Neurosurgery and ICU by 6NaX84

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									Neurosurgery and ICU
       Wilson Ho
       July 2009
 Neuro-physiology
 ICP monitoring
 Severe head injury
 Brain tumor
 Hemorrhagic stroke
 hyponatremia
Neuro - physiology
       Monroe - Kellie Principle
 Skull   is a rigid box
     Brain 80%
     Blood 10%
     CSF 10%


 Expansionof one component is at the
 expense of the other components
Monroe-Kellie Principle




   Volume-Pressure Curve
   Normal ICP ~ 4 –15mmHg
             Auto-regulation
   The brain’s ability to change the diameter of its blood
    vessels automatically over a range of normal BP to
    maintain a constant cerebral blood flow (CBF) in
    response to its metabolic needs.

   The Brain can effectively auto-regulate its
    hemodynamics when BP is 60-170mmHg & ICP <30
    mmHg

   CBF is Normally 750 ml/min
                       Auto-regulation curve


CBF
                                                              Slope not zero




                  10           50                      140   mmHg


Critical closing P.                                                 CPP

                        Cerebral Perfusion Pressure = MAP - ICP
Auto-regulation compromised
Systemic factors
   MAP < 50 mmHg
       poor perfusion – ischemia

   MAP > 170 mmHg
       Arteries unable to constrict – hyperaemia – increase ICP


Local factors
       Head Injuries
       Tumors
       vascular lesions
       increases metabolic activities
       Prolonged  ICP > 30 mmHg
  Cerebral Perfusion Pressure
 CPP = MAP – ICP
 MAP = DBP + 1/3 (SBP – DBP)


 60-150mmHg   range. CPP should be
 maintained > 65 mm Hg for adequate
 blood supply to brain
ICP monitoring
              ICP monitoring
 Indications


     Suspected raised intracranial pressure
     Unable to monitor clinically
     CSF retention
     Post op condition
                   ICP monitoring
   Intraventricular
       Monitoring
       Therapeutic


   Parenchymal
       Easy installation


   Subdural / epidural
       Inaccurate
       Rarely used
ICP monitoring
         ICP Catheter problems
                      Ensure all connections are tight
   Infection         No leakage of CSF
                      Regular changes of scalp dressing
   Over - drainage   Keep drainage bag at proper level
                      Minimize manipulations
                      Poor wave-form
                      Empty bag regularly
   Blockage          Early removal
                      Unavoidable
   Disconnection     Avoid kinking of tubings
                      Inform immediately
   Bleeding
                      Double check with water column
   Inaccuracy        Re-calibrate
   Pull out          Inaccurate when no CSF around catheter
                      Can be dangerous
    accidentally      Especially for confused patients
   Management of raised ICP
 Blocked  ?
 Need re-calibration ?
 Sedated enough ?
 Proper ventilation ?
 Trend of ICP ?
 Other parameters & physical signs
 CT brain
            To lower ICP
   Level of bed
   Sedation / paralysis
   Controlled hyperventilation
   Osmotic diuresis – Mannitol / Glycerol
   Maintain adequate systemic BP
   Let out CSF from EVD
   Surgery
       Removal of mass lesion
       Decompressive craniectomy
Severe head injury
                General Principles
   To prevent “secondary insults” to the brain

   Primary insult
       Damage sustained during impact
Severe Head Injury GCS (3-8)
 SECONDARY BRAIN DAMAGE
    Cerebral Swelling
         Medical / Surgical means
    Herniation
         Removal of hematoma and contusion
    Cerebral ischemia
         Maintain adequate perfusion and oxygenation
    Infection
         CSF leak, open brain trauma
    Convulsion
         Anti-convulsants
Herniation - “cone”
    Patients needing ICU care
 Close  monitoring
 Multi-system trauma
 Depressed conscious level
 Likely to deteriorate
 Post operative patient
 Potential candidates for organ donation
              Pathology
   Cerebral Contusion
       Lobes and poles against skull bone

   Intracranial hematoma
       Epidural hematoma
       Subdural hematoma

   Skull fracture
       Vault – open / close
       Skull base

   Diffuse axonal injury
          General Principle
 Small contusion / hematoma can be
  absorbed
 Cerebral swelling peak around day 7 - 10
 Remove lesions with mass effect
 Monitor & maintain CPP
 Prevent Seizure
 Prevent hyperthermia
Cerebral Contusion
Within 1st hour   After 6 hours
Epidural Hematoma
Acute Subdural hematoma
 Basal skull fracture

 Clinicalsuspicion
 Confirmed by CT scan
 CSF fistula
 NO nasal gastric tube
Brain tumor
                  Brain tumor
 Primary
     Glioma
 Secondary     – more common
     Lung / colon / breast / kidney


 Supra-tentorial    / Infra-tentorial
 compartment
      Post operative ICU care
 Electiveresection
 Rarely emergency resection
 Large raw area for large tumors
 Prevent STRUGGLING / HYPERTENSION


     Steroid
     Anticonvulsant
  Posterior fossa tumor

 Cerebellarmetastatic tumor
 Nerve sheath tumor
 Brainstem tumor
Acoustic Neuroma
Respiratory problem / Aspiration problem
Check gag reflex / consult speech therapist
Pituitary Tumor
              Pituitary Tumor
 Functional
     Acromegaly / Cushing disease
 Nonfunctional
     Visual symptoms / Mass effect


 Transphenoidal     removal
     Microscopic / Endoscopic approach
        Post operative monitoring
   Visual acuity, visual field
       Residual tumor hemorrhage
       Optic nerve / chiasm injury


   CSF leakage

   Excessive urine output
       Usually temporary
Hemorrhagic stroke
                ICH
 10% Treated surgically
 Small hematoma
     Absorb spontaneously
 Large   hematoma
     Vegetative
 Medium     sized hematoma
     Possible surgical intervention
        Common ICH
 Capsular  / thalamic hemorrhage
 Intra-ventricular hemorrhage
 Cerebellar hemorrhage
 Brainstem hemorrhage
USG guided aspiration
            Post op ICU care
 Risk   of re-hemorrhage
     Large raw area created by hematoma
 Keep sedated
 Prevent HYPERTENSION
     Low ICP
 Continue   anticonvulsant
Subarachnoid hemorrhage
Subarachnoid Hemorrhage
  Head injury
  Cerebral aneurysms
   Aneurysmal
Subarachnoid H’age
Aneurysmal Subarachnoid H’age
                ICU Care

 Close  monitoring
 Maintain normal BP
 Calm
 Start Nimodipine / Anticonvulsant
 Angiogram / CT angiogram


 Early   / delay surgery
 Aneurysmal hemorrhage
 Mass effect -   EVD / Craniotomy
 Hydrocephalus   -    EVD / Shunt
 Rebleeding -    Clipping / Coiling
 Seizure     -   Anticonvulsant
 Vasospasm -     Nimodipine / Triple H
Clipping of aneurysm
Coiling of aneurysm
   Cerebral Vasospasm / Delayed
Ischemic Neurological Deficit (DIND)

 Delayed    cerebral ischemia
     most common cause of death and disability
      after SAH


 Over 17-40% SAH patients, death or
  major deficits
         Why vasospasm?

Oxyhaemoglobin

   Free oxygen radicals
   Lipid peroxidation
   Activation of protein kinase C, phospholipase
    C and A2
   Accumulation of diacylglycerol
   Release of endothelin-1
   Tonic state of smooth muscle contraction
Factors that increases the risk of
              DIND
  Amount    of subarachnoid blood and
     frequency of SAH

    Poor clinical SAH grades
    Antifibrinolytic drugs
    Hypotension
    Inappropriate treatment of hyponatraemia
    Hypovolaemia
    Hyperthermia
    Increased ICP
Transcranial Doppler
Mean MCA Velocity (cm/s)   300




                           200




                           100




                             0
                                 D1 D2 D3 D4 D5 D6 D7 D8 D9 D10 D11 D12 D13
                                                  SAH Day
Management of Vasospasm
   Optimize ICU support, prevent hypotension,
    hyponatraemia, anaemia, hyperthermia, raised ICP

   Triple H therapy
       Hypertension, hypervolaemia, haemodilution


   Drugs
       Nimodipine
       Magnesium sulphate?
       Tirilazad mesylate?


   Angioplasty
Angioplasty for vasospasm
         Summary

 Dedicated  ICU care
 Aware of vasospasm
 Daily TCD
 Early detection and aggressive
  treatment (angioplasty)
 Hyponatremia in neurosurgery
 Common     in

    Traumatic brain injury
    Aneurysmal subarachnoid hemorrhage
    Transsphenoidal surgery for pituitary tumor
 Hyponatremia in neurosurgery
 Syndrome      of inappropriate ADH secretion
 (SIADH)

 Cerebral    salt wasting (CSW)

     Hyponatremia
     High urine to serum osmolality ratio
     High urinary sodium level
               Hyponatremia
 SIADH
     expanded extracellular volume (ECV) due to
      water retention


 CSW
     Contracted ECV due to renal salt wasting
           Mechanism of CSW
 Postulation


     Disruption of neural input to the kidney

     Increased in circulating natriuretic factor –
      ANP / BNP
                      Treatment
 SIADH – fluid restriction
 CSW – salt & fluid replacement


        Wrong diagnosis, wrong treatment

   SIADH
       given IV saline, worsening of hyponatremia

   CSW
       Fluid restriction – further ECV contraction
    Pituitary transsphenoidal
              surgery


 Mechanical  manipulation / disruption of
 pituitary gland and pituitary stalk
         DI Tri-phasic response
   4-8 day period of DI

   1-14 days of
    excessive release of
    ADH

   Permanent DI
            Diabetes Insipidus

   ADH deficiency

   Polyuria (>5ml/Kg/hr)

   Urine / plasma osmolality ratio <1.5

   Hypernatremia

   Treatment – sodium & fluid replacement,
    DDAVP
                  DI & CSW
 DI   & Cerebral salt wasting can co-exist
     Give DDAVP alone for increased urine output
     Increase in free water resorption
     Exacerbation of hyponatremia
     May lead to cerebral oedema

 Don’t   just act on high urine output
     Check sodium level, plasma / urine osmolality
     Replace sodium, fluid and DDAVP
           Delayed hyponatremia
 SIADH like syndrome
 5 days post transsphenoidal surgery
 Nausea, vomiting, headache, malaise, dizziness


   Pathophysiology
       Surgical manipulation causing release of ADH
       Adrenocortical insufficiency

   Low dose hydrocortisone – decreased ADH
    secretion
          the end
        thank you

wilsonho@ns.org.hk

								
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