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NURS 2280 (11)


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Dalhousie University
NURS 2280
Shauna Houk

Altered Neurological Function: Brain Injury and Neurodegenerati ve Disease Lorri Giffin RN MN-NP Geriatric Medicine CDHA March 1, 2011 Objectives • Understand that neurological deterioration can be acute(injury) or insidious(disease) • Explore basic concepts of brain injury including presentation, management and outcomes • Discuss Parkinson’s disease ..features, diagnosis and treatment • Review types of dementia, clinical features and treatment of AD Using Case Study Approach Review for each T opic: • Definition • Epidemiology • Pathophysiology • Clinical Features • Evaluation and management CASE #1 B.W . • J.W. 34 yr male struck head on snow/ice while snowboarding with his children • Brief LOC on scene, ambulatory shortly after, felt disoriented and dizzy for 15 min following, vomited x1 • Presents to ED 4 hrs later with persistent occipital headache, mild nausea • In triage in ED 36.8,HR 78,RR16, 138/80 and GCS 15 Mild TBI/Concussion: Definition • occurs with head injury due to contact and/or acceleration/deceleratio n forces • defined as mild by a GCS score of 13 to 15, measured ~ 30 minutes after injury • concussion as a trauma- induced alteration in mental status that may or may not involve loss of consciousness • Rapid onset of short-lived impairment of neurologic function that resolves spontaneously • Neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than structural injury • Typically associated with normal imaging studies Mild TBI/Concussion: Epidemiology • 70-90% of all treated brain injuries are mild • Incidence of hospital-treated patients with mild traumatic brain injury is about 100- 300/100,000 Canada • However, much mild TBI is not reported/treated and the true population-based rate is probably above 600/100,000. • Mild traumatic brain injury is more common in males 2.0:1 to 2.8:1 Estimates of the relative causes of TBI are as follows: • mvc (45%) • falls (30%) • occupational accidents (10%), • recreational accidents (10%) • assaults (5%) In the elderly, falls are more likely the cause,MVC are more common in the young Pathophysiology • Mild TBI may result in cortical contusions due to coup and contrecoup injuries • Milder degrees of axonal damage are postulated to play a role • Disruption of axonal neurofilament organization impairs axonal transport leading to axonal swelling, Wallerian degeneration, and transection • Release of excitatory neurotransmitters acetylcholine, glutamate, and aspartate, and the generation of free radicals may contribute to secondary injury Clinical Features Hallmarks of concussion are confusion and amnesia which may be apparent immediately after the head injury or may appear several minutes later • The amnesia almost always involves loss of memory for the traumatic event but frequently includes loss of recall for events immediately before (retrograde amnesia)and after the head trauma (Anterograde amnesia) • Amnesia also may be evidenced by the patient repeatedly asking a question that has already been answered • Inability to focus attention • Disorientation (walking in the wrong direction, unaware of time, date, place) • Slurred or incoherent speech (making disjointed or incomprehensible statements) • Gross observable incoordination (stumbling, inability to walk tandem/straight line) • Emotionality out of proportion to circumstances (appearing distraught, crying for no apparent reason) • Memory deficits (exhibited by patient repeatedly asking the same question that has already been answered or inability to memorize and return three of three words and three of three objects for five minutes Acute Evaluation/Manage ment • Obtain details of event..mechanism of injury,length of time decreased LOC, witnessed?, seizure activity? etc. • Neurologic assessment and mental status testing • +/- Neuroimaging The Canadian CT Head Rule Requires a head CT for patients with mild TBI and any one of the following: • GCS <15 two hours after injury • Suspected open or depressed skull fracture • Any sign of basilar skull fracture: hemotympanum, raccoon eyes , Battle's sign, or cerebrospinal fluid leak, oto- or rhinorrhea • Two or more episodes of vomiting • 65 years of age or older • Amnesia before impact of 30 or more minutes • Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from ≥3 feet or ≥5 stairs) Observation Observation is recommended for min of 24 hours after a mild TBI d/t of the risk of intracranial complications should be awakened from sleep every two hours and avoid strenuous activity for at least 24 hours The following warning signs should prompt the caregiver to seek immediate reassessment: • Inability to awaken the patient • Severe or worsening headaches • Somnolence or confusion • Restlessness, unsteadiness, or seizures • Difficulties with vision • Vomiting, fever, or stiff neck • Urinary or bowel incontinence • Weakness or numbness involving any part of the body Back to the case..B.W • Neurological exam=N, mental status=N • CT ..? • Follow up? Case #2 J.T • J.T 24 yr male was assaulted outside bar, struck repeatedly in the head. He fell to the ground unconscious. Seizure activity present at scene • On arrival to ED J.. was awake, restless and combative, PERLA, GCS=10 • After initial assessment in ED G.T became somnolent then unresponsive GCS= 7 Traumatic brain injury (TBI) • leading cause of death in North America for individuals between the ages of 1 and 45 • survivors live with significant disabilities, resulting in major socioeconomic burden as well • In 2000, the economic impact of TBI in the US was estimated to be $9.2 billion in lifetime medical costs and $51.2 billion in productivity losses TBI Epidemiology • Rates of TBI are highest in the very young (age 0-4) and in adolescents and young adults (15 to 24 years) • Peak in incidence in the elderly (age >65 years) • Approx 78% of TBI are treated in ED (mild) 19 % of pts require hosp and 3% are fatal • Hospitalization rates are highest in patients > 65 yrs Classification • TBI is a heterogeneous disease • TBI can lead to several pathologic injuries, most of which can be identified on neuroimaging: •Skull fracture •Epidural hematoma •Subdural hematoma •Subarachnoid hemorrhage •Intraparenchymal hemorrhage •Cerebral contusion •Intraventricular hemorrhage •Focal and diffuse patterns of axonal injury with cerebral edema Pathophysiology • Primary brain Injury — Primary brain injury occurs at the time of trauma. Common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury, and blast waves, they all result from external mechanical forces transferred to intracranial contents. The damage that results includes a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling • Diffuse axonal injury (DAI):shearing multiple small lesions seen within white matter tracts DAI typically present with profound coma without elevated intracranial pressure (ICP), and often have poor outcome • Cerebral contusions : most common,often seen in the basal frontal and temporal areas • Extra-axial ( outside the substance of the brain) hematomas are generally encountered when forces are distributed to the cranial vault and the most superficial cerebral layers. These include epidural, subdural, and subarachnoid hemorrhage. Secondary Brain Injury • Cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours/days: • Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell membranes • Electrolyte imbalances • Mitochondrial dysfunction • Inflammatory responses • Apoptosis • Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury Management of acute severe TBI: ED Treatment and diagnostic assessment is done according to the ATLS (Advanced T rauma Life Support) protocol: • Adequate oxygenation (PaO2 >60 mm Hg) and blood pressure support (systolic BP >90 mm Hg) continue to be priorities • Vital signs including heart rate, blood pressure, respiratory status pulse ox, and temp require ongoing monitoring • A neurologic exam completed asap to determine the clinical severity of the TBI,GCS is commonly used to assess and communicate neurologic status A GCS score of 8 or lower is considered a severe TBI. Neurologic status should be continuously assessed. Deterioration is common in the initial hours after the injury • The patient should be assessed for other systemic trauma • CBC, electrolytes, glucose, coagulation parameters, blood alcohol level, and urine toxicology should be checked • Typically Intubation/line placement …neuroimaging..ICP monitor insertion Management of acute severe TBI: ICU • ICP monitor/drain insertion if not already done • Decompressive craniotomy • General medical care — Maintenance of BP (systolic >90 mm Hg) and oxygenation (PaO2 >60 mm Hg) remain priorities • prevention of deep venous thrombosis (DVT) • Nutritional support • Head of be
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