Increased insensible water loss in newborn infants nursed under radiant heaters.
(1/165)
Urine osmolality was studied in 38 babies nursed in conventional incubators or cots and 18 nursed under an overhead radiant heat shield. Among 50 babies receiving a similar fluid intake in the first 48 hours of life mean urinary osmolality was significantly higher in the radiant heater group. In babies weighing less than 1500 g a trend towards higher urinary osmolalities was recorded in those nursed under radiant heaters even though they had received amost double the fluid intake of the incubator group. Severe hypernatraemia occurred in four of the five babies weighing less than 1000 g who were nursed under radiant heaters but in none of the seven babies of similar birth weight nursed in incubators. These findings are consistent with previous observations of an increase in insensible water loss in babies nursed under radiant heaters and emphasise the importance of providing enough extra water for these infants and the need for close monitoring of their fluid balance. The latter may be done at the bedside by measuring urinary specific gravity with a hand refractometer. (+info)
Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake.
(2/165)
We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension. (+info)
Hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism.
(3/165)
We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca. (+info)
Neonatal hypernatremic dehydration associated with breast-feeding malnutrition: a retrospective survey.
(4/165)
BACKGROUND: Hypernatremic dehydration in neonates is a potentially devastating condition. Recent reports have identified breast-feeding malnutrition as a key factor in its pathophysiology. METHODS: Using a theoretical framework for breast-feeding kinetics, a retrospective chart review of all neonates less than 28 days of age who were seen at either British Columbia's Children's Hospital or the Vancouver Breastfeeding Centre between 1991-1994 was conducted to identify and classify possible causes of breast-feeding malnutrition among neonates who developed hypernatremic dehydration. RESULTS: Twenty-one cases hypernatremic dehydration were identified. Infant weight loss ranged from 8% to 30% of birth weight, and serum sodium levels ranged from 146 mmol/L to 207 mmol/L. In each case, maternal or infant factors (e.g., poor breast-feeding technique, lactation failure following postpartum hemorrhage and infant suckling disorders associated with cleft palate or ankyloglossia) that could interfere with either lactation or breast-feeding dynamics and account for insufficient breast milk intake were identified. INTERPRETATION: Prenatal and in-hospital screening for maternal and infant risk factors for breast-feeding malnutrition combined with early postpartum follow-up to detect excessive infant weight loss are important for the prevention of neonatal hypernatremic dehydration. (+info)
Hyponatremia and hypernatremia in the elderly.
(5/165)
Management of abnormalities in water homeostasis is frequently challenging. Because age-related changes and chronic diseases are often associated with impairment of water metabolism in elderly patients, it is absolutely essential for clinicians to be aware of the pathophysiology of hyponatremia and hypernatremia in the elderly. The sensation of thirst, renal function, concentrating abilities and hormonal modulators of salt and water balance are often impaired in the elderly, which makes such patients highly susceptible to morbid and iatrogenic events involving salt and water. Clinicians should use a systematic approach in evaluating water and sodium problems, utilizing a comprehensive history and physical examination, and a few directed laboratory tests to make the clinical diagnosis. Furthermore, clinicians should have a clear appreciation of the roles that iatrogenic interventions and lapses in nutrition and nursing care frequently play in upsetting the homeostatic balance in elderly patients, particularly those who are in longterm institutional and inpatient settings. (+info)
Isosorbide in treatment of infantile hydrocephalus.
(6/165)
This paper reports the experiences of the second clinical trial in the use of isosorbide in the treatment of 34 selected cases of infantile hydrocephalus of all types. Subject to careful biochemical monitoring of serum electrolyte, urea, and acid-base balance, treatment with 2 g/kg body weight 6-hourly is safe. Side effects are immediately eliminated by interrupting therapy. With lower dosage, prolonged maintenance therapy was possible, for as long as 11 months, without side effects and with need for much less frequent biochemical monitoring. Isosorbide effectively prevented the need for shunt therapy in 10 of 34 patients, including 3 infants with uncomplicated congenital hydrocephalus of moderate degree and infants whose hydrocephalus was associated with spina bifida and whose cerebral mantle was between 20 to 25 mm. In posthaemorrhagic and postmeningitic hydrocephalus valuable time was gained before shunt therapy until the infant and his CSF were fit for operation. (+info)
Successful treatment in the patient with serum sodium level greater than 200 mEq/L.
(7/165)
Hypernatremia developing in nonhospitalized adults is predominantly a disease of the elderly and mentally handicapped patients, possibly revealing inadequate nursing care of these patients. It has long been claimed that the duration of hypernatremia and its rate of correction are correlated with improvement in patients' neurologic status. Since there are only a handful of cases with serum sodium levels greater than 200 mEq/L until recently, it is not clear at what rate plasma sodium concentration can be safely normalized in severe hypernatremic patients. We report a case of severe hypernatremia with survival. This patient underwent rapid correction of serum sodium concentration during the management of this metabolic derangement using isotonic solution. (+info)
Hypokalaemia and paralysis.
(8/165)
It is not uncommon for patients to present to the emergency room with severe weakness and a markedly low plasma potassium concentration. We attempted to identify useful clues to the diagnosis of hypokalaemic periodic paralysis (HPP), because its acute treatment aims are unique. We retrospectively reviewed charts over a 10-year period: HPP was the initial diagnosis in 97 patients. Mean patient age was 29+/-1.1 and the male:female ratio was 77:20. When the final diagnosis was HPP (n=73), the acid-base state was normal, the urine K(+) concentration was low, and the transtubular K(+) concentration gradient (TTKG) was <3. In patients with thyrotoxic periodic paralysis (TPP) (n=39), hypokalaemia was very commonly accompanied by hypophosphataemia (1.9+/-0.1 mg/dl). A clinical diagnosis of sporadic periodic paralysis (SPP) was made if hyperthyroidism and a family history of HPP were both absent (n=29). One subgroup of patients with HPP had a severe degree of hypernatraemia (167+/-5.0 mmol/l, n=3). There were only two patients with familial periodic paralysis (FPP). In 24 patients, the initial diagnosis was HPP, but subsequent studies failed to confirm this diagnosis. Each of these patients had an acid-base disorder, a high rate of renal K(+) excretion in the presence of hypokalaemia, and a TTKG of close to 7. With respect to therapy, much less K(+) was given to patients with HPP, yet 1:3 subsequently had a plasma K(+) concentration that eventually exceeded 5.0 mmol/l. Using plasma acid-base status, phosphate and K(+) excretion parameters allows a presumptive diagnosis of HPP with more confidence in the emergency room. (+info)