Transcript Module 7
Module 7 Neurology W.Pawliuk MPH MSNEd RN CEN Key Assessment Components Family history, genetic risk Current health problems Level of consciousness/orientation Memory and attention Language, higher levels of cognition Cranial nerve assessment Sensory function Motor function Cerebellar function Glasgow Coma Scale Assessment of the Nervous System Subjective data Important health information Past health history Medications Surgery or other treatments Assessment of the Nervous System (cont’d) Functional Health Patterns Health Perception–Health Management Pattern Nutritional-Metabolic Pattern Elimination Pattern Activity-Exercise Pattern Sleep-Rest Pattern Cognitive-Perceptual Pattern Self-Perception–Self-Concept Pattern Role-Relationship Pattern Sexuality-Reproductive Pattern Coping–Stress Tolerance Pattern Value-Belief Pattern Assessment of the Nervous System (cont’d) Objective data Physical examination Mental status Cranial nerves Olfactory nerve Optic nerve Oculomotor, trochlear, and abducens nerves Trigeminal nerve Facial nerve Acoustic nerve Glossopharyngeal and vagus nerves Spinal accessory nerve Hypoglossal nerve Fig. 56-16 Assessment of the Nervous System (cont’d) Physical examination (cont’d) Motor system Sensory system Light touch Pain and temperature Vibration sense Position sense Cortical sensory functions Reflexes Fig. 56-17 Fig. 56-18 Fig. 56-19 Diagnostic Studies of the Nervous System Cerebrospinal fluid analysis Lumbar puncture Radiologic studies Cerebral angiography Electrographic studies Electroencephalography Electromyography and nerve conduction studies Evoked potentials Intracranial Pressure Skull has three essential components Brain tissue Blood Cerebrospinal fluid (CSF) Components of the Brain Intracranial Pressure Intracellular and extracellular fluids of brain tissues make up 78% of the volume Blood makes up 12% Remaining 10% is CSF Balance of these components maintains the ICP under normal conditions Intracranial Pressure (Cont’d) Factors that influence ICP Arterial pressure Venous pressure Intraabdominal and intrathoracic pressure Posture Temperature Blood gases (CO2 levels) Intracranial Pressure (Cont’d) Degree to which these factors ↑ ICP depends on the ability of the brain to accommodate to the changes Regulation and Maintenance Normal intracranial pressure Pressure exerted by the total volume from the brain tissue, blood, and CSF Modified Monro-Kellie doctrine: Describes relatively constant volume within skull structure Regulation and Maintenance (Cont’d) Normal intracranial pressure (cont’d) If volume in any one of the components increases within cranial vault and volume from another component is displaced, the total intracranial volume will not change Regulation and Maintenance (Cont’d) Normal compensatory adaptations Alteration of CSF absorption or production Displacement of CSF into spinal subarachnoid space Dispensability of the dura Ability to compensate is limited If volume increase continues, ICP rises Regulation and Maintenance (Cont’d) Measuring ICP Can be measured in Ventricles Subarachnoid space Epidural space Brain parenchymal tissue Regulation and Maintenance (Cont’d) Measuring ICP (cont’d) Pressure transducer Normal ICP: 0 to 15 mm Hg Cerebral Blood Flow Definition The amount of blood in milliliters passing through 100 g of brain tissue in 1 minute About 50 ml/min per 100 g of brain tissue Cerebral Blood Flow (Cont’d) Autoregulation of cerebral blood flow (CBF) Automatic alteration in diameter of cerebral blood vessels to maintain constant blood flow to brain Ensures a consistent CBF to provide the metabolic needs of brain tissue and maintain cerebral perfusion pressure Cerebral Blood Flow (Cont’d) Cerebral perfusion pressure (CPP) Pressure needed to ensure blood flow to the brain CPP = MAP – ICP Normal is 70 to 100 mm Hg <50 mm Hg is associated with ischemia and neuronal death Cerebral Blood Flow (Cont’d) Factors affecting cerebral blood flow CO2 O2 Hydrogen ion concentration Cerebral Edema Increased accumulation of fluid in the extravascular spaces of brain tissue Three types of cerebral edema Vasogenic Cytotoxic Interstitial Cerebral Edema (Cont’d) Vasogenic cerebral edema Most common type Occurs mainly in white matter Associated with changes in the endothelial lining of cerebral capillaries Cerebral Edema (Cont’d) Cytotoxic cerebral edema Results from local disruption of functional integrity of cell membranes Occurs mainly in gray matter Cerebral Edema (Cont’d) Interstitial cerebral edema Result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus Can also be caused by enlargement of the extracellular space as a result of systemic water excess Mechanisms of Increased ICP Causes Mass lesion Cerebral edema Head injury Brain inflammation Metabolic insult Increased Intracranial Pressure Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. Mechanisms of Increased ICP (Cont’d) Sustained increase in ICP results in brainstem compression and herniation of brain from one compartment to another Herniation Clinical Manifestations Change in level of consciousness Result from changes in CBF Change in vital signs Cushing’s triad Systolic hypertension with widening pulse pressure Bradycardia Altered respirations Ocular signs Compression of CN III (oculomotor) results in pupil dilation Clinical Manifestations (Cont’d) ↓ In motor function Decerebrate posturing (extensor) Indicates more serious damage Decorticate posturing (flexor) Decorticate and Decerebrate Posturing Clinical Manifestations Headache Often continuous and worse in the morning Vomiting Not preceded by nausea Projectile Complications Two major complications of uncontrolled increased ICP Inadequate cerebral perfusion Cerebral herniation Tentorial herniation Uncal herniation Cingulate herniation Diagnostic Studies Aimed at identifying underlying cause MRI CT Cerebral angiography EEG Brain tissue oxygenation measurement Diagnostic Studies (Cont’d) Aimed at identifying underlying cause (cont’d) ICP measurement Transcranial Doppler studies Evoked potential studies PET Measurement of ICP ICP monitoring used to guide clinical care when at risk for increased ICP Those admitted with a Glasgow Coma Scale of 8 or less Those with abnormal CT scans or MRI Measurement of ICP (Cont’d) The gold standard for ICP monitoring is the ventriculostomy LICOX brain tissue oxygenation catheter Jugular venous bulb catheter Potential Placements of ICP Monitoring Devices Measurement of ICP Infection is always a serious consideration with ICP monitoring ICP should be measured as a mean pressure at the end of expiration Waveform should be recorded Shaped similar to arterial pressure trace ICP Monitor Waveforms Measurement of ICP Inaccurate readings can be caused by CSF leaks Obstruction in catheter Differences in height of bolt/transducer Kinks in tubing Incorrect height of drainage system relative to patient’s reference point Measurement of ICP (Cont’d) With catheter, it is possible to control ICP by removing CSF Careful monitoring of the volume of CSF drained is essential Intermittent Drainage System Collaborative Care Adequate oxygenation PaO2 maintenance at 100 mm Hg or greater ABG analysis guides the oxygen therapy May require mechanical ventilator Collaborative Care (Cont’d) Drug Therapy Mannitol Corticosteroids Barbiturates Antiseizure drugs Collaborative Care (Cont’d) Nutrition Increased ICP leads to hypermetabolic and catabolic state Traumatic Brain Injury (TBI) Blow or jolt to head May be result of head penetration by foreign object Primary Brain Injury Open vs. closed head injuries Mild, moderate, severe classification Fractures Coup and Contrecoup Injury Acceleration-Deceleration Injury Epidural Hematoma Epidural hematoma Arterial bleeding into the space between the dura and the inner skull Subdural Hematoma Venous bleeding into space beneath dura and above arachnoid Most commonly from tearing of bridging veins within cerebral hemispheres or from laceration of brain tissue Bleeding occurs more slowly, symptoms mirror those of epidural hematoma Patient in MVA with TBI Priority interventions: Assessment Priority nursing care in ED Surgical intervention Postsurgical care Discharge teaching Traumatic Brain Injury Skull Fractures Figure 13-14. Skull fractures. A, Linear; open, depressed; basilar; and comminuted fractures. B, View of base of skull with fractures. (From Barker E. Neuroscience Nursing: A Spectrum of Care. 3rd ed. St. Louis: Mosby; 2008.) 61 Traumatic Brain Injury Classifications Primary Direct injury to brain from impact Coup injury Contrecoup injury Types Concussion Contusion Penetrating injuries Diffuse axonal injuries Hematomas Complications Intracranial bleeding 62 Secondary Consequence of initial trauma Inflammatory response Release of cytokines Vasogenic edema Traumatic Brain Injury Pathophysiology of secondary brain injury. Ca++, Calcium; ICP, intracranial pressure. 63 Traumatic Brain Injury Hematomas Types of hematomas. A, Subdural (takes on contour of brain). B, Epidural. C, Intracerebral. (From Barker E. Neuroscience Nursing: A Spectrum of Care. 3rd ed. St. Louis: Mosby; 2008.) 64 Traumatic Brain Injury Management Nursing Medical/Surgical Neurological assessment Same as increased intracranial Glasgow Coma Scale Airway assessment ICP monitoring Hemodynamic monitoring Interventions to control elevated ICP Evaluation of diagnostic tests 65 pressure Several surgical procedures Craniotomy Bone fragments Evacuation hematoma Foreign body removal Spinal Cord Injuries Hyperflexion Hyperextension Axial loading or vertical compression (e.g., caused by jumping) Excessive head rotation beyond its range Penetration (e.g., caused by bullet or knife) Spinal Cord Injuries (cont’d) Spinal Cord Injuries (cont’d) Common Spinal Cord Syndromes Central cord syndrome Anterior cord syndrome Posterior cord lesion Brown-Séquard syndrome Common Spinal Cord Syndromes (cont’d) Clinical Manifestations Generally direct result of trauma that causes cord compression, ischemia, edema, and possible cord transection Related to level and degree of injury Patient with an incomplete lesion may demonstrate a mixture of symptoms Clinical Manifestations (Cont’d) Higher the injury, the more serious the sequelae Proximity of cervical cord to medulla and brainstem Movement and rehabilitation potential related to specific locations of spinal cord injury Clinical Manifestations (Cont’d) Immediate postinjury problems include Maintaining a patent airway Adequate ventilation Adequate circulating blood volume Preventing extension of cord damage (secondary damage) Clinical Manifestations Respiratory System Respiratory complications closely correspond to level of injury Cervical injury Above level of C4 Presents special problems because of total loss of respiratory muscle function Mechanical ventilation is required to keep patient alive Clinical Manifestations Respiratory System (Cont’d) Cervical injury (cont’d) Below level of C4 Diaphragmatic breathing if phrenic nerve is functioning Spinal cord edema and hemorrhage can affect function of phrenic nerve and cause respiratory insufficiency Hypoventilation almost always occurs with diaphragmatic breathing Clinical Manifestations Respiratory System (Cont’d) Cervical and thoracic injuries cause paralysis of Abdominal muscles Intercostal muscles Patient cannot cough effectively Leads to atelectasis or pneumonia Clinical Manifestations Respiratory System (Cont’d) Artificial airway provides direct access for pathogens Important to ↓ infections Pulmonary edema may occur in response to fluid overload Clinical Manifestations Cardiovascular System Any cord injury above level T6 greatly ↓ the influence of the sympathetic nervous system Bradycardia occurs Peripheral vasodilation results in hypotension Relative hypovolemia exists due to ↑ in venous capacitance Think neurogenic shock !!!!! Clinical Manifestations Cardiovascular System (Cont’d) Cardiac monitoring is necessary Peripheral vasodilation ↓ Venous return of blood to heart ↓ Cardiac output IV fluids or vasopressor drugs may be required to support BP Clinical Manifestations Urinary System Urinary retention common Bladder is atonic and overdistended Indwelling catheter inserted Increased risk of infection Bladder may become hyperirritable Loss of inhibition from brain Reflex emptying Clinical Manifestations Gastrointestinal System If cord injury is above T5, primary GI problems related to hypomotility Decreased GI motor activity contributes to development of Paralytic ileus Gastric distention Nasogastric tube may relieve gastric distention Clinical Manifestations Gastrointestinal System (Cont’d) Stress ulcers common Intraabdominal bleeding may occur Difficult to diagnose Indications of bleeding Continued hypotension despite treatment Decreased hemoglobin and hematocrit Positive hemocult test Expanding girth may also be noted Clinical Manifestations Gastrointestinal System (Cont’d) Less voluntary neurogenic control over bowel results in a neurogenic bowel Injury level of T12 or below Bowel is areflexic ↓ Sphincter tone Clinical Manifestations Gastrointestinal System (Cont’d) As reflexes return Bowel becomes reflexic Sphincter tone is enhanced Reflex emptying occurs Clinical Manifestations Integumentary System Consequence of lack of movement is skin breakdown Pressure ulcers can occur quickly Can lead to major infection or sepsis Clinical Manifestations Thermoregulation Poikilothermism Adjustment of body temperature to room temperature Occurs in spinal cord injuries because sympathetic nervous system interruption prevents peripheral temperature sensations from reaching hypothalamus Clinical Manifestations Thermoregulation (Cont’d) With spinal cord disruption, there is also Decreased ability to sweat Decreased ability to shiver Degree of poikilothermism depends on level of injury Clinical Manifestations Metabolic Needs Nasogastric suctioning may lead to metabolic alkalosis ↓ Tissue perfusion may lead to acidosis Monitor electrolyte levels until suctioning is discontinued and normal diet is resumed Clinical Manifestations Metabolic Needs (Cont’d) Loss of body weight is common Nutritional needs much greater than expected for immobilized person Positive nitrogen and high-protein diet Prevents skin breakdown and infection Decreases rate of muscle atrophy Clinical Manifestations Peripheral Vascular Problems Deep vein thrombosis (DVT) problem Pulmonary embolism a leading cause of death DVT assessments Doppler examination Impedance plethysmograph Measurement of legs and thigh girth Diagnostic Studies Complete spine films are performed to assess for vertebral fracture CT scan may be used to assess stability of injury, location, and degree of bone injury MRI used where there is unexplained neurologic deficit Comprehensive neurologic examination Collaborative Care Initial goals are to Sustain life Prevent further cord damage Systemic and neurogenic shock must be treated to maintain BP At cervical level, all body systems must be maintained until full extent of damage is known Collaborative Care (Cont’d) Thoracic and lumbar vertebrae injuries Systemic support less intense Respiratory compromise not as severe Bradycardia is not a problem Specific problems treated symptomatically Collaborative Care (Cont’d) After stabilization, history is obtained Emphasis on how injury occurred Extent of injury as perceived by patient immediately after event Collaborative Care (Cont’d) Assessment Test muscle groups with and against gravity Note spontaneous movement Sensory examination Position sense and vibration Collaborative Care (Cont’d) Assessment (cont’d) Brain injury may have occurred—assess history for Unconsciousness Signs of concussion Increased intracranial pressure Musculoskeletal injuries Trauma to internal organs Collaborative Care Nonoperative Stabilization Focused on stabilization of injured spinal segment and decompression Through traction or realignment Eliminate damaging motion at injury site Intended to prevent secondary damage Collaborative Care Surgical Therapy Criteria for early surgery Cord decompression may result in ↓ secondary injury Evidence of cord compression Progressive neurologic deficit Compound fracture Bony fragments Penetrating wounds of spinal cord or surrounding structures Collaborative Care Surgical Therapy (Cont’d) Common surgical procedures Decompression laminectomy by anterior cervical and thoracic approaches with fusion Posterior laminectomy with use of acrylic wire mesh and fusion Insertion of stabilizing rods Collaborative Care Drug Therapy Methylprednisolone (MP) Administered early and in large doses there is greater recovery of neurologic function Was a standard of care, but MP increases risk of complications, cost, hospital stay Now a treatment option No benefit 8 hours postinjury Collaborative Care Drug Therapy (Cont’d) Vasopressor agents Used in acute phase Maintain mean arterial pressure Drug interactions may occur Pharmacologic agents Used to treat specific autonomic dysfunctions Nursing Assessment Subjective Data Past health history Health perception–health management Activity-exercise Cognitive-perceptual Coping–stress tolerance Nursing Assessment (Cont’d) Objective Data General: Poikilothermism Integumentary: Neurogenic shock Respiratory: Lesions at C1-3 Cardiovascular: Lesions above T5 GI: Decreased or absent bowel sounds Urinary: Retention, flaccid bladder Nursing Diagnoses Impaired gas exchange Decreased cardiac output Impaired skin integrity Constipation Impaired urinary elimination Nursing Diagnoses (Cont’d) Impaired physical mobility Risk for autonomic dysreflexia Ineffective coping Interrupted family process Planning Overall goals Maintain an optimal level of neurologic functioning Have minimal to no complications of immobility Learn skills, gain knowledge, and acquire behaviors to care for self Return to home and community Nursing Implementation Health Promotion Identify High-risk populations Counseling Education Support legislation on seat belt use, helmets for motorcyclists/bicyclists, child safety seats Nursing Implementation (Cont’d) Nursing Interventions Education Counseling Maintaining appointments Referral to programs Recreation and exercise programs Alcohol treatment programs Smoking cessation programs Spinal and Neurogenic Shock Spinal shock Temporary neurologic syndrome Characterized by ↓ Reflexes Loss of sensation Flaccid paralysis below level of injury Experienced by ~50% of people with acute spinal cord injury Spinal and Neurogenic Shock (Cont’d) Spinal shock (cont’d) Syndrome lasts days to months May mask potential postinjury neurologic function Active rehabilitation may begin Spinal and Neurogenic Shock (Cont’d) Neurogenic shock Loss of vasomotor tone caused by injury Characterized by hypotension and bradycardia (important clinical cues) Spinal and Neurogenic Shock (Cont’d) Neurogenic shock (cont’d) Loss of sympathetic nervous system innervation causes Peripheral vasodilation Venous pooling ↓ Cardiac output ASIA Impairment Scale American Spinal Injury Association (ASIA) impairment scale Commonly used for classifying severity of impairment resulting from spinal cord injury ASIA Impairment Scale (Cont’d) Combines assessment of motor and sensory function Determines neurologic level and completeness of injury Useful for Recording changes in neurologic status Identifying appropriate functional goals for rehabilitation ASIA Impairment Scale (Cont’d) ASIA Impairment Scale (Cont’d) Overview of Anatomy and Physiology Endocrine glands and hormones The endocrine system is composed of a series of ductless glands It communicates through the use of hormones Hormones are chemical messengers that travel though the bloodstream to their target organ Overview of Anatomy and Physiology Pituitary gland—“master gland” Anterior pituitary gland Posterior pituitary gland Thyroid gland Parathyroid gland Adrenal gland Adrenal cortex Adrenal medulla Pancreas Figure 11-2 (From Thibodeau, G.A., Patton, K.T. [2008]. Structure and function of the body. [13th ed.]. St. Louis: Mosby.) Pituitary hormones. Diabetes Insipidus Etiology/pathophysiology Transient or permanent metabolic disorder of the posterior pituitary Deficiency of antidiuretic hormone (ADH) Primary or secondary Diseases of the Posterior Pituitary Diabetes insipidus Insufficiency of ADH Polyuria and polydipsia Partial or total inability to concentrate the urine Neurogenic Insufficient amounts of ADH Nephrogenic Inadequate response to ADH Psychogenic Disorders of the Pituitary Gland Diabetes insipidus Clinical manifestations/assessment Polyuria; polydipsia May become severely dehydrated Lethargic Dry skin; poor skin turgor Constipation Medical management/nursing interventions ADH preparations Limit caffeine due to diuretic properties Diseases of the Posterior Pituitary Syndrome of inappropriate antidiuretic hormone secretion (SIADH) Hypersecretion of ADH For diagnosis, normal adrenal and thyroid function must exist Clinical manifestations are related to enhanced renal water retention, hyponatremia, and hypo-osmolality Interesting YouTube Videos (cut-n-paste) http://www.youtube.com/watch?v=lXwk5p OIsoY http://www.youtube.com/watch?v=LqP http://www.youtube.com/watch?v=CUaEwgf KOEc http://www.youtube.com/watch?v=pN http://www.youtube.com/watch?v=mtdBGO vj-No http://www.youtube.com/watch?v=wl http://www.youtube.com/watch?v=mAGozj9 BP_E http://www.youtube.com/watch?v=wl http://www.youtube.com/watch?v=K9BYEO 9725k http://www.youtube.com/watch?v=0sHLqKu Ve_g http://www.youtube.com/watch?v=zD6HM mc0QmA http://www.youtube.com/watch?v=pl9KJkl WUlE 7f103cSU vEpmUcDss YiDxNcMdc YiDxNcMdc&list=PLE4074619D70E637 9 http://www.youtube.com/watch?v=B6 G8DCGC3I&list=PLE4074619D70E6379 http://www.youtube.com/watch?v=ElE ONHSKKSY http://www.youtube.com/watch?v=SE5 IbNdTJfg