Updated Fall 2009 by John Nation, RN, MSN

Neurosensory: Altered Cerebral Function and Increased intracranial pressure (IICP)
Updated Fall 2009 by John Nation, RN, MSN From the notes of Charlene Morris, RN, MSN & Marnie Quick, RN, MSN, CNRN

Overview of Today’s Lecture
Discuss altered cerebral function Anatomy and physiology Definition of common terms Neurological assessment techniques Increased intracranial pressure Clinical manifestations Interventions Nursing concerns

Have you read Lewis pages 1467- 1481?
Yes No Abstain

Brain A & P: Brain Anatomy Ventricles of the Brain

Flow of CSF: Produced by filtration of the blood by the choroid plexus of each ventricle flows inferiorly through the lateral ventricles, intraventricular foramen, third ventricle, cerebral aqueduct, fourth ventricle and subarachnoid space and to the blood.

Altered Cerebral Function: Arousal/cognition (LOC) Patho/assessment
Reticular Activating System (RAS) – Reticular Formation - meshwork of gray cell within brainstem extending to the thalamus. Controls wakefulness, arousal and alertness. Reticular Activating System- You Tube Cerebral cortex outer layer of gray cell bodies of brain. Controls cognition, thought process.

Altered Cerebral Function: What is Consciousness?
Consciousness (Merriam- Webster): waking life (as that to which one returns after sleep, trance, or fever) in which one's normal mental powers are present “the ether wore off and the patient regained consciousness” Dynamic state Continuum from awareness of self and environment to unawareness Consciousness to deep coma Coma- prolonged unconsciousness

Causes of Changes in LOC
Alcohol intoxication Drug intoxication (particularly opiates, narcotics, sedatives, and anti-anxiety or seizure medications) Arrhythmia Brain disorders Central nervous system diseases Lack of oxygen (hypoxia) Abnormal blood sugars (diabetic coma) Electrolyte or mineral imbalance Exposure to heavy metals or hydrocarbons Extreme fatigue or sleep deprivation Ketoacidosis Head trauma Heart failure Hypoglycemia (low blood sugar) Increased carbon dioxide levels (hypercarbia) often seen in emphysema Infection Low blood pressure (hypotension) Metabolic disorders Thyroid or adrenal gland disorders Seizures such as those related to epilepsy Shock Stroke Source: National Institute of Health

Causes of Coma: Coma can be caused by:
Traumatic brain injuries. Brain injuries that result from traffic collisions or acts of violence are the most common cause of comas. Stroke. Acute loss of blood flow to the brain followed by swelling or no blood flow to a major part of the brainstem can result in a coma. Diabetes. Blood sugar levels that get too high (hyperglycemia) and stay too high or get too low (hypoglycemia) and stay too low can cause coma. Source: Mayo Clinic:

Causes of Coma (Cont’d):
Lack of oxygen. People who have escaped drowning or been resuscitated after a heart attack may not awaken due to lack of blood flow and oxygen to the brain. Infections. Encephalitis and meningitis are infections that cause inflammation of the brain, spinal cord or the tissues that surround the brain. Severe cases of either encephalitis or meningitis can result in a coma. Toxins. Exposure to toxins, such as carbon monoxide or drug overdoses, can cause brain damage and coma. Source: Mayo Clinic:

Altered Levels of Consciousness: Definitions of Terms
Lethargy - a slight reduction in alertness, less aware of what is happening around them and think more slowly. Obtundation - a moderate reduction in alertness or clouding of consciousness. Stupor - an excessively long or deep sleeplike state. Arousal is brief by vigorous stimulation, such as repeated shaking, loud calling, pinching. Coma - is a state of complete unresponsiveness, cannot be aroused, in a deep coma lacks avoidance of pain. Some reflexes may be present.

Altered Cerebral Function: Assessment of arousal/cognition (LOC)
Is the patient alert? Assess to person/place/time/event (A&O x 4) Respond to verbal stimuli? Respond to painful stimuli? Purpose: shows the brain receives the impulse, interprets it, and responds Types of painful stimuli: Trapezius pinch- grasp at least two inches of trapezius muscle. Squeeze and twist. Supraorbital pressure- carefully applied upward pressure on the ridge along the upper portion of the bony orbital structure Pressure on finger nails Sternal rub- not considered appropriate Is the patient unresponsive? A-----V-----P-----U!

Trapezius Pinch

Injury reported as secondary to sternal rub.

Descending Response to pain stimuli
Pushes your hand away Pulls away from pain site General movement Flexion Extension No response

Decorticate posturing- abnormal flexion Decerebrate posturing- abnormal extension

Glasgow Coma Scale Chart both total and sub scores to indicate where the deficits are. Also not why..periorbital edema may make opening eyes impossible. Also chart the patient’s best effort not necessarily the first response. A score of 13 to 14 indicates mild deficit. A score between 9 and 12 points to moderate deficit, and a score of 8 or less indicates severe coma.

Assessment of Vital Signs
Temperature - hypothalamus pressure can lead to alterations in body temperature Cushing’s triad – caused by edema & increased intracranial pressure 1) Increased systolic BP 2) Decreased pulse rate 3) Irregular respirations

Eleven Twelve Thirteen Fourteen
A 44 y/o male presents to the ED after a motor vehicle accident. When you ask him where he is, he opens his eyes and states “work” before closing his eyes again. He states that his abdomen hurts, and he points to the specific location when you ask. What is his GCS? Eleven Twelve Thirteen Fourteen

Lethargy is defined as a deep sleep like state where the patient is aroused only with loud noise or painful stimuli. True False

Assessment of arousal/cognition - Respiratory
Respiratory- changes occur as brainstem is being compressed Yawning & sighing Cheyne-Stokes – crescendo-decrescendo with apnea Central Neurogenic hyperventilation Apneustic breathing – Pauses in inspiration and expiration Cluster breathing – irregular deep to shallow with apnea Ataxic respirations - grossly irregular

Respiratory Irregularities

Cranial Nerves

Assessment of arousal/cognition Pupillary light reflex
Occipital lobe Brain stem Sensory: CN 2 - Optic Motor: CN 3 - Occulomotor Note pupil size; darken room; shine light in and note reaction and size Compare pupil size, shape, movement, and reactivity. CN III compressed pupil on that/ipsilateral side dilates. Pin point pupils – pons or meds. Fixed pupil unresponsive to light – IICP, nerve injury, previous surgery, or mydriatic eye gtts.

Assessment of arousal/cognition Pupillary light reflex
PERRLA- “Pupils equal, round, reactive to light and accommodation” Anisocoria: The two pupils are not of equal size. Light-near dissociation, refers to a condition where the light reflex is absent or abnormal but the near response is intact. There is no clinical condition in which the light reflex is present and the near response is absent. Amaurotic: blind eye still has consensual response

Assessment Arosual/cognition EOM’S & Brain stem function
Eye movement- CN 3,4,6 In Deep COMA- test EOM’s by Oculocephalic reflex Doll’s eyes- Sensory- CN 8; Motor- CN 3,4,6 Good Dolls eyes: eyes move in opposite direction of head movement – intact brain stem at Pons & nerves Bad/negative Dolls eyes: eyes do not move head turned Eye movement 3,4,& 6 also tests brain stem function Corneal reflex – CN 5 & 7 How tested with spinal cord injury?

Assessment arousal/cognition Additional Motor Assessment
Ability to move, strength, and symmetry Grips, arm strength, & drift Planter flexion, dorsiflexion, & leg strength Coordination Finger to nose, heel up and down shin Planter Reflex- Babinski testing Meningeal signs- Brudzinski, nuchal rigidity Motor- squeeze nurse’s hands, palmar drift, raise foot off bed Resistance to movement during ROM or movement to painful stimuli also indicate ability to move and strength

Planter Reflex and Babinski testing
Babinski's reflex – present when the great toe flexes toward the top of the foot and the other toes fan out after the sole of the foot has been firmly stroked. Postitive response indicates damage to nerve paths connecting the spinal cord and the brain (corticospinal tract) Abnormal after the age of 2.

Meningeal signs- Brudzinski, nuchal rigidity
One of the physically demonstrable symptoms of meningitis is Brudzinski's sign. Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.

Meningitis signs- Kernig’s sign
Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

Neuro assessment - Sensation
Dull vs. sharp – use broken tongue depressor or cotton tip applicator Include face, hands, arms, abdomen, feet, and legs

Neuro Assessment Videos
Lewis DVD

A RN needs an order from a physician to conduct a neurological assessment on a patient showing new symptoms of a CVA. True False

Altered cerebral function Nursing assessment for Cerebral Dysfunction
Terms used to describe LOC Description more important than term Health history- drugs/head injury/metabolic Physical exam- modify as individual cooperation Neuro Vital Signs LOC, V/S, Pupils, Strength/Movement, Sensation Glasgow coma scale NIH Stroke Scale – want low score NIH Stroke Scale pdf

Common manifestations/Complications Coma states and brain death
Irreversible coma- persistent vegetative state Does not have functioning cerebral cortex Caused by anoxia or severe brain injury Sleep-wake cycles; chew/swallow/cough, no tracking Locked-in Syndrome (not true coma) Functioning RAS & cortex; pons level interference Aware, communicate with eyes Brain death Loss of all brain function- flat EEG, no blood flow

Prognosis of individual with altered cerebral functioning
Outcome varies according to underlying cause and pathologic process The longer the individual unconscious, the longer has absent Doll’s eyes; the poorer the cognitive recovery Residual mental problems typically outweigh the physical

Altered Cerebral Function Therapeutic Interventions
Diagnostic tests- to R/O & identify cause of altered cerebral function CT, MRI, EEG, blood work Medications- vary according to problem Overdose; fluid/electrolyte replacement; antibiotics Surgery- (Ex. tumors, intracranial bleeds) Other- airway/vent; treat IICP; enteral feeding

MRI of the brain EEG CT of the head X- Ray of the head
Your patient becomes disoriented and reports a severe headache. Which diagnostic test would you expect the physician to order first? MRI of the brain EEG CT of the head X- Ray of the head

Which of the below options would be your priority nursing diagnosis for a patient with altered cerebral function? Risk for aspiration Ineffective tissue perfusion Ineffective airway Risk for imbalance nutrition

Altered Cerebral Functioning: Pertinent Nursing problems
Identify the priorities: Impaired physical mobility Risk for aspiration Ineffective coping- Family Ineffective tissue perfusion (cerebral) Risk for impaired skin integrity Ineffective airway Risk for imbalanced nurtition Alteration in breathing pattern Home care

Increased Intracranial Pressure (IICP)

Increased Intracranial Pressure- Overview
Normal ICP Control Autoregulation Causes of Increased ICP Clinical Manifestations Diagnostic Studies Monitoring Increased ICP Treatment

ICP Skull is a closed box with three essential components: blood 12%, brain tissue 78%, and cerebrospinal fluid (CSF) 10% Normally, arterial pressure, venous pressure, intraabdominal and intrathoracic pressure, posture, temperature, and blood gases keep ICP relatively constant

Monro-Kellie hypothesis
Brain tissue, blood, and CSF are mostly constant in volume If the volume of one component increases, another component will be displaced In total, the intracranial pressure will not change while compensation is possible (ex. Change in CSF production or absorption, vasoconstriction or dilation, compression or distention of brain tissue) The ability to accommodate change is limited

Measuring Increased ICP
Normal ICP is 0 to 15 mm Hg Usually treated once above 20 mm Hg

Cerebral Blood Flow (CBF)
Cerebral Blood Flow- amount of blood in mls passing through 100g of brain tissue in 1 minute Global CBF is 50ml/min Normal blood flow 25ml/min in white matter Normal blood flow 75 ml/min in gray matter Brain requires constant supply of oxygen and glucose Brain uses 20% of oxygen and 25% of glucose

Autoregulation Autoregulation- the automatic adjustment in diameter of cerebral blood vessels to maintain constant blood flow despite changes in blood pressure Autoregulation is not effective with a MAP less than 50 mm Hg Autoregulation is not effective with a MAP greater than 150 mm Hg

Autoregulation (Cont’d)
Cerebral Perfusion Pressure (CPP)- pressure needed to ensure blood flow to the brain CPP= MAP- ICP Normal CPP is 70 to 100 mm Hg CPP < 50 mm Hg causes ischemia and neural death CPP< 30 mm Hg is not compatible with life

Factors Affecting Cerebral Blood Flow
Increased PaCO2 dilates cerebral vessels Decreased PaCO2 constricts cerebral vessels, increases cerebrovascular resistance, reduces CBF, and decreases ICP Decreased cerebral O2 tension dilates cerebral vessels Cardiac or respiratory arrest Diabetic coma Infections Encephalopathies

Cerebral Edema- Increased accumulation of fluid in extravascular spaces of brain tissue Results in increased tissue volume Caused by brain abscess, brain tumor, hematoma, hemorrhage, contusion, posttraumatic brain swelling, meningitis, enephalitis, anoxic and ischemic episodes, cerebral infarction, venous thrombosis, lead or arsenic intoxication, hepatic encephalopathy, uremia Three types: vasogenic, cytotoxic, and interstitial (more than one type can occur at the same time)

Cerebral Edema (Cont’d)
Vasogenic Cerebral Edema- Most common Changes in endothelial lining of cerebral capillaries allow leakage of macromolecules into extravascular space Fluid flows to extravascular space due to osmotic gradient Can be caused by tumors, abscesses, and toxins

Cytotoxic Cerebral Edema- Occurs most often in gray matter Lesions or trauma cause cerebral hypoxia, sodium depletion, and syndrome of inappropriate antidiuretic hormone (SIADH Fluid then shifts from extracellular space directly into the cells

Interstitial Cerebral Edema- Periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus

Causes of Increased ICP
Aneurysm rupture and subarachnoid hemorrhage Brain tumor Encephalitis Hydrocephalus Hypertensive brain hemorrhage Intraventricular hemorrhage Meningitis Severe head injury Subdural hematoma Status epilepticus Stroke Source: National Institute of Health

Stages of Compliance with IICP
Compensation is effective & autoregulation present – CSF, Blood, and Brain Compliance less effective & increase risk for IICP Any small increase in volume causes great increase in ICP, loss of autoregulation & Cushing's triad Herniation

Increased Intracranial Pressure (IICP) Cerebral edema/hydrocephalus
Cerebral edema- Increases the volume of brain tissue which can cause herniation Hydrocephalus- Build up of CSF inside the skull

Health history- assess brain involvement Physical exam-
Increased intracranial pressure (IICP): Nursing assessment specific to IICP Health history- assess brain involvement Physical exam- Altered cerebral function assessment Frequency depends on potential IICP Early sign- change in LOC 3rd Cranial nerve compression- pupil dilation, no response to light, ptosis of the eyelid on ipsilateral side as lesion Papilledema, projectile vomiting, vision changes, seizures Late sign- Cushing’s Traid – Widening pulse pressure (increasing SBP & decreasing DBP) decreased HR, and irregular respiratory pattern

Increased Intracranial Pressure (IICP): Therapeutic Interventions
Diagnostic tests- CT Scan MRI PET EEG Angiography Transcranial doppler studies ECG CBC, Coags, BMP, ABGs, drug screen Barbiturate Coma – pentobarbital or Pentothal longer acting Propofol – short acting, permits ability to do neuro checks Can do pupil checks even in medication coma Need to treat B/P less than 90 or 100 systolic or Cerebral Perfusion Pressure 70 or 80 also treat B/P > 150 in some cases some suggest permitting B/P to be higher MED coma can lead to low B/P treatment is considered a failure if: Hypotention not responsive to cardiac inotropes, peripheral vasopressors, or intravenous fluid therapy (cardiac isotopes: dopamine, dobutamine, epinephrine) (peripheral vasopressors: ephedrine, phenylephrine) (IV fluids: packed RBCs, albumine, hetastarch, LR) The temperature of the body is regulated by neural feedback mechanisms which operate primarily through the hypothalmus. The hypothalmus contains not only the control mechanisms, but also the key temperature sensors. Under control of these mechanisms, sweating begins almost precisely at a skin temperature of 37°C and increases rapidly as the skin temperature rises above this value. The heat production of the body under these conditions remains almost constant as the skin temperature rises. If the skin temperature drops below 37°C a variety of responses are initiated to conserve the heat in the body and to increase heat production. These include Vasoconstriction to decrease the flow of heat to the skin. Cessation of sweating. Shivering to increase heat production in the muscles. Secretion of norepinephrine, epinephrine, and thyroxine to increase heat production In lower animals, the erection of the hairs and fur to increase insulation.

Increased Intracranial Pressure (IICP): Therapeutic Interventions (Cont’d)
Medications- Osmotic diuretic (Mannitol) Sometimes loop diuretic (Lasix) Antiseizure medications (Dilantin) Corticosteroids (Decadron) (brain tumors, bacterial meningitis) Proton pump inhibitor (Protonix) GI prophylaxis Vasoactive drugs to maintain MAP Barbituates Sedation

ICP monitoring LICOX cath – brain tissue oxygenation of frontal white matter PbtO2 Normal PbtO2 is mmHg LICOX Catheter Jugular venous bulb cath SjvO2 indicates brain tissue removal of O2 from blood Normal SjvO2 is 60% to 80% <50 to 55% of O2 in venous blood indicates impairment of flow and brain taking out more O2 than normal ICP Waveforms (P1, P2, & P3) see Lewis p. 1474 P1 arterial pulse wave should be highest P2 is intracranial compliance – if higher than P1 compliance is compromised P3 is the venous pulsation and should be the lowest

Intracranial pressure monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated, and plateau waves. At high ICP the P2 peak is higher than the P1 peak, and the peaks become less distinct and plateau.

ICP Monitoring (Cont’d) Pg 1473
Intraventricular Monitoring: Considered gold standard of ICP monitoring Surgically placed into ventricular system Has drainage bag, pressure transducer, and three way stopcock Accurate, can drain CSF Infection occurs in up to 20% of patients Risk of hemorrhage during placement (2%)

ICP Monitoring (Cont’d)
Intraparenchymal Monitoring: Inserted into brain parenchyma via small hole drilled in skull Thin cable with fiberoptic transducer at the tip Easier to place, lower risk of infection, lower risk of bleed Cannot drain CSF Not as accurate Mechanically complex design carries greater risk of failure

Subarachnoid Monitoring: Hollow screw placed through skull into dura Dura is then punctured, allowing CSF to communicate with the transducer Frequently clog and are considered unreliable Rarely used

Epidural Monitoring: Rest against the dura after passing through the skull Often inaccurate and are of limited clinical utility Used for coagulopathic patients with hepatic encephalopathy

Noninvasive Monitoring- Tissue resonance analysis (TRA)- ultrasound-based method Transcranial doppler Intraocular pressure Tympanic membrane displacement None of above have demonstrated reproducible clinical success at this time

ICP Monitoring New Approaches to ICP Monitoring

Intraventricular and subarachnoid monitoring devices for IICP

Ineffective tissue perfusion: cerebral
Increased intracranial pressure (IICP): Pertinent Nursing Problems and Interventions Ineffective tissue perfusion: cerebral Assess/report sign IICP Adequate airway Promote venous drainage Control environment stimuli Plan nursing care – avoid clustering care Avoid Valsalva’s maneuver If bone flap out post op- assess & position Assess external shunts/drains

A patient has ICP monitoring with an intraventricular catheter
A patient has ICP monitoring with an intraventricular catheter. A priority nursing intervention for the patient is : Aseptic technique to prevent infection Maintain the bed in Trendelenburg position Removal of CSF to maintain normal ICP Sampling CSF to determine abnormalities

A patient with an intracranial problem does not open his eyes to any stimulus, has no verbal response except mutturing when stimulated, and flexes his arm in response to painful stimuli. The GCS is: six eight nine eleven

Match the following treatment for increased ICP with it’s effect: Oxygen administration
Decreased cerebral metabolism Prevention of hypoxia Decreased volume of brain water Cerebral arterial vasoconstriction Decreased lesion edema

Match the following treatment for increased ICP with its effect: Mild hyperventilation

Match the following treatment of increased ICP with its effect: Osmotic diuretics

Match the following treatment of increased ICP with its effect: Dexamethasone (Decadron)

Match the following treatment for increased ICP with its effect: Barbiturates

VP shunt (a narrow piece of tubing) is surgically placed in the ventricle of the brain to drain CSF to the abdomen where it is absorbed by the body. CSF Shunt

After VP Shunt Surgery There is mild pain involved with this surgery. Acetaminophen (Tylenol ) or ibuprofen may be used for postoperative discomfort. You will be in the hospital for days. Once you are eating and drinking, and there are no complications, you will be able to go home. You will have a follow-up appointment in the neurosurgery clinic in 7-10 days. Your head dressing and staples will be removed at that time. After discharge, you may resume your regular activities unless you are told otherwise. In the future, you will need antibiotics before dental work and other invasive procedures.

After VP Shunt Surgery (Cont’d)
When to Call your Neurosurgeon or Nurse Practitioner Sometimes a shunt malfunctions by becoming clogged, disconnected, or infected. If this happens, you may experience any of the following signs and symptoms: Redness, pain or swelling of the skin along the length of the shunt or at the incision sites Drainage from the incision Fever greater than 101.5° F-usually within the first six months of surgery Irritability or excessive sleepiness Nausea or vomiting Recurring headaches Blurred or double vision Sudden or gradual change in personality Rubbing of the head Weakness Balance or coordination problems

Brain Herniation

Cingulated Herniation - a
Brain Herniation Cingulated Herniation - a Cingulate gyrus slips under falx cerebri Usually caused tumor or bleed Non life threatening

Uncal or Lateral Herniation - b
Brain Herniation Uncal or Lateral Herniation - b Uncus of temporal lobe slips through notch of tentorium and compresses the ipsilateral CN 3, brainstem, & vital centers Life threatening

Central or Transtentorial Herniation - c
Brain Herniation Central or Transtentorial Herniation - c Caused by: downward pressure on mid structures of cerebrum or general cerebral edema which compresses the brainstem Life threatening – compresses RAS & vital centers Abnormal heart rhythms, disturbances or cessation of breathing, cardiac arrest, and death

Extracranial Herniation - d
Brain Herniation Extracranial Herniation - d Occurs with displacement of brain through a cranial defect. Usually Non-life threatening

Infratentorial (subtentorial or Tonsillar) Herniation - e
Brain Herniation Infratentorial (subtentorial or Tonsillar) Herniation - e Downward displacement of infratentorial structures through the foramen magnum Life threatening

The End!

Updated Fall 2009 by John Nation, RN, MSN

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