Fluent Essays

Answer the question on the slide 53 with responses of 30 to 50 words using APA format. acute_brain_disorders_ch_44.pptx Unformatted Attachment Preview Acute brain disorders Chapter 44 Module objectives • Describe etiology of disorders of the neurologic system. • Explain clinical signs and symptoms of disorders that affect the neurologic system. How does the brain sustain injury? • Primary brain injury • As a result of the direct insult/injury • Secondary brain injury • Progressive damage or damage that evolves over time • Critical factor which determines • Neuronal cell fate after injury • Or, what is the degree of adenosine triphosphate (ATP) depletion? Ischemia vs. hypoxia • Ischemia (decreased blood flow) is a contributing factor either as the primary insult or as part of the secondary response • Ischemia results in immediate neurologic dysfunction because of inability of neurons to generate ATP needed for energy-requiring processes Remember ischemia = ‘I want oxygen’ • Ischemia and hypoxia (decreased oxygen at cellular level) usually occur together • Neuronal tissue highly sensitive to oxygen deprivation Failure at the cellular level • Neurons have remarkable ATP requirement and limited capacity for anaerobic metabolism during ischemia • Dependent on glucose for ATP production • Stores very little glycogen • About 5 to 10 minutes without oxygen irreversible brain damage • Two mechanisms can cause brain cell death • Anaerobic metabolism • Deterioration of ion gradients Anaerobic metabolism in the brain • Anaerobic metabolism • Causes mitochondrial dysfunction • Pyruvate converted to lactate • Hydrogen ions lead to cellular acidosis, which affects neuronal integrity • Inadequate energy supply leads to deterioration • Anoxic depolarization causes potassium to leave the cell and sodium, chloride, and calcium ions to enter leading to injury and death Ischemic cascade causing brain injury Brain regulation • The body normally provides steady supply of oxygen and nutrients to brain cells and removes metabolic wastes • Normally influenced by • pH • Carbon dioxide • Oxygen in the arterial blood • Injury causes imbalance; • Local or global impairment; • Any interference with vessel dilation leads to ischemia • Impaired vasoconstriction mechanisms cause hyperperfusion & edema formation Intracranial pressure • Premise of Monro-Kellie is • The brain self-regulates pressures and adapts as needed • With brain injury, the ability to selfregulate is impaired • Increased intracranial pressure (ICP) can occur due to • Space-occupying lesions/tumors • Vasogenic or cytotoxic edema • Obstruction of or excessive production of CSF If I have increased ICP, what would you see? Headache Nausea/vomiting Altered LOC Blurred vision Papilledema (swelled optic disk) Impaired pupillary response Help me! • As ICP rises, neural tissue and blood vessels are compressed • If unrelieved (remember the Monro-Kellie doctrine), the brain will find a pathway for relief of pressure • Herniation – protruded brain tissue through opening in brain • Types vary Let’s prevent that • Management • Based on brain imaging such as • CT or MRI • • • • Surgical or medical management Monitoring of ICP and cerebral perfusion pressure (CPP) If lesion or hematoma, remove it! If pressure needs relief remove cerebrospinal fluid (CSF) • Treatment is focused on maintaining cerebral oxygenation “ A change in level of consciousness (LOC) is the most sensitive indicator of altered brain function Marsh & Banasik, (2019), p. 900 Super important to know!! ” Assessing LOC • LOC can fluctuate in brain injury— essential to assess frequently • May have orders to perform neuro assessment every hour • Complete loss of consciousness = coma • Assessment tool is Glasgow Coma Scale (GCS) for acute brain injury • Mild injury >12; moderate injury 9-12; severe injury <8 Need to know GCS and ranking of severity Motor response • Most powerful predictor of patient outcome • Decorticate posturing • Decerebrate posturing Q&A What would be the GCS value for a patient who opens his eyes when the nurse calls his name, does not know where he is or that it is nighttime, and purposefully moves his head away when the nurse applies pressure to his eyebrow ridge? a. 8 b. 10 c. 12 d. 14 Q&A A patient’s posturing is characterized by abnormal flexion of the arms and wrists with the legs and feet extended and internally rotated. How does the nurse document this finding? a. Decerebrate b. Diffuse c. Dysconjugate d. Decorticate Cranial nerve assessments • Pupil reflex—CN II and III • Changes in size, shape, reactivity early indication of ICP and brain herniation • Eye movements – CN III, IV, VI • May be impaired with increased ICP • Client may be nystagmus, dysconjugate movement and ocular palsies • Impaired reflex implies brainstem dysfunction • “Doll’s eyes” maneuver – rotate client’s head from side to side Oculovestibular reflex • Normal eyes turn in opposite direction of head rotation • Cold calorics – inject cold water into ear canal • Normal response = tonic deviate of both eyes to side irrigated • Cornea reflex – touch cornea with wisp of cotton to elicit a blink • Absence of blink = severely impaired brain Traumatic brain injury (TBI) Facts about TBI • Leading cause of death & disability in United States • Most are due to transportation-related accidents, falls, firearms, sports • Severity of TBI classified by GCS • Mild: GCS 13-15 • Moderate: GCS 9-12 • Severe: GCS 8 or below Types of TBI • Primary injury • Focal • Polar • Diffuse • Intracranial hematomas • Epidural • Subdural • Subarachnoid Primary injury • Results from initial injury/trauma on brain cells • Focal injury is localized at site of injury • Polar injury is caused by acceleration/deceleration movement of brain in skull, resulting in a double injury • Diffuse injury = movement of brain in skull resulting in widespread axonal injury Mechanism of injury • Concussion • Mild TBI– most common • Alteration or loss of consciousness (<30 mins) – no evidence of brain injury on imaging • S/sx • • • • • • Headache N/V Dizziness Fatigue Blurred vision Cognitive/emotional disturbances • Contusion (AKA bruise) • Area of brain on imaging = tissue damage • Necrosis, laceration, bruise Hematomas • Intracranial hematoma • • • • Localized collection of blood in cranial vault Disruption of vasculature May expand slow or quickly Compresses brain structures and increases ICP • Types • Epidural • Subdural • Subarachnoid Epidural hematoma • Between dura and skull • Usually arterial injury = rapid onset of symptoms • Presentation • Primary injury minor – brief period of altered LOC then normal cognition, but LOC rapidly deteriorates • Diagnosis • CT scan • Treatment • Surgical removal of hematoma Subdural hematoma • Blood between dura and outer arachnoid • Involves bridging veins; symptom onset slower • Acute – within 24 hrs of injury • Subacute – increased ICP (headache, vomiting, blurred vision) 2-10 days after • Chronic – prone to rebleeding • Diagnosis • CT or MRI • Treatment • Remove tissue and clot Subarachnoid hematoma • Blood between pia mater and arachnoid membrane • Rupture of bridging veins in the subarachnoid space • Most commonly associated with • Cerebral aneurysms • Arteriovenous malformation (AVM) • Arterial in origin • Blood spreads through CSF causing • • • • Meningeal irritation Hydrocephalus‘ Headache & vasospasm Ischemia Secondary injury to brain • Body response to initial injury may cause more harm than initial injury • • • • Ischemia Hypoxic events Vasogenic/neurogenic edema Brain swelling & increased ICP • Ruptured vessels can rebleed or spasm • CSF drainage can be occluded Treatment 1. Ensure cardiopulmonary stability (ABCs) 2. Obtain radiographic images of head/neck a. Evaluate need for surgery 3. Maintain a. b. c. d. Normothermia Normal CO2 levels (PaCO2) Normal serum glucose Normal intravascular volume 4. For acutely elevated ICP a. Administer mannitol (osmotic diuretic) b. Provide sedation c. Mild hypothermia d. Mild hyperventilation Treatment • For severely elevated ICPs • • • • • Invasive monitoring Diuretics Hypertonic saline Moderate hyperventilation Barbiturate coma • Open head injuries • Prophylactic antibiotics • Basilar skull fractures • CSF can leak out from nose or ears • Bilateral periorbital hematomas (black eyes—AKA raccoon eyes) • Bruising under ears (Battle’s sign) Stroke Cerebrovascular disease • Abnormalities in cerebral perfusion • Indications are • Transient ischemic attacks (TIA) Most common • Ischemic stroke • Hemorrhagic stroke • Stroke (or cerebrovascular accident [CVA]) • Sudden onset • Neurologic dysfunction • Brain ischemia/infarction • Fifth leading cause of death in U.S. • Males affected more than females • Risk factors similar to other atherosclerotic disorders • • • • • • HTN DM Hyperlipidemia Smoking Older age Family history Ischemic stroke • Sudden occlusion of cerebral artery due to thrombus formation or emboli • Thrombotic strokes d/t atherosclerosis and coagulopathies • Embolic strokes d/t cardiac dysfunction or dysrhythmias (a fib) • Clinical manifestations • Contralateral hemiplegia • Hemisensory loss • Contralateral visual field blindness • Treatment • Re-establish perfusion to the brain cells • Needs to be within 3 hours of symptom onset for maximal effectiveness • New term: • Penumbra = area of ischemic but viable cells surrounding the infarct A nurse is asked about the definition for penumbra. How should the nurse reply? Q&A • • • • It is a lack of sensory information from the paralyzed side. It is the ischemic but viable cells surrounding the infarct area. It is the abnormal shunting of blood into the arteriovenous mass. It is the excessive accumulation of cerebral spinal fluid in the brain. Copyright © 2019, Elsevier Inc. All rights reserved. 37 Ischemic stroke • If neuro deficits completely resolve – consider TIA • Neuro symptoms typically last only minutes, but may last up to 24 hrs • Symptoms will resolve without any neuro deficits • Important warning signs of thrombotic stroke • Indicate significant risk for subsequent stroke • Treatment = daily aspirin, carotid endarterectomy or angioplasty if ≥ 70\% occlusion Hemorrhagic stroke • Usually due to severe, chronic hypertension • Secondary injury is much higher with this type of stroke • Associated with higher morbidity and mortality • Bleeding into brain tissue which then exerts pressure on surrounding tissue Stroke treatment • Ensure cardiovascular stability • Obtain head CT ASAP • Institute ICP monitoring and management Stroke treatment ISCHEMIC HEMORRHAGIC • Minimize size of infarct • Manage blood pressure • Preserve neurologic functioning • ‘Permissive’ hypertension • Interventions • • • • Thrombolytics Anticoagulants/antiplatelets Carotid endarterectomy Angioplasty/stent placement • Do not want to dramatically drop BP • May need surgery to remove hematoma Sequelae of stroke Language deficits • Aphasia • Expressive • receptive Cognitive deficits -Impaired spatial relationship skills Sensory disturbances • Loss of sensory input on contralateral side Motor deficits • Loss of function in contralateral side Memory or impaired judgment Other factors attributed to stroke • Cerebral aneurysm & arteriovenous malformations (AVM) most common cause of subarachnoid hemorrhage • Aneurysm • Arterial lesion leading to dilation and ballooning • Associated with high blood pressure, acute alcohol intox, recreational drug use (esp. cocaine) • Can be congenital defect • Most often in Circle of Willis Cerebral aneurysm • Clinical manifestations • • • • Severe headache Photophobia N/V Stiff neck • Diagnosis • CT, MRI, lumbar puncture • Treatment • Surgical stabilization of aneurysm, such as • Clipping or embolization • Medically manage • Maintain BP and blood volume normal to high • Calcium channel blocker (Nimodipine) Other factors attributed to stroke • AVM • Capillary system eventually becomes congested mass of vessels that could burst • Clinical manifestations • Seizure, neuro dysfunction • Treatment • • • • Surgical removal Radiation therapy Irradiation Glue embolization (cutting off blood supply) CNS infections CNS infections • Organisms may gain access to the CNS through the bloodstream, direct extension from a primary site or along peripheral and cranial nerves, or through maternalfetal exchange • Risk factors: • • • • • • Immunocompromised Debilitation Poor nutrition Radiation Steroid therapy Contact with vectors • Meningitis and cerebral abscess commonly associated with bacterial infections; encephalitis usually viral. Meningitis • Bacteria usually reach the CNS via the bloodstream or extension from cranial structures like sinuses or ears • Most common bacteria are Streptococcus pneumonia • Bacteria invade leptomeninges; accumulation of inflammatory exudate can result in obstructive hydrocephalus • Classic presentations: headache, fever, stiff neck (meningismus), and signs of cerebral dysfunction (confusion, delirium) • Diagnosis: lumbar puncture • Treatment: intravenous antibiotic therapy and supportive measures; corticosteroids? • Prevention: vaccinations for Hib and N. meningitidis Encephalitis • Inflammation of the brain commonly caused by West Nile virus, western equine encephalitis, and herpes simplex • Typical presentation of West Nile includes fever, HA, malaise, muscle pain, and/or rash; for herpes: fever, headache, seizure, confusion, stupor, and coma • Diagnosis: CT, MRI, lumbar puncture • Treatment: supportive with control of symptoms, including antipyretics, antiviral, steroids, anti-seizure medications, fluid resuscitation Brain Abscess • Localized collection of pus within the brain parenchyma • Usually from pus forming bacteria (pyogenic) • Presents as space-occupying lesion and typically with signs of infectious etiology • Treatment: drainage and/or excision of the abscess with IV antibiotic therapy Case study J.S. is a 72-year-old woman with a long history of atherosclerosis. One afternoon, her grandson found her sitting in a chair staring blankly into space. She was leaning to the right, drooling, and had been incontinent of urine. She was able to focus her eyes on him when he spoke to her, but she was unable to verbalize a response. She was transported to the local hospital and diagnosed with a stroke. 52 Questions • What questions could be asked of J.S.’s family to help determine the cause of her stroke as thrombotic, embolic, or hemorrhagic (i.e., questions to assess risk factors for each type of stroke)? • Based on the scenario described above, which brain hemisphere (left or right) suffered the ischemic damage? What other manifestations of this stroke location would likely be apparent? • What medical therapies might be used to manage this current stroke and/or to prevent another one? • What information might be appropriate to give J.S.’s family about the expected recovery process after stroke? ... Purchase answer to see full attachment