Medical Complications of
Eating Disorders
Margherita Mascolo, MD
Assistant Professor of Medicine
U i
University
i off Colorado
C l d S
School
h l off Medicine
M di i
Lead Physician, ACUTE Center for Eating Disorder at
Denver Health
Learning Objectives:
Define anorexia nervosa and bulimia nervosa
How to identifyy at risk patients
p
Appropriate work up
When to transfer patients to a higher level of
care
• Common
C
medical
di l complications
li i
off anorexia
i
nervosa and bulimia nervosa
•
•
•
•
Epidemiology of Anorexia
Nervosa
• In Western industrialized countries, the prevalence is 0.3 - 4%
of the female population and 0.1% of the male population
• Mortality is the highest of any psychiatric diagnosis
– 0.56% per year
– 12 times higher than the annual death rate for women 15-24
15 24
years of age
– Roughly
g y one third are due to cardiac complications;
p
;
average age of death is 34 years
– Up to 30% of affected patients do not achieve sustainable
recovery
What is Anorexia Nervosa?
• Defined by four criteria from DSM-IV
DSM IV
– Refusal to maintain body weight at or above 85% of that
p
for height
g
expected
– Intense fear of gaining weight or becoming fat, even though
underweight
– Disturbance
b
in the
h perception off one’s body
b d weight
h for
f
shape
– In postmenarchal women,
women the absence of three consecutive
menstrual periods
– Subtypes: restrictive or binge/purge
Anorexia Nervosa
Epidemiology of Bulimia
Nervosa
• Prevalence is between 1-2% of the female population
et e p
prevalence
e a e ce for
o females
e a es iss betwee
between 1.1
. aand
d
• Lifetime
4.2%
g
• Onset between 13 and 20 yyears of age
• Ten times more common in females than males
What is Bulimia Nervosa?
• Defined by the DSM IV as:
– Recurrent episodes of binge eating
– Recurrent, inappropriate compensatory behavior to
prevent weight gain
– These behaviors occur an average
g of twice a week for
three months
– Self evaluation is influenced by body shape and
weight
– The disturbance does not only occur during periods
off anorexia
i nervosa
Risk Factors for Eating
Disorders
• Female > male (2-3:1)
• Peaks at ages 13-14 and 17-18
– Byy age
g 14,, 60-70% of ggirls are trying
y g to reduce
weight
• Highest
g
incidence in Western societies
– Independent of race or ethnicity
Risk Factors for Eating
Disorders
• Personal history of DM type I, cystic fibrosis,
d
depression,
i anxiety
i disorder,
di d ADHD,
ADHD PTSD
PTSD,
and OCD
• Family history positive for: obesity,
depression, anxiety, other eating disorders
• Social history: dancers, body builders, models,
actors
Symptoms of Eating Disorders
Anorexia Nervosa
Amenorrhea
Depression
Fatigue/weakness
Abdominal pain
Constipation
Bloating/fullness with
eating
i
• Dry skin
• Cold intolerance
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Bulimia Nervosa
Irregular menses
Palpitations
Acid reflux
Fatigue/weakness
C ti ti /di h
Constipation/diarrhea
Upper and lower ext edema
Frequent sore throat
Sensitive teeth
Swollen cheeks
Depression
Signs of Eating Disorders
•
•
•
•
•
•
•
Anorexia Nervosa
Hypothermia/hypotension/
bradycardia
y
Dry skin
Brittle hair and nails
Lanugo hair
Cold and cyanotic hands
and feet
Lower ext edema
Cardiac murmur ((MVP))
•
•
•
•
•
•
•
Bulimia Nervosa
Calluses on back of hand
Salivary gland hypertrophy
Dental erosion/caries
Mouth ulcers
Edema
Abdominal bloating
Cardiac arrhythmias
The SCOFF Questionnaire
1. Do you make yourself Sick because you feel
uncomfortably full?
y have lost Control over how much
2. Do yyou worryy you
you eat?
pounds in a three
3. Have yyou recentlyy lost Over 14 p
month period?
4. Do you believe yourself to be Fat when others say
you are too thin?
5. Would you say that Food dominates your life?
The SCOFF Questionnaire
• Ask all patients 10 – 40 years old in high risk
groups
• Count one point for every “yes” answer
• Score of ≥ 2 likely anorexia nervosa or bulimia
nervosa
Work up
Work-up
•
•
•
•
•
•
•
•
•
Height and weight
CBC with diff
Chem 7 with mag and phosph
LFT’s
TSH
UA
FOBT
EKG
DEXA if disease
di
for
f ≥ 6 months
h
When to Hospitalize?
For Anorexia Nervosa:
– Inpatient care below 75% of
ideal body weight
– Severe organ dysfunction:
cardiac (arrhythmias),
gastrointestinal,l electrolyte,
l
l
hematologic
– Worsening weight loss with
severely
l restricted
d caloric
l
intake (at risk for refeeding
syndrome)
For Bulimia Nervosa:
–
–
–
–
Potassium <2.2 mmol/L
Bicarbonate > 40 mmol/L
Excessive edema
History of edema with
cessation of purging
behaviors
DISEASE SPECTRUM
IBW calculation:
Women: 100 lbs for first 5 feet then 5
lb ffor each
lbs
h additional
ddi i l iinch
h
Men: 106 lbs for first 5 feet then 6 lbs
for each additional inch
Mild
Moderate
Severe
Ideal Body Weight
(IBW) %
Inpatient
p
treatment
40%
50%
60%
70%
Outpatient
p
treatment
80%
90%
100%
•Anorexia nervosa diagnosed
at 85% of IBW
Medical Complications
• Differ depending on the type of eating disorder
– In anorexia, the medical complications are the
direct result of starvation and weight loss
– In bulimia, they correlate with the mode and
frequency of purging
Medical Complications of
Anorexia Nervosa
•
•
•
Metabolic
– Refeeding syndrome
– Plateau effect
– Hypercortisolemia
Gastrointestinal
– Gastroparesis
– Constipation
– Hepatitis
– Hypoglycemia
– Superior mesenteric artery
syndrome
– Pancreatitis
P
titi
Electrolyte dysfunction
– Hyponatremia
– Volume contraction
•
•
•
Cardiac
– Bradycardia
– Tachycardia
– The QT question
– Congestive
C
ti heart
h t ffailure
il
– Hypotension
Endocrine
– Amenorrhea
– Osteoporosis
– Cortisol and “the belly”
– Thyroid function
Hematologic
– Pancytopenia
Refeeding Syndrome
• Caused by life-threatening shifts in fluid and
electrolytes
y as a starved person
p
begins
g to eat
• Seen initially in unintentional refeeding of WWII
victims who died of cardiovascular complications
p
• Replicated in Keys’ “Minnesota Experiment”
• Rediscovered with the introduction of TPN
Refeeding Syndrome
• As a starvingg p
person is beingg fed,, the bodyy shifts from a
catabolic to an anabolic state
– From fat to carbohydrate metabolism
• Glucose in the food stimulates insulin release which drives
phosphate and potassium intracellularly
– Lowers serum levels of both K and Phosph
– In addition, insulin decreases sodium excretion in the
distal tubule leading to edema
• Newly synthesized cells use these electrolytes as well as
magnesium as building blocks thus further depleting serum
levels
Refeeding Syndrome
• Hypophosphatemia causes depletion of ATP and 2,3-DPG
which lead to
– Diaphragmatic muscle fatigue
– Respiratory failure
– Rhabdomyolysis
– Seizure
– CHF (depressed myocardial contractility)
• Fall is seen in the first 2-3 days of refeeding and may last up to 12 weeks
k
• Aggressive replacement of phosphorus is crucial
• Po route is the best absorbed and patients may need up to 3
gm per day of potassium acid phosphate
Refeeding Syndrome
• Hypokalemia may lead to
– Rhabdomyolysis
– Seizures
– Cardiac arrhythmias
• Fall
ll in potassium is seen more acutely
l over the
h first
f
24-48
44
hours of refeeding and also corrects much faster (over the first
2-3 days)
y)
– May replace IV or po
Refeeding Syndrome
• Edema
– Insulin mediated, NOT related to albumin/oncotic
pressure
• Causes increased retention of sodium and thus water in
the distal tubule
– Occurs within the first few days of refeeding and resolves
within a few weeks
– Treatment consists of low sodium diet, leg elevation, and
slow increase of calories
Refeeding Syndrome
Wh is
Who
i at Risk?
Ri k?
National
N
i l Institute
I i
for
f Clinical
Cli i l E
Excellence
ll
(NICE) Guidelines
G id li
for
f
Management of Refeeding Syndrome:
One or more of the following:
-OR-
· BMI < 16 kg/m2
· Unintentional weight loss of >15% in
the pprevious 3-6 months
· Little or no nutritional intake for >10
days
· Low levels of potassium, phosphorus,
or magnesium before refeeding
Two or more of the following:
· BMI <18.5 kg/m2
· Unintentional weight loss of >10% in
the pprevious 3-6 months
· Little or no nutritional intake for > 5
days
· History of alcohol abuse or drugs
including insulin,
insulin chemotherapy,
chemotherapy
antacids, or diuretics
National Institute for Health and Clinical Excellence. Guideline for the Management of Refeeding Syndrome (Adults), 2nd edition, NHS Foundation Trust, 2009
Refeeding Syndrome
• How to prevent?
p
– Recognize at risk patients
– Correct electrolyte disturbances prior to initiating
nutritional support
– “Start low and go slow” with kcals based on pt’s basal
energy expenditure (BEE)
– Increase kcals slowly (by 300-400kcals) every three days
and check daily chem 10 for the first week of refeeding
– Low salt diet and leg elevation to prevent/treat edema
Hypoglycemia
• Maybe due starvation or refeeding
• In starvation:
– Due to depleted glycogen stores in the liver and lack of
substrates for gluconeogenesis
• In refeeding:
– Due to glucose load stimulating insulin secretion and
overwhelmingg the alreadyy depleted
p
hepatic
p
glycogen
g y g stores
• Can be life-threatening if not recognized
Hypoglycemia
• Treatment:
– Nutritional support (i.e. KCALS!!!)
– Check FSBG q 4 hours for the first 24-48 hours of
refeeding
– +/+/ D5NS in order to maintain serum glucose above 70
• May need dextrose for up to 24- 48 hours
Cardiac Complications
• The heart in the severelyy malnourished patients
p
loses mass
which leads to decreased cardiac output
– May lead to acute heart failure if overwhelmed with the
i
increased
d circulating
i l ti bl
blood
d volume
l
presentt during
d i
refeeding
– Hypokalemia
yp
and hypophosphatemia
yp p p
mayy lead to
arrhythmias and decreased contractility
– Cardiac mortality is likely due to QT dispersion and low
h
heart
rate variability
i bili
• All hospitalized patients should have a baseline EKG and be
kept on telemetry
Hepatitis
• Abnormalites in LFT’s are common in the severely
malnourished state and maybe due to starvation or refeeding
• The mechanism for hepatitis of starvation is apotosis or
autophagy
– May see transaminases up to 30 x upper limit of normal
– Treatment is continued nutritional support and
normalization of liver function returns within 1-2 weeks
into refeeding
Hepatitis
• Steatohepatitis
p
of refeedingg is manifested byy increasingg
AST/ALT during the initial phases of refeeding
– Likely due to dextrose causing fat accumulation
– Treatment for this is decreased feeding rate/kcals
• Serial liver ultrasounds can aid in differentiation
– Normal sized liver is indicative of starvation hepatitis
• CONTINUE pushing kcals
– Enlarging liver is indicative of refeeding hepatitis
• SLOW down kcal intake
Bone Marrow Suppression
• Severe malnutrition causes suppression of the bone marrow
and replacement of its matrix with one that does not produce
cells
ll
– Serous fat atrophy
• Trilinear hypoplasia:
yp p
anemia,, leukopenia,
p
, and
thrombocytopenia are very common
• Bone marrow function fully recovers with weight restoration
Amenorrhea
• Caused byy downregulation
g
of the hypothalamicpituitary-gonadal axis
• Axis normalizes when
% of IBW and
within 90%
menses likely return within
6 months of achieving that
weight
Gastroparesis
• Occurs as a consequence of kcal restriction and loss of at least 10
to 20 pounds
• Symptoms include bloating, nausea, flatus, and abdominal pain
that’s
h ’ more pronounced
d after
f meals
l
• Treatment:
– Avoidance of high fiber diet
– Weight restoration (resolves when within 80% of IBW)
– Small, more frequent meals with kcals in liquid form
– Use of reglan 30 minutes prior to meals helps speed up transit
time through the GI tract and alleviate symptoms
• 2.5
2 5 to 5 mg prior to meals
Osteoporosis
• Occurs solely in anorexia and usually begins early in disease
course and
d progresses quickly
i kl
• Peak bone mass is achieved by the end of the second decade
which is the time when anorexia manifests itself
• These patients never reach peak bone mass thus their
osteoporosis is severe and resistant to treatment
– Trabecular bone is affected more than cortical
• Duration of amenorrhea is the best predictor of bone density
– A baseline DEXA should be performed 6 months after the
cessation of menses
g restoration leadingg to activation of the hypothalamicyp
• Weight
pituitary-gonadal axis is the best treatment
Osteoporosis
Adolescents
with AN
Women with
AN
Osteopenia
52%
90%
Osteoporosis
25%
38%
Bruni, et al. Open
p issues in anorexia nervosa: prevention
p
and therapy of bone loss. Ann N Y Acad Sci, 2006.
Osteoporosis
• Treatment:
• Estrogen
g replacement
p
and exercise are neither
protective nor therapeutic
• Bisphosphonates have questionable benefit and can
cause harm
h
to neonates (for
(f patients that
h weight
h
restore)
• All patients should be placed on Calcium and have
adequate vitamin D levels (25-OH vit D above 30)
Anorexia Nervosa Pearls
• Patients at < 70% IBW should undergo refeeding in a
hospitalized setting with professionals familiar with such
patients
ti t
• Refeeding syndrome can be deadly and patients should be
closelyy monitored
• “Start low and go slow” with kcalories
• Most medical complications, except osteoporosis, do resolve
with weight restoration
Medical Complications of
Bulimia
l
Nervosa
•
•
•
•
Metabolic
– Electrolyte imbalance
– Dehydration
Renal
– Acute kidney injury
– Edema: total body, pulmonary,
cerebral
Gastrointestinal
– Constipation
– Esophageal rupture
– GERD
– Cathartic colon
Sialadenitis
•
•
Dental erosion
Cardiac
– Arrhythmias
– Diet pill toxicity: palpitations,
hypertension
– Emetine cardiotoxicity
– Mitral valve prolapse
•
Endocrine
– Irregular menses
– Mineralocorticoid excess
•
Pulmonary Mediastinal
Pulmonary-Mediastinal
– Aspiration pneumonitis
– Pneumomediastinum
PseudoBartter’ss Syndrome
PseudoBartter
• Case:
– 18 yr female with AN-binge purge subtype who vomits 3-4
times daily presented to ACUTE complaining of abdominal
pain and bloating
– Height 5’3”
5 3 with a weight of 72
72.66 lbs ( 63% IBW)
– Labs
• Na: 124 mmol/L
• K: 1.6 mmol/L
• Bicarbonate: 52 mmol/L
PseudoBartter’ss Syndrome
PseudoBartter
• Chronic volume depletion
from purging (vomiting,
l ti
laxatives,or
di ti )
diuretics)
causes upregulation of
aldosterone by the renalangiotensin-aldosterone
system
• Aldosterone retains salt and
water at the expense of
potassium and acid
PseudoBartter’ss Syndrome
PseudoBartter
• Renal retention of salt and water (due to high circulating
aldosterone) leads to low serum potassium and high
bi b t (metabolic
bicarbonate
( t b li alkalosis/contraction
lk l i / t ti alkalosis)
lk l i )
• In order to downregulate, or “shut off” aldosterone, volume
restoration is keyy
• Aggressive volume resuscitation may lead to acute congestive
heart failure or severe edema so with most other things in
these
h patients,
i
fluids
fl id are to be
b administered
d i i
d slowly,
l l D5NS at
50cc/hr for 1-2 days
PseudoBartter’ss Syndrome
PseudoBartter
• Potassium repletion
p
is futile unless concomitant volume
restoration is in progress
– May place KCl in D5NS
• Because aldosterone is a hormone, its downregulation may
take up to 2-3 weeks
– Spironolactone maybe given in these patients for the first 2
weeks of cessation of purging behaviors in order to block
the action of aldosterone while waiting for the axis to shut
i lf off
itself
ff
– Spironolactone is an aldosterone inhibitor, provides mild
diuresis, and as a potassium
potassium-sparing
sparing diuretic aids in the
correction of hypokalemia
PseudoBartter’ss Syndrome
PseudoBartter
• Dose of spironolactone is 25-50mg daily for 1 to 2 weeks
• In addition to volume restoration +/- use of spironolactone,
patients should
– Be on a low salt diet (< 3gm of salt per day)
– Elevate legs
– Be patient as the edema will resolve within two to three
weeks of cessation of purging
p g g
GERD
• Commonly seen in BN given vomiting
• Symptom severity does not predict the occurrence of Barrett’s
esophagus but chronicity does
• No need for endoscopy unless “red flags” occur such as
dysphagia anemia
dysphagia,
anemia, or persistent dyspepsia despite treatment
• Proton pump inhibitors are more effective for healing
esophagitis than are histamine-2 receptor blockers
• Metoclopromide may also be used 30 minutes prior to meals
to decrease the frequency of vomiting
Constipation
• Weight loss may lead to slow colonic transit and low caloric
intake may lead to reflex hypofunctioning of the colon
• Worsened by electrolyte abnormalities such as hypokalemia
and volume depletion
• Cathartic colon syndrome
• consequence of laxative abuse
• permanent damage to colonic nerves leading to further constipation
and
d slower
l
ttransit
it ti
time
Constipation
• Counsel patients about the ineffectiveness of laxatives for weight
loss
• Reassure patients that bowel function will normalize again after
p to several
laxatives have been discontinued but mayy take up
weeks
• Remind patients that per Rome criteria, “normal bowel function”
is anything more than 2 bowel movements per WEEK!
• Polyethylene glycol (Miralax), an osmotic laxative, has been the
most successful in such patients. Avoid any stimulant laxative
(senna)
• If constipation persists and becomes bothersome, glycerin
suppositories are very helpful
Sialoadenosis
• Hypertrophy of the salivary glands in response to chronic
purging
• Seen about three days after cessation of vomiting
• Can be very distressing for patients given their body image
issues
• Painful at times
• Recedes within a few weeks of p
purging
g g cessation
Sialoadenosis
Sialoadenosis
Sialoadenosis
• Treatment:
– Cessation of vomiting
– Application of warm compresses to the glands
– Sucking sour/tart candies in order to stimulate saliva
production, clear the ducts, and decompress the glands
– NSAIDs
– In extreme cases, pilocarpine (parasympathetic muscarinic
receptor
p agonist
g
that increases saliva p
production)) maybe
y
used
• 5 mg TID
Bulimia Nervosa Pearls
• Stop
pp
purging
g g behaviors
• Slowly restore volume in order to shut off hormonal
mechanisms responsible for edema and electrolyte
abnormalities
b
liti
• Judiciously use spironolactone in select cases
• Do not treat constipation with stimulant laxatives but with
osmotic laxaties such as polyethylene glycol or suppositories
• Treat GERD with PPIs
• Treat sialadenosis with warm compresses and sour candy
• Complications will resolve with weight restoration
Questions?????