Part V Nutrition

Chapter 58: Refeeding Syndrome

Chapter 59: Malnutrition
Chapter 60: Overweight and Obesity

Josselle S. Calienta MD
Table of contents

01 Chapter 58: Refeeding Syndrome

02 Chapter 59: Malnutrition

Section C

03 Chapter 60: Overweight and Obesity

 58
Refeeding
Syndrome
 Occur if high-energy feeding is
started too soon or too vigorously,
and it may lead to sudden death with
signs of heart failure
 Occurs in malnourished individuals
as a result of untimely, overzealous
oral, enteral, or parenteral (highest
risk) feeding
 Onset is usually 24-48 hours after the
start of high energy feeding and is
characterized by breathlessness,
rapid pulse, increased venous
pressure, rapid enlargement of the
liver, and watery diarrhea
Signs and Symptoms

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Pathophysiology
Management
1. Stabilization phase - providing maintenance amounts of energy
and protein and correcting electrolyte imbalances and
micronutrient deficiencies
2. Transition phase - controlled transition to high-energy feeding

Treatment with a single parenteral dose of digoxin and furosemide

has been useful.
 59
Malnutrition
Definitions

Failure to thrive Malnutrition

Children who are not Undernutrition and is defined as an imbalance between

growing as expected nutrient requirements and intake or delivery that then results
in deficits—of energy, protein, or micronutrients—that may
negatively affect growth and development
Clinical Manifestations

 Inadequate weight-for–
corrected age, failure to gain
adequate weight over a period
of time (weight gain velocity),
height velocity, weight for-
height, body mass index (BMI),
and developmental outcomes
ETIOLOGY AND
DIAGNOSIS of
MALNUTRITION
The most common mechanisms for illness-related causes of insufficient
growth include

(1) failure to ingest sufficient

calories, or starvation

(2) increased nutrient losses

(3) increased metabolic demands, as

seen in extensive burn injuries

(4) altered nutrient

Etiology and Diagnosis

 A complete history should include a detailed nutritional, family, and

prenatal history; the quantity, quality, and frequency of meals; and further
information regarding the onset of the growth failure.
 A comprehensive physical examination is necessary to elicit underlying
etiologies
 Additional measurements that are useful for following the progress of the
acutely malnourished child are mid-upper arm circumference (MUAC)
and hand-grip strength.
Treatment
Mild – Outpatient

 Caloric supplementation – oral feeds

 Speech therapy if with history of difficulty of

oral feeds

 If a child has not responded after 2-3 months

of outpatient management, consider
hospitalization for potential initiation of
nasogastric tube feeds
Treatment
Mild – Outpatient
Moderate to Severe

 Hospitalization – to avoid refeeding

syndrome

 Caloric supplementation

 In general - Multivitamin supplementation

should be given to all to meet the
recommended dietary allowance as well as
increased micronutrient demands with catch- The same anthropometric measures used
to diagnosis malnutrition should be used to
up growth.
measure progress and recovery from the
malnourished state.
 60
Overweight and
Obesity
Epidemiology

Mercury
 According to the National Health and Nutrition Examination Survey
(NHANES), 2013–2014, 34% of children 2-19 yr old were overweight or
obese, with 17% in the obese range. Risk for obesity in children 2-19 yr old
varies significantly by race/ethnicity, with >20% for minority children
compared with 15% for white children. Across all racial groups, higher
maternal education confers protection against childhood obesity.
 Risk factors Protective factor
 The first 1000 days, the period from  Breastfeeding is modestly
conception to age 2 yr, are increasingly protective for obesity based
recognized as a modifiable period related to on dose and duration.
risk for childhood obesity.
 Parental obesity
 Prenatal factors, including high
preconceptual weight, gestational weight
gain, high birthweight, and maternal
smoking
 Infants with high levels of negative reactivity
(temperament)
Definition

 Obesity is defined using the body mass index (BMI), an excellent

proxy for more direct measurement of body fat
 BMI = weight in kg/(height in meters)2
 Obesity and overweight are defined using BMI percentiles for
children ≥2 yr old and weight/length percentiles for infants <2 yr
old.
 The criterion for obesity is BMI ≥95th percentile and for overweight
is BMI between 85th and 95th percentiles.
 Etiology
 Individual adiposity is the result of a complex interplay among genetically
determined body habitus, appetite, nutritional intake, physical activity (PA),
and energy expenditure.
Environmental changes

● The food environment has changed dramatically related to

urbanization and the food industry.
● As fewer families routinely prepare meals, foods prepared
by a food industry have higher levels of calories, simple
carbohydrates, and fat.
● These changes, in combination with marketing pressure,
have resulted in larger portion sizes and increased snacking
between meals.
● The increased consumption of high-carbohydrate beverages,
including sodas, sport drinks, fruit punch, and juice, adds to
these factors.
Environmental changes

● Sleep plays a role in risk for obesity. Over the last 4 decades, children
and adults have decreased the amount of time spent sleeping. Reasons
for these changes may relate to increased time at work, increased time
watching television, and a generally faster pace of life.
● Chronic partial sleep loss can increase risk for weight gain and obesity,
with the impact possibly greater in children than in adults.
● In studies of young, healthy, lean men, short sleep duration was
associated with decreased leptin levels and increased ghrelin levels,
along with increased hunger and appetite
Genetics

● FTO gene at 16q12 – increased energy intake

● Melanocortin-4 receptor (MC4R) deficiency - early-onset
obesity and food-seeking behavior
● Proopiomelanocortin (POMC) deficiency, a prohormone
precursor of adrenocorticotropic hormone (ACTH) and
melanocyte-stimulating hormone (MSH), resulting in adrenal
insufficiency, light skin, hyperphagia, and obesity.
● Prader-Willi syndrome is characterized by insatiable appetite
and food seeking.
Endocrine and Neural Physiology

● Monitoring of “stored fuels” and short-term control of

food intake (appetite and satiety) occurs through
neuroendocrine feedback loops linking adipose tissue, the
gastrointestinal (GI) tract, and the central nervous system
(CNS)
● GI hormones, including cholecystokinin, glucagon-like
peptide 1, peptide YY, and vagal neuronal feedback
promote satiety.
● Ghrelin stimulates appetite.
Endocrine and Neural Physiology

● Adipose tissue provides feedback regarding energy storage levels to

the brain through hormonal release of adiponectin and leptin.
● Adipocytes secrete adiponectin into the blood, with reduced levels
in response to obesity and increased levels in response to fasting.
● Reduced adiponectin levels are associated with lower insulin
sensitivity and adverse CV outcomes.
● Leptin is directly involved in satiety; low leptin levels stimulate
food intake, and high leptin levels inhibit hunger in animal models
and in healthy human volunteers.
Endocrine and Neural Physiology

● Numerous neuropeptides in the brain,

including peptide YY (PYY), agouti-
related peptide, and orexin, appear to
affect appetite stimulation, whereas
melanocortins and α-melanocortin–
stimulating hormone are involved in
satiety
Comorbidities

 Type 2 diabetes
 Hypertension
 Hyperlipidemia Metabolic syndrome
 Nonalcoholic fatty liver
disease (NAFLD)

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 Insulin resistance Chronic inflammation
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Evaluation
 Examination of the growth chart reveals the severity,
Mercury
duration, and timing of obesity onset.

 Children who are overweight (BMI in 85–95 th

percentile) are less likely to have developed comorbid
conditions than those who are obese (BMI ≥95th
percentile).
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 Those with a BMI ≥99th percentile are more likely to
have coexisting medical problems.
Evaluation

Mercury

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Intervention
 Based on behavior change theories,
treatment includes specifying target
behaviors, self-monitoring, goal
setting, stimulus control, and
promotion of self-efficacy and self-
management skills
 Behavior changes associated with
improving BMI include drinking lower
quantities of sugar-sweetened
beverages, consuming higher-quality
diets, increasing exercise, decreasing
screen time, and self-weighing.
Intervention
 It is important to begin with clear
recommendations about appropriate
caloric intake for the obese child
 Surgery
 The American Pediatric Surgical Association
guidelines recommends that surgery be considered
only in children with complete or near-complete
skeletal maturity, a BMI ≥40, and a medical
complication resulting from obesity, after they
have failed 6 mo of a multidisciplinary weight
management program.
 Surgical approaches include the Roux-en-Y and the
adjustable gastric band
 Nutritional complications of bariatric surgery
include malabsorption and vitamin (A, B1, B2, B6,
B12, D, E, K) and mineral (copper, iron) deficiencies
that require supplementation.
Prevention
Prevention
Rapid-Onset Obesity With
Hypothalamic Dysfunction,
Hypoventilation, and
Autonomic
Dysregulation (ROHHAD)
● A rare, poorly understood disease of childhood onset, the first sign
of which is sudden, rapid, and extreme weight gain in a previously
healthy child
● The diagnosis is initially considered after the observation of rapid-
onset obesity (15-20 lb gain) after age 1.5 yr, accompanied by at
least 1 additional sign of hypothalamic dysfunction.
● Central hypoventilation may not be present at diagnosis but will
develop over time, and artificial ventilatory support will be required
at least during sleep, if not 24 hr/ day.
Clinical Manifestation

● The initial symptoms present between ages 18 mo and 7 yr.

● Typically, the 1st symptom observed is rapid-onset obesity, with
weight gain of 15-20 lb in 6-12 mo. This is a sign of hypothalamic
dysfunction.
● The 2nd common sign of HD, seen in most ROHHAD patients, is
disordered water balance, including hyper- and hyponatremia and
both adipsia and polydipsia.
● Sleep-disordered breathing (SDB) is one of the key symptoms,
often manifesting as one of the most severe features of the
phenotype, with the greatest potential for fatal complications.
Clinical Manifestation
● Obstructive sleep apnea
● All ROHHAD patients will eventually develop central alveolar
hypoventilation, requiring artificial ventilatory support
● All ROHHAD patients have symptoms of autonomic nervous
system (ANS) dysregulation - most common manifestations are
ophthalmologic, including pupillary dysfunction, strabismus, and
alacrima.
● Neural crest tumors are observed in at least 40% of ROHHAD
patients, most frequently ganglioneuromas and
ganglioneuroblastomas of the chest or abdomen; rarely a
neuroblastoma has been reported
Clinical Manifestation

● Most patients do not have behavioral

or psychologic disorders. For those
who do, however, the disorders can
be quite severe, including anxiety,
depression, rage, lethargy, irritability,
aggressiveness, psychosis, and
obsessive-compulsive disorder.
Diagnosis

● The diagnostic criteria: rapid-onset obesity after 1.5 years of age,

central hypoventilation beginning after age 1.5 yr, and ≥1 of the
following signs of HD: disordered water balance,
hyperprolactinemia, failed GH stimulation test, central
hypothyroidism, corticotropin deficiency, and altered onset of
puberty.
● Additionally, it should be confirmed that no CCHS-related
PHOX2B gene mutation is present, to rule out a diagnosis of
CCHS or LO-CCHS.
Treatment

● There is currently no cure for

ROHHAD. Rather, treatment
consists of early identification,
meticulous monitoring, and
symptomatic management of
the various symptoms as they
develop.
Thank you!!!