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INTRACRANIAL PRESSURE : Hydrocephalus, Meningitis, Head Injury, Brain Tumors Fall 2009

INTRACRANIAL PRESSURE : Hydrocephalus, Meningitis, Head Injury, Brain Tumors Fall 2009. WHY DOES IT HAPPEN?. Brain tissue + blood + CSF = skull volume. MONROE-KELLIE HYPOTHESIS. Because of the limited space for expansion within the skull

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INTRACRANIAL PRESSURE : Hydrocephalus, Meningitis, Head Injury, Brain Tumors Fall 2009

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  1. INTRACRANIAL PRESSURE:Hydrocephalus, Meningitis, Head Injury, Brain Tumors Fall 2009

  2. WHY DOES IT HAPPEN? • Brain tissue + blood + CSF = skull volume

  3. MONROE-KELLIE HYPOTHESIS • Because of the limited space for expansion within the skull • An in any one of the components a change in the volume of the other

  4. COMPENSATION • Shifting of CSF • INCREASED absorption of CSF • DECREASED cerebral blood volume

  5. WITHOUT COMPENSATION • ICP will rise • DECREASED cerebral perfusion stimulates edema shifts brain tissue Through openings in the rigid dura HERNIATION DEATH

  6. DECREASED CEREBRAL BLOOD FLOW • ICP REDUCES CEREBRAL BLOOD FLOW ISCHEMIA CELL DEATH • SYSTEMIC RESPONSE: Vasomotor centers stimulated BP accompanied by slow bounding pulse and respiratory irregularities

  7. EFFECTS OF CO2 ON CEREBRAL BLOOD FLOW • CO2 partial pressure cerebral vasodilation leads to INCREASED cerebral blood flow and ICP • CO2 partial pressure cerebral vasoconstriction

  8. BODY’S COMPENSATION FOR CEREBRAL EDEMA • GOAL: MAINTAIN BLOOD FLOW AND PREVENT TISSUE DAMAGE • Autoregulation: brain changes the diameter of its blood vessels automatically to maintain a constant cerebral blood flow during alterations in systemic blood pressure • Decreasing production and flow of CSF

  9. CUSHING’S RESPONSE • Seen when cerebral blood flow decreases significantly • With ischemia vasomotor centers increases arterial pressure to overcome the ICP • Sympathetic response causes a rise in systolic BP, widening pulse pressure and reflex slowing of the heart rate • MUST HAVE IMMEDIATE INTERVENTION • CAN RECOVER AT THIS POINT IF TREATED RAPIDLY

  10. CUSHING’S TRIAD • At a certain volume and pressure the brains ability to autoregulate becomes ineffective leading to ischemia and infarction • See in patient: mental status changes and bradycardia, hypertension and bradypnea • IF NO INTERVENTION leads to HERNIATION OF THE BRAIN STEM

  11. HERNIATION OF THE BRAIN STEM • Shifting of brain tissue • Area that is shifted has pressure on it • Resulting in decreased blood supply • Resulting in cerebral ischemia • Resulting in INFARCTION and BRAIN DEATH

  12. PATHOLOGIC CONDITIONS THAT CAUSE IIP • Head injury, CVA • Brain tumor • Intracranial surgery • Meningitis • Encephalitis • Subarchnoid hemorrhage

  13. EARLY SYMPTOMS OF IIP • ***change in LOC: Slowing of speech Delay in response to verbal suggestions Irritability, Restlessness, resp effort • Changes in pupils • Weakness in one extremity/ 1 side of body • Headache constant increasing in intensity

  14. LATE SYMPTOMS OF IIP • Deterioration of LOC leading to coma • Sluggish, unequal response of pupils to light • HR ; RR ; bradycardia to tachycardia • BP and temperature rise • Pulse pressure widens • irregular respiratory pattern: Cheyne Stokes • Projectile vomiting • Hemiplegia, decorticate/decerebrate posturing, bilateral flaccidity before death • Loss of brain stem reflexes

  15. Neurologic Nursing Assessments • LOC • Pupil response • VS • Motor activity

  16. ASSESSMENT OF LEVEL OF CONSCIOUSNESS Indication of the highest level of cerebral activity EVALUATION IS DONE BY: • Determining degree of alertness • Orientation to person, place, time • Ability to awaken • Degree of lethargy • Status of reflexes (gag, swallow, etc)

  17. ASSESSMENT OF PUPILS • Determines reaction to light • NORMAL: the pupils constrict rapidly and equally to light (PERLA) • ABNORMAL: unequal reaction, abnormal position of pupils

  18. ASSESSMENT OF VS INDICATING IIP • Pulse decreases • Respiration decreases • BP increases • Temperature increases

  19. ASSESSMENT OF MOTOR ACTIVITY • Watch hand and feet movement • Have pt squeeze your fingers • Look for change in facial muscles • Look for inequality of motor strength, generalized weakness, tremors, ataxia

  20. ASSESSEMENT OF TEMPERATURE • Increased temperature indicates increased intracranial pressure • CAUSE: irritation or damage to temperature regulating mechanism in brainstem

  21. SEIZURE PRECAUTIONS • Pad side rails • Have oxygen and suction available • Observe for seizures

  22. ASSESSMENT/DIAGNOSTICS • CT scan • MRI • PET (positive emission tomography)

  23. MANAGEMENT • GOAL IS TO RELIEVE INCREASED ICP HOW? • cerebral edema • volume of CSF • cerebral blood volume while maintaining cerebral perfusion

  24. MONITOR ICP • Intraventricular catheter (ventriculostomy) • Subarachnoid bolt • Epidural/subdural catheter • Fiberoptic transducer-tipped catheter placed in subdural space or the ventricle

  25. GOALS: decreasing cerebral edema • Administer osmotic diuretics mannitol(Osmitrol) • Administer coricosteroids dexamethasone (Solumedrol, Medrol) • Restrict fluids • Drain CSF

  26. GOAL: maintaining cerebral perfusion • GOAL: Improve cardiac output • HOW: Using fluid volume and inotropic agents (dobutamine hydrochloride) • EFFECTIVENESS OF CARDIAC OUTPUT OUTCOME ASSESSED INDICATING SUCCESS AT : cerebral perfusion pressure maintained at greater than 70 mm Hg

  27. GOAL: Reducing CSF and intracranial blood volume • Use of drains to remove CSF • This reduces ICP and restores cerbral perfusion pressure • CAUTION: overdrainage causes collapse of the ventricles

  28. GOAL: controlling fever • Fever increases cerebral metabolism and increases cerebral edema • Antipyretics • Cooling blankets

  29. GOAL: maintaining oxygenation • Maintain oxygenation • Monitor arterial blood gases

  30. GOAL: Reducing metabolic demands • Reduce cellular metabolic demands • Administer barbiturates: nembutal, pentothal, diprivan • Administer opiods (morphine sulfate or fentanyl citrate) with ventilated clients to decrease agitation • Administer paralyzing agents vercuronium bromide or cisatracurium (Nimbex): agitation. Must be used with sedation/analgesia

  31. ASSESSMENTS NOTED WITH ICP BASED ON LOCATION IN BRAIN • ICP on frontal lobes leads to Cheyne Stokes respirations • ICP in the midbrain causes hyperventilation • ICP in the lower portion of the brain stem (pons and medulla) leads to irregular respirations and eventually apnea

  32. NURSING CARE TO MAINTAIN PATENT AIRWAY

  33. NURSING CARE TO OPTIMIZE CEREBRAL TISSUE PERFUSION

  34. CAUSES OF INCREASED ICP

  35. HYDROCEPHALUS • Condition present at birth or resulting from other cause in which there is an abnormal amount of CSF volume in the intracranial cavity. • The fluid accumulates in the ventricles of the brain

  36. TYPES OF HYDROCEPHALUS INTERNAL NON-COMMUNICATING: • Blockage within the ventricles keeping the CSF from going to the subarachnoid space CAUSES: • developmental malformations • Neoplasms • Infections • trauma

  37. TYPES OF HYDROCEPHALUS CONTINUED INTERNAL COMMUNICATING HYDROCEPHALUS: • Occurs when the obstruction is in the subarachnoid cistern at the base of the brain or in the subarachnoid space. • There is no blockage in the ventricles • Fluid pathways are open • Fluid is not absorbed into the spinal subarachnoid space

  38. S & S OF HYDROCEPHALUS EARLY • Increased head circumference • Bulging fontanels • Cranial sutures separate • Signs of increased ICP

  39. S & S OF HYDROCEPHALUS • LATE: • Macewen’s sign (cracked pot) • Setting sun sign (bulging eyes, schlera visible above iris) • Opisthtonus (arched back) • Frontal bossing (forehead enlargement)

  40. TREATMENT OF HYDROCEPHALUS • Correction of cause of obstruction • Ventricular shunting procedures

  41. SHUNTS • Ventricular catheter with a oneway flow valve and a distal catheter • Designed to open at a predetermined pressure and close when the pressure falls below that level • Allows the CSF to go into the general circulation

  42. Types of shunts • Ventriculoperitoneal (VP) – one of choice • OLDER FORMS: • Ventriculpleural • ventriculoatrial

  43. PROBLEMS WITH SHUNTS • Infections • Tubing becomes kinked, plugged or separates • Needs to be replaced when grows

  44. POSTOP NURSING CARE • Position on unoperated side to prevent pressure on the shunt valve • Keep flat to prevent too rapid reduction of intracranial fluid (when the ventricular size is reduced too fast the cerebral cortex pulls away from the dura and produces a subdural hematoma)

  45. COMPLICATIONS • SHUNT INFECTION: look for inflammation at the operative site and along the shunt tract and increased intracranial pressure symptoms • TREATMENT: intraventricular and IV antibiotics • SHUNT OBSTRUCTIONS: look for S & S of increased intracranial pressure • TREATMENT: return to surgery

  46. Other causes of IICP: MENINGITIS DEFINED: Infection of pia mater, arachnoid membrane and CSF filled subarachnoid space due to bacteria, virus, or fungal organism

  47. S & S OF MENINGITIS • NEONATE: hypothermia or fever depending upon maturity, refuse to eat, poor muscle tone • INFANTS: fever and high pitched cry, headache, bulging fontanel • CHILDREN/ADOLESCENTS: fever, photophobia, headache, nuchal rigidity, positive Kernigs and Brudzinski’s signs

  48. SIGNS AND SYMPTOMS COMMON TO ALL AGES • Irritability • Seizures • vomiting

  49. DIAGNOSIS OF MENIGITIS LP: CSF examined Pressure measured • Normal: 0 to 15 mm Hg • Increased ICP: greater than 15 mm Hg CSF sent to lab to identify organism • Gram stain (preliminary identification • Blood Cell Count: increased WBC • Glucose: decrease in glucose • Protein: increase in protein

  50. TREATMENT OF MENINGITIS • Antibiotics after LP and sending of CSF • Penicillin (ampicillin, piperacillin) • Cephalosporins (cetriaxone sodium, defotasime sodium) • Vancomycin hydrochloride alone or with Rifampin • Dexamethasone given 15-20 min befoe first dose of antibiotic and every 6 hours for next 4 days

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