Table 4.
Physiopathology and main clinical features of the RFS
Pathophysiological mechanisms | Clinical manifestations |
---|---|
Hypophosphatemia | |
Increased phosphate consumption due to enhanced production of phosphorylated intermediates for glycolysis, the Krebs cycle, and the electron transport chain to produce adenosine triphosphate and 2,3-diphosphoglycerate | Impaired cardiac and respiratory functions (i.e., tachycardia and tachypnea) |
Neurologic symptoms (i.e., confusion, somnolence, lethargy, coma, paresthesia, seizures) | |
Hematologic disorders (i.e., hemolysis, dysfunction of platelets and leukocytes, thrombocytopenia) | |
Hypoxia (due to impaired oxygen release from 2,3- diphosphoglycerate) | |
Muscular disorders (i.e., weakness, rhabdomyolysis, decreased cardiac contractility, myalgia) | |
Hypokalemia | |
Intracellular shift of potassium by insulin stimulation of the Na + /K + ATPase | Cardiac arrhythmias |
Impairment of potassium reuptake in the nephron (role of hypomagnesemia) | Neurologic symptoms (i.e., weakness, hyporeflexia, respiratory depression, and paralysis) due to impaired transmission of electrical impulses |
Hypomagnesemia | |
Not completely clear Intracellular shift of magnesium after carbohydrate feeding |
Increased renal losses of potassium |
Cardiac arrhythmias (i.e., torsade de pointes, atrial fibrillation, ventricular arrhythmias) | |
Electrocardiograph changes (i.e., prolonged QT and PR, widened QRS) | |
Abdominal discomfort (i.e., anorexia, diarrhea, nausea, vomiting) | |
Neuromuscular symptoms (i.e., tremor, paraesthesia, tetany, seizures, irritability, confusion, weakness, ataxia) | |
Thiamine deficiency | |
Increased consumption of thiamine by glucose metabolism enzymes | Neurologic disorders or dry beriberi, Wernicke encephalopathy and Korsakoff’s syndrome (i.e., ataxia, disturbance of consciousness, oculomotor abnormalities, symptoms of acute peripheral neuropathy, coma) |
Cardiovascular disorders or wet beriberi (i.e., peripheral edema, heart failure) | |
Metabolic acidosis (due to glucose conversion to lactate) | |
Sodium and fluid retention | |
Renal sodium and fluid retention due to insulin antinatriuretic properties (after carbohydrate feeding) | Peripheral edema |
Pulmonary edema and heart failure (due to increased vasoconstriction and peripheral resistance by sodium stimulation of noradrenaline and angiotensin II) | |
Hyperglycemia | |
Increased tissue resistance to endogenous glucose | Metabolic acidosis |
Hypercapnia, respiratory failure, and risk of fatty liver due to lipogenesis (stimulated by insulin) |
ATP adenosine triphosphate