INTRACRANIAL PRESSURE Hydrocephalus Meningitis Head Injury Brain Tumors

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 tissue Through 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 CO 2 ON CEREBRAL BLOOD FLOW • CO 2 partial pressure cerebral vasodilation leads to INCREASED cerebral blood flow and ICP • CO 2 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 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

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 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)

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 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 ICP HOW? 1. cerebral edema 2. volume of CSF 3. cerebral blood volume while maintaining cerebral perfusion

MONITOR ICP 1. Intraventricular catheter (ventriculostomy) 2. Subarachnoid bolt 3. Epidural/subdural catheter 4. 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 fluids 4. 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 oxygenation 2. Monitor arterial blood gases

GOAL: Reducing metabolic demands 1. Reduce cellular metabolic demands 2. Administer barbiturates: nembutal, pentothal, diprivan 3. 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 hyperventilation 3. 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 space CAUSES: • 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 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

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 skull OPEN: 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 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

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 response Each 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