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Raised intra cranial pressure
 

Raised intra cranial pressure

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RAISED ICT IS AN IMPORTANT ONE IN CASE OF CVAs THERE MAY BE FALSE LOCALISING SIGNS//

RAISED ICT IS AN IMPORTANT ONE IN CASE OF CVAs THERE MAY BE FALSE LOCALISING SIGNS//

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    Raised intra cranial pressure Raised intra cranial pressure Presentation Transcript

    • WEL-COME
    • DEPARTMENT OF INTERNAL MEDICINE
    • PIVOTAL ROLE IN CRITICAL CARE MANAGEMENT RAISED INTRACRANIAL PRESSURE
    • INTRODUCTION
      • What is intracranial pressure?
      • Pressure within the cranial cavity (within a rigid structure) Skull /cranialvault exerted by the intracranial contents .
    • Normal Intracranial Pressure
      • 5 – 15 mmHg in adult at rest
      • <20mmHg usually in most
      • In recumbent posture – 8mmHg or 110 mmH 2 0
      • Zero in standing posture due to transmission of CSF column to the lumbar region.
    • A View of CSF
      • 1 0 function of CSF in mechanical one – water jacket.(1500gm of brain tissue  50gm in CSF)
      • Average intracranial volume is 1700ml
      • Volume of brain is 1200-1400ml
      • CSF Volume 70 – 160ml (104ml-mean)
      • Spinal subarachanoid space 10-20ml of CSF
      • Average rate of CSF formation is
        • 21-22 ml/hr
        • 0.35ml/min
        • 500ml/day
        • renewed 4 or 5 times daily
      • Main site of formation of CSF – choroid plexure floor of the lateral, third, fourth ventricle
      • Blood brain barrier – is formed by
        • Endothelium of the choroidal, brain capillaries
        • Plasma membrane, adventitia of these vessels, pericapillary foot processes of astrocytes
        • CSF has “sink action” Davson’s term
        • CSF third circulation by “WILLIAM HARVEY” (Blood, Lymph)
    • Raised ICP
      • Part of compartmental syndrome
      • Persistent elevation of > 20mmHg for > 10min is raised ICP
      • > 30mmHg – poor prognosis .
    • MONRO – KELLIE DOCTRINE
      • An increase in the volume of any one of the three components brain, blood, CSF must be at the expense of the other two beyond the autoregulation.
      • Brain is least compressible among the three.
      • Cerebral blood flow is autoregulated
      • Autoregulation persist until cerebral prefusion pressure is in range of 60-160 mmHg
      • If CPP <60mmHg --  CBF
    • CUSHING TRIAD
      • Hypertension
      • Bradycardia
      • Irregular respiration
      • Later phenomenon of raised ICT
    • Intracranial Pressure causes
      • Intracranial Masses
      • Blockage of CSF
      • Haemorrhage
      • Hypertensive encephalopahty
      • Venous Sinus thrombosis
      • Hyperadrenalism
      • Attitude sickness
      • Tetracycline
      • Vit-A intoxication
      • Cerebral or Extracerebral mass
        • Tumor
        • Massive infraction with edema
        • Contusion
        • Parenchymal
        • SDH : EDH
        • Abscess
      • General Brain Swelling
        • Anoxia, Acute hyponatremia
        • A hepatic failure
        • Hypertensive encephalopathy
        • Reye syndrome
      •  Venous Pressure
        • Heart Failure
        • Obs. Of superior mediastinum Jugular veins
        • Cerebral vein thrombosis
      • Obstruction to flow and absorption of CSF
        • Hydrocephalus
        • Meningitis – usual cause
        • If at absorption surface – the ventricles remain normal in size.
      •  Volume of CSF
        • Meningits ; SAH
      •  CSF production
        • Choroid plexus tumors
        • In children hydrocephalus
    • TYPES OF CEREBRAL EDEMA
      • Cytotoxic
        • Cerebral swelling  cellular engorgement  neuron, glia
        • Is due to ischemia
      • Vasogenic edema
        • Accumalation of extracellular fluid
        • Defective BBB
        • Leaky capillaries
        • Seen in metastases, gliomas, meningiomas
    • Changes in CRANIUM
      • Sub falcine hermation
        • Shift of cingulate gyrus of one hemisphere under the falxcerebri to contra lateral side.
        • Septum pellucidum may shift from midline.
      • Uncal Herniation
      • Tentorial – Mid brain
      • Tonsillar – Foramen magnum
    • CLINICAL FEATURES Headache
      • Worse in early morning, lying down
      • Increased on coughing, straining, bending
      • Improves through the day, ambulation
      • Associated with vomiting
      • Relieved by analgesia
      • Dull ache
      • Often mild
      • Reason :
        • relative hypercarbic, hypoxia state during sleep may be responsible for exacerbation on waking up
        • Compression of pain sensitive vascular structures
    • Clinical Signs of herniation
      • Brain stem compression
        • Loss of pupillary activity
        • Impairment of eye movements
        • Hyperventilation
        • Motor posturing flexion or extension
      • Herniation is often is rapidly fatal
      • Vomiting with / without Nausea
        • Projectile
        • Due to irritation of the vagal nuclei in the floor of fourth ventricle by the  ICP
        • Relieves headache Temporarily
      • Double vision, Blurred vision
        • Due to III, VI CN palsies
      • Frontal Lobe
        • Personality changes
        • Unsteadiness of gait
        • Incontinence of urine
      • Right side hemiplegia, garbled speech – dominant temporal lobe .
      • Lethargy, drowsiness
      • Unconsciousness – COMA
      • Papilloedema – due to CSF shunted into optic nerve sheaths, may be the only sign of increased CSF / increased ICP
      • Arterial hypertension
      • Fever
    •  
    • Investigations
      • CT Scan with Contrast
      • MRI with Contrast
        • Except cerebral abscess
      • Technetium brain scan – destructive skull vault, skull base lesions
      • EEG – Cerebral abscess, focal slow waves seen
      • Skull Film- not useful in hemispherical tumors
      • Routine tests
      • Angiography, volumetric MRI
      • Lumbarpuncture only after imaging
      • Biopsy
    • SPECIFIC INVESTIGATIONS
      • Invasive intracranial pressure monitoring
        • Extradural <1%, baseline drift
        • Subdural
        • Intraparenchymal, accurate 1%, breakage
        • Intraventricular can also be used for drainage, increased inflammation rate
      • Cisternography
      • Transfontametry
      • Transcranial doppler flow velocity
    • IMMEDIATE MEASURES Rapidly effective are
      • Elevate head end by 30-45 0 – straight head position
        • Head elevation -  JVP,  venous outflow
        • Sharp head angulation - avoided
      • Hyperventilation – Acute lowering of ICP
        • 16-20 cycles / min (ventilated) / Ambu bag by face mask
        • Action < 30min
        • Diminishes in 1-3 hr
        • Tapered over 6-12 hr
        • Sudden cessation leads to increased ICP
      • Hyperventilation should be such that PCo 2 < 30mmHg
      • If < 25mmHg – exacerbate cerebral ischemia by causing excessive vasoconstriction .
      • Mannitol
        • Biphasic action
        •  ICP by cerebral dehydrating effect
        • RAPID infusion is imp.
        •  Brain volume – by osmotic gradient
        • Osmotic diuretic – free water clearance
      • 20% mannitol 1g/kg loading dose
      • Every 4-6hrs @ 0.25 – 0.5g/kg
      • It should be given over 10min
      • Action in 10-20min lasts for 3-6 hrs
        • Disadvantages:
          • Congestive cardiac failure – due to volume contraction
          • Hypokalemia– serum electrolytes every 6hrs
          • Hyperosmolarity
          • ATN
          • Sudden rebound increased ICP
          • Normal saline (0.9%) should be given
          • No action if > 315m osm/kg , maintain <300 or <280
      • Drainage of CSF
        • 5-10ml of CSF to be removed
      • Use of steroids
        • Dexamethasone 4-6mg 6 th Hrly
    • Neurosurgical procedures
      • Craniotomy
      • Ventriculostomy
      • Placement of ICP monitor
    • ICP monitors
      • Ventricular monitors
        • External drainage can be done
        • High infection rate
        • Increased after 5 days
      • Intraparenchymal
        • It is fibroptic , acurate, 1% infectgion, inflexible, Breakage
      • Epiudural Transudes
        • Superficial to dura
        • <1% infection
        • Baseline drift (>5-10mmHg)
      • Normal Intracranial Pressure 50-200cmH2O (4-15mmHg)
      • Jugular venous pressure is normally principle determinant of ICP
      • Initially as volume is added to the intracranial space, minimal increase in pressure occurs – Highly compliant nature of intra cranial contents
      • As intracranial volume increases CSF is displaced through foramen magnum blood is displaced from compressed brain tissue
      • Loss of compliance
      • Further increase in intracranial volume leads to dramatic elevation of ICP
    • CEREBRL PERFUSION PRESSURE
      • Important determinant of CBF
      • CPP = MABP – ICP
      • In presence of auto regulation, CBF is maintained at a constant level across a wide range of CPP ( 50-150mmHg)
      • In presence of injury auto regulation impaired
      • CBF directly proportional to CPP
      • CPP should be maintain 70-120mmHg
      • <70mmHg secondary hypoxic ischemic damage
      • > 120mmHg break through hyperperfusion
    • ICP WAVEFORMS
      • Effects of systemic arterial, venous pressure on intracranial contents
      • Initial offered deflection systemic arterial pressure wave
      • two types
        • Lundberg A waves
        • Plateau waves – Dangerous elevation of ICP 20-80mmHg
      • Global Hypokinesia
      • Lundberg B waves
        • Less amplitude 20mmHg
        • 1-5minutes
        • Less Dangerous
        • Marker of abnormal auto regulation
    • Respiration pattern
      • No localizing value
        • Depressed inspiration - Severe Coma
        • Cheyne stokes respiration – Hyperventilation & Apnea, Bihemispheric lesions, Metabolic encephalopathy, stable breathing pattern,
        • Doesnot imply impending respiratory arrest
        • Hyperventilation – Systemic diseases , Meatabolic acidosi, Hepatic encephalopathy,
        • Central neurogenic hyperventilation, CNS Lymphoma, Brain stem damage
      • Localizing value
      • Apneustic breathing – Prolonged inspirtory phase, apnea – pontine damage
      • Cluster breathing , shallow hyperventilation, cerebellar damage
      • Ataxic (biot’s ) breathing – irregular choatic , medullary respiratory centre, apnea
    •  
      • What is Kernohans notch?
      • What is lymphatic blood supply of brain?
      • What is Queckenstedt test?
      • Where is megalencephaly seen?
      • What are late signs of late intracranial pressure?
      • Where is hyperventilation useful?
    • GENERALIZED TREATMENT
      • Sedation, Paralysis – needs intubation
        • Morphine IV 2.5mg every hrly
        • Fenatanyl IV 50mg/ml
          • 25-100mg IVP –rapid control
          • Infusion 4mg/250ml NS @ 5ml /hr
        • Propofol IV 10mg/ml – reversible
          • 5-50mcg/kg/min
      • BP management
        • if CPP > 120mmHg
        • if ICP > 20mmHg
        • maintain CPP > 70mmHg by treatment of hypertension
        • Labetalol IV 5mg/ml -  1  1 blocker 20 – 80 mg every 10-20minutes
        • Nicardpine IV 25mg / 250 ml Ns @5ml /Hr
        • Increase BP by Dopamine 800mg/500ml NS
      • Seizures
        • Iv.Phenytoin 25mg/min slowly
        • Iv. Diazepam resp.depression
        • Iv.Lorazepam
        • Theopental
      • Fever
        • Acetaminophem 650mg every 4hrly
        • Indomethacin 25 mg every 6hrly
      • Blood glucose – Between 70-140mg/dl
      • Na + > 140mmol/L
      • Avoid fluid overload, dehydration
      • High caloric feeds
      • Hyperosmolar isovolemia needed
      • Foley’s catheter
    • SPECIFIC TREATMENT
      • Decompressive surgery
        • Removal of temporal bone on non dominent side acouste neuroma
      • Chemotherapy
      • Diuretics
      • Pentobarbital coma – refractory cases
      • - may cause hypotension
      • - 10 -20mg /kg flaccid coma
      • - EEG every 24-48hrs
      • Hemicraniectomy
    • PROGNOSIS
        • Poor Prognosis – CPP < 60mmHg > 20min
        • Refractory to Pentobarbital coma
        • Motor response – to pain is imp prognostic sign flexor response
    • Idiopathic Intracranial Hypertension
      • Pseudo tumor cerebri
      • Marked papilloedema
      • No increased ventricular size
      • Obese young women
      • Headache, visual blurring
      • VI cranial nerve palsy
      • CSF Pressure increased
      • Imaging is normal
      • It is due to decreased absorption of CSF
      • Treatment
        • Steroids , Acetazolamide, shunting
    • Normal Pressure Hydrocephalus
      • Enlarged cerebral ventricles
      • No cortical atrophy
      • Dementia
      • Urinary incontinence
      • gait apraxia
      • CSF pressure Normal
      • Treatment
        • Lumbarpuncture
        • Sudden increase in pressure on infusion of normal saline
        • shunt
    • ICP WAVES
      • Lundberg A waves (Plateau waves)
        • Dangerous elevation of ICP
        • 20 – 80 mmHg
        • 5min -1hr in duration
        • Associated with 60mmHg CPP
      • Lundberg B waves
        • 10 – 20 mmHg
        • 1 – 5 min
        • Less dangerous
        • Intracranial compliance
      • A – Pathologic
      • B – Arterial
      • C - Respiratory
    • Step wise approach
      • ICP Monitor ventriculostomy versus parenchymal
      • Goals
        • ICP < 20mmHg
        • CPP > 60mmHg
      • ICP > 20-25mmHg for > 5min
      • Drain CSF via ventriculostomy (If in place)
      • Elevate head end of bed –midline head position
      • Maintain (serum osmolality < 320mosml)
      • Glucocorticoids
      • Sedation
      • Paralysis
      • Hyperventilation
      • Pressor therapy
    • Refractory Cases
        • Phentobarb coma
        • Hypothermia
        • Hyperventilation
        • Hemicraniectomy
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    • Headings
      • Defination
      • Normal Values
      • Brief descripation of CSF
      • Autoregulation of CBF
      • Evaluation of raised ICP
      • Monas Kellie Doctrine
      • Cushing Traid
      • Changes in ICP
      • Changes in Cranium
      • Types of Cerebral Edema
      • Causes
      • Clinical features
      • Investigations
      • Teatment
      • ProtocolN.Pressure hydrocephalus
      • Idiopathic intracranial HTN
      • Prognosis
    • References
      • Harrison's Principles of Internal Medicine 18 th edi.
      • Adam and Uietor’s Principles of Neurology 7 th edi.
      • Cecil text book of Medicine 22 nd edi.
      • On call neurology – Marshall , meych
      • Neurology investigations – Hugher
      • Kumar and clarck clinical medicine – 5 th edi.
      • Oxford prionciples of critical card
      • API text book of medicine – 8 th edi.
      • Davidson & Principles , practice of Medicine 20 th edi.
      • Bailey and Love – 25 th edi.
      • Klashmigton manual of clinical therapeutics
      • Youtube.com
      • Newscience.com
      • Thanks to Dr.John Israel
          • Prof & Head of Medicine
      • One Thing about experience ins that when you don’t have very much
      • You’re apt to get a lot there is a big differences between nearly right exactly right
      • Coming together is beginning
      • Keeping together is progress
      • Working together is success.
      • Success is where preparation and opportunity meet.