1 / 50

Medical Nutrition Therapy in Neurological Disorders Part 1

Medical Nutrition Therapy in Neurological Disorders Part 1. Nutrition and Neurologic Disease. May have nutritional etiologies resulting from deficiency or excess May be nonnutritional in origin but have significant nutritional implications. Stroke Statistics.

sezja
Télécharger la présentation

Medical Nutrition Therapy in Neurological Disorders Part 1

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Medical Nutrition Therapy in Neurological Disorders Part 1

  2. Nutrition and Neurologic Disease • May have nutritional etiologies resulting from deficiency or excess • May be nonnutritional in origin but have significant nutritional implications

  3. Stroke Statistics • Stroke is the third leading cause of death ranking behind diseases of the heart and cancers • Killed 150,147 people in 2004; females accounted for 60.9 percent of stroke deaths. • About 5,700,000 stroke survivors are alive today. 2,400,000 are males and 3,300,000 are females. • Data from GCNKSS studies show that about 700,000 people suffer a new or recurrent stroke each year. About 500,000 of these are first attacks and 200,000 are recurrent attacks. (GCNKS studies) http://www.americanheart.org/presenter.jhtml?identifier=4725accessed online 11-16-07

  4. Stroke Statistics • From 1992 to 2002 the death rate from stroke declined 13.8 percent, but the actual number of stroke deaths rose6.9 percent. • A leading cause of functional disability – 15-30% permanently disabled Primary Prevention of Ischemic Stroke, AHA/ASA Guideline, Stroke 2006;37:1583-1633, accessed online 11-16-06

  5. Non-Modifiable Age Gender Low Birth Weight Race/ethnicity Genetic factors Modifiable Hypertension Exposure to cigarette smoke Diabetes Atrial fib and other cardiac conditions Dislipidemia (ischemic stroke) Post-menopausal hormone therapy Poor diet Obesity/body fat distribution Inactivity Risk Factors for Ischemic Stroke Primary Prevention of Ischemic Stroke, AHA/ASA Guideline, Stroke 2006;37:1583-1633, accessed online 11-16-06

  6. Pathophysiology of Stroke • 85% of strokes caused by a thromboembolic event (related to atherosclerosis, hypertension, diabetes, gout) • Embolic stroke: cholesterol plaque is dislodged from vessel, travels to the brain, blocks an artery • Thrombotic stroke: cholesterol plaque within an artery ruptures, platelets aggregate and clog a narrow artery

  7. Nutrition-Related Factors and Stroke Risk (BMI = body mass index)

  8. Thromboembolic Stroke

  9. Hemorrhagic Stroke • Intraparenchymal hemorrhage: prevalence of hypertension is 80%; vessel inside the brain ruptures • Subarachnoid hemorrhage (SAH): ruptured aneurism in the subarachnoid space; or due to head trauma • 15% of all strokes

  10. Hemorrhagic Stroke

  11. Medical Treatment for Stroke • Thrombolytic or “clot-busting” drugs to restore perfusion to affected areas within 6 hours of onset of stroke • Controlling intracranial pressure (ICP) while maintaining sufficient perfusion of the brain

  12. Nutritional Management in Stroke • Primary prevention • Acute management (screening for dysphagia and nutritional risk) • Intervention for swallowing disorders via consistency changes

  13. AHA Guidelines for Primary Prevention of CVD and Stroke: 2006 Update • Smoking: complete cessation (Class I, evidence level B • Avoid exposure to environmental tobacco smoke (Class IIA, evidence C) • BP control: goal <140/90 mmHg with lower targets in some subgroups (<130/80 in diabetes) Goldstein et al, Primary Prevention of Ischemic Stroke, Stroke 2006;37:1583-1633)

  14. AHA Guidelines for Primary Prevention of CVD and Stroke: 2006 Update • Blood lipid mgt: • NCP III guidelines for pts who have not had a stroke and have high TC or non-HDL-C w/ high TG • Pts with known CAD and high risk HTN even w/ normal LDL treat with lifestyle/statin (Class I, evidence A) • Rec wt loss, ↑ physical activity, smoking cessation, niacin or gemfibrozil (Class IIA, evidence B) Goldstein et al, Primary Prevention of Ischemic Stroke, Stroke 2006;37:1583-1633)

  15. AHA Diet/Lifestyle Guidelines for Primary Prevention of CVD/Stroke: 2006 Update • Reduced intake of sodium and increased intake of potassium to lower blood pressure (Class I, evidence A) • Recommended sodium intake <2.3g/day; potassium >4.7g/day • DASH diet emphasizing fruits, vegetables, lowfat dairy products is recommended to lower BP (Class I, evidence A) • High fruit and vegetable intake may lower risk of stroke (Evidence C) • Wt reduction is recommended because it lowers BP • Increased physical activity (>30 minutes of moderate-intensity activity daily) Pearson et al. (Circulation. 2002;106:388-391.)

  16. Lipids and Stroke • Cholesterol is a very weak risk factor for ischemic stroke, in contrast to CAD • Cholesterol reduction with diet and nonstatin drugs is not effective in stroke prevention, although reductions in levels of cholesterol are modest • Statins produce a statistically significant 25% reduction in the risk of stroke Briel M, et al Am J Med 2004;117:596-606

  17. Lipids and Stroke in MRFIT

  18. Lipids and Stroke: ARIC Study • Cohort study of 14,175 men and women • After 10-year followup, there were weak and inconsistent associations between ischemic stroke and LDL-C, HDL-C, apo-B, apo-A-1, triglycerides • Most consistent relationship was lower risk in women with higher HDL and higher risk with lower TG Shahar E, et al. Stroke, 2003;34:623-631

  19. Lipids and Stroke • Problem may be the heterogenicity of stroke, although even when looking at homogeneous ischemic stroke, relationship is weak • The protective effect of statins may be due to their non-cholesterol-lowering effects.

  20. Relationship Between Fat/Cholesterol and Stroke Risk • Dietary cholesterol, MFA, PUFA not related to risk of stroke • Low intake of SFA and animal protein associated with  risk of intraparenchymal hemorrhage • In DCCT trial, intensive treatment lowered LDL, TC and TG and cerebrovascular events

  21. Guidelines for Management of Acute Stroke Rehab (AHA/ASA) • Dysphagia occurs in 45% of all hospitalized stroke patients; can lead to aspiration pneumonia and death. • Malnutrition is present in 15% of patients admitted to the hospital, and this percentage doubles during the first week after stroke. • A bedside swallow screening should be completed before oral intake (Evidence Level=B). • If the patient’s swallow screening is abnormal, a complete bedside swallow examination is recommended (Evidence Level=I). AHA/ASA Endorsed Veterans Affairs/Department of Defense Clinical Practice Guideline for the Management of Adult Stroke Rehabilitation Care (Stroke. 2005;36:2049.)

  22. Dysphagia Treatment- AHA/ASA • Dysphagia treatment may involve posture changes, heightening sensory input, swallow maneuvers, active exercise programs, or diet modifications. • Dysphagia management may include nonoral feeding and psychological support. • At this time, it is unclear how dysphagic patients should be fed after acute stroke. AHA/ASA Endorsed Veterans Affairs/Department of Defense Clinical Practice Guideline for the Management of Adult Stroke Rehabilitation Care (Stroke. 2005;36:2049.)

  23. Dysphagia Treatment- AHA/ASA • The literature supports the use of tube feeding for patients who cannot sustain sufficient oral caloric and/or fluid intake to meet nutritional needs. • Limited evidence suggests that percutaneous endoscopic gastrostomy feeding compares favorably with nasogastric tube feeding (Evidence Level=B). AHA/ASA Endorsed Veterans Affairs/Department of Defense Clinical Practice Guideline for the Management of Adult Stroke Rehabilitation Care (Stroke. 2005;36:2049.)

  24. FOOD (Feed or Ordinary Diet) Trial • Tested feeding strategies after acute stroke including oral supplementation, early vs delayed NG feeding, and NG vs PEG feeding • Poor baseline nutritional status is associated with worse outcomes at 6 months. • This relationship persists after adjustment for pt’s age, prestroke functional level, living conditions, and severity of stroke. AHA/ASA Guidelines for the Early Management of Patients with Ischemic Stroke. (Stroke. 2005;36:916.)

  25. FOOD (Feed or Ordinary Diet) Trial • Found no benefit to routine oral supplementation of post-stroke patients who had not been identified as malnourished (1) • Early tube feeding was associated with an absolute reduction in risk of death of 5.8% (p=0.09) and a reduction in death or poor outcome of 1.2% (p=0.7) (2) • PEG feeding (vs NG) was associated with an absolute increase in risk of death of 1.0%, p=0.9) and an increased risk of death or poor outcome of 7.8% (p=0.05). 1: Lancet. 2005 Feb 26-Mar 4;365(9461):755-63. 2: Lancet. 2005 Feb 26-Mar 4;365(9461):764-72

  26. AHA Guidelines for Early Management of Pts with Ischemic Stroke • A poor nutritional status was associated with an increased risk of infections including pneumonia, gastrointestinal bleeding, and pressure sores. • These data provide a strong rationale for assessment of the patient’s nutritional status at the time of admission. AHA/ASA Guidelines for the Early Management of Patients with Ischemic Stroke. (Stroke. 2005;36:916.)

  27. Alzheimer’s Disease • Most common form of dementia • Increases exponentially after age 40 • Prevalence in white males at age 100 is 41.5% • Higher prevalence in women (3X) due to lower mortality

  28. Symptoms of Alzheimer’s Disease • Forgetfulness: may forget recent events, activities, names of familiar people or things (anomia). • Forget how to do simple tasks, such as brushing teeth, brushing hair • Get lost in familiar surroundings • Repeat words spoken by others (echolalia) • Loss of comprehension (agnosia)

  29. Symptoms of Alzheimer’s Disease (cont) • Motor skills deteriorate: loss of reflexes and shuffling gait • Bowel and bladder control lost • Limb weakness and contractures • Intellectual activity ceases • Vegetative state

  30. Alzheimer’s Disease Risk Factors • Age: risk doubles every five years after age 65 • Family history: early onset strongly hereditary; late onset has a genetic component • Those with a parent or sibling with AD are 2-3 times more likely to develop AD

  31. Alzheimer’s Disease Risk Factors • Head injury • Down syndrome • Low level of education • Female gender

  32. Alzheimer’s Disease Prevention: Research Areas •  AD risk is associated with CVD, hypertension, diabetes •  AD risk associated with exercise, staying mentally active, social engagement • Research ongoing into use of antioxidants (vitamins E and C), ginkgo biloba • Research into estrogen and AD suggests that estrogen treatment in postmenopausal women may  risk of dementia

  33. Treatment of Alzheimer’s Disease • No drug can stop or reverse AD • Some drugs may slow progress (tacrine (Cognex®), donepezil (Aricept®), rivastigmine (Exelon®), or galantamine (Razadyne®) • Other medications may treat symptoms such as sleeplessness, agitation, wandering, anxiety, and depression National Institutes on Aging, Alzheimer’s Disease Education and Referral Center http://www.alzheimers.org/treatment.htm

  34. Nutritional Consequences of Alzheimer’s Disease • Weight loss is common possibly due to  activity (pacing) • Decreased independence and impaired self-feeding • Inability to recognize hunger, thirst and satiety • Meals forgotten as soon as eaten or may not be eaten at all • Inability to recognize food when presented • Risk for dehydration

  35. MNT in Alzheimer’s Disease • Vitamin-mineral supplementation; assure intake of antioxidants • Minimize distractions at mealtime (turn off radio or television) • Place foods on small plates and give one at a time • Serve food on plates of contrasting color

  36. MNT in Alzheimer’s Disease • Model use of eating utensils, provide verbal cues • Allow patient to use eating utensils as long as possible • Finger foods may be helpful, but monitor for swallowing problems and choking • Frequent snacks, nutrient-dense foods, nutritional supplements may be helpful

  37. Practical Interventions for Eating-Related Behavioral Problems Common in Individuals with Dementia

  38. Practical Interventions for Eating-Related Behavioral Problems Common in Individuals with Dementia

  39. Migraine Headache • Thought to be vascular in origin • Throbbing, episodic, and intense • History of intercurrent nausea, vomiting, photophobia, visual or olfactory auras • Treated with NSAIDs, sympathomimetics, seritonin agonists; prophylaxis with calcium channel blockers, beta-adrenergic blockers, serotonin antagonists

  40. Migraine Headache • Headaches may be triggered by food • Varies by individual and tolerance thresholds vary over time • No general recommendations about food avoidance • Foods often cited are citrus fruits, tea, coffee, pork, chocolate, milk, nuts, vegetables, cola drinks • Evaluate through food and symptom diary

  41. Myasthenia Gravis (MG) • Autoimmune disorder of the neuromuscular junction • Body makes antibodies to acetylcholine receptors; make them unresponsive to Ach • Nervous system signal to the muscle is garbled • Relapsing and remitting weakness and fatigability; diplopia, facial muscle weakness, dysphagia (33%)

  42. Myasthenia Gravis (MG) Medical Treatment • Anticholinesterases inhibit acetylcholesterase and increase the amount of Ach • Removal of the thymus gland • Corticosteroids

  43. Myasthenia Gravis (MG) MNT • Nutritionally dense foods at the beginning of meals before the patient tires • Small frequent meals • Time medication with feeding to facilitate optimal swallowing • Limit physical activity before meals • Don’t encourage food consumption when patient is tired; may aspirate

  44. Wernicke-Korsakoff syndrome MNT Cause • Chronic thiamin deficiency with continued carbohydrate ingestion Treatment • Thiamin • Adequate hydration • Diet liberal in high-thiamin foods • Eliminate ETOH • Dietary protein may need to be restricted

  45. Amyotrophic Lateral Sclerosis • Also called Lou Gehrig’s Disease • Most common motor system disease • Progressive denervation atrophy and weakness of muscles • Both upper and lower motor neurons are lost in the spinal cord, brain stem, and motor cortex • Progresses to death in 2 to 6 years

  46. Amyotrophic Lateral Sclerosis • Prevalence constant throughout the world • Men affected more than women • Age of onset mid-50s (40-70) • Cause unknown • 5% familial, rest sporadic

  47. Amyotrophic Lateral Sclerosis Presentation • Muscle weakness commences in the legs and hands and progresses to the proximal arms and oropharynx • Voluntary skeletal muscles are at risk for atrophy and complete loss of function • Spasticity of jaw muscles resulting in slurred speech • Dysphagia, difficulty chewing  weight loss • Death from respiratory failure

  48. Amyotrophic Lateral Sclerosis Nutritional Implications • Dysphagia, chewing, swallowing problems • Decreased body fat, lean body mass, nitrogen balance and increased REE as death approaches • Late stage patients may not tolerate PEG placement d/t respiratory compromise • Initiate discussions about whether to place a feeding tube early in disease process • Enteral feedings do not prolong life

  49. Amyotrophic Lateral Sclerosis MNT • Correlates with ALS Severity Scale (pp 1102-1103) • Emphasize fluids as patients may limit fluids d/t toileting difficulties • Get baseline weight; 10% loss  increased risk • Modify consistency as eating problems develop using easy-chew foods, thickened liquids, using small frequent meals, cool food temperatures

  50. Amyotrophic Lateral Sclerosis MNT • If nutrition support is planned, use EN • Initiate early rather than later; dehydration occurs before malnutrition • Purpose of nutrition support should be to enhance quality of life • Eventually patients will not be able to manage oral secretions

More Related