AACN PCCN Webinar Session 4 Neurology & Behavioral Presenter: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, CEN Independent Clinical Nurse Specialist & Education Consultant [email protected] Session 4: Neurology & Behavioral Table of Contents Neurology ........................................................................................................................................ 2 Behavioral ..................................................................................................................................... 13 1 Session 4: Neurology & Behavioral Neurology I. INTRODUCTION PCCN Test Plan Neurology, Multisystem, Behavioral: 15% a. Cerebrovascular Malformation (including aneurysm, AV malformation) b. Encephalopathy (e.g., hypoxic-ischemic, metabolic, edema, infectious, hepatic) c. Intracranial Hemorrhage (e.g., subarachnoid, epidural, encephalitis) d. Seizure Disorders e. Stroke (cerebrovascular accident)  Ischemic (embolic)  Hemorrhagic  Transient Ischemic Attack (TIA) II. ANATOMY & PHYSIOLOGY a. Skull b. Brain c. Meninges: Dur Mater, Arachnoid, Pia Mater d. Cerebrum e. Brain Stem f. Cerebellum g. Cranial Nerves h. Blood Vessels i. Cerebral Spinal Fluid j. Spinal Cord k. Peripheral Nerves III. NEURO ASSESSMENT (Included for Review) a. Level of Consciousness (LOC) b. Glasgow Coma Scale (GCS) 3-15  Eye Opening - 1- 4 points  Best Verbal Response – 1- 5 points  Best Motor Response – 1- 6 points 2 Session 4: Neurology & Behavioral c. Pupils  Size: Sympathetic & Parasympathetic, CN II & III  Shape  Symmetry  Reaction to Light  Extra Ocular Movement: CNIII, IV  Abnormal Pupillary Findings o Nonreactive, midposition: Midbrain Damage o Nonreactive Pinpoint: Pons Damage o Reactive, Small & Equal: Damage Affecting Sympathetic Innervation o One Fixed & Dilated Pupil: Same side CN III compression or injury o Bilateral Fixed & Dilated Pupils: Severe Brain Compression, Ischemia and/or Anoxia d. General Observation  Behavior  Mood/Affect  Appearance  Communication Pattern and Style  Organized Flow of Thoughts e. Motor & Sensory f. Cognitive Function  Orientation  Memory & Retention  Attention  Abstract Reasoning  Judgment g. Language & Communication  Aphasias o Expressive Aphasia (Brocca’s) – Dominant Frontal Lobe o Receptive Aphasia (Wernicke’s) – Dominant Temporal Lobe h. Respiratory Patterns  Cheyne-Strokes Breathing: Problem in Cerebral Hemispheres, Diencephelon or Basal Ganglia  Neurogenic Hyperventilation: Midbrain or Upper Pons Problems  Apneustic Breathing: Pons Lesion (prolonged inspiration with pauses) 3 Session 4: Neurology & Behavioral Cranial Nerves # Cranial Nerve function assessment I Olfactory  Smell  Evaluate Ability to Identify Odors II Optic  Vision  Evaluate Sight III Occulomotor  Eye Movement  Evaluate Eye Movement  Pupil Constriction  Towards Nose  Elevation of Eye Lid  Up and In, Down and In IV Trochlear  Eye Movement  Evaluate Eye Movement  Downward and Inward V Trigeminal  Sensation to Face  Tighten Jaw (Clench Teeth)  Muscles of Mastication  Corneal Reflex VI Abducens  Eye Movement  Evaluate Eye Movement  Laterally Outward VII Facial  Muscles of Face  Demonstrate Facial Expressions  Taste Anterior Tongue  Show Teeth VIII Acoustic  Vestibular – Balance  Evaluate Hearing  Cochlear – Hearing IX Glossopharyngeal  Pharyngeal Reflex (gag)  Swallow  Taste Posterior Tongue  Evaluate Gag  Swallowing X Vagus  Parasympathetic Innervation  Assessed with Glossopharyngeal  Swallowing XI Spinal Accessory  Sternocleidomastoid &  Shrug Shoulders Trapezius Muscle Movement  Rotate Head XII Hypoglossal  Movement of Tongue  Check Speech IV. STROKE: TIME IS BRAIN Definitions a. Stroke: Permanently impaired central nervous system (CNS) tissue/functioning due to impaired cerebrovascular perfusion b. Transient Ischemic Attack (TIA): Lasts for minutes to hours. No detectable dysfunction or tissue damage c. Penumbra: Viable but not functioning neuronal cells. This area may recover and not progress to stroke 4 Session 4: Neurology & Behavioral Risk Factors a. Age b. Hypertension c. Atrial Fibrillation d. Dyslipidemia e. Diabetes Mellitus f. Coronary Artery Disease g. Sedentary Lifestyle h. Smoking i. Obesity j. Valvular Disease Causes of Ischemic Stroke a. Thrombotic  Atherosclerosis  Vasculitis  Arterial Dissection  Hematologic Disorders b. Embolic  Cardiogenic  Athero-thrombotic Arterial Source  Unknown Source: Hypercoagulable State Initial Assessment a. Goals  Rapid Assessment  Initiate Treatment b. Assessment  ABC’s  Vital Signs  Cardiac Monitor  Accurate Event History  Presentation (language, motor, sensory) c. Common Stroke Signs: Sudden  Rarely Loss Consciousness  Asymmetrical Facial Expression  Weakness on One Side of the Body  Numbness on One Side of the Body  Difficulty Speaking or Understanding 5 Session 4: Neurology & Behavioral  Difficulty Walking  Visual Difficulty: Homonymous Hemianopia, visual field cut same side as stroke  Severe, Unexplained Headache d. Tests  CT Scan (no contrast)  MRI  Transcranial Doppler  Blood Work Ischemic Stroke Care a. Hypertension  Normal Response to Stroke  Usually Resolves in 3-4 days  Some HTN is Good  Only tx if SBP >220, DBP > 140 or MAP >130  Unless t-PA: SBP > 185, DBP > 110 b. Do Not Lower Blood Pressure > 10 % per hour c. Activase (alteplase or rt-PA)  Only FDA Approved Drug Therapy  Within 3 Hrs of Onset and 4.5 Hrs for some patients  Dose 0.9 mg/kg  10% Bolus Over 1Minute  Remainder of Dose Over 1 Hour  No ASA, Heparin, etc x 24 Hours d. Interventions  Treat Hypotension  Treat Hyperthermia (Keep < 37.50 C)  Maintain Serum Glucose 80 - 150  Monitor ABG’s and Pulse Ox  Protect Airway  Initially Flat Until Hemodynamically Stable HOB > 450  NPO  Swallowing Study Hemorrhagic Stroke (Intracerebral Hemorrhage) a. Bleeding into Tissue/Parenchyma b. Commonly From Hypertension c. Signs & Symptoms  Severe Headache, N/V, Loss of Consciousness  Retinal Hemorrhage  Similar to Ischemic Strokes  Localized Blood Seen on CT 6 Session 4: Neurology & Behavioral d. Bleeding into the Subarachnoid Area e. Often Due to a Ruptured Aneurysm or AVM f. Often Due to Trauma  Epidural – Arterial  Subdural – Venous: Acute, Subacute, Chronic  Intercranial  Subarachnoid  Hematomas Aneurysm a. Types  Fusiform  Berry  Saccular b. Rupture  Bleeds into the Subarachnoid Space  Bleeding Continues Until Tamponade Occurs and Thrombus Forms Arteriovenous Malformation (AVM) A congenital abnormal linkage between an artery and vein. When ruptured or leaking will present the same as an intracerebral hemorrhage. Assessment a. “Worst Headache of My Life” b. N/V c. Loss of Consciousness d. Nucal Rigidity and Photophobia e. Focal Deficits f. Clinical Findings Similar to Ischemic Strokes g. Ventricular and/or Subarachnoid Blood Seen on CT h. CSF from LP Positive for Blood i. Hydrocephalus Might Occur j. Hyponatremia Might Occur  SIADH  DI Medical Management a. Diagnostic Work up  CT/MRI  Cerebral Angiogram  MRA  Transcranial Doppler  Lumbar Puncture  Laboratory Assessment 7 Session 4: Neurology & Behavioral b. Strict Control of Blood Pressure c. Pre-Repair -- MAP 80-90, BPS < 140  Sodium Nitroprusside (Nipride)  Normodyne (Labetalol)  Hydralazine (Apresoline)  Aneurysm Precautions  Pain Relief d. Post-Repair: Vasospasm – Major Concern  Triple H Therapy (trending out of favor 2012) o Hypertensive -- MAP 120-150  Phenylephrine (Neosynephrine)  Dopamine Hydrochloride (Dopamine)  Norepinephrine Bitartrate (Levophed) o Hemodilutional -- Hct of 30-33 o Hypervolemic -- CVP of 8-12  Calcium Channel Blockers  Nimodipine: 60 mg PO q 4 hours for 21 days  NO Heparin, Coumadin, or ASA V. ENCEPHALITIS: INFLAMMATION OF THE BRAIN Etiology (usually viral) a. Herpes Simplex 1 b. Arbovirus (Mosquitoes) c. West Nile, Eastern and Western Equine, St. Louis d. Enterovirus e. Polio, Coxsackie's f. Measles, Mumps, Rabies g. Cytomegalovirus, Varicella-Zoster h. Immunocompromised Clinical Presentation a. Personality Changes b. Behavioral Changes c. Altered LOC d. Focal Neurologic Deficits e. Hallucinations (olfactory and gustatory)  Classic Sign of Herpes Encephalitis 8 Session 4: Neurology & Behavioral Management a. ABCs b. Supportive Care c. Herpes Simplex 1 Encephalitis, Acyclovir d. Seizure Management e. Fever Management f. Pain Management VI. ENCEPHALOPATHY Generalized or Global Mental Status Dysfunction Etiology a. Direct Pathology in Brain  Cerebral Blood Flow Disruptions  Structural Changes/Injuries  Concussive Brain Injury  Electrical Activity Changes  Neurotransmitter Changes  Ischemic Injuries to Tissue b. Indirect Pathology  Toxin Buildup (renal, Hepatic)  Metabolic Imbalance  Severe Systemic Hypertension  Hypo/Hyper Glucose (acute and chronic)  Chronic Alcohol Abuse (Wernicke’s) Clinical Presentation Not a specific disease but results from neurological or systemic disorders. S&S are directly related to primary cause. a. Change in: LOC, Behavior, Personality, Memory b. Renal Insufficiency Symptoms c. Liver Dysfunction Symptoms Management a. ABCs b. Seizure Precautions/Prevention/Management c. Safety Concerns/Issues 9