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Unformatted text preview: Neurological Emergencies Emergencies
Presented by Barbara Robinette, RN, BSN, MICN Cerebral Dynamics Cerebral The brain requires a constant supply of O2 and glucose. glucose. The brain makes up 2% of the total body weight, but The consumes 25% of the body’s total O2 and glucose consumes requirements. requirements. Primary source of energy for the brain is glucose Primary converted to ATP. converted When ATP levels drop to 55% of normal we see When difficulty with speech, behavior, memory, judgment, and personality. and At 40-45%…Brain cells die(& are not regenerated) Causes of ATP Failure Causes Circulatory arrest: the brain’s supply of O2 is depleted in 10 seconds. depleted Metabolism switches to anaerobic-lactic acid Metabolism builds up, blood volume increases, and the blood brain barrier opens. blood 15 times more glucose is needed to produce 15 ATP with more lactic acid build up. ATP Causes of ATP Failure(cont.) ATP Seizure- rapid cellular firing in the brain cause Seizuretoxins to spill out. toxins Seizure activity depletes ATP Blood flow increases 250-300% to meet Blood metabolic needs. metabolic Status Epilepticus is emergent d/t ATP Status depletion. depletion. Causes of ATP Failure(cont.) Causes SZ does not have to have a motor component to SZ deplete ATP- don’t just paralyze deplete Treat immediately with a benzodiazepine Treat (Lorazepam/Ativan) (Lorazepam/Ativan) Check levels, then treat with an Anti-convulsantCheck phenytoin/Dilantin, valproic acid/Depakote, or carbamazepine/Tegretol. carbamazepine/Tegretol. Dilantin is mixed in NS & needs an In-Line Filter. Do Dilantin not hang as IVPB-needs its own main line in a pump (as do ALL IV Drips). (as Causes of ATP Failure(cont.) Failure Hyperthermia- increases metabolism (10% per Hyperthermia1ºC above 37.5ºC) 1ºC Hypoxia- PaO2 <60mmHg or O2 sat<90% causes inc blood flow. This inc risk of edema and ischemic injury. Maintain PaO2 90-100 and mmHg to nourish despite edema and ischemia. mmHg Hypotension (map<50mmHg)- inadequate Hypotension delivery of blood to meet metabolic needs. delivery Intracranial Pressure (ICP) Intracranial ICP-dependent on 3 volumes: the Brain, CSF, ICP-dependent and Blood and CSF and Blood can vary; if one increases the CSF other compensates, so the brain experiences little change. little As ICP increases, compensatory mechanisms As are depleted. are Brain contents shift and eventually can Brain herniate through the tentorial opening. herniate Increased Intracranial Pressure Increased As ICP increases, CPP decreases Increased cerebral ischemia & potential Increased hypoxia hypoxia Cerebral ischemia: >CO2 and < O2 in cerebral vessels vessels CO2 causes vasodilatation- counteracts CO2 compensatory mechanisms. compensatory Cerebral Perfusion Pressure (CPP) Cerebral CPP is the most important measure to maintain CPP = MAP - ICP Adequate CPP (>70-80mmHg) enables well Adequate oxygenated blood to flow to injured or ischemic areas. ischemic CPP is raised by increasing the MAP or CPP decreasing ICP decreasing MAP is raise in a normovolaemic pt with MAP norepinephrine or dopamine norepinephrine Causes of Increased ICP Causes Increase in brain volume: space occupying Increase lesion (tumor) or cerebral edema lesion Change in blood flow: obstruction of venous Change outflow, hyperemia, or hypercapnia outflow, Increase in CSF: hydrocephalus, subarachnoid Increase hemorrhage, choroid plexus papilloma hemorrhage, Neurological Subjective Assessment Assessment Sequence of onset & Sequence development of neuro symptoms symptoms Consciousness Mentation- memory, Mentationcognitive ability cognitive Personality changes Communication- speech, Communicationhearing, & comprehension hearing, Vision- decreased acuity, Visiondiplopia diplopia Injury of fall Headache Seizures Altered sensation Vomiting Motor abilityMotor weakness (paresis) paralysis (plegia) loss of coordination Tremors twitching. Neurological Objective Assessment: LOC LOC Alert- pt responds immediately to minimal external Alertstimuli stimuli Lethargic- state of drowsiness, requires increased Lethargicstimulus to be awakened stimulus Obtunded- duller indifference to stimuli, and Obtundedminimally maintained minimally Stuporous- Aroused only by vigorous and continuous Stuporousexternal stimuli external Comatose- Vigorous stimulation fails to produce any Comatosevoluntary neural response voluntary Neurological Objective Assessment: Motor Function Motor Muscle Strength: Hand grasp Pronator drift (10 sec.) Pedal push & pull Leg drift (5 sec.) Response to noxious stimuli Response (nail bed pressure or pinch inner arm or leg) inner Muscle Tone: evaluate Muscle opposition to passive movement movement Hypotonia Flaccidity Hypertonia Spasticity Rigidity Localizes Withdraws Abnormal flexion (decorticate Abnormal posturing)- may be spontaneous or in response to stimulus stimulus Abnormal extension Abnormal (decerebrate posturing)-may be spontaneous or in response to stimulus to Neurological Objective Assessment: Pupils and Eyes Pupils Pupils respond even with neuromuscular blocking Pupils agents agents Pupillary function assessment: Size Shape Reactivity to light Conscious- track through 6 fields Unconscious- (IF C-SPINE is CLEARED) Assess if UnconsciousOculocephalic (Doll’s Eyes) reflex is intact. Lack of response (not intact) indicates significant brainstem injury. response Eye movement (CN III, IV, & VI) Neurological Objective Assessment: Neurological Vital Signs Blood Pressure: Cerebral autoregulation (controls cerebral blood flow) is Cerebral lost with any type of intracranial injury- inc blood flow » inc cerebral blood volume » increased ICP inc Systemic hypertension common with intracranial injury Medulla & vagus nerve provide parasympathetic control of Medulla heart-when stimulated this lower brainstem system produces bradycardia produces Abrupt ICP- dysrhythmias (PVC’s, AV blocks, & V-fib) Bradycardia, systolic hypertension, & bradypnea Heart Rate and Rhythm: Cushing’s Triad Neurological Objective Assessment: Respiratory Pattern Respiratory Cheyne-Stokes: Rhythmic crescendo & decrescendo, brief apnea Bilateral deep cerebral lesions, some cerebellar lesions Very deep, very rapid, no apnea Lesions in midbrain & upper pons Prolonged inspiratory &/or expiratory pause of 2-3 sec. Irregular gasping with long apnea Lower pons & upper medulla Irregular deep and shallow irregular apnea Lesions on Medulla Central neurogenic hyperventilation: Apneustic: Cluster breathing: Ataxic Respirations Neurological Objective Assessment: Early Signs Assessment: LOC: More stimulation required to get the same response Loss of finer detail of orientation Speech less distinct Altered memory RESTLESSNESS Suddenly quiet Pupils- sluggish (usually unilateral & ipsilateral to lesion) Motor function- usually contralateral, pronator drift, loss of Motor motor strength, increased tone motor Vital signs occasionally tachycardic occasional hypertensive swings Neurological Objective Assessment: Late Signs Assessment: LOC- arousable only with deep pain or LOCunarousable unarousable Pupils- fixed or dilated Motor response- dense hemi-paresis, Motor posturing, no response posturing, Vital signs- Cushing's triad (widened pulse Vital pressure), abnormal respirations pressure), Diagnostic Procedures Diagnostic Skull & spine films CT- noninvasive visualization of structures MRI- structural & biochemical abnormalities, detects MRInecrotic or ischemic tissue, distinguishes white matter changes changes Cerebral angiography- evaluates cerebral circulation Myelography-evaluate spinal canal, subarachnoid Myelography-evaluate space around spinal cord, & spinal nerve roots space Planning and Intervention Planning HOB elevated to 30-45º Head and neck in midline position Calm environment Limit visitors/stmuli Limit activity No vagal maneuvers Restrict suppositories Planning and Intervention (cont.) Planning Monitor ABC’s Medical decompression- Diuretics, increase venous Medical outflow outflow Hyperventilation only in cerebral HTN Hyperventilation Ensure adequate CPP- increase MAP Monitor I&O- foley Vasopressors- Nitroprusside, Norepinephrine, Vasopressorsdopamine dopamine Frequent neuro checks Medical Management: Airway Medical Severely brain injured pts should be intubated Hyperventilation should only be used in an Hyperventilation acute inc ICP episode, may cause vasoconstriction vasoconstriction CO2 causes vasodilatation- ventilate to normal CO2 level (PaCO2 4.0 kPA/30mmHg) CO Mannitol Mannitol First, decreases viscosity of blood improving First, cerebral blood flow cerebral Second, creates osmotic gradient which draws Second, water out of neurons water In prolonged use, Mannitol molecule cross In into cerebral interstitial space exacerbating cerebral edema cerebral Best as bolus for acute reduction of ICP Medical Management: IV Therapy Medical Keep normovolemic (hypovolemic pt have inc Keep risk of hypotention » decreased CPP) risk Do not give D5W- free water decreases serum Do osmolality » increased water content of brain. osmolality Elevated blood sugar level- brain produces Elevated lactic acid » lowers tissue pH » inc ischemia lactic Medical Management: Medical Sedation and Anaesthesia ICP rises with valsalva-type maneuvers Sedation is necessary for adequate ventilationSedation benzodiazepines benzodiazepines Analgesia is also required- narcotics, diprivan Neuromuscular blockers may be usedNeuromuscular succinylcholine,vecuronium succinylcholine,vecuronium Concussion Concussion Traumatic reversible neurological deficitTraumatic temporary loss of consciousness with some retrograde amnesia retrograde Cause- rapid acceleration/deceleration Causestimulus or sudden blow to the skull stimulus Shock waves from the blow cause the Shock Reticular activating system to stop temporarily reversing in minutes to hours reversing Concussion: Concussion: Planning & Interventions Bed rest Pt education: S/S of increased ICP Post concussion syndrome: HA, dizzy, Post tinnitus, diplopia, inability to concentrate, memory disturbances, personality changes, lower energy level lower Skull fracture Skull Linear Fx: most Linear common(70%)-usu benign unless crosses major vascular channel major Depressed skull fx: Depressed damages cerebral tissue by compression or laceration & retaining bony fragments which may set focus for Sz may Basilar Skull Fx: Basilar Cranial nerve involvment. where it occurs effects clinical picture picture S/S: raccoon sign, battle S/S: sign (usu after 24 hours), CSF leaks (otorrhea, rhinorrhea), sweet or salty taste in back of throat. back Skull Fracture Skull Skull Fracture Skull Basilar Skull Fracture Basilar What is wrong with this picture? What Raccoon sign = Raccoon Basilar Skull fracture Basilar NEVER PLACE NEVER NGT IN THE NOSE OF A PT WITH A BASILAR SKULL FRACTURE FRACTURE Results of Incorrect NGT Placement Placement Skull Fracture GSW Skull Epidural Hematoma Epidural Collection of blood between the dura and the Collection skull skull Usually d/t laceration of the middle meningeal Usually artery associated with temporal skull fractures artery Progresses rapidly- Increased ICP, breain Progresses shifts, and uncal herniation (medial portion of temporal lobe, uncus, herniate down through tentorial opening tentorial 50% mortality Epidural Hematoma Epidural Subdural Hematoma Subdural Collection of blood between the dura mater Collection and subarachnoid layer and Veins that bridge the subdural space are torn Classified by onset: acute- <48 hrs, subacuteClassified 2-14 days, chronic- >14 days 2-14 Caused by anything from a hard sneeze to Caused head trauma head Most common in children and elderly Subdural Hematoma Subdural Subdural Hematoma Subdural Acute Subdural and Subacute Subdural Hematomas. Diffuse Axonal Injury (DAI) Diffuse Wide spread disruption of neurological Wide function caused by microscopic damage to axons axons Sudden acceleration/deceleration stimulus Sudden creates sheering force greatest where density difference is greatest- at gray-white Matter junction junction Diffuse Axonal Injury (DAI) Diffuse Cerebral Contusion Cerebral Actual bruising of the brain tissue Petechial hemorrhages & extravasation of Petechial fluid from the vessels fluid Focal ischemia and edema Potential infarction/necrosis Contrecoup injury- rebound injury Meningitis Meningitis Two thirds of bacterial meningitis are <15 yrs, Two with peak incidence from 3-12 months with Primary illness may weaken immune system Primary for secondary meningitis infection for Usually presents as “Not acting right,” with Usually headache, fever, irritability, N/V/D, bulging fontanelle fontanelle Dx by Lumbar puncture, CBC, Blood cultures Treated w antibiotics, possibly corticosteroids THE END THE
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This note was uploaded on 03/25/2010 for the course PAR 100 taught by Professor Alan during the Spring '10 term at Miramar College.
- Spring '10