of the basilar artery  Duret hemorrhages
  29. 29. Tonsillar herniation Pressure and Push of tonsils against FM closing of 4th ventricle Medullary compression can occur suddenly Respiratory arrest.
  30. 30. Upward brainstem herniation  Rapidly expanding post. Fossa lesion  Vermis and midbrain pushed upwards  Compressing the dorsal midbrain ,blood vessels and the cerebral aqueduct.  Impaired upgaze , LOC and acute hydrocephalus.
  31. 31. Symptoms: • Headache - usually frontal and classically worse after lying down. • Vomiting - classically early morning, and without associated nausea. • Blurred vision. signs: • Tense fontanelle in infants. • Depressed conscious state. • Cushing'striad: hypertension, bradycardia,apnoea. • Pupillary changes: uni or bilateral pupillary dilation. • VI nerve palsy (false localising sign). • Papilloedema - may not be present if increase in ICP is of recent onset (< 24 hrs). CLINICAL FEATURES OF INTRACRANlAL HYPERTENSION 
  33. 33. Indications for ICP monitoring  Trauma and ICH are the two prime indications for ICP monitoring.  The classic indication is in the patient in a coma with a Glasgow Coma Scale score of 8 or less.  Perioperative ICP monitoring :undergone tumor or arteriovenous malformation resection and are at risk for cerebral edema with an inability to follow a clinical neurological examination.  Selected non neurosurgical cases where risk of raised ICP.
  34. 34. Ideal ICP monitor • Nils Lundberg outlined the basic requirements for an ICP monitor • Minimal trauma during placement • Negligible risk for infection • No CSF leakage, easy to handle, reliable • Able to continue to function during various diagnostic and therapeutic procedures
  35. 35. Various monitors
  36. 36.  American National Standard for Intracranial Pressure Monitoring Devices, specifies that  ICP monitoring device should have A pressure range between 0 and 100 mm Hg, Accuracy of 2 mm Hg in the range of 0 to 20 mm Hg Maximal error of 10% in the range of 20 to 100 mm Hg
  37. 37. External Ventricular Drain  An external ventricular drain (EVD), or ventriculostomy drain, connected to an external strain gauge is currently the “gold standard” for measuring ICP.  ADVANTAGES Serves also as a therepeutic device low cost most accurate ,
  38. 38. Disdvantages  Accurate placement of an EVD may be difficult.  In some patients, it is simply not possible to place an EVD.  Complications include malposition(4-20%)  occlusion (8%)  hemorrhage(1.1%)  And infection (8.8%)
  40. 40. The ICP waveforms recorded with EVD  normally pulsatile  . Left ventricular contraction contributes the cardiac component.  During inspiration , there is a fall in ICP and rise in ICP during expiration.
  41. 41.  waveform of highest frequency consist of as many as five smaller peaks.  the percussion wave (W1)  the tidal wave (W2)  the dicrotic wave (W3)
  42. 42. Lundberg's classification of ICP waves.  A waves or plateau waves  B waves  C waves  Lundberg N: Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Neurol Scand 1960; 36(Suppl 49):1- 193
  43. 43. A WAVES or PLATEAU WAVES Steep raise in ICP to 50-80 mm Hg Duration 2-20 minutes  Result of an increase in cerebrovascular blood volume due to vasodilation.  Plateau waves are a normal compensatory response to decreases in CPP
  44. 44. Lundberg B waves  Short elevations of A modest nature (10 to 20 mm hg) that occur at A frequency of 0.5 to 2 hz/S  Thought to relate to vasodilation secondary to respiratory fluctuations in paco2  Questionable clinical significance
  45. 45. C waves  Are more rapid sinusoidal fluctuations occurring approximately every 10 seconds  Corresponding to traube-hering-mayer fluctuations in arterial pressure
  46. 46. FIBEROPTIC INTRACRANIAL PRESSURE MONITOR  Fiberoptic devices for ICP monitoring in which the catheter tip measures the amount of light reflected off a pressure-sensitive diaphragm .  The most widely studied fiberoptic device is the Camino fiberoptic ICP monitoring device (Integra Neuroscience, Plainsboro, NJ).
  47. 47. Adavntages Disadvantages  Ease of insertion.  Accuracy  low complication rate  Zero drift.  Mechanical problems (breakage or dislocation)
  48. 48. The subarachnoid screw (bolt)  A subdural screw or bolt is a hollow screw that is inserted through a hole drilled in the skull. It is placed through dura mater.  This allows the sensor to record from inside the subdural space.
  49. 49. Bolt Drill bit Driver
  50. 50. Advantages  Does not penetrate the brain.  Lower risk of infection than the intraventricular catheter  It is easier to place.  It is unable to drain CSF  The accuracy is questionable.
  51. 51. MINIATURE STRAIN GAUGE TRANSDUCER Codman MicroSensor ICP Transducer ,the prototype. It has a microchip pressure sensor at the tip of a flexible nylon cable that produces different electricity based on pressure
  52. 52. Advantages Disadvanteges  can be placed in various compartments, including the ventricle, parenchyma, and subdural space  Less accurate.
  53. 53. Spiegelberg Parenchymal Transducer  using an Air-Pouch mounted in the tip region of a dual lumen probe.  One lumen transmits the pressure to the Brain- Pressure Monitor. The second lumen is used for drainage of CSF.
  54. 54. Emerging Technology  To measure compliance, the monitor injects a small amount of air into the air balloon pouch and measures the pressure response to this change in volume  Compliance Monitor
  55. 55. Noninvasive Intracranial Pressure Monitoring  optic nerve sheath diameter (ONSD), which can be measured by ultrasound, correlates with ICP.  demonstrated a strong linear relationship between ONSD and ICP.  But the critical value of ONSD for detecting elevated ICP (ICP >20 mm Hg) is different in the various studies, thus limiting its potential use at this time
  56. 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. 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. 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  Reye’s syndrome  Stroke  Reye’s syndrome  Increase in CSF volume  Hydrocephalous  Choroids plexus palpilloma  Increased blood volume  Vascular malformations  Cerebral venous thrombosis  Meningitis, encephalitis
  59. 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. 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. 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. 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. 63. Respiratory care  Avoid hypoxia (PaO2 <60mmhg or O2 sat< 90%)  Ventilate to normocarbia( avoid prophylactic hyperventilation)  Optimal respiratory management is crucial for control of ICP.  Mechanical ventilation also can have adverse effects on ICP.  Adjusting ventilator settings ( PEEP)
  64. 64. Fever control  potent vasodilator and Fever-induced dilation of cerebral vessels can increase CBF and may increase ICP  worsens neurologic injury 1. 1.Jones PA, Andrews PJD, Midgley S, et al. Measuring the burden of secondary insults in head-injured patients during intensive care. J Neurosurg Anesth. 1994;6:4–14.
  65. 65. Blood pressure control  Avoid hypotension –normalize intravascular volume.  Use pressors if needed.  Control hypertension if present.
  66. 66. Treatment of anemia  It is reported of patients with severe anemia presenting with symptoms of increased ICP and signs of papilledema, which resolve with treatment of the anemia 1 . Biousse V, Rucker JC, Vignal C, et al. Anemia and papilledema. Am J Ophthalmol. 2003;135:437–46.
  67. 67. Seizure control  Seizures can increase cerebral metabolic rate and ICP.  Control of seizures found to increase the outcome in severe traumatic brain injury. Lee ST, Lui TN, Wong CW, et al. Early seizures after severe closed head injury. Can J Neurol Sci. 1997;24:40–3.
  68. 68. Sedation and analgesia  Agitation and pain may significantly increase blood pressure and ICP.  Light sedation and good analgesia
  69. 69. Prophylactic hypothermia Schwab, S. et al. "Moderate Hypothermia in the Treatment of Patients with Severe Middle Cerebral Artery Infarction." American Heart Association. July 31, 1998, pg. 2461-2466
  70. 70. Measures for refractory intracranial hypertension  Heavy sedation and paralysis  Hyperosmolar therapy  Hyperventilation  Barbiturate coma  Steroids  Prophylactic hypothermia  Surgical treatment
  71. 71. Heavy sedation and paralysis  Intracranial hypertension caused by agitation, posturing, or coughing can be prevented by sedation and nondepolarizing muscle relaxants that do not alter cerebrovascular resistance.  morphine and lorazepam for analgesia/sedation and cisatracurium or vecuronium as a muscle relaxant.
  72. 72. DRAWBACKS  Interferes in examination.  Myopathy  Polyneuropathy  Prolonged neuromuscular blockade.
  73. 73.  Can minimize these complications by  Limiting the use and dose  Train-of-four monitoring  Measuring creatine phosphokinase daily  Stopping thedrug daily to evaluate response.
  74. 74. Hyperosmolar therapy  Mannitol  isolated from the secretions of the plant flowering ash and called manna after its resemblance to the Biblical food.  Today, mannitol is commercially produced by catalytic hydrogenation of fructose, sucrose (invert sugar), or glucose-fructose syrups.  Schwarz, 1994; Ojamo et al., 2000
  75. 75.  An osmotic diuretic  alcohol of the 6C sugar mannose  confined to the extracellular space  only slightly metabolized and rapidly excreted by the kidney.  Mannitol induces diuresis by elevating the osmolarity of the glomerular filtrate and thereby hindering tubular reabsorption of water.  Excretion of sodium and chloride is also enhanced  Time to action 1-5min, peak at 20-60min; ICP returns to baseline by 4hours
  76. 76. Mannitol osmotherapy in brain  Mannitol does not cross the blood brain barrier so an elevated plasma osmolality due to a infusion of hypertonic mannitol is effective in removing fluid from the brain. This is called 'mannitol osmotherapy'.  The brain cells also compensate for the presence of continued hypertonicity by the intracellular production of 'idiogenic osmoles'. The effect is to increase intracellular tonicity and allow brain cell volume to return towards normal presumably with improvement of intracellular functions despite the continued hypertonicity.
  77. 77. Blood viscosity autoregulation of CBF  Influences intracranial compliance: hence improvement in neurological status can occur despite little measurable effect on ICP.  autoregulation is mediated through alterations in the level of adenosine in response to oxygen availability changes in cerebral tissue.  The decrease in blood viscosity after mannitol administration leads to an improved oxygen transport to the brain.
  78. 78.  . When autoregulation is intact, more oxygen leads to decreased adenosine levels, resulting in vasoconstriction  The decrease in resistance to flow from the decreased blood viscosity is balanced by increased resistance from vasoconstriction, so that CBF remains the same
  79. 79. A test dose of mannitol should be given prior to instituting therapy for patients with marked oliguria or those believed to have inadequate renal function.
  80. 80. Adverse effects  Acute adverse haemodynamic effects  - variable effects on BP following a bolus of mannitol  - Hypotension.  - the acute vasodilatory effect of mannitol  decrease in plasma pH  release of ANP  histamine release from basophils  direct impairment of contractile properties of vascular smooth muscle
  81. 81.  Dehydration and Electrolyte Disturbances  - osmotic diuretics result in excess net free water clearance  - sodium imbalance  - other electrolytes imbalance :potassium, phosphate and magnesium  - cardiac arrhythmias and neuromuscular complications are common
  82. 82. Rebound phenomena  - definition is any unexpected rise in ICP after the administration of osmotherapy  - explanation : due to penetration of osmotically active particles into the brain, their accumulation creating an osmotic gradient favouring movement of water into the brain, and oedema formation
  83. 83. other possible mechanisms  rapid volume depletion stemming from overzealous administration of osmotic diuretics  overly rapid administration of hypotonic fluids to patients after a prolonged period of hyperosmolar dehydration  in the former case, volume depletion sets the stage for hyperviscosity and haemodynamic compromise leading to reactive cerebral hyperaemia  - in the latter case, a CNS adjusted to the hyperosmolar state is suddenly exposed to plasma of reduced osmolality
  84. 84. •Opens the BBB, and mannitol that has crossed the BBB may draw fluid into the CNS which can aggravate vasogenic cerebral edema'''. It should be tapered to prevent ICP rebound" • Corticosteroids + phenytoin + mannitol may cause hyperosmolar nonketotic state wit •High doses of mannitol carries the risk of acute renal failure •Large doses prevents diagnosing DI Cautions with mannitol
  85. 85. Glycerol  Trivalent alcohol.  Used systemically and orally to decrease the ICP.  Not metabolically inert. Partially metabolised to CO2 and water.  Oral Glycerol decreases the ICP in 30-60min.  DOSAGE: 1.2gm/kg, maintainence 0.5-1gm/kg every 3-4 hrs  IV Preparation: 10% glycerol in 0.4 N saline  Complications: Hemolysis, hemoglobinuria, renal failure and hyperosmolar coma.
  86. 86.  the addition of glycerol to mannitol avoids rebound edema likely to be observed with the intravenous administration of only mannitol.  This comnbination stiategy is able to enlance the diffusion of water from cerebrospinal fluid back into plasma by elevating the osmolality of the plasma
  87. 87. Hypertonic saline  ICP reduction best with 23.4 % saline 10%, 7.2% and 3% have also been used Dosage of 3% saline 1-2ml/kg Q12h. over 5 min.  ICP reduction best with 23.4 % saline but ill- sustained  has a clear advantage over mannitol in hypovolemic and hypotensive patients. Qureshi et al. Critical Care Medicine, 26(3) (1998) Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain
  88. 88. Hypertonic saline Mechanism of action:  Membrane stabilizing effect helps in preserving BBB.  Direct vasodilatation of pial vessels  Reduction of blood viscosity due to enhancement of the intravascular volume  Rapid absorption of cerebrospinal fluid  Restoration of the normal membrane potentials  Local dehydration of brain tissue
  89. 89. Complications  Coma, seizures and rebound phenomenon.  Systemic effects: CCF , Hypokalemic acidosis.  Deranged platelet aggregation  Phlebitis and renal failure Hypertonic saline
  90. 90. Hyperventilation  Decreases paco2,  Induce constriction of cerebral arteries by alkalinizing the CSF.  Reduction in cerebral blood volume decreases ICP.
  91. 91.  hyperventilation (HPV) to pco2. " 30-35 mm Hg  Used only for  short periods for acute neurologic deterioration  or chronically for documented IC-HTN unresponsive to sedation, paralytics, CSF drainage and osmotic therapy
  92. 92. do not use prophylactically avoid aggressive hyperventilation (pCO<25 mm Hg)
  93. 93. Loop diuretics Used in conjunction with mannitol to treat raised ICP. Furosemide works synergitically with mannitol  remove free water  appropriate in patients with fluid overload  decreases CSF production  decreases edema in pathological areas(disrupted BBB)  oncodiuretic therapy: albumin infusion followed by furosemide (no hyperosmolality or hypernatremia)
  94. 94. Steroids  Dexamethasone is the most widely used  Steroids are effective in reducing ICP in tumors.  No proven benefit in Head injured patients.  In cerebral ischemia they may worsen outcome direct steroid toxicity increase glucose levels which increases lactic acid levels.
  95. 95. Steroids  Mechanism of action: Reduction in CSF production Membrane stabilization & restoration of BBB Reduction in ICP secondary to antiedema action Improves CSF bulk outflow at arachnoid villi  Dosage: Dexamehtasone 10mg loading dose 4mg Q6H
  96. 96. Barbiturate therapy  Barbiturate protect brain from anoxic, ischemic and vasogenic cerebral edema.  Useful in reducing ICP resistant for other methods of treatment.  Mechanism of action: Uncouples brain metabolism and CBF Reduces CMRO2 permitting tolerance of a degree of ischemia or anoxia => lower demand for CBF =>reduces the CBV and hence reduces the ICP. Free radical scavenger
  97. 97.  Dosage: 10mg/kg adminstered over 30min. followed by 1-5mg/kg to maintain a serum concentration of 3.5 – 4.5mg/100ml or 10 – 20min of burst suppression Barbiturate therapy
  98. 98.  Major disadvantage: Hypotension, (treated with dopamine), myocardial depression  Administration in ICU with arterial line BP and CVP monitors  Euvolemia to be ensured  Pressor support if required Barbiturate therapy
  99. 99.  Causes a decrease in ICP by reducing the CMRO2 and depression of metabolic requirements.  Body temp has to to be reduced to 32.8deg. Fall in ICP was average of 45% to a maximum of 80%..  Still controversial  Moderate hypothermia can help to control critically elevated ICP values in severe space-occupying edema after MCA stroke and may improve clinical outcome in these patients1.  At 27deg C: cardiac arrhythmias  Problems during rewarming: seizures, drowsiness, coma Hypothermia
  100. 100. Surgical treatment  Resection of mass lesions  Acute epidural and subdural hematomas , brain abscess, tension pneumocephalus and tumors etc need to be removed
  101. 101. Ventriculostomy  CSF drainage  Works immediately by removal of CSF  long-term benefit by allowing edema fluid to drain into the ventricular system
  102. 102. Complications  Infection  Haemorrhage  Brain parenchymal damage  Seizure  Needle porencephaly  Upward transtentorial herniation
  103. 103. Operative decompression  External decompression: Decompressive craniectomy.  Reports suggest that decompressive craniectomy effectively reduces ICP in most (85%) patients with intracranial hypertension refractory to conventional medical treatment Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006;104:469–79. Polin RS, Shaffrey ME, Bogaev CA, et al. Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery. 1997;41:84–92.
  104. 104.  Brain oxygenation measured by tissue PO2 and blood flow estimated by middle cerebral artery flow velocity also are usually improved after decompressive craniectomy . Stiefel MF, Heuer GG, Smith MJ, et al. Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension. J Neurosurg. 2004;101:241–7. Bor-Seng-Shu E, Hirsch R, Teixeira MJ, et al. Cerebral hemodynamic changes gauged by transcranial Doppler ultrasonography in patients with posttraumatic brain swelling treated by surgical decompression. J Neurosurg. 2006;104:93–100.
  105. 105. Decompressive craniectomy Complications:  Infection  Subdural/ subgaleal hygroma  Enhancement of brain edema with fresh haemorrhages Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006;104:469–79.
  106. 106. thank you
  107. 107. References 1. Youmans Neurological Surgery, 6th Edition By H. Richard Winn, Md 2. Plum And Posner’s Diagnosis Of Stupor And Coma ,4th Edition 3. Neurosurgery By, Setti S. Rengachary, Robert H. Wilkins 4. Goodman & Gilman's The Pharmacological Basis Of Therapeutics - 11th Ed. (2006)
  108. 108. Questions  1. first systematic recording of ICP done by a)Guilalmaue b)Janny c)Neil lundberg d) all of the above
  109. 109.  2. the level of CPP under which CBF would impair is a)50mmhg b)40mmhg c)60mmhg d)30mmhg
  110. 110.  3.The territory of infarcts seen in uncal herniation a)ACA territory b)PCA territory c)MCA territory d)none
  111. 111.  4. The limiting factor for therapy barbiturate is a)respiratory depression b)hypotension c)hypertension d)all the above
  112. 112.  5.Factor associated with incidence of infection in EVD  a)insertion of IVC in neuro intensive care unit b)previous IVC c)use of steroids d) none
  113. 113.  6.most significant problem of fiberoptic ICP monitor is a) infection b)breakage c)zero drift d)bleeding
  114. 114.  method of ICP monitor in patients with massive edema with slit ventricles a)subarachnoid bolt b)parenchymal monitor c)both d)EVD
  115. 115.  8.the best method of ICP monitor in coagulopathy patients is a)subararachnoid bolt b)EVD monitor c)parenchymal transducer d)TCD
  116. 116.  9.During mannitol administration , to prevent renal failure the serum osmolality should be below a)320 m osm b)280m osm c)350 mosm d)250 m osm
  117. 117.  10.the minimum diametre of decompressive craniectomy flap is a)12 cm b)20 cm c)15cm d)25 cm