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

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

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WHY DOES IT HAPPEN?. Brain tissue blood CSF = skull volume. MONROE-KELLIE HYPOTHESIS. Because of the limited space for expansion within the skullAn in any one of the components a change in the volume of the other. . . COMPENSATION. Shifting of CSF INCREASED absorpt

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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




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

51. TREATMENT OF MENINGITIS Isolation for 24 hours after initiation of antibiotics Strict I & O q 1-2 hr: avoid overhydration to prevent cerebral edema Control seizures Control fever

52. NURSING CARE Decrease environmental stimuli Keep room quiet No pillow (nuchal rigidity) Seizure precautions Cautious handling of neck VS, NS, LOC q 1-2 hr Observe for S&S of IICP NPO if decreased LOC

53. EXPOSURE TO MENIGITIS CDC recommends treating children/parents /health care workers exposed to bacterial meningitis with RIFAMPIN SIDE EFFECTS: nausea, vomiting, diarrhea, HA, dizziness, orange urine, permanent orange discoloration of contact lenses; cannot be given to pregnant women and interferes with contraceptives Or Cipro or rocephin

54. VACCINATION Recommended as adjunct to antibiotic when exposed if living with person who develops meningitis Also recommended for children and at risk adults to avoid meningitis

55. HEAD INJURY CLOSED: no break in skull OPEN: break in skull

56. GRADES OF HEAD INJURY GRADE I: MILD HEAD INJURY – momentary loss of consciousness, not admitted to hospital GRADE II: patient has momentary loss of consciousness, lethargy, confusion, hemiparesis, admitted, require surgery GRADE III: SEVERE HEAD INJURY – patient unable to follow simple commands, have serious neurologic damage, dilated pupils and posturing; without rapid attention pt may die

57. TYPES OF HEAD INJURY CONCUSSION: transitory impairment of neurological function resulting from mechanical force and release of enzymes CONTUSSION: brain bruise caused by a blow with a blunt object HEMATOMA: bleeding within the brains layers

58. EPIDURAL OR EXTRADURAL HEMATOMAS Arterial blood collects between the dura and skull Patient loses consciousness and regains it temporarily Vomiting Hemiparesis Pupil changes Then rapid deterioration TREATMENT: removal of hematoma via craniotomy

59. SUBDURAL HEMATOMA Venous bleeding below the dura Accompanied by increased intracranial pressure ACUTE: develops within several days after injury; surgery needed SUBACUTE: develops within a few days to 3 weeks; surgery needed CHRONIC: develops weeks to months after injury

60. COMPLICATIONS OF HEAD INJURY Cerebral edema Diabetes insipidus SIADH (syndrome of inappropriate antidiuretic hormone) Stress ulcer Epilepsy Meningitis Hyperthermia/Hypothermia

61. MEDICAL TREATMENT OF HEAD INJURY Decrease ICP with mannitol (diuretic) and steroids Antibiotics to prevent meningitis Keep dehydrated to avoid increase in fluid level

62. SURGICAL TREATMENT OF HEAD INJURY Craniotomy: used to relieve ICP, , control hemorrhage, remove tumor, aneurysm or old hematoma Supratentorial approach infratentorial approach Burr holes: used to remove clot

63. NUTRITION FOLLOWING HEAD INJURY Stress and steroids increase catabolism To avoid muscle wasting patient receives tube feedings or hyperalimentation

64. ASSESSMENTS OF HEAD INJURY PATIENT Assess airway LOC (level of consciousness) Pupils reactivity: brisk, reactive, sluggish size: look for differences in size indicating brainstem dysfunction

65. ASSESSMENTS CONTINUED Assess for movement Check for sensation Assess hand grasps Assess for S & S of IICP Assess for respiratory changes Assess for VS changes Assess for headache

66. GLASCOW COMA SCALE Used to evaluate neurologic status of patients who have had a head injury Based on an assessment of: Eyes open Best motor response Verbal response Each category gets assigned a number

67. POSTOPERATIVE CARE CRANIOTOMY Assess respiratory function Suction, C&DB q 2 hrs, ventilator Assess neurologic function, LOC, S&S of IICP Strict I&O Seizure precautions Assess for CSF leak from ear, nose drainage, Assess for S&S of meningitis

68. POSTOPERATIVE CARE: POSITIONING Position HOB 30 degrees (supratentorial); on back or unoperative side Position flat for infratentorial procedure with patient on either side

69. POSTOP CRANIOTOMY CARE CONTINUED Assess for intracranial bleeding Assess for GI bleeding; provide anatacids and histamine blockers Assess for DI/SIADH Assess for headache; provide Tylenol and Codeine Assess for emotional response and knowledge deficit

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