single tertiary-level neonatal unit. Patients Preterm infants given parenteral nutrition (PN) in the first postnatal week during two discrete 6-month. In neonatology, it has been proposed as a useful marker for both a diagnosis and an indication of the severity of metabolic bone. PDF | On Jan 1, , André Couto Carvalho and others published Raquitismo hipofosfatemia ligado ao X. Hallazgo de una nueva mutation en.
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Hypophosphatemia in critically ill children. The purpose of this paper is to review clinical studies on hypophosphatemia in pediatric intensive care unit patients with a view to verifying prevalence and risk factors associated with this disorder. Hipfoosfatemia terms included critically ill, pediatric intensive care, trauma, sepsis, infectious diseases, malnutrition, inflammatory response, surgery, starvation, respiratory nipofosfatemia, diuretic, steroid, antiacid therapy, mechanical ventilation.
The search period covered those clinical trials published from January to January Studies hipofosfqtemia endocrinological disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were not included in this review.
Out of 27 studies retrieved, only 8 involved pediatric patients, and most of these were case reports. One clinical trial and one retrospective study were identified. The commonly associated factors in most patients with hypophosphatemia were refeeding syndrome, neonnatal, sepsis, trauma, and diuretic and steroid therapy.
Given the high prevalence, clinical manifestations, and multiple risk factors, the early identification of this disorder in critically ill children is crucial for adequate replacement therapy and also to avoid complications. Pediatric intensive care unit. Os termos utilizados para pesquisa foram: Despite the fact that monitoring of sodium, potassium, and calcium ions is part of the routine of intensive care unit services, little attention has been devoted to phosphorus during the follow-up of critically ill patients.
Required for many biological functions, phosphorus plays an important part in metabolism as a main intracellular anion, hipofosfatemiw constituent, and component of phosphorylated intermediate compounds, and phosphorus is also a component in cellular membranes, nucleic acids, and nuclear proteins.
Approximately hipofpsfatemia of phosphorus is the recommended daily allowance for healthy adults, with an average of mg for normal children. Phosphorus is absorbed in greater proportions in the jejunum, mainly by passive transport.
Phosphorus is also present in soft tissues in the form of phospholipids, phosphoglycides, and phosphoproteins. Similar to that of calcium, homeostasis of phosphorus also involves direct participation of the intestine, bones, and kidneys, being maintained by the action of Vitamin D 1. Vitamin D acts in the intestine, increasing both calcium and phosphorus absorption.
Phosphatemia, however, is practically controlled by renal excretion. PTH secretion, stimulated by a decrease in calcium serum levels, acts in renal reabsorption, reducing urinary excretion of calcium while simultaneously inhibiting the tubular reabsorption of phosphorus. Conversely, when calcium levels are high, calcitonin is released, acting in reverse neontal, i. Normal blood concentrations for phosphorus in children aged 5 or under are shown hipfoosfatemia Table 1.
The lower limits are cut-off points for diagnosis of hypophosphatemia. The same classification as for adults is used in children over 5 years old.
Hypophosphatemia in critically ill children
In adults, hypophosphatemia is classified as mild The decreasing of the body’s stores and increased consumption of phosphorus can explain the onset of hypophosphatemia in malnourished patients. In critically ill patients, hypophosphatemia results from chronic phosphate depletion and cellular redistribution. The first mechanism involves situations such as insufficient intake over prolonged periods malnutritionreductions in intestinal absorption antiacid therapyand increases in urinary losses diuretic therapy.
The redistribution condition, for its part, besides being more frequent in these hjpofosfatemia, is commonly responsible for triggering the more severe form of hypophosphatemia. Respiratory alkalosis, high blood concentrations of stress hormones insulin, glucagon, adrenalin, cortisoland refeeding syndrome are the main conditions contributing to phosphate redistribution within the organism. In the majority of cases, the symptoms related to hypophosphatemia are nonspecific, such as fatigue and irritability.
The aim of this study was to carry out a review of the literature on the prevalence, risk factors, and clinical conditions associated with hypophosphatemia hipofoscatemia critically ill children.
The following criteria were used to select the included neojatal Those studies concerning endocrine disorders, genetic syndromes, rickets, renal diseases, anorexia nervosa, alcohol abuse, and prematurity were excluded. A total of 27 articles were retrieved; of these, only 8 were related to pediatric age groups, where these comprised 1 prospective clinical study, 16 1 retrospective, 17 1 abstract, 18 and 5 case reports.
Hypophosphatemia varied according to clinical diagnosis as follows: The case reports described the onset of hypophosphatemia in malnourished children during refeeding; 10,19 in adolescents with diagnosed bone tumor, 20 and severe encephalic cranial trauma. Among the clinical studies, hypophosphatemia was detected in over half of patients assessed. The results also showed hypophosphatemia to be a transitory condition during the acute phase of infection, stabilizing before C-reactive protein concentration becomes normalized.
Despite this, it is important to make clear that the sample did not include critically ill patients, such subjects being more susceptible to the deleterious effects of hypophosphatemia. The risk factors most often associated with hypophosphatemia were refeeding, 10,19 malnutrition, 10,17 infection, 16 sepsis, 4,23,24 trauma, 21 and diuretics 9,25 and steroids use.
Severe hypophosphatemia and its hipofosfqtemia complications has been referred to as refeeding syndrome, especially in malnourished patients who have been re-fed rapidly and inappropriately through enteral or parenteral nutrition.
In this syndrome, besides phosphorus depletion, changes generally occur in the serum levels of potassium and magnesium, as well in hydric balance, glycose metabolism, and vitamin deficiencies, particularly thiamin.
Refeeding syndrome has received little recognition or study in clinical practice, especially in the pediatric population. Questions remain with regard to this issue, since not all patients undergoing refeeding, even without electrolyte supplements, develop the syndrome.
In critically ill, malnourished patients, the serum level of phosphorus prior to refeeding is usually normal. However, as the body’s total stores become depleted, there is a risk of developing hypophosphatemia as the supply of nutrients increases cell uptake of phosphorus for synthesis of the phosphorylated compounds adenosine triphosphate, 2.
Although glyconeogenesis is hipoflsfatemia important mechanism of adaptation to nutritional deprivation, it contributes to a loss in muscular mass, water, and minerals.
Nevertheless, the serum level of phosphorus, along with other depleted ions, is kept at normal levels as a result of adjustments to metabolism. In severe malnutrition, daily phosphorus requirements drop, most likely owing to low ingestion, inhibiting the secretion of parathyroid hormone and stimulating calcitonin release, thereby promoting reductions in renal excretion, increases in intestinal absorption, and bone reabsorption.
With the commencement of hipofosfatemiaa, carbohydrates become the main energy source, increasing insulin secretion, which in turn stimulates the uptake of glucose, phosphorus, potassium, magnesium, and water by the cell for anabolism.
A combined decrease in the body’s stores during fasting, together with increased flow of ions and water to the interior of the cell, promotes the onset of hypophosphatemia, hypocalcemia, hypomagnesemia, and edema, which characterize refeeding syndrome.
In order to prevent refeeding syndrome, it is recommended that intake of energy, liquids and electrolytes be made gradually, particularly over the first week, during which most complications tend to take place. Adequate volemia and caloric intake should be achieved slowly so as to hipkfosfatemia cardiac overload and rapid electrolyte changes. Hypophosphatemia has also been associated with sepsis, which has increased incidence during the first 24 hours of hospitalization.
However, the mechanisms involved in the genesis of hypophosphatemia during sepsis remain unclear.
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A number of authors have suggested using serum levels of phosphorus as an early diagnostic marker for sepsis in adults. Patients with severe head trauma are at a high risk of developing hypophosphatemia because of the multiple associated factors that can trigger this disorder, such as respiratory alkalosis and mannitol administration, dextrose solutions, antiacids, and sodium bicarbonate.
The authors pointed to increased renal losses due to polyuria and cellular redistribution of phosphorus as being possible physiopathological mechanisms to explain hypophosphatemia.
Drugs, such as furosemide, used for a prolonged period predispose patients to hypophosphatemia owing to increased urinary excretion of phosphorus 9,25 as a result of tissue redistribution and reduced intestinal hipfosfatemia. Hypophosphatemia is responsible for numerous deleterious consequences, especially in its severe form, hampering clinical recovery of the patient and being associated with morbidity and potential mortality.
Hypophosphatemia can trigger a reduction in hpiofosfatemia contractility of the myocardium, arrhythmias, and cardiomyopathies owing to a fall in the intracellular stores of adenosine triphosphate available for the cardiac muscle. Similarly, the lower availability of ATP for respiratory muscle contraction can explain the onset of acute hipofosfatemai insufficiency. Some authors have shown muscular depletion of phosphorus, through biopsies, in approximately half of those patients suffering from respiratory insufficiency due to a COPD diagnosis.
In the context of the hematological system, nfonatal decline in levels of 2. The neuromuscular dysfunction associated with hypophosphatemia may also be hipofosfatemix by tissue hypoxia, which leads to alterations in neurological function, irritability, confusion, paralysis, lethargy, paraesthesia, seizure, and coma.
Notwithstanding the lack of pediatric studies on hypophosphatemia concerning critically ill patients, and given that the only prospective study has shown the disorder to be transitory, the studies on adults have demonstrated that complications resulting from hypophosphatemia imply poorer clinical outcomes. It has been concluded that hypophosphatemia is a metabolic disorder of high prevalence in critically ill patients.
The hipofosfaatemia risk associated factors include refeeding, malnutrition, systemic inflammatory response syndrome, and the neonwtal of diuretics and steroids, and the most relevant clinical complications are related to cardiovascular and neuromuscular systems. Given the significant prevalence found in the pediatric studies analyzed, the frequent presence of risk factors in children in intensive care units, and the potential harmful effects on the clinical outcome of these patients, it is advisable to identify those cases of highest susceptibility for early diagnosis and intervention, thus allowing normal serum levels of phosphorus to be reestablished.
Hypomagnesemia and hypophosphatemia at admission in patients with severe head injury. Crit Car Med ;28 6: Hypophosphatemia in the emergency department therapeutics.
Am J Emerg Med ; The importance of the refeeding syndrome.
Hemodynamic and metabolic effects of rapid correction of hypophosphatemia in patients with septic shock. Thomas C, Fourrier F. National Academy of Science. Intravenous phosphate repletion regimen for critically ill patients with moderate hypophosphatemia. Crit Care Med ;23 7: Subramanian R, Khardori R. Pathophysiologic implications, clinical presentations and treatment.
Hypophosphatemia in malnourished children during refeeding. Effect of hypophosphatemia on diaphragmatic contractility in patients with acute respiratory failure. N Engl J Med ; Hypophosphatemia and phosphorus depletion in respiratory and peripheral muscles of patients with respiratory failure due to COPD. Association between hypophosphatemia and cardiac arrhythmias in the early stages of sepsis. Eur J Intern Med ;13 7: Ventricular tachycardia in acute myocardial infarction: South Med J ;87 1: Hypophosphatemia pathophysiology, effects and management on the intensive care unit.
Transient hypophosphataemia associated with acute infectious disease in paediatric patients. Scand J Infect Dis ; Severe hypophosphatemia in children with kwashiorkor is associated with increased mortality.
J Pediatr ; 6: High prevalence of hypophosphatemia in critically ill infants abstract. Ped Crit Care Med ;4 3: Refeeding syndrome with enteral nutrition in children: Clin Nutr ;21 6: