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Malnutrition
N=502 consecutive admission
Malnutrition was present in ~24% of hospitalized patients.
The prevalence of malnutrition was significantly higher in
malignant diseases (50.9 vs. 21.0%, p < 0.0001).
High prevalence rates >30% were observed in subgroups of
Incidence
Unknown
No universal definition
Wide variety of clinical manifestation
How?
Administration of a glucose load by any route
(but classically with intravenous glucose
solutions or TPN) leads to intracellular
electrolyte shifts and sodium retention which
are responsible for most of the clinical
manifestations of RFS
Crook MA, Hally V, Panteli JV: The importance of the refeeding syndrome. Nutrition
2001;17:6327
Mallet M: Refeeding syndrome. Age Ageing 2002;31:656
Syndrome
Acute electrolyte abnormalities
Fluid retention
Dysfunction of various organ systems
potentially fatal
occur with any form of nutrition (oral,enteral, or
parenteral) in patients who are malnourished
from any cause.
Pathophysiology
During a period of suboptimal oral intake there will be loss
of :
lean tissue mass
water
minerals
Pathophysiology
In addition, increased tissue anabolism leads to increased cellular
demand for phosphorus, glucose, potassium and water.
Synthesis of adenosine triphosphate, 2,3-diphosphoglycerate, and
creatine phosphokinase may also contribute to phosphorus
depletion.
Carbohydrate loading also leads to sodium and water retention,
which results in volume expansion and edema, which can lead to
circulatory overload and heart failure.
Hyperglycemia is common and can lead to osmotic diuresis,
acidosis, and increased susceptibility to bacterial infection
Marinella MA: Refeeding syndrome, in Frequently Overlooked Diagnoses in Acute Care. 2003
Soloman DM, Kirby DF: The refeeding syndrome: A review. JPEN J Parenter Enteral Nutr 1990;14:907
Marik PE, Bedigian MK: Refeeding hypophosphatemia in critically ill patients in an intensive care unit. Arch Surg 1996;
131:10437
Pathophysiology
Also, hypophosphatemia may lead to
decreased erythrocyte adenosine triphosphate levels
resulting in increased cell membrane rigidity
hemolytic anemia
Thrombocytopenia
Clinical menifestations
Cardiac*
Arrhythmias
Congestive heart failure
Pulmonary
Dyspnea
Respiratory failure
Neurologic
Seizures
Weakness
Paraesthesias
Delirium
Guillain-Barre
Musculoskeletal
Rhabdomyolysis
Myalgia
Hematologic
Hemolytic anemia
Thrombocytopenia
Immunologic
Infection
Metabolic
Metabolic acidosis
Hyperglycemia/insulin resistance
Renal
Acute tubular necrosis
Myoglobinuria
Hemoglobinuria
*major
cause of mortality
Patients at risk
Prolonged starvation/poor
intake
Dysphagia
Vomiting
Diarrhea
Surgery
Nasogastric suction
Alcoholism
Cancer chemotherapy
Homelessness
Anorexia nervosa
Depression
Diagnosis
Recognition of the syndrome and having a high index of
suspicion in at-risk patients
especially those with little or no oral intake for several days
Eg. a patient transferred to our ward from a medical or surgical floor
may have a recent history of vomiting, diarrhea, or nil orally status
and on reinstitution of oral or enteral feeding, may develop RFS.
Eg. Recent poor oral intake for several days develop symptoms of
confusion, weakness, dyspnea, tachycardia, paresthesias
Laboratory evidence of
hypophosphatemia
hypokalemia,
hypomagnesemia
hyperglycemia
Treatment
Recognizing patients at risk
Reinstituting nutrition slowly*
orally, enterally or parenterally
JC: From malnutrition to refeeding during anorexia nervosa. Curr Opin Clin Nutr Metab
Care 1998;1:4815
Treatment
severe hypoK+ (2.5 mEq/liter)
IV KCL via a central vein.
Significant hypoMg2+
24 g of intravenous magnesium sulfate
Conclusions
RFS is an underappreciated common cause of lifethreatening electrolyte derangements in
hospitalized patients. It can be fatal.
Risks for developing RFS include (malnourished)
Conclusions
At risk patients (malnourished) should be
regularly monitor
serum phosphorus, potassium, magnesium,
glucose and clinical volume status.