Transcript Refeeding Syndrome - St. Joseph Mercy Oakland

Interventions for Addressing Medical
Complications Related to
Outpatient Refeeding and Intake Regulation
October 14, 2016
St. Joseph Mercy Health System
Eating Disorder Conference
Allison Laurie, PMHNP-BC
Overview/Objectives
•
•
•
•
Define refeeding syndrome (RFS)
Identify patients at risk for RFS
Describe the pathophysiology of starvation
Identify the main pathophysiologic
features/clinical manifestations of RFS
• Discuss prevention of RFS
• Identify recommended treatment & standards
of care
• Case review
2
Background
• Refeeding is the cornerstone of treatment for
patients with anorexia nervosa
• Essential to prevent serious or even fatal
medical complications of starvation
• Starvation induced cognitive deficits can
preclude efficacy of psychotherapies
• Weight restoration is not without risk for the
patient; must be balanced against the
potentially fatal complications of the refeeding
syndrome.
3
Refeeding Syndrome Overview
• Clinical complications that occur as a
result of fluid and electrolyte shifts
during nutritional rehabilitation of
malnourished patients
• May result in cardiac arrhythmia,
cardiac failure or arrest, hemolytic
anemia, delirium, seizures, coma,
and sudden death
Garber, A. K., Sawyer, S. M., Golden, N. H., Guarda, A. S., Katzman, D. K., Kohn, M. R., Le Grange, D., Madden, S., Whitelaw, M. & Redgrave, G. W. (2016). A systematic
review of approaches to refeeding in patients with anorexia nervosa. International Journal of Eating Disorders.
4
Risk Factors
•
•
•
•
•
Directly related to the amount of weight loss during the
current episode, and the rate of weight restoration.
Patients at <70 percent of IBW, or those who have lost
weight most rapidly, are at greatest risk for the syndrome.
Inpatient hospitalization recommended if patient has <70
percent of IBW for initial stage of nutritional
replenishment.
Other risk factors: low phosphate, potassium, or
magnesium prior to refeeding; little to no nutritional
intake for previous 5 to 10 days.
Highest risk within first 2 weeks of refeeding. Risk
progressively dissipates over the next few weeks.
Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 336(7659), 1495-1498.
5
Pathogenesis of Starvation
Starvation/malnutrition
Insulin concentrations decrease, glucagon increases
Gluconeogenesis, protein and fat catabolism (for glucose
synthesis)
Weight loss
Water, vitamin, and mineral depletion
6
Consequences of Starvation
• Decreased insulin and increased glucagon
secretion.
• Switch from glucose toward ketone bodies as a
source of energy.
• Glycogen stores used
• BMR decreases
• Brain adapts to using ketones
• Atrophy of all organs
• Reduced lean body mass
• Abnormal liver function
7
Refeeding Syndrome
8
Clinical Manifestations
• Symptoms of RFS are variable and may be
unpredictable.
• Nausea/vomiting
• Lethargy
• Respiratory insufficiency
• Cardiac failure
• Hypotension
• Arrhythmias
• Delirium
• Coma
• Fatality
Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 336(7659),
1495-1498.
9
Clinical Manifestations of Electrolyte
Abnormalities Associated with RFS
•
•
•
•
•
Phosphate
Potassium
Magnesium
Sodium
Vitamins/Thiamine
Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 336(7659), 1495-1498.
10
Phosphate
• Pathogenesis:
• Begins with depletion of stores during starvation
• Upon intake of glucose with refeeding, release of
insulin triggers cellular uptake of phosphate
• Insulin additionally causes cells to produce a
variety of depleted molecules that require
phosphate (ATP), which further deplete body’s
stores of phosphate.
• Lack of phosphate results in tissue hypoxia and
resultant myocardial dysfunction, respiratory
failure, etc.
11
Clinical Manifestations of
Hypophosphatemia
- Normal range: 0.8-1.45 mmol/l
- Cardiovascular: heart failure, arrhythmia, hypotension,
cardiomyopathy, shock, death.
- Renal: acute tubular necrosis, metabolic acidosis
- Skeletal: rhabdomyolysis, weakness, myalgia,
diaphragm weakness.
- Neurologic: delirium, coma, seizures, tetany
- Endocrine: hyperglycemia, insulin resistance,
osteomalacia
- Hematologic: hemolysis, thrombocytopenia, leukocyte
dysfunction
12
Potassium
• Pathogenesis:
• Also depleted in starvation
• Serum concentration may be normal
• With the change to anabolism upon
refeeding, potassium is taken up into cells as
they increase in volume and number, and as
a direct result of insulin secretion
• Result is hypokalemia
• Causes derangements in the electrochemical
membrane potential.
13
Clinical Manifestations of Hypokalemia
- Normal Range 3.5-5.1 mmol/l
- Cardiovascular: hypotension, ventricular arrhythmias,
cardiac arrest, bradycardia, or tachycardia
- Respiratory: hypoventilation, respiratory distress,
respiratory failure
- Skeletal: weakness, fatigue, muscle twitching
- GI: diarrhea, nausea, vomiting, anorexia, paralytic
ileus, constipation
- Metabolic: metabolic acidosis
14
Magnesium
• Another predominantly
intracellular cation
• Important cofactor for must
enzyme systems including oxidative
phosphorylation and ATP
• production
• Necessary for structural integrity of
DNA, RNA, and ribosomes.
• Affects membrane potential,
deficiency can lead to cardiac
dysfunction & neuromuscular
complications.
15
Clinical Manifestations of Hypomagnesemia
- Normal Range: 0.77-1.33mmol/l
- Cardiovascular: arrhythmias, T wave alternans
- Respiratory: hypoventilation, respiratory distress,
respiratory failure
- Neuromuscular: weakness, fatigue, muscle cramps,
ataxia, vertigo, paresthesia, hallucinations, depression,
convulsions
- GI: abdominal pain, diarrhea, vomiting, loss of appetite,
constipation
- Hypocalcemia
- *Many cases of hypomagnesemia do not manifest until
late
16
Sodium
• Pathogenesis:
• Changes in carbohydrate metabolism have a
profound effect on sodium and water
balance
• Introduction of carbohydrate to a diet leads
to a rapid decrease in renal excretion of
sodium and water.
• If fluid repletion is instituted to maintain a
normal urine output, pts may rapidly
develop fluid overload.
17
Clinical Manifestations of Hyponatremia
•
•
•
•
•
Normal Range: 136-145 mmol/l
Cardiovascular: heart failure, arrhythmia
Respiratory: respiratory failure,
pulmonary edema
Renal: renal failure
Skeletal: muscle cramps, fatigue, fluid
retention, swelling (edema).
©2015
18
Vitamins/Thiamine
• Thiamine is an essential coenzyme in
carbohydrate metabolism.
• Deficiencies can result in
• Korsakoff’s syndrome:
• Retrograde and anterograde amnesia,
confabulation
• Wernicke’s encephalopathy:
• Ocular abnormalities, ataxia, confusion,
hypothermia, coma
• Particular concern in alcoholism
* Vitamin deficiencies may also result in
• CHF, lactic acidosis, beriberi disease, and
muscle weakness.
©2015
19
Cardiovascular Complications
Most fatalities occur due to cardiac complications
•
•
Impaired contractility, decreased stroke volume, heart failure, and
arrhythmias
Atrophy of the heart during starvation results in
heightened vulnerability for fluid overload and heart
failure.
• Sodium and fluid retention can lead to volume
overload
• Echo, ECG, and cardiology consult as indicated by
pt’s clinical status
•
©2015
20
Preventing RFS
Identification of high risk patients
• One or more of the following (NICE guidelines):
•
•
Little to no intake for >10 days
•
Body mass index (kg/m2) <16
•
Weight loss of >15% in the past three to six months
•
Low levels of potassium, phosphate, or magnesium before
feeding
Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 336(7659), 1495-1498.
©2015
21
Preventing RFS
Identification of high risk patients:
• Or the patient has two or more of the following:
•
•
Body mass index <18.5
•
Unintentional weight loss >10% in the past 3 to 6 months
•
Little or no nutritional intake for >5 days
•
History of alcohol misuse or drugs including insulin,
chemotherapy, antacids or diuretics.
Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 336(7659), 1495-1498.
©2015
22
Preventing RFS
Patients are at highest risk for RFS in the first two
weeks of nutritional replenishment and weight
gain.
• Historically, the standard of care for refeeding
patients with AN is to initiate at low caloric levels,
and advance slowly.
• Example: Start at 1,200 calories per day
(kcal/day) and advance by about 200 calories
every other day.
•
©2015
23
When to Hospitalize?
Criteria for admission vary by region, age, and the
type of treatment facility.
• Some published positions and guidelines have
suggested that hospital admission is warranted in
the presence of:
•
•
Vital sign abnormalities (bradycardia, hypotension,
orthostatic HR/BP, and hypothermia)
•
Failure to respond to lower levels of care, suicidality, or
other severe psychiatric symptoms
•
Severe malnourishment (BMI<15kg/m2)
©2015
24
Preventing RFS
Monitoring the patient clinically and
biochemically during the refeeding process.
• Proactive correction of electrolyte
abnormalities (particularly phosphorus
levels)
• Monitoring for and treating cardiovascular
complications.
•
©2015
25
When Not to Hospitalize
For some patients, weight restoration can
be achieved successfully outside of the
hospital.
• Alternative treatment settings include
partial hospitalization, residential
programs, intensive outpatient
programs.
• Non-inpatient settings are cost-effective
for long-term nutritional rehabilitation.
•
©2015
26
How to Refeed
In mild and moderately malnourished patients,
lower calorie refeeding is too conservative.
• In severely malnourished patients, there is
insufficient evidence to support changing the
current standard of care for refeeding.
• Standard recommendations for the
macronutrient composition of refeeding is 2535% fat, 15-20% protein, 50-60% carbohydrate.
•
Garber, A. K., Sawyer, S. M., Golden, N. H., Guarda, A. S., Katzman, D. K., Kohn, M. R., Le Grange, D., Madden, S., Whitelaw, M. & Redgrave, G. W. (2016). A systematic review of approaches to refeeding in patients with anorexia nervosa.
International Journal of Eating Disorders.
©2015
27
Treating RFS
Reduce nutritional support
• Correct hypophosphatemia, hypokalemia, and
hypomagnesemia.
• Patients with marked edema, or a serum
phosphorus <2mg/dL should be hospitalized to
intravenously correct electrolyte deficiencies, and
for close monitoring.
• Continuous telemetry may be needed to monitor
cardiopulmonary physiology.
•
Garber, A. K., Sawyer, S. M., Golden, N. H., Guarda, A. S., Katzman, D. K., Kohn, M. R., Le Grange, D., Madden, S., Whitelaw, M. & Redgrave, G. W.
(2016). A systematic review of approaches to refeeding in patients with anorexia nervosa. International Journal of Eating Disorders.
©2015
28
Case Review
A 40-year-old woman with a history of anorexia had suffered several
complications of the condition in the past, including electrolyte disorders,
arrhythmias, amenorrhea, osteoporosis, depression and progressive social
isolation. Before admission, she had lost further weight to 40 kg (BMI
13.5 kg/m2). Prior to admission, she resumed eating several large meals a day.
On admission, she had ankle edema and hypotension (95/70 mm Hg). Serum
concentrations of phosphate, magnesium and potassium were low and the ECG
showed sinus bradycardia (51 b.p.m.) and a prolonged QT interval (490 ms).
Within 4 h of admission and continuation of oral nutrition and, despite oral
supplements of vitamins and electrolytes, she developed muscle weakness and
drowsiness. The ECG showed short runs of ventricular tachycardia. i.v.
supplementation of electrolytes and minerals was started and the serum
electrolyte concentrations returned to normal within 2 days, with resolution of
the muscle weakness and the ventricular tachycardia. However, the QT interval
remained prolonged at 460 ms.
©2015
29
Key Points
Severe anorexia nervosa with a very low BMI is a common cause of the
refeeding syndrome in hospital practice. In this case, refeeding was begun
by the patient herself and was continued after hospital admission.
In severe and prolonged malnutrition, there may be cardiac atrophy as well
as electrolyte abnormalities, including sinus bradycardia and a prolonged
QT interval (Heymsfield et al., 1978; Powers, 1982). These changes make
the heart more vulnerable to hypophosphatemia and hypokalemia with
ventricular arrhythmias and sudden death (Isner et al., 1985; Beumont and
Large, 1991), especially, if the QT interval exceeds 470 ms (Cooke et al.,
1994). It should also be remembered that the concomitant abuse of
diuretics, laxatives and alcohol by anorectic patients may exacerbate
electrolyte and vitamin deficiencies. It is, therefore, important to be alert to
the danger of the refeeding syndrome in patients with these problems.
©2015
30
Questions?
©2015
31