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 intra cranial pressure

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

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