Medical Nutrition Therapy in Neurological Disorders Part 1

Nutrition and Neurologic Disease

• May have nutritional etiologies resulting May have nutritional etiologies resulting from deficiency or excessfrom deficiency or excess

• May be nonnutritional in origin but have May be nonnutritional in origin but have significant nutritional implicationssignificant nutritional implications

Stroke Statistics• Stroke is the third leading cause of death ranking Stroke is the third leading cause of death ranking

behind diseases of the heart and cancersbehind diseases of the heart and cancers• Killed 150,147 people in 2004; Killed 150,147 people in 2004; females accounted females accounted

for 60.9 percent of stroke deaths. for 60.9 percent of stroke deaths. • About 5,700,000 stroke survivors are alive today. About 5,700,000 stroke survivors are alive today.

2,400,000 are males and 3,300,000 are females. 2,400,000 are males and 3,300,000 are females. • Data from GCNKSS studies show that about Data from GCNKSS studies show that about

700,000 people suffer a new or recurrent stroke 700,000 people suffer a new or recurrent stroke each year. About 500,000 of these are first attacks each year. About 500,000 of these are first attacks and 200,000 are recurrent attacks. and 200,000 are recurrent attacks. (GCNKS (GCNKS studies)studies)

http://www.americanheart.org/presenter.jhtml?identifier=4725accessed online 11-16-07

Stroke Statistics

• From 1992 to 2002 the death rate from From 1992 to 2002 the death rate from stroke declined 13.8 percent, but the stroke declined 13.8 percent, but the actual number of stroke deaths rose 6.9 actual number of stroke deaths rose 6.9 percentpercent. . 

• A leading cause of functional disability – A leading cause of functional disability – 15-30% permanently disabled15-30% permanently disabled

Primary Prevention of Ischemic Stroke, AHA/ASA Guideline, Stroke 2006;37:1583-1633, accessed online 11-16-06

Risk Factors for Ischemic StrokeNon-ModifiableNon-Modifiable• AgeAge• GenderGender• Low Birth WeightLow Birth Weight• Race/ethnicityRace/ethnicity• Genetic factorsGenetic factors

ModifiableModifiable• HypertensionHypertension• Exposure to cigarette smokeExposure to cigarette smoke• DiabetesDiabetes• Atrial fib and other cardiac Atrial fib and other cardiac

conditionsconditions• Dislipidemia (ischemic stroke)Dislipidemia (ischemic stroke)• Post-menopausal hormone Post-menopausal hormone

therapytherapy• Poor dietPoor diet• Obesity/body fat distributionObesity/body fat distribution• InactivityInactivity

Primary Prevention of Ischemic Stroke, AHA/ASA Guideline, Stroke 2006;37:1583-1633, accessed online 11-16-06

Pathophysiology of Stroke

• 85% of strokes caused by a thromboembolic event 85% of strokes caused by a thromboembolic event (related to atherosclerosis, hypertension, diabetes, (related to atherosclerosis, hypertension, diabetes, gout)gout)• Embolic stroke: cholesterol plaque is dislodged Embolic stroke: cholesterol plaque is dislodged

from vessel, travels to the brain, blocks an from vessel, travels to the brain, blocks an arteryartery

• Thrombotic stroke: cholesterol plaque within an Thrombotic stroke: cholesterol plaque within an artery ruptures, platelets aggregate and clog a artery ruptures, platelets aggregate and clog a narrow arterynarrow artery

Nutrition-Related Factors and Stroke Risk

Nutrition-Related Factors and Stroke Risk

(BMI = body mass index)

Thromboembolic Stroke

Hemorrhagic Stroke

• Intraparenchymal hemorrhage: prevalence Intraparenchymal hemorrhage: prevalence of hypertension is 80%; vessel inside the of hypertension is 80%; vessel inside the brain rupturesbrain ruptures

• Subarachnoid hemorrhage (SAH): ruptured Subarachnoid hemorrhage (SAH): ruptured aneurism in the subarachnoid space; or due aneurism in the subarachnoid space; or due to head traumato head trauma

• 15% of all strokes15% of all strokes

Hemorrhagic Stroke

Medical Treatment for Stroke

• Thrombolytic or “clot-busting” drugs to Thrombolytic or “clot-busting” drugs to restore perfusion to affected areas within 6 restore perfusion to affected areas within 6 hours of onset of strokehours of onset of stroke

• Controlling intracranial pressure (ICP) Controlling intracranial pressure (ICP) while maintaining sufficient perfusion of while maintaining sufficient perfusion of the brainthe brain

Nutritional Management in Stroke

• Primary preventionPrimary prevention• Acute management (screening for Acute management (screening for

dysphagia and nutritional risk)dysphagia and nutritional risk)• Intervention for swallowing disorders via Intervention for swallowing disorders via

consistency changesconsistency changes

AHA Guidelines for Primary Prevention of CVD and Stroke: 2006 Update

• Smoking: complete cessation (Class I, Smoking: complete cessation (Class I, evidence level Bevidence level B

• Avoid exposure to environmental tobacco Avoid exposure to environmental tobacco smoke (Class IIA, evidence C)smoke (Class IIA, evidence C)

• BP control: goal <140/90 mmHg with lower BP control: goal <140/90 mmHg with lower targets in some subgroups (<130/80 in targets in some subgroups (<130/80 in diabetes)diabetes)

Goldstein et al, Primary Prevention of Ischemic Stroke, Stroke 2006;37:1583-1633)

AHA Guidelines for Primary Prevention of CVD and Stroke: 2006 Update

• Blood lipid mgt: Blood lipid mgt: • NCP III guidelines for pts who have not had a NCP III guidelines for pts who have not had a

stroke and have high TC or non-HDL-C w/ stroke and have high TC or non-HDL-C w/ high TG high TG

• Pts with known CAD and high risk HTN even Pts with known CAD and high risk HTN even w/ normal LDL treat with lifestyle/statin (Class w/ normal LDL treat with lifestyle/statin (Class I, evidence A)I, evidence A)

• Rec wt loss, Rec wt loss, ↑ physical activity, smoking ↑ physical activity, smoking cessation, niacin or gemfibrozil (Class IIA, cessation, niacin or gemfibrozil (Class IIA, evidence B)evidence B)

Goldstein et al, Primary Prevention of Ischemic Stroke, Stroke 2006;37:1583-1633)

AHA Diet/Lifestyle Guidelines for Primary Prevention of CVD/Stroke: 2006 Update

• Reduced intake of sodium and increased intake of Reduced intake of sodium and increased intake of potassium to lower blood pressure (Class I, evidence A)potassium to lower blood pressure (Class I, evidence A)

• Recommended sodium intake <2.3g/day; potassium Recommended sodium intake <2.3g/day; potassium >4.7g/day>4.7g/day

• DASH diet emphasizing fruits, vegetables, lowfat dairy DASH diet emphasizing fruits, vegetables, lowfat dairy products is recommended to lower BP (Class I, evidence products is recommended to lower BP (Class I, evidence A)A)

• High fruit and vegetable intake may lower risk of stroke High fruit and vegetable intake may lower risk of stroke (Evidence C)(Evidence C)

• Wt reduction is recommended because it lowers BPWt reduction is recommended because it lowers BP• Increased physical activity (Increased physical activity (>>30 minutes of moderate-30 minutes of moderate-

intensity activity daily)intensity activity daily)Pearson et al. (Circulation. 2002;106:388-391.)

Lipids and Stroke

• Cholesterol is a very weak risk factor for Cholesterol is a very weak risk factor for ischemic stroke, in contrast to CADischemic stroke, in contrast to CAD

• Cholesterol reduction with diet and Cholesterol reduction with diet and nonstatin drugs is not effective in stroke nonstatin drugs is not effective in stroke prevention, although reductions in levels of prevention, although reductions in levels of cholesterol are modestcholesterol are modest

• Statins produce a statistically significant Statins produce a statistically significant 25% reduction in the risk of stroke25% reduction in the risk of stroke

Briel M, et al Am J Med 2004;117:596-606

Lipids and Stroke in MRFIT

Lipids and Stroke: ARIC Study

• Cohort study of 14,175 men and womenCohort study of 14,175 men and women• After 10-year followup, there were weak After 10-year followup, there were weak

and inconsistent associations between and inconsistent associations between ischemic stroke and LDL-C, HDL-C, apo-ischemic stroke and LDL-C, HDL-C, apo-B, apo-A-1, triglyceridesB, apo-A-1, triglycerides

• Most consistent relationship was lower risk Most consistent relationship was lower risk in women with higher HDL and higher risk in women with higher HDL and higher risk with lower TGwith lower TG

Shahar E, et al. Stroke, 2003;34:623-631

Lipids and Stroke

• Problem may be the heterogenicity of Problem may be the heterogenicity of stroke, although even when looking at stroke, although even when looking at homogeneous ischemic stroke, relationship homogeneous ischemic stroke, relationship is weakis weak

• The protective effect of statins may be due The protective effect of statins may be due to their non-cholesterol-lowering effects.to their non-cholesterol-lowering effects.

Relationship Between Fat/Cholesterol and Stroke Risk• Dietary cholesterol, MFA, PUFA not Dietary cholesterol, MFA, PUFA not

related to risk of strokerelated to risk of stroke• Low intake of SFA and animal protein Low intake of SFA and animal protein

associated with associated with risk of intraparenchymal risk of intraparenchymal hemorrhagehemorrhage

• In DCCT trial, intensive treatment lowered In DCCT trial, intensive treatment lowered LDL, TC and TG and cerebrovascular LDL, TC and TG and cerebrovascular eventsevents

Guidelines for Management of Acute Stroke Rehab (AHA/ASA)• Dysphagia occurs in 45% of all hospitalized stroke Dysphagia occurs in 45% of all hospitalized stroke

patients; can lead to aspiration pneumonia and patients; can lead to aspiration pneumonia and death.death.

• Malnutrition is present in 15% of patients Malnutrition is present in 15% of patients admitted to the hospital, and this percentage admitted to the hospital, and this percentage doubles during the first week after stroke.doubles during the first week after stroke.

• A bedside swallow screening should be completed A bedside swallow screening should be completed before oral intake (Evidence Level=B). before oral intake (Evidence Level=B).

• If the patient’s swallow screening is abnormal, a If the patient’s swallow screening is abnormal, a complete bedside swallow examination is complete bedside swallow examination is recommended (Evidence Level=I). 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.)

Dysphagia Treatment- AHA/ASA

• Dysphagia treatment may involve posture Dysphagia treatment may involve posture changes, heightening sensory input, changes, heightening sensory input, swallow maneuvers, active exercise swallow maneuvers, active exercise programs, or diet modifications. programs, or diet modifications.

• Dysphagia management may include Dysphagia management may include nonoral feeding and psychological support. nonoral feeding and psychological support.

• At this time, it is unclear how dysphagic At this time, it is unclear how dysphagic patients should be fed after acute stroke.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.)

Dysphagia Treatment- AHA/ASA

• The literature supports the use of tube feeding for The literature supports the use of tube feeding for patients who cannot sustain sufficient oral caloric patients who cannot sustain sufficient oral caloric and/or fluid intake to meet nutritional needs. and/or fluid intake to meet nutritional needs.

• Limited evidence suggests that percutaneous Limited evidence suggests that percutaneous endoscopic gastrostomy feeding compares endoscopic gastrostomy feeding compares favorably with nasogastric tube feeding (Evidence favorably with nasogastric tube feeding (Evidence Level=B). 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.)

FOOD (Feed or Ordinary Diet) Trial

• Tested feeding strategies after acute stroke Tested feeding strategies after acute stroke including oral supplementation, early vs including oral supplementation, early vs delayed NG feeding, and NG vs PEG delayed NG feeding, and NG vs PEG feeding feeding

• Poor baseline nutritional status is associated Poor baseline nutritional status is associated with worse outcomes at 6 months.with worse outcomes at 6 months.

• This relationship persists after adjustment This relationship persists after adjustment for pt’s age, prestroke functional level, for pt’s age, prestroke functional level, living conditions, and severity of stroke. living conditions, and severity of stroke.

AHA/ASA Guidelines for the Early Management of Patients with Ischemic Stroke. (Stroke. 2005;36:916.)

FOOD (Feed or Ordinary Diet) Trial• Found no benefit to routine oral supplementation Found no benefit to routine oral supplementation

of post-stroke patients who had not been identified of post-stroke patients who had not been identified as malnourished (1)as malnourished (1)

• Early tube feeding was associated with an absolute Early tube feeding was associated with an absolute reduction in risk of death of 5.8% (p=0.09) and a reduction in risk of death of 5.8% (p=0.09) and a reduction in death or poor outcome of 1.2% reduction in death or poor outcome of 1.2% (p=0.7) (2)(p=0.7) (2)

• PEG feeding (vs NG) was associated with an PEG feeding (vs NG) was associated with an absolute increase in risk of death of 1.0%, p=0.9) absolute increase in risk of death of 1.0%, p=0.9) and an increased risk of death or poor outcome of and an increased risk of death or poor outcome of 7.8% (p=0.05). 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

AHA Guidelines for Early Management of Pts with Ischemic Stroke

• A poor nutritional status was associated A poor nutritional status was associated with an increased risk of infections with an increased risk of infections including pneumonia, gastrointestinal including pneumonia, gastrointestinal bleeding, and pressure sores. bleeding, and pressure sores.

• These data provide a strong rationale for These data provide a strong rationale for assessment of the patient’s nutritional status assessment of the patient’s nutritional status at the time of admission. at the time of admission.

AHA/ASA Guidelines for the Early Management of Patients with Ischemic Stroke. (Stroke. 2005;36:916.)

Alzheimer’s Disease

• Most common form of dementiaMost common form of dementia• Increases exponentially after age 40Increases exponentially after age 40• Prevalence in white males at age 100 is Prevalence in white males at age 100 is

41.5%41.5%• Higher prevalence in women (3X) due to Higher prevalence in women (3X) due to

lower mortalitylower mortality

Symptoms of Alzheimer’s Disease• Forgetfulness: may forget recent events, Forgetfulness: may forget recent events,

activities, names of familiar people or activities, names of familiar people or things (anomia). things (anomia).

• Forget how to do simple tasks, such as Forget how to do simple tasks, such as brushing teeth, brushing hairbrushing teeth, brushing hair

• Get lost in familiar surroundingsGet lost in familiar surroundings• Repeat words spoken by others (echolalia)Repeat words spoken by others (echolalia)• Loss of comprehension (agnosia)Loss of comprehension (agnosia)

Symptoms of Alzheimer’s Disease (cont)• Motor skills deteriorate: loss of reflexes and Motor skills deteriorate: loss of reflexes and

shuffling gaitshuffling gait• Bowel and bladder control lostBowel and bladder control lost• Limb weakness and contracturesLimb weakness and contractures• Intellectual activity ceasesIntellectual activity ceases• Vegetative stateVegetative state

Alzheimer’s Disease Risk Factors• Age: risk doubles every five years after age Age: risk doubles every five years after age

6565• Family history: early onset strongly Family history: early onset strongly

hereditary; late onset has a genetic hereditary; late onset has a genetic componentcomponent

• Those with a parent or sibling with AD are Those with a parent or sibling with AD are 2-3 times more likely to develop AD2-3 times more likely to develop AD

Alzheimer’s Disease Risk Factors• Head injuryHead injury• Down syndromeDown syndrome• Low level of educationLow level of education• Female genderFemale gender

Alzheimer’s Disease Prevention: Research Areas AD risk is associated with CVD, AD risk is associated with CVD,

hypertension, diabeteshypertension, diabetes AD risk associated with exercise, staying AD risk associated with exercise, staying

mentally active, social engagementmentally active, social engagement• Research ongoing into use of antioxidants Research ongoing into use of antioxidants

(vitamins E and C), ginkgo biloba(vitamins E and C), ginkgo biloba• Research into estrogen and AD suggests Research into estrogen and AD suggests

that estrogen treatment in postmenopausal that estrogen treatment in postmenopausal women may women may risk of dementia risk of dementia

Treatment of Alzheimer’s Disease• No drug can stop or reverse ADNo drug can stop or reverse AD• Some drugs may slow progress (Some drugs may slow progress (tacrine tacrine

(Cognex®), donepezil (Aricept®), (Cognex®), donepezil (Aricept®), rivastigmine (Exelon®), or galantamine rivastigmine (Exelon®), or galantamine (Razadyne®)(Razadyne®)

• Other medications may treat symptoms Other medications may treat symptoms such as sleeplessness, agitation, wandering, such as sleeplessness, agitation, wandering, anxiety, and depressionanxiety, and depression

National Institutes on Aging, Alzheimer’s Disease Education and Referral Center http://www.alzheimers.org/treatment.htm

Nutritional Consequences of Alzheimer’s Disease• Weight loss is common possibly due to Weight loss is common possibly due to activity activity

(pacing)(pacing)• Decreased independence and impaired self-Decreased independence and impaired self-

feedingfeeding• Inability to recognize hunger, thirst and satietyInability to recognize hunger, thirst and satiety• Meals forgotten as soon as eaten or may not be Meals forgotten as soon as eaten or may not be

eaten at alleaten at all• Inability to recognize food when presentedInability to recognize food when presented• Risk for dehydrationRisk for dehydration

MNT in Alzheimer’s Disease

• Vitamin-mineral supplementation; assure Vitamin-mineral supplementation; assure intake of antioxidantsintake of antioxidants

• Minimize distractions at mealtime (turn off Minimize distractions at mealtime (turn off radio or television)radio or television)

• Place foods on small plates and give one at Place foods on small plates and give one at a timea time

• Serve food on plates of contrasting colorServe food on plates of contrasting color

MNT in Alzheimer’s Disease

• Model use of eating utensils, provide verbal Model use of eating utensils, provide verbal cuescues

• Allow patient to use eating utensils as long Allow patient to use eating utensils as long as possibleas possible

• Finger foods may be helpful, but monitor Finger foods may be helpful, but monitor for swallowing problems and chokingfor swallowing problems and choking

• Frequent snacks, nutrient-dense foods, Frequent snacks, nutrient-dense foods, nutritional supplements may be helpfulnutritional supplements may be helpful

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

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

Migraine Headache

• Thought to be vascular in originThought to be vascular in origin• Throbbing, episodic, and intenseThrobbing, episodic, and intense• History of intercurrent nausea, vomiting, History of intercurrent nausea, vomiting,

photophobia, visual or olfactory aurasphotophobia, visual or olfactory auras• Treated with NSAIDs, sympathomimetics, Treated with NSAIDs, sympathomimetics,

seritonin agonists; prophylaxis with calcium seritonin agonists; prophylaxis with calcium channel blockers, beta-adrenergic blockers, channel blockers, beta-adrenergic blockers, serotonin antagonistsserotonin antagonists

Migraine Headache

• Headaches may be triggered by foodHeadaches may be triggered by food• Varies by individual and tolerance Varies by individual and tolerance

thresholds vary over timethresholds vary over time• No general recommendations about food No general recommendations about food

avoidanceavoidance• Foods often cited are citrus fruits, tea, Foods often cited are citrus fruits, tea,

coffee, pork, chocolate, milk, nuts, coffee, pork, chocolate, milk, nuts, vegetables, cola drinksvegetables, cola drinks

• Evaluate through food and symptom diaryEvaluate through food and symptom diary

Myasthenia Gravis (MG)

• Autoimmune disorder of the neuromuscular Autoimmune disorder of the neuromuscular junctionjunction

• Body makes antibodies to acetylcholine Body makes antibodies to acetylcholine receptors; make them unresponsive to Achreceptors; make them unresponsive to Ach

• Nervous system signal to the muscle is Nervous system signal to the muscle is garbledgarbled

• Relapsing and remitting weakness and Relapsing and remitting weakness and fatigability; diplopia, facial muscle fatigability; diplopia, facial muscle weakness, dysphagia (33%)weakness, dysphagia (33%)

Myasthenia Gravis (MG) Medical Treatment• Anticholinesterases inhibit Anticholinesterases inhibit

acetylcholesterase and increase the amount acetylcholesterase and increase the amount of Achof Ach

• Removal of the thymus glandRemoval of the thymus gland• CorticosteroidsCorticosteroids

Myasthenia Gravis (MG) MNT

• Nutritionally dense foods at the beginning Nutritionally dense foods at the beginning of meals before the patient tiresof meals before the patient tires

• Small frequent mealsSmall frequent meals• Time medication with feeding to facilitate Time medication with feeding to facilitate

optimal swallowingoptimal swallowing• Limit physical activity before mealsLimit physical activity before meals• Don’t encourage food consumption when Don’t encourage food consumption when

patient is tired; may aspiratepatient is tired; may aspirate

Wernicke-Korsakoff syndrome MNT

CauseCause• Chronic thiamin deficiency with continued Chronic thiamin deficiency with continued

carbohydrate ingestioncarbohydrate ingestion

TreatmentTreatment• ThiaminThiamin• Adequate hydrationAdequate hydration• Diet liberal in high-thiamin foodsDiet liberal in high-thiamin foods• Eliminate ETOHEliminate ETOH• Dietary protein may need to be restrictedDietary protein may need to be restricted

Amyotrophic Lateral Sclerosis

• Also called Lou Gehrig’s DiseaseAlso called Lou Gehrig’s Disease• Most common motor system diseaseMost common motor system disease• Progressive denervation atrophy and Progressive denervation atrophy and

weakness of musclesweakness of muscles• Both upper and lower motor neurons are Both upper and lower motor neurons are

lost in the spinal cord, brain stem, and lost in the spinal cord, brain stem, and motor cortexmotor cortex

• Progresses to death in 2 to 6 yearsProgresses to death in 2 to 6 years

Amyotrophic Lateral Sclerosis

• Prevalence constant throughout the worldPrevalence constant throughout the world• Men affected more than womenMen affected more than women• Age of onset mid-50s (40-70)Age of onset mid-50s (40-70)• Cause unknownCause unknown• 5% familial, rest sporadic5% familial, rest sporadic

Amyotrophic Lateral Sclerosis Presentation• Muscle weakness commences in the legs and Muscle weakness commences in the legs and

hands and progresses to the proximal arms and hands and progresses to the proximal arms and oropharynxoropharynx

• Voluntary skeletal muscles are at risk for atrophy Voluntary skeletal muscles are at risk for atrophy and complete loss of functionand complete loss of function

• Spasticity of jaw muscles resulting in slurred Spasticity of jaw muscles resulting in slurred speechspeech

• Dysphagia, difficulty chewing Dysphagia, difficulty chewing weight loss weight loss• Death from respiratory failureDeath from respiratory failure

Amyotrophic Lateral Sclerosis Nutritional Implications• Dysphagia, chewing, swallowing problemsDysphagia, chewing, swallowing problems• Decreased body fat, lean body mass, nitrogen Decreased body fat, lean body mass, nitrogen

balance and increased REE as death approachesbalance and increased REE as death approaches• Late stage patients may not tolerate PEG Late stage patients may not tolerate PEG

placement d/t respiratory compromiseplacement d/t respiratory compromise• Initiate discussions about whether to place a Initiate discussions about whether to place a

feeding tube early in disease processfeeding tube early in disease process• Enteral feedings do not prolong lifeEnteral feedings do not prolong life

Amyotrophic Lateral Sclerosis MNT• Correlates with ALS Severity Scale (pp 1102-Correlates with ALS Severity Scale (pp 1102-

1103)1103)• Emphasize fluids as patients may limit fluids d/t Emphasize fluids as patients may limit fluids d/t

toileting difficultiestoileting difficulties• Get baseline weight; 10% loss Get baseline weight; 10% loss increased risk increased risk• Modify consistency as eating problems develop Modify consistency as eating problems develop

using easy-chew foods, thickened liquids, using using easy-chew foods, thickened liquids, using small frequent meals, cool food temperaturessmall frequent meals, cool food temperatures

Amyotrophic Lateral Sclerosis MNT• If nutrition support is planned, use ENIf nutrition support is planned, use EN• Initiate early rather than later; dehydration Initiate early rather than later; dehydration

occurs before malnutritionoccurs before malnutrition• Purpose of nutrition support should be to Purpose of nutrition support should be to

enhance quality of lifeenhance quality of life• Eventually patients will not be able to Eventually patients will not be able to

manage oral secretionsmanage oral secretions