N utritional Management in Anorexia Nervosa 10/14/2013

10/14/2013
Nutritional Management in
Anorexia Nervosa
Nutritional Management in
Anorexia Nervosa
 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?
Rattanachaiwong S.
Subjective Global Assessment
Body mass index
A
Classification
Normal
Overweight
Obesity
WHO criteria
Asia-Pacific criteria
<18.5
<18.5
18.5-24.9
18.5-22.9
25-29.9
23-24.9
≥30
≥25
• Obesity grade 1
30-34.9
25-29.9
• Obesity grade 2
35-39.9
≥30
• Morbid obesity
≥40
-
C
การรับประทานอาหาร
• ทานได้ปกติ
• ทานได้ลดลง แต่มากกว่า
¾ ของปกติ
• เปลี่ยนมาทานโจ๊ก หรือข้าวต้ม • เปลี่ยนมาทานแต่น้าๆ
• ทานได้ลดลง แต่มากกว่า ½ • ทานได้ลดลง <1/2 ของปกติ
ของปกติ
น้าหนัก
• เท่าเดิมหรือเพิ่มขึน
• ลดลงแต่เพิ่มขึนแล้ว
• ลดลง <5% ใน 1 เดือน
• ลดลง <
​ 10%ใน 6 เดือน
อาการของทางเดิน
อาหาร (ท้องเสีย,
อาเจียน)
• ไม่มีอาการ
• มีอาการ < 2สัปดาห์แต่เป็น
• มีอาการน้อยกว่า 2
ทุกวัน
สัปดาห์และไม่ได้เป็นตลอด
การท้างาน
• ท้างานได้ปกติ
• ท้างานได้ลดลง แต่ยัง
ช่วยเหลือตัวเองได้
• ต้องมีคนช่วย
ตรวจร่างกาย
• ปกติดี
• BMI > 18.5
kg/m2
• Edema
• BMI < 18.5 kg/m2
• Ascites
• BMI < 17.5 kg/m2
 BMI = bogy weight(kg)/ height(m)2
Underweight
B
• ลดลง >5% ใน 1 เดือน
• ลดลง >
​ 10%ใน 6 เดือน
• มีอาการมากกว่า 2 สัปดาห์
Subjective Global Assessment
SGA class
การแปลผล
A
ไม่มี หรือมีความเสี่ยงน้อยที่จะเกิดภาวะทุพโภชนาการ
B
มีความเสี่ยงสูงที่จะเกิดภาวะทุพโภชนาการ ต้องติดตามอย่างใกล้ชิด
C
มีภาวะทุพโภชนาการอย่างรุนแรง
Nutritional Therapy
in Anorexia Nervosa
1
10/14/2013
NICE guidelines
for treatment of eating disorders 2004
“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)
Markers of decompensation
Treasure J, et al. Lancet. 2010 Feb 13;375(9714):583-93.
Markers of decompensation
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.
Nutritional management in AN
 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
Treasure J, et al. Lancet. 2010 Feb 13;375(9714):583-93.
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10/14/2013
Refeeding syndrome
Thiamin as coenzyme
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
Thiamin as coenzyme
Nutritional management in AN
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
(2030 ml/kg/day)
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
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/multi-mineral supplement in oral form is
recommended for people with anorexia nervosa during
both inpatient and outpatient weight restoration.” (C)
Vitamin B3
(mg)
16
14
10
40
20
-
Vitamin B5
(mg)
5
5
3
10
-
-
 Vitamin 200% RDI
 +additional thiamin 100 mg/day for refeeding syndrome
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
NICE guidelines
for treatment of eating disorders 2004
“In some cases treatment with a multi-
 Mineral and trace element 100% RDI
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10/14/2013
Refeeding induce an increased in REE
in malnourished AN
Aim for weight gain
Treasure J, et al.
Lancet 2010
National Institute for Clinical
Excellence (NICE) 2004
Outpatient
Inpatient
250-450 g /wk
1 kg /wk
0.5 kg /wk
0.5-1 kg /wk
Modern Nutrition in Health
and Disease 10th edition
P<0.001
P<0.001
Resistant to weight gain!!
Mean REE:FFM control group 131±15
~ 1-2 kg /wk
“Why did my patients not gain weight?”
Van Wymelbeke V, et al. Am J Clin Nutr. 2004 Dec;80(6):1469-77.
NICE guidelines
for treatment of eating disorders 2004
“It is often unfair to accuse most of
these AN patients of discarding their food
when they do not gain body weight.”
Any roles of parenteral nutrition?
“Total parenteral nutrition should not be used
for people with anorexia nervosa, unless there is
significant gastrointestinal dysfunction.” (C)
Van Wymelbeke V
For our case
 Actual body weight (ABW)
 Height
 Ideal body weight (IBW) = height-110
or ideal body weight at BMI 20 kg/m2
38 kg
156 cm
= 46 kg
= 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
Conclusions
 Re-establish normal eating behavior
 AN- aware of refeeding syndrome, volume overload
 Micronutrients supplement in malnourished patients
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Medical complications of eating disorders
Thank you
 Hypercholesterolemia in
anorexia nervosa
Blendis LM, et al. Postgrad Med J. 1968 Apr;44(510):327-30.
Proposed mechanism of
hypercholesterolemia in AN






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)
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.
Thank you
The reciprocal pattern of cholesterol level in AN
Serum
cholesterol
BW
Blendis LM, et al. Postgrad Med J. 1968 Apr;44(510):327-30.
Medical Complications
of Eating disorders
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Medical complications of eating disorders
Medical complications of eating disorders
Skin
 Russell’s sign








Xerosis
Lanugo-like body hair
Telogen effluvium
Acne
Acrocyanosis
Carotenoderma
Pruritis
Purpura
scar/callus formation over the dorsal surface of the
hand, as the hand is used to stimulate the gag reflex to induce
vomiting
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
Medical complications of eating disorders
Medical complications of eating disorders
Endocrine : DM type 1
Gastrointestinal
 somes report higher prevalence of AN among DM type 1
 EDs increase risk of microvascular complications
 worsen QoL in DM type 1








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
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
Medical complications of eating disorders
Medical complications of eating disorders
Cardiovascular and pulmonary
Skeletal system









arrhythmia ; the most common cause of death
prolonged QT
bradycardia
pneumomediastinum
 spontaneous chest pain, may mimic acute MI
osteopenia
osteoporosis
Low body weight predicts low bone mineral density
Only weight restoration alone may not effective
? Bisphosphonate + calcium + vitamin D
 acrocyanosis
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
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10/14/2013
Medical complications of eating disorders
Laboratory changes in AN
Increase
Hematology
 hemoconcentration due to hypovolemia
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
Mitchell JE, et al. Curr Opin Psychiatry. 2006 Jul;19(4):438-43.
Elevation of Liver function test
in Anorexia nervosa





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
Harris RH, et al. Int J Eat Disord. 2013; 46(4):369-74.
Elevation of Liver function test
in Anorexia nervosa
50% decrease within 2 and 5 days
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Elevation of Liver function test
in Anorexia nervosa
maximal elevation usually
occur at the lowest body
weight point
4500
4000
3500
3000
2500
AST
2000
ALT
1500
calorie tintake
1000
500
0
Day 0
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Day 22
Day 28
Day 35
Day 40
Day 48
Adapted from Harris RH, et al. Int J Eat Disord. 2013;46(4):369-74.
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10/14/2013
Elevation of Liver function test
in Anorexia nervosa
Elevation of Liver function test
in Anorexia nervosa
Proposed pathogenesis
 ischemia
 low glutathione level with resultant oxidant stress
 starvation-induced hepatocyte autophagy
 hepatic fat and glucose deposit (after refeeding)
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
Harris RH. Int J Eat Disord. 2013;46(4):369-74.
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Autophagy
Diffuse hepatocytic swelling
Centriobular fibrosis and atrophy
Low organelle-density hepatocyte
Autophagosome sequestring
cytoplasmic components
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
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
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Rautou PE, J Hepatol. 2010;53(6):1123-34.
Starvation-induced hepatocyte autophagy
Autophagy
 well-known survival strategy under stress condition
 supply macromolecules for biosynthesis during nutrientdeprivation
 help to delay cell apoptosis
 also can kill a cell “autophagic death”
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
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Starvation-induced hepatocyte autophagy
Approach to abnormal LFT in AN
Abnormal LFT
exclude other causes
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
Ultrasound / CT upper abdomen
small liver, no fatty liver
• continue feeding
• should improve in 2-5 days
Rautou PE, J Hepatol. 2010;53(6):1123-34.
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
large liver, fatty liver
• probably due to overfeed
• consider reduction in calorie
feed
Adapted from Harris RH, et al. Int J Eat Disord. 2013; 46(4):369-74.
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
9
10/14/2013
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
Medical complications of eating disorders
Rautou PE, et al. Gastroenterology. 2008;135(3):840-8
10