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
• An in any one of the components a change in the volume of the
other
COMPENSATION
• Shifting of CSF• INCREASED absorption of CSF• DECREASED cerebral blood volume
WITHOUT COMPENSATION
• ICP will rise• DECREASED cerebral perfusion
stimulates edema shifts brain tissueThrough openings in the rigid dura HERNIATION DEATH
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
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
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
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
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
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
PATHOLOGIC CONDITIONS THAT CAUSE IIP
• Head injury, CVA• Brain tumor• Intracranial surgery• Meningitis• Encephalitis• Subarchnoid hemorrhage
EARLY SYMPTOMS OF IIP
• ***change in LOC: Slowing of speechDelay in response to verbal suggestionsIrritability, Restlessness, resp effort• Changes in pupils• Weakness in one extremity/ 1 side of body• Headache constant increasing in intensity
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
Neurologic Nursing Assessments
• LOC• Pupil response• VS• Motor activity
ASSESSMENT OF LEVEL OF CONSCIOUSNESS
Indication of the highest level of cerebral activityEVALUATION IS DONE BY:• Determining degree of alertness• Orientation to person, place, time• Ability to awaken• Degree of lethargy• Status of reflexes (gag, swallow, etc)
ASSESSMENT OF PUPILS
• Determines reaction to light• NORMAL: the pupils constrict rapidly and
equally to light (PERLA)• ABNORMAL: unequal reaction, abnormal
position of pupils
ASSESSMENT OF VS INDICATING IIP
• Pulse decreases• Respiration decreases• BP increases • Temperature increases
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
ASSESSEMENT OF TEMPERATURE
• Increased temperature indicates increased intracranial pressure
• CAUSE: irritation or damage to temperature regulating mechanism in brainstem
SEIZURE PRECAUTIONS
• Pad side rails• Have oxygen and suction available• Observe for seizures
ASSESSMENT/DIAGNOSTICS
• CT scan• MRI• PET (positive emission tomography)
MANAGEMENT
• GOAL IS TO RELIEVE INCREASED ICPHOW?1. cerebral edema2. volume of CSF3. cerebral blood volume while maintaining
cerebral perfusion
MONITOR ICP
1. Intraventricular catheter (ventriculostomy)2. Subarachnoid bolt3. Epidural/subdural catheter4. Fiberoptic transducer-tipped catheter placed
in subdural space or the ventricle
GOALS: decreasing cerebral edema
1. Administer osmotic diuretics mannitol(Osmitrol)
2. Administer coricosteroids dexamethasone (Solumedrol, Medrol)
3. Restrict fluids4. Drain CSF
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
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
GOAL: controlling fever
• Fever increases cerebral metabolism and increases cerebral edema
• Antipyretics• Cooling blankets
GOAL: maintaining oxygenation
1. Maintain oxygenation2. Monitor arterial blood gases
GOAL: Reducing metabolic demands
1. Reduce cellular metabolic demands 2. Administer barbiturates: nembutal, pentothal,
diprivan3. Administer opiods (morphine sulfate or fentanyl
citrate) with ventilated clients to decrease agitation
4. Administer paralyzing agents vercuronium bromide or cisatracurium (Nimbex): agitation. Must be used with sedation/analgesia
ASSESSMENTS NOTED WITH ICP BASED ON LOCATION IN BRAIN
1. ICP on frontal lobes leads to Cheyne Stokes respirations
2. ICP in the midbrain causes hyperventilation3. ICP in the lower portion of the brain stem
(pons and medulla) leads to irregular respirations and eventually apnea
NURSING CARE TO MAINTAIN PATENT AIRWAY
NURSING CARE TO OPTIMIZE CEREBRAL TISSUE PERFUSION
CAUSES OF INCREASED ICP
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
TYPES OF HYDROCEPHALUS
INTERNAL NON-COMMUNICATING:• Blockage within the ventricles keeping the CSF from
going to the subarachnoid spaceCAUSES: • developmental malformations• Neoplasms• Infections• trauma
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
S & S OF HYDROCEPHALUS
EARLY• Increased head circumference• Bulging fontanels• Cranial sutures separate• Signs of increased ICP
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)
TREATMENT OF HYDROCEPHALUS
• Correction of cause of obstruction• Ventricular shunting procedures
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
Types of shunts
• Ventriculoperitoneal (VP) – one of choice
• OLDER FORMS:• Ventriculpleural• ventriculoatrial
PROBLEMS WITH SHUNTS
• Infections• Tubing becomes kinked, plugged or separates• Needs to be replaced when grows
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)
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
Other causes of IICP: MENINGITIS
DEFINED: Infection of pia mater, arachnoid membrane and CSF filled subarachnoid space due to bacteria, virus, or fungal organism
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
SIGNS AND SYMPTOMS COMMON TO ALL AGES
• Irritability• Seizures• vomiting
DIAGNOSIS OF MENIGITISLP: CSF examinedPressure measured• Normal: 0 to 15 mm Hg• Increased ICP: greater than 15 mm HgCSF sent to lab to identify organism• Gram stain (preliminary identification• Blood Cell Count: increased WBC• Glucose: decrease in glucose• Protein: increase in protein
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
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
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
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
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
HEAD INJURY
CLOSED: no break in skullOPEN: break in skull
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
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
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
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
COMPLICATIONS OF HEAD INJURY
• Cerebral edema• Diabetes insipidus• SIADH (syndrome of inappropriate antidiuretic
hormone)• Stress ulcer• Epilepsy• Meningitis• Hyperthermia/Hypothermia
MEDICAL TREATMENT OF HEAD INJURY
• Decrease ICP with mannitol (diuretic) and steroids
• Antibiotics to prevent meningitis• Keep dehydrated to avoid increase in fluid
level
SURGICAL TREATMENTOF 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
NUTRITION FOLLOWING HEAD INJURY
• Stress and steroids increase catabolism• To avoid muscle wasting patient receives tube
feedings or hyperalimentation
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
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
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 responseEach category gets assigned a number
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
POSTOPERATIVE CARE: POSITIONING
• Position HOB 30 degrees (supratentorial); on back or unoperative side
• Position flat for infratentorial procedure with patient on either side
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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