refeeding syndrome (dhyta).doc

8/10/2019 REFEEDING SYNDROME (dhyta).doc

1/8

REFEEDING SYNDROME

Definisi

The term refeeding syndrome (RS) is used in order to describe the metabolic

alterations that occur when administering nutrition, whether by oral, enteral, or

parenteral means, to severely malnourished or food-deprived individuals The

fundamental condition in RS is severe hypophosphataemia, which is accompanied by

fluid balance abnormalities, carbohydrate metabolism alterations, certain vitamin

deficiencies such as thiamine deficiency, as well as hypopotassaemia and

hypomagnesaemia !linically, this signifies the appearance of neurological,

respiratory, cardiovascular, haematological, and other abnormalities a few days after

resuming feeding, which increases patient morbidity and even mortality

Epidemiologi

"irst reports of the syndrome appeared in the #$%&s after observations of

malnourished prisoners of war who developed cardiac and neurological symptoms

soon after the recommencement of feeding There is no internationally agreed

definition of RS 'n & !roo et al referred to a syndrome of severe electrolyte and

fluid shifts associated with metabolic abnormalities in malnourished patients

undergoing refeeding, whether orally, enterally, or parenterally

*s there is no strict definition, it is not surprising that the incidence of RS is unclear

Robust epidemiological studies are lacing in part due to the absence of accepted

diagnostic criteria or internationally agreed guidelines for detecting RS +ost

published data from prospective and retrospective case series do not reflect overall

incidence

Faktor Risiko

'dentification of high ris patients is crucial

*ny patient with negligible food intae for more than five days is at ris of

developing refeeding problems

atients with anoreia nervosa

atients with chronic alcoholism

.ncology patients
http://flipper.diff.org/app/items/info/3385http://flipper.diff.org/app/items/info/3385


2/8

ostoperative patients

/lderly patients (comorbidities, decreased physiological reserve)

atients with uncontrolled diabetes mellitus (electrolyte depletion, diuresis)

atients with chronic malnutrition0o +arasmus

o rolonged fasting or low energy diet

o +orbid obesity with profound weight loss

o 1igh stress patient unfed for 23 days

o +alabsorptive syndrome (such as inflammatory bowel disease, coeliac

disease, chronic pancreatitis, cystic fibrosis, short bowel syndrome)

Patogenesis
http://en.wikipedia.org/wiki/Marasmushttp://flipper.diff.org/app/items/info/1572http://flipper.diff.org/app/items/info/1572http://en.wikipedia.org/wiki/Marasmushttp://flipper.diff.org/app/items/info/1572http://flipper.diff.org/app/items/info/1572


3/8

Patofisiologi

Prolonged fasting

'n early starvation, blood glucose levels decline, resulting in a decrease in insulin and

an increase in glucagon levels This stimulates glycogenolysis in the liver and

lipolysis of triacetylglycerol in fat reserves producing fatty acids ("*s) and glycerol

which are used by tissues for energy and converted to etone bodies in the liver *s

glycogen reserves then become depleted, gluconeogenesis is stimulated in the liver,

utilising amino acids (derived from the breadown of muscle), lactate and glycerol

resulting in the synthesis of glucose for use by the brain and red blood cells The main

result of these changes is that the body switches the main energy course from

carbohydrate to protein and fat The basal metabolic rate decreases by as much as &4


4/8

%5

6uringprolonged fasting, hormonal and metabolic changes are aimed at preventing

protein and muscle breadown The tissues decrease their use of etone bodies, and

use fatty acids as their main energy source This results in an increase in blood levels

of etone bodies, stimulating the brain to switch from glucose to etone bodies as its

main energy source The liver decreases its rate of gluconeogenesis, due to the

reduced need for glucose by the brain, thus preserving muscle protein which is its

source of amino acids 6uring the period of prolonged starvation, several intracellular

minerals become severely depleted 1owever, serum concentrations of these minerals,

including phosphate, may remain normal This is because these minerals are mainly in

the intracellular compartment, which contracts during starvation 'n addition, there is

a reduction in renal ecretion

Refeeding

The reintroduction of nutrition to a starved or fasted individual results in a rapid

decline in both gluconeogeneis and anaerobic metabolisms This is mediated by the

rapid increase in serum insulin that occurs on refeeding 'nsulin stimulates

glycogen, fat, and protein synthesis This process re7uires minerals such as phosphate

and magnesium and cofactors such as thiamine 'nsulin stimulates the absorption of

potassium into the cells through the sodium-potassium *Tase symporter, which also

transports glucose into the cells +agnesium and phosphate are also taen up into the

cells 8ater follows by osmosis 6epleted intracellular stores and a large

concentration gradient ensure a rapid fall in the etracellular concentration of these

ions .smotic neutrality must be maintained resulting in the retention of sodium and

water Reactivation of carbohydrate-dependent metabolic pathways increases demand

for thiamine, a cofactor re7uired for cellular en9ymatic reactions The deficiencies of

phosphate, magnesium, potassium, and thiamine occur to varying degrees and have

different effects in different patients


5/8

Manifestasi Klinis

Hypophosphatemia

The predominant manifestation of refeeding syndrome is hypophosphatemia

rapidly progressive The phosphate is essential for cell function 't has a structural role

as a component maing up phospholipids, nucleoproteins and nucleic acids: it plays a

ey part in metabolic pathways, such as glycolysis and oidative

phosphorilation, and it is implicated in the control of en9ymatic processes through

protein phosphorilation

hosphate acts as a cofactor of glyceraldehyde-;-phosphate dehydrogenase

Therefore, in the event of hypophosphataemia, it decreases production of ,;diphosphoglycerate (,;-6#%

mg?d@, or at higher levels if the decrease is rapid, and they are very apparent when

levels are ># mg?d@


6/8

Severe hypophosphataemia induces significant alterations on the neurological,

cardiac, respiratory, and haematological levels, and can lead to death The mortality

rate in patients with severe hypophosphataemia is ;&5

Hypopotassaemia

otassium has various physiological functions and contributes to the maintenance

of membrane potential and the regulation of glycogen and protein synthesis

1ypopotassaemia alters the transmembrane action potential, resulting in its

hyperpolarisation and altered muscle contractility 8e spea of mild to moderate

hypopotassaemia when serum potassium levels are between % and ;% m/7?@ The

patient may present gastrointestinal symptoms, such as nausea, vomiting, and

constipation as well as weaness 'f it is untreated, it can progress to severe

hypopotassaemia (serum potassium >% m/7?@) with the appearance of

neuromuscular dysfunction and disorders affecting myocardial contractility and signal

conduction Severe hypopotassaemia provoes electrocardiographic changes The

patient may present cardiac arrhythmias, from atrial tachycardia, bradycardia,

atrioventricular bloc and ventricular etrasystoles to tachycardia, ventricular

fibrillation, and even sudden death

Hypomagneasemia

't acts as a cofactor of numerous en9ymes and participates in regulating different

biochemical reaction, such as oidative phosphorylation 1ypomagnesaemia is

fre7uent in critically ill patients, and it is associated with increased morbidity and

mortality Aormal serum levels are between #= and % mg?d@ (&B%-# mmol?@)

atients with mild to moderate hypomagnesaemia (serum magnesium level between #

and #% mg?d@) are generally asymptomatic, which is not the case for those with

severe hypomagnesaemia (serum levels ># mg?d@) 't has diverse clinical

manifestations0 neuromuscular dysfunction, electrocardiographic changes, cardiac

arrhythmias, and even death

Thiamine deficiency

Thiamine or vitamin C is a hydrosoluble vitamin which is necessary for

carbohydrate metabolism because it acts as a cofactor for pyruvate dehydrogenase and

transetolases


7/8

+alnourished patients have vitamin several changes, including hypotiaminemia

'n advanced stages may induce brain disorders such as 8ernice-Dorsaoff

syndrome, also observed in obese undergoing bariatric operations

Thiamine deficiencycauses an increase in blood levels of pyruvate, which is

transformed into lactate This ecessive lactate formation gives rise to lactic acidosis

Thiamine deficiency can lead to the appearance of heart failure

Pencegahan

*ll guidelines recommend that vitamin supplementation should be started

immediately, before and for the first #& days of refeeding !irculatory volume should

also be restored .ral, enteral, or intravenous supplements of the potassium,

phosphate, calcium, and magnesium should be given unless blood levels are high

before refeeding

/lectrolyte levels should be measured once daily for one wee, and at least

three times in the following wee Erinary electrolytes could also be checed to help

assess body losses and to guide replacement
http://flipper.diff.org/app/items/info/4251http://flipper.diff.org/app/items/info/4251


8/8

Terapi

'f a patient is diagnosed with RS, nutrition therapy must be discontinued immediately

Treatment will include taing the necessary supplementary steps (treating

cardiovascular and respiratory manifestations, etc) and correcting electrolytic

anomalies 'n the event of neurological changes, a dose of #&& mg 'F thiamine must

also be administered Autrition may be reintroduced when the patient is asymptomatic

and stable * slow pace is recommended when resuming feeding (approimately %&5

of the pace that had been followed previously), with gradual increases over G to %

days, supplementing electrolytes and vitamins appropriately and carefully monitoring

the patient

refeeding syndrome (dhyta).doc

Documents