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Raised icp

The document discusses the historical understanding and physiological mechanisms of intracranial pressure (ICP). It notes that George Kellie in 1823 helped define the closed box concept of the skull. The key points are: 1) ICP is maintained by a balance between brain tissue, blood, and cerebrospinal fluid volumes within the fixed skull space. 2) Common causes of increased ICP include brain tumors, hemorrhages, edema from injuries or infections. 3) Monitoring devices include external ventricular drains and fiberoptic monitors, though all have advantages and disadvantages. 4) Increased ICP can cause herniation and shift brain tissues, reducing blood flow and oxygen, potentially leading to

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DR.THIRUMAL Moderator: Dr.A.RAJESH
 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these premises be true, it does not then appear very conceivable how any portion of the circulating fluid can ever be withdrawn from within the cranium, without its place being simultaneously occupied by some equivalent; or how anything new or exuberant can be intruded without an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
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
HISTORICAL REVIEW
Understanding of the CSF circulation — MAGENDIE who described a small foramen in the floor of the fourth ventricle 175 years ago.
ALEXANDER MONRO &GEORGE KELLIE((1823-24, Scotland) ) defined closed box concept
 (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
 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
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.
 (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).
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
Intracranial Pressure  Skull has three essential components  Brain tissue 78% (1400ml)  Blood 12% (75-100ml)  CSF 10% (75-100ml)
 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.
 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
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
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
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
ICP-Volume Curve 100 0 40 60 80 20 Volume ICP mm Hg ICP controlled due to compensation Small volume marked ICP
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,
 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
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—.
Definition of herniation Herniation of brain tissue from one compartment (separated by calvarial and /or dural boudaries) to another.
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
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
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
Uncal herniation  ipsilateral fixed and dilated pupil  impaired level of consciousness  Hemiparesis  Visual disturbances  PCA infarcts
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
Rostrocaudal brainstem deterioration  Downward displacement of the midbrain or pons  Stretches the medial perforating branches of the basilar artery  Duret hemorrhages
Tonsillar herniation Pressure and Push of tonsils against FM closing of 4th ventricle Medullary compression can occur suddenly Respiratory arrest.
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.
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 
RAISED ICP ICP>MAP CERBRAL ISCHEMIA ACTIVATION OF ANS HYPERTENSION&TACHYCARDIA BARORECEPTORS & VAGUS NERVE STIMULATION BRADYCARDIA RAISED ICP BRAINSTEM COMPRESSION IRREGULAR BREATHING AND APNOEA
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.
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
Various monitors
 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
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 ,
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%)
Factors affecting the complications with EVD  VENUE OF PLACEMENT  EXTENDED TUNNELING  PROPHYLACTIC CATHETER EXCHANGE  PROPHYLACTIC ANTIBIOTIC USE  ANTIBIOTIC-IMPREGNATED CATHETER
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.
 waveform of highest frequency consist of as many as five smaller peaks.  the percussion wave (W1)  the tidal wave (W2)  the dicrotic wave (W3)
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
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
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
C waves  Are more rapid sinusoidal fluctuations occurring approximately every 10 seconds  Corresponding to traube-hering-mayer fluctuations in arterial pressure
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).
Adavntages Disadvantages  Ease of insertion.  Accuracy  low complication rate  Zero drift.  Mechanical problems (breakage or dislocation)
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.
Bolt Drill bit Driver
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.
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
Advantages Disadvanteges  can be placed in various compartments, including the ventricle, parenchyma, and subdural space  Less accurate.
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.
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
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
 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.
 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.
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
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
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
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
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.
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)
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.
Blood pressure control  Avoid hypotension –normalize intravascular volume.  Use pressors if needed.  Control hypertension if present.
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.
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.
Sedation and analgesia  Agitation and pain may significantly increase blood pressure and ICP.  Light sedation and good analgesia
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
Measures for refractory intracranial hypertension  Heavy sedation and paralysis  Hyperosmolar therapy  Hyperventilation  Barbiturate coma  Steroids  Prophylactic hypothermia  Surgical treatment
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.
DRAWBACKS  Interferes in examination.  Myopathy  Polyneuropathy  Prolonged neuromuscular blockade.
 Can minimize these complications by  Limiting the use and dose  Train-of-four monitoring  Measuring creatine phosphokinase daily  Stopping thedrug daily to evaluate response.
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
 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
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.
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.
 . 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
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.
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
 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
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
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
•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
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.
 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
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
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
Complications  Coma, seizures and rebound phenomenon.  Systemic effects: CCF , Hypokalemic acidosis.  Deranged platelet aggregation  Phlebitis and renal failure Hypertonic saline
Hyperventilation  Decreases paco2,  Induce constriction of cerebral arteries by alkalinizing the CSF.  Reduction in cerebral blood volume decreases ICP.
 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
do not use prophylactically avoid aggressive hyperventilation (pCO<25 mm Hg)
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)
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.
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
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
 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
 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
 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
Surgical treatment  Resection of mass lesions  Acute epidural and subdural hematomas , brain abscess, tension pneumocephalus and tumors etc need to be removed
Ventriculostomy  CSF drainage  Works immediately by removal of CSF  long-term benefit by allowing edema fluid to drain into the ventricular system
Complications  Infection  Haemorrhage  Brain parenchymal damage  Seizure  Needle porencephaly  Upward transtentorial herniation
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.
 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.
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.
thank you
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)
Questions  1. first systematic recording of ICP done by a)Guilalmaue b)Janny c)Neil lundberg d) all of the above
 2. the level of CPP under which CBF would impair is a)50mmhg b)40mmhg c)60mmhg d)30mmhg
 3.The territory of infarcts seen in uncal herniation a)ACA territory b)PCA territory c)MCA territory d)none
 4. The limiting factor for therapy barbiturate is a)respiratory depression b)hypotension c)hypertension d)all the above
 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
 6.most significant problem of fiberoptic ICP monitor is a) infection b)breakage c)zero drift d)bleeding
 7.best method of ICP monitor in patients with massive edema with slit ventricles a)subarachnoid bolt b)parenchymal monitor c)both d)EVD
 8.the best method of ICP monitor in coagulopathy patients is a)subararachnoid bolt b)EVD monitor c)parenchymal transducer d)TCD
 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
 10.the minimum diametre of decompressive craniectomy flap is a)12 cm b)20 cm c)15cm d)25 cm
Raised icp

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Raised icp

  • 1.
  • 2.
     If thesepremises 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  Todiscuss 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.
  • 5.
    Understanding of theCSF circulation — MAGENDIE who described a small foramen in the floor of the fourth ventricle 175 years ago.
  • 6.
    ALEXANDER MONRO &GEORGEKELLIE((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 Lydenmeasures 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 introducedLP 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) -MARIOBROCK 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: <-2 mm Hg
  • 12.
    Intracranial Pressure  Skullhas three essential components  Brain tissue 78% (1400ml)  Blood 12% (75-100ml)  CSF 10% (75-100ml)
  • 13.
     Principle buffersin 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.
     Brain candistort 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.
    Monroe-Kelly doctrine:  thesummarized 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  Thebrain 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 mmHg ICP controlled due to compensation Small volume marked ICP
  • 19.
    Autoregulation of cerebralblood 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 perfusionpressure (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.
    Cerebral edema  Netincrease 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—.
  • 23.
    Definition of herniation Herniationof brain tissue from one compartment (separated by calvarial and /or dural boudaries) to another.
  • 24.
    SEVEN MAJOR PATTERNSOF 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
  • 25.
    falcine herniation occurs whenan 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
  • 26.
    LATERAL DISPLACEMENT OFTHE 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
  • 27.
    Uncal herniation  ipsilateralfixed and dilated pupil  impaired level of consciousness  Hemiparesis  Visual disturbances  PCA infarcts
  • 28.
    Central transtentorial  Comadue to impairment of the ascending arousal system at the diencephalic level  Pituitary stalk may become partially avulsed, causing diabetes insipidus  Midbrain involvement- perinaud syndrome
  • 29.
    Rostrocaudal brainstem deterioration  Downwarddisplacement of the midbrain or pons  Stretches the medial perforating branches of the basilar artery  Duret hemorrhages
  • 30.
    Tonsillar herniation Pressure andPush of tonsils against FM closing of 4th ventricle Medullary compression can occur suddenly Respiratory arrest.
  • 31.
    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.
  • 32.
    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.
    RAISED ICP ICP>MAP CERBRAL ISCHEMIA ACTIVATIONOF ANS HYPERTENSION&TACHYCARDIA BARORECEPTORS & VAGUS NERVE STIMULATION BRADYCARDIA RAISED ICP BRAINSTEM COMPRESSION IRREGULAR BREATHING AND APNOEA
  • 34.
    Indications for ICPmonitoring  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.
  • 35.
    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
  • 36.
  • 37.
     American NationalStandard 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
  • 38.
    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 ,
  • 40.
    Disdvantages  Accurate placementof 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%)
  • 41.
    Factors affecting thecomplications with EVD  VENUE OF PLACEMENT  EXTENDED TUNNELING  PROPHYLACTIC CATHETER EXCHANGE  PROPHYLACTIC ANTIBIOTIC USE  ANTIBIOTIC-IMPREGNATED CATHETER
  • 42.
    The ICP waveformsrecorded 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.
  • 43.
     waveform ofhighest frequency consist of as many as five smaller peaks.  the percussion wave (W1)  the tidal wave (W2)  the dicrotic wave (W3)
  • 44.
    Lundberg's classification ofICP 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
  • 46.
    A WAVES orPLATEAU 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
  • 47.
    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
  • 48.
    C waves  Aremore rapid sinusoidal fluctuations occurring approximately every 10 seconds  Corresponding to traube-hering-mayer fluctuations in arterial pressure
  • 49.
    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).
  • 51.
    Adavntages Disadvantages  Easeof insertion.  Accuracy  low complication rate  Zero drift.  Mechanical problems (breakage or dislocation)
  • 52.
    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.
  • 53.
  • 55.
    Advantages  Does notpenetrate 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.
  • 56.
    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
  • 57.
    Advantages Disadvanteges  canbe placed in various compartments, including the ventricle, parenchyma, and subdural space  Less accurate.
  • 58.
    Spiegelberg Parenchymal Transducer  usingan 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.
  • 59.
    Emerging Technology  Tomeasure 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
  • 60.
    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
  • 61.
     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.
  • 62.
     Tympanic membranedisplacement 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.
  • 63.
    Common Causes ofraised 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
  • 64.
    Intracranial hypertension secondaryto 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
  • 65.
    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
  • 66.
    General care tominimize intracranial hypertension  Optimizing cerebral venous outflow  Respiratory care  Fever control  Blood pressure control  Treatment of anemia  Seizure control  Sedation and analgesia
  • 67.
    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.
  • 68.
    Respiratory care  Avoidhypoxia (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)
  • 69.
    Fever control  potentvasodilator 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.
  • 70.
    Blood pressure control Avoid hypotension –normalize intravascular volume.  Use pressors if needed.  Control hypertension if present.
  • 71.
    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.
  • 72.
    Seizure control  Seizurescan 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.
  • 73.
    Sedation and analgesia Agitation and pain may significantly increase blood pressure and ICP.  Light sedation and good analgesia
  • 74.
    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
  • 75.
    Measures for refractory intracranialhypertension  Heavy sedation and paralysis  Hyperosmolar therapy  Hyperventilation  Barbiturate coma  Steroids  Prophylactic hypothermia  Surgical treatment
  • 76.
    Heavy sedation andparalysis  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.
  • 77.
    DRAWBACKS  Interferes inexamination.  Myopathy  Polyneuropathy  Prolonged neuromuscular blockade.
  • 78.
     Can minimizethese complications by  Limiting the use and dose  Train-of-four monitoring  Measuring creatine phosphokinase daily  Stopping thedrug daily to evaluate response.
  • 79.
    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
  • 80.
     An osmoticdiuretic  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
  • 81.
    Mannitol osmotherapy inbrain  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.
  • 82.
    Blood viscosity autoregulationof 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.
  • 83.
     . Whenautoregulation 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
  • 84.
    A test doseof mannitol should be given prior to instituting therapy for patients with marked oliguria or those believed to have inadequate renal function.
  • 85.
    Adverse effects  Acuteadverse 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
  • 86.
     Dehydration andElectrolyte 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
  • 87.
    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
  • 88.
    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
  • 89.
    •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
  • 90.
    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.
  • 91.
     the additionof 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
  • 92.
    Hypertonic saline  ICPreduction 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
  • 93.
    Hypertonic saline Mechanism ofaction:  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
  • 94.
    Complications  Coma, seizuresand rebound phenomenon.  Systemic effects: CCF , Hypokalemic acidosis.  Deranged platelet aggregation  Phlebitis and renal failure Hypertonic saline
  • 95.
    Hyperventilation  Decreases paco2, Induce constriction of cerebral arteries by alkalinizing the CSF.  Reduction in cerebral blood volume decreases ICP.
  • 96.
     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
  • 97.
    do not useprophylactically avoid aggressive hyperventilation (pCO<25 mm Hg)
  • 98.
    Loop diuretics Used inconjunction 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)
  • 99.
    Steroids  Dexamethasone isthe 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.
  • 100.
    Steroids  Mechanism ofaction: 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
  • 101.
    Barbiturate therapy  Barbiturateprotect 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
  • 102.
     Dosage: 10mg/kgadminstered 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
  • 103.
     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
  • 104.
     Causes adecrease 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
  • 105.
    Surgical treatment  Resectionof mass lesions  Acute epidural and subdural hematomas , brain abscess, tension pneumocephalus and tumors etc need to be removed
  • 106.
    Ventriculostomy  CSF drainage Works immediately by removal of CSF  long-term benefit by allowing edema fluid to drain into the ventricular system
  • 107.
    Complications  Infection  Haemorrhage Brain parenchymal damage  Seizure  Needle porencephaly  Upward transtentorial herniation
  • 108.
    Operative decompression  Externaldecompression: 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.
  • 109.
     Brain oxygenationmeasured 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.
  • 110.
    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.
  • 111.
  • 112.
    References 1. Youmans NeurologicalSurgery, 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)
  • 113.
    Questions  1. firstsystematic recording of ICP done by a)Guilalmaue b)Janny c)Neil lundberg d) all of the above
  • 114.
     2. thelevel of CPP under which CBF would impair is a)50mmhg b)40mmhg c)60mmhg d)30mmhg
  • 115.
     3.The territoryof infarcts seen in uncal herniation a)ACA territory b)PCA territory c)MCA territory d)none
  • 116.
     4. Thelimiting factor for therapy barbiturate is a)respiratory depression b)hypotension c)hypertension d)all the above
  • 117.
     5.Factor associatedwith incidence of infection in EVD  a)insertion of IVC in neuro intensive care unit b)previous IVC c)use of steroids d) none
  • 118.
     6.most significantproblem of fiberoptic ICP monitor is a) infection b)breakage c)zero drift d)bleeding
  • 119.
     7.best methodof ICP monitor in patients with massive edema with slit ventricles a)subarachnoid bolt b)parenchymal monitor c)both d)EVD
  • 120.
     8.the bestmethod of ICP monitor in coagulopathy patients is a)subararachnoid bolt b)EVD monitor c)parenchymal transducer d)TCD
  • 121.
     9.During mannitoladministration , to prevent renal failure the serum osmolality should be below a)320 m osm b)280m osm c)350 mosm d)250 m osm
  • 122.
     10.the minimumdiametre of decompressive craniectomy flap is a)12 cm b)20 cm c)15cm d)25 cm

Editor's Notes

  • #28 some impairment of ocular motility by thisstage, some degree of exophoria ispresent in most people when they are not completelyawake.However, examining oculocephalicresponses by rotating the head usually willdisclose eye movement problems
  • #41 Infection most often related to duration of catheter placement , infection rate significantly increased after 5 days of palcement.
  • #42 find a reduction in CSF and systemic infection in the group that received prolonged antibiotic prophylaxis.[33] It should be noted that infections that develop in patients who receive prolonged or broad-spectrum antibiotic prophylaxis, or both, for EVD placement are often caused by more virulent microorganisms such as Candida and gram-negative organisms.[32-34] Currently, the “Guidelines for the Management of Severe Traumatic Brain Injury” does not recommend antibiotic prophylaxis for EVD placement/catheterization.significantly reduce bacterial adhesion versus controls in vitro and in animal models.[36] In one randomized controlled trial, Zabramski and coworkers showed that a catheter impregnated with minocycline and rifampin reduced the infection rate significantly from 9.4% to 1.3
  • #44 The percussion wave is the most constant in amplitude and derives from pulsations in large intracranial arteries.[9] The tidal wave has a more variable shape and is thought to arise from brain elastance. The tidal wave and the dicrotic wave are separated by the dicrotic notch, which corresponds to the dicrotic notch in the arterial pulse waveform.
  • #50 it is possible to insert the probe into a region with pathology as well.t is possible to insert the ICP monitor even in patients with severely compressed ventricles or those with a significant midline shift.
  • #52 The most significant problem of the Camino fiberoptic device is zero drift. The device is first zeroed to atmospheric pressure (usually at room temperature) and then inserted into the brain parenchyma. Recalibration cannot be performed unless the transducer is removed from the patient, zeroed, and then reinserted. Zero drift then occurs over time, which will lead to an erroneous ICP reading. According to the manufacturer, the drift for the first 24 hours should be only 2 mm Hg and then should be 1 mm Hg for the first 5 days. However, clinical studies have shown that the daily drift is significantly larger than the manufacturer&apos;s specification. Daily drift rates of 0.5 to 3.2 mm Hg have been reported, and the maximal drift reported in most studies is usually greater than 20 mm Hg (positive or negative).[41,43-45] In most clinical series, recalibration was often needed, and this was often discovered when the clinical picture did not match the ICP reading or a negative ICP reading appeared on the monitor.[43],[45] However, there has been no report of erroneous ICP reading resulting in clinical mismanagement, such as missing an enlarging mass lesion
  • #67 Prevention or treatment of factors that may aggravate or precipitate intracranial hypertension is a cornerstone of neurologic critical care. Specific factors that may aggravate intracranial hypertension include obstruction of venous return (head position, agitation), respiratory problems (airway obstruction, hypoxia, hypercapnia), fever, severe hypertension, hyponatremia, anemia, and seizures
  • #68 WITH ELEVATION MAP REDUCED AND ICP ALSO REDUCED HENCE CBF IS CONSTANT.J Trauma. 2004 Oct;57(4):687-93; discussion 693-5.Decompressivelaparotomy to treat intractable intracranial hypertension after traumatic brain injury
  • #69 which may be needed to improve oxygenation, can increase ICP by impeding venous return and increasing cerebral venous pressure and ICP, and by decreasing blood pressure leading to a reflex increase of cerebral blood volume.
  • #70 Fever increases metabolic rate by 10% to 13% per degree Celsius
  • #71 . If the decision is made to treat systemic hypertension, the choice of antihypertensive agent is important. Vasodilating drugs, such as nitroprusside, nitroglycerin, and nifedipine, can be expected to increase ICP and may reflexively increase plasma catecholamines, which may be deleterious to the marginally perfused injured brain. Sympathomimetic-blocking antihypertensive drugs, such as β-blocking drugs (labetalol, esmolol) or central acting α-receptor agonists (clonidine), are preferred because they reduce blood pressure without affecting the ICP. Agents with a short half-life have an advantage when the blood pressure is labile.
  • #72  [PubMed] reported of patients with severe anemia presenting with symptoms of increased ICP and signs of papilledema, which resolve with treatment of the anemia The mechanism is thought to be related to the marked increase in CBF that is required to maintain cerebral oxygen delivery when anemia is severe.
  • #77 Although a disadvantage of this therapy is that the neurologic examination cannot be monitored closely, the sedatives and muscle relaxants can be interrupted once a day, usually before morning rounds, to allow neurologic assessments.
  • #78 Myopathy is associated with the use of neuromuscular blocking agents, particularly in combination with corticosteroids [46]. Polyneuropathy has been observed in patients with sepsis and multiple organ failure. Prolonged neuromuscular blockade is seen in patients with multiple organ failure especially with kidney and liver dysfunction