Breastfeeding-associated hypernatremia: are we missing the diagnosis?

OBJECTIVES: To assess the incidence and complications of breastfeeding-associated hypernatremic dehydration among hospitalized neonates. STUDY DESIGN: A retrospective study was conducted at Children's Hospital of Pittsburgh over a 5-year period, to identify otherwise healthy term and near-term (> or =35 weeks of gestation) breastfed neonates (<29 days of age) who were admitted with serum sodium concentrations of > or =150 mEq/L and no explanation for hypernatremia other than inadequate milk intake. RESULTS: The incidence of breastfeeding-associated hypernatremic dehydration among 3718 consecutive term and near-term hospitalized neonates was 1.9%, occurring for 70 infants. These infants were born primarily to primiparous women (87%) who were discharged within 48 hours after birth (90%). The most common presenting symptom was jaundice (81%). Sixty-three percent of infants underwent sepsis evaluations with lumbar puncture. No infants had bacteremia or meningitis. Infants had hypernatremia of moderate severity (median: 153 mEq/L; range: 150-177 mEq/L), with a mean weight loss of 13.7%. Nonmetabolic complications occurred for 17% of infants, with the most common being apnea and/or bradycardia. There were no deaths. CONCLUSION: Hypernatremic dehydration requiring hospitalization is common among breastfed neonates. Increased efforts are required to establish successful breastfeeding.

Preventing neurological complications from dysnatremias in children.

Dysnatremias are among the most common electrolyte abnormalities encountered in hospitalized patients. In most cases, a dysnatremia results from improper fluid management. Dysnatremias can occasionally result in death or permanent neurological damage, a tragic complication that is usually preventable. In this manuscript, we discuss the epidemiology, pathogenesis and prevention and treatment of dysnatremias in children. We report on over 50 patients who have suffered death or neurological injury from hospital-acquired hyponatremia. The main factor contributing to hyponatremic encephalopathy in children is the routine use of hypotonic fluids in patients who have an impaired ability to excrete free-water, due to such causes as the postoperative state, volume depletion and pulmonary and central nervous system diseases. The appropriate use of 0.9% sodium chloride in parenteral fluids would likely prevent most cases of hospital-acquired hyponatremic encephalopathy. We report on 15 prospective studies in over 500 surgical patients that demonstrate that normal saline effectively prevents postoperative hyponatremia, and hypotonic fluids consistently result in a fall in serum sodium. Hyponatremic encephalopathy is a medical emergency that should be treated with hypertonic saline, and should never be managed with fluid restriction alone. Hospital-acquired hypernatremia occurs in patients who have restricted access to fluids in combination with ongoing free-water losses. Hypernatremia could largely be prevented by providing adequate free-water to patients who have ongoing free-water losses or when mild hypernatremia (Na>145 mE/l) develops. A group at high-risk for neurological damage from hypernatremia in the outpatient setting is that of the breastfed infant. Breastfed infants must be monitored closely for insufficient lactation and receive lactation support. Judicious use of infant formula supplementation may be called for until problems with lactation can be corrected.

Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.