Nutritional Management in Eating Disorders S..pdf · Medical complications of eating disorders...

10/14/2013

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Nutritional Management in

Anorexia Nervosa Rattanachaiwong S.

Nutrition screening and assessment

BMI, SGA (subjective global assessment)

Nutrition therapy

Who should be admitted?

How to prescribe diet & micronutrients?

What is the aim of treatment?

Nutritional Management in Anorexia Nervosa

Body mass index

BMI = bogy weight(kg)/ height(m)2

Classification WHO criteria Asia-Pacific criteria

Underweight <18.5 <18.5

Normal 18.5-24.9 18.5-22.9

Overweight 25-29.9 23-24.9

Obesity ≥30 ≥25

• Obesity grade 1 30-34.9 25-29.9

• Obesity grade 2 35-39.9 ≥30

• Morbid obesity ≥40 -

A B C

การรับประทานอาหาร • ทานได้ปกต ิ

• ทานได้ลดลง แต่มากกว่า

¾ ของปกต ิ

• เปลี่ยนมาทานโจ๊ก หรือข้าวต้ม

• ทานได้ลดลง แต่มากกว่า ½ ของปกต ิ

• เปลี่ยนมาทานแต่น ้าๆ

• ทานได้ลดลง <1/2 ของปกต ิ

น ้าหนัก • เท่าเดิมหรอืเพิ่มขึ น

• ลดลงแต่เพิ่มขึ นแล้ว • ลดลง <5% ใน 1 เดือน

• ลดลง <10%ใน 6 เดือน • ลดลง >5% ใน 1 เดือน

• ลดลง >10%ใน 6 เดือน

อาการของทางเดิน

อาหาร (ทอ้งเสยี,

อาเจียน)

• ไม่มีอาการ

• มีอาการน้อยกวา่ 2 สัปดาห์และไม่ได้เป็นตลอด

• มีอาการ < 2สัปดาห์แต่เป็นทุกวัน

• มีอาการมากกว่า 2 สัปดาห ์

การท้างาน • ท้างานได้ปกต ิ • ท้างานได้ลดลง แต่ยัง

ช่วยเหลอืตัวเองได ้• ต้องมีคนช่วย

ตรวจร่างกาย • ปกติด ี

• BMI > 18.5

kg/m2

• Edema • BMI < 18.5 kg/m2

• Ascites • BMI < 17.5 kg/m2

Subjective Global Assessment

SGA class การแปลผล

A ไม่มี หรือมีความเสี่ยงน้อยที่จะเกิดภาวะทุพโภชนาการ

B มีความเสี่ยงสูงที่จะเกิดภาวะทุพโภชนาการ ต้องติดตามอย่างใกล้ชิด

C มีภาวะทุพโภชนาการอย่างรุนแรง

Subjective Global Assessment

Nutritional Therapy in Anorexia Nervosa

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“Most people with anorexia nervosa should be

treated on an outpatient basis.” (C)

“Inpatient treatment should be considered for

people with anorexia nervosa whose disorder is associated with high or moderate physical risk.” (C)

NICE guidelines for treatment of eating disorders 2004 Indications for admission

American Psychiatric Association, 2000

- BMI < 16 kg/m2 - weight loss more than 20%

Modern Nutrition in Health and Disease 10th edition (2006)

- dangerously low BMI - metabolic complications - suicidality/ self injurious behavior - pregnancy - DM type 1

National Institute for Clinical Excellence (NICE) 2004

- patient not improve with appropiate outpatient outpatient treatment

- moderate to high physical risk - risk of suicide or self-harm

Markers of decompensation

Treasure J, et al. Lancet. 2010 Feb 13;375(9714):583-93.





3 regular meals a day

aim total calorie 30-35 kcal/ kg actual body weight/day

aim total protein 1.2-1.5 g/kg ideal body weight/day

expanding food repertoire

avoiding diet foods : fat-free, sugar-free products

limit weighing to once a week

aware of refeeding syndrome

Nutritional management in AN

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Refeeding syndrome

hypokalemia

hypophosphatemia

hypomagnesemia

Thiamin deficiency

Clinical presentations peripheral edema, cardiac arrhythmia, neuromuscular weakness,

nystagmus, gaze palsies, gait ataxia, internuclear ophthalmoplegia, psychosis (Wernicke-Korsakoff syndrome), heart failure, pulmonary congestion, lactic acidosis

Refeeding syndrome

Thiamin as coenzyme

Thiamin as coenzyme

Prevention of refeeding syndrome

correct electrolytes imbalance before feeding (K, Mg, PO4)

start with low calorie first

slow titration +500 kcal every 2-3 days

Thiamin 100 mg IV OD x 3 days

recheck for electrolytes abnormalities during calorie titration

restrict fluid to sufficient to maintain renal function (20-30 ml/kg/day)

Nutritional management in AN Diet prescription : first phase

calorie specific example

Treasure J, et al. Lancet 2010

5-10 kcal/kg/day low salt high phosphate

milk-based product

Modern Nutrition in Health and Disease 10th edition (2006)

1000-1200 kcal/day low salt

“In some cases treatment with a multi-vitamin/multi-mineral supplement in oral form is recommended for people with anorexia nervosa during both inpatient and outpatient weight restoration.” (C)

Vitamin 200% RDI

+additional thiamin 100 mg/day for refeeding syndrome

Mineral and trace element 100% RDI

NICE guidelines for treatment of eating disorders 2004

Male RDA

Female RDA

MTV tablet

Centrum Bco tablet

B1-6-12

Vitamin B1 (mg)

1.2 1.1 5 2.25 5 100

Vitamin B2 (mg)

1.3 1.1 2 3.2 2 -

Vitamin B3 (mg)

16 14 10 40 20 -

Vitamin B5 (mg)

5 5 3 10 - -

Vitamin B6 (mg)

1.7 1.5 1 3 2 5

Folic (mg)

0.4 0.4 0.1 0.4 - -

Vitamin B12 (mcg)

2.4 2.4 1 9 - 65

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Outpatient Inpatient

Treasure J, et al. Lancet 2010

250-450 g /wk 1 kg /wk

National Institute for Clinical Excellence (NICE) 2004

0.5 kg /wk 0.5-1 kg /wk

Modern Nutrition in Health and Disease 10th edition

~ 1-2 kg /wk

Aim for weight gain

“Why did my patients not gain weight?”

Refeeding induce an increased in REE in malnourished AN

Van Wymelbeke V, et al. Am J Clin Nutr. 2004 Dec;80(6):1469-77.

Mean REE:FFM control group 131±15

P<0.001 P<0.001

Resistant to weight gain!!

“It is often unfair to accuse most of these AN patients of discarding their food

when they do not gain body weight.” Van Wymelbeke V

Any roles of parenteral nutrition?

“Total parenteral nutrition should not be used

for people with anorexia nervosa, unless there is significant gastrointestinal dysfunction.” (C)

NICE guidelines for treatment of eating disorders 2004

Actual body weight (ABW) 38 kg

Height 156 cm

Ideal body weight (IBW) = height-110 = 46 kg

or ideal body weight at BMI 20 kg/m2 = 20x1.56x1.56

= 48 kg

Aim TC 30-35 kcal/ABW/day = 1140-1330 kcal/day

Aim TP 1.2-1.5 g/IBW/day =55.2-69 g/day

Day 1 400-500 kcal/day + thiamin 100 mg IV ODx3days

MTV 1x2, Bco 1x2

titrate 500 kcal q 2-3 days, F/U electrolytes

For our case

Re-establish normal eating behavior

AN- aware of refeeding syndrome, volume overload

Micronutrients supplement in malnourished patients

Conclusions

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Thank you

Medical complications of eating disorders

Hypercholesterolemia in anorexia nervosa

Blendis LM, et al. Postgrad Med J. 1968 Apr;44(510):327-30.

Cholesterol-riched food during binge behavior (AN-B)

Low FT4/ or FT3 (lead to decrease hepatic LDL receptor)

Mobilization of body fat during phase of weight loss

Increase flux of peripheral cholesterol to liver

Decreased hepatic LDL receptor

Reduced bile acid formation (AN-R)

Proposed mechanism of hypercholesterolemia in AN

Weinbrenner T, et al. Br J Nutr. 2004 Jun;91(6):959-69. Nestel PJ. J Clin Endocrinol Metab. 1974 Feb;38(2):325-8.

Ohwada R, et al. Int J Eat Disord. 2006 Nov;39(7):598-601.

The reciprocal pattern of cholesterol level in AN

Blendis LM, et al. Postgrad Med J. 1968 Apr;44(510):327-30.

Serum cholesterol

BW

Thank you Medical Complications

of Eating disorders

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Skin

Xerosis

Lanugo-like body hair

Telogen effluvium

Acne

Acrocyanosis

Carotenoderma

Pruritis

Purpura


Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.

Russell’s sign


scar/callus formation over the dorsal surface of the hand, as the hand is used to stimulate the gag reflex to induce vomiting

Endocrine : DM type 1

somes report higher prevalence of AN among DM type 1

EDs increase risk of microvascular complications

worsen QoL in DM type 1



Gastrointestinal

gastric dilatation

gastric mucosal necrosis

delayed gastric emptying

gastric motor dysfunction

impaired sense of hunger and satiety

delayed small bowel transit time

constipation

Case report : pancreatitis, necrotizing colitis



Cardiovascular and pulmonary

arrhythmia ; the most common cause of death

prolonged QT

bradycardia

pneumomediastinum

spontaneous chest pain, may mimic acute MI

acrocyanosis



Skeletal system

osteopenia

osteoporosis

Low body weight predicts low bone mineral density

Only weight restoration alone may not effective

? Bisphosphonate + calcium + vitamin D



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Hematology

hemoconcentration due to hypovolemia



Laboratory changes in AN

Increase Decrease

HCO3 (metabolic alkalosis) Cholesterol (TC, LDL, HDL) Aminotransferase enzymes Cortisol Hyperamylasemia Hypercarotenemia CETP activity Ketone bodies Apo-A1, B, C2, C3, E

K (hypokalemia) Na (hyponatremia) BUN, Cr FT4, FT3 Gonadotropin hormone

rare complication of AN

more likely to occur in BMI < 12 kg/m2

elevation of aminotransferase enzymes (AST, ALT)

can vary from mild to severe

liver decompensation, coagulopathy, hyperbilirubinemia and fulminant liver failure have been reported

peak level may occur after initiation of nutritional therapy

Elevation of Liver function test in Anorexia nervosa

Harris RH, et al. Int J Eat Disord. 2013; 46(4):369-74. Rautou PE, et al. Gastroenterology. 2008;135(3):840-8


Rautou PE, et al. Gastroenterology. 2008;135(3):840-8

50% decrease within 2 and 5 days

0

500

1000

1500

2000

2500

3000

3500

4000

4500

Day 0 Day 22 Day 28 Day 35 Day 40 Day 48

AST

ALT

calorie tintake


Adapted from Harris RH, et al. Int J Eat Disord. 2013;46(4):369-74.

maximal elevation usually occur at the lowest body weight point

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Proposed pathogenesis

ischemia

low glutathione level with resultant oxidant stress

starvation-induced hepatocyte autophagy

hepatic fat and glucose deposit (after refeeding)


Harris RH. Int J Eat Disord. 2013;46(4):369-74.

Histological findings and immunostaining

swelling and clarified hepatocyte

glycogen depletion (PAS staining)

centrilobular liver cell atrophy associated with mild sinusoidal fibrosis

ceroid pigment, predominant in centrilobular zone

autophagosomes in 4/12 cases

no significant hepatocellular necrosis, congestion

no markers of apoptosis found




Diffuse hepatocytic swelling Centriobular fibrosis and atrophy

Autophagosome sequestring cytoplasmic components

Low organelle-density hepatocyte

Autophagy

Rautou PE, J Hepatol. 2010;53(6):1123-34.

Starvation-induced hepatocyte autophagy

Autophagosome

double-membrane vesicle

sequestering other cytoplasmic components e.g. mitochondria, endoplasmic reticulum

fusion with pre-existing lysosomes

result in low density of organelles in hepatocyte

may lead to autophagic cell death


Autophagy

well-known survival strategy under stress condition

supply macromolecules for biosynthesis during nutrient-deprivation

help to delay cell apoptosis

also can kill a cell “autophagic death”



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Rautou PE, J Hepatol. 2010;53(6):1123-34.

Approach to abnormal LFT in AN

Adapted from Harris RH, et al. Int J Eat Disord. 2013; 46(4):369-74.

Abnormal LFT

Alcohol, drugs and toxin Viral hepatitis : HBsAg, Anti-HBs, Anti-HBc, Anti-HCV, Anti-HAV Autoimmune hepatitis : ANA, anti-smooth muscle Ab, anti-LKM Wilson disease : serum ceruloplasmin

exclude other causes

Ultrasound / CT upper abdomen

small liver, no fatty liver large liver, fatty liver

• continue feeding • should improve in 2-5 days

• probably due to overfeed • consider reduction in calorie

feed









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