Hyponatremia (<135 mmol/L), typically associated with an elevated anti-diuretic hormone level, is common among children admitted with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. The main consequences of acute hyponatremia include cerebral edema and Ayus-Arieff pulmonary edema. A widespread belief is that, in children with pneumonia or bronchiolitis, hyponatremia results from inappropriate anti-diuresis. By contrast, the pathogenic role of extracellular fluid volume depletion or decreased effective circulating blood volume is underscored. Considering the prevalence of hyponatremia, sodium determination is advised on admission in children diagnosed with bronchiolitis, pneumonia, or pulmonary exacerbation of cystic fibrosis. There is no necessity to do anything beyond reassessing the appropriateness of fluid therapy in cases with mild (130-134 mmol/L) hyponatremia. In children with sodium <130 mmol/L, the underlying etiology is sometimes evident from history and physical findings. Given that clinical assessment of fluid volume status is difficult in hyponatremia, further laboratory evaluation is often required in these patients. An increase in sodium level ≤6 mmol/L per day is currently considered the therapeutic goal in all cases. Emergency correction with a 2 mL/kg body weight bolus of 3.0% saline over 10-15 min intravenously is advised in cases with severe symptoms due to hyponatremia and in cases with symptoms, even if mild, due to a rapid-onset (<48 h) of hyponatremia (two additional doses are administered if the patient's condition does not improve).
BackgroundIntravenous fluids are commonly prescribed in childhood. 0.9 % saline is the most-used fluid in pediatrics as resuscitation or maintenance solution. Experimental studies and observations in adults suggest that 0.9 % saline is a poor candidate for fluid resuscitation. Although anesthesiologists, intensive care specialists, perioperative physicians and nephrologists have been the most active in this debate, this issue deserves some physiopathological considerations also among pediatricians.ResultsAs compared with so-called “balanced” salt crystalloids such as lactated Ringer, administration of large volumes of 0.9 % saline has been associated with following deleterious effects: tendency to hyperchloremic metabolic acidosis (called dilution acidosis); acute kidney injury with reduced urine output and salt retention; damaged vascular permeability and stiffness, increase in proinflammatory mediators; detrimental effect on coagulation with tendency to blood loss; detrimental gastrointestinal perfusion and function; possible uneasiness at the bedside resulting in unnecessary administration of more fluids. Nevertheless, there is no firm evidence that these adverse effects are clinically relevant.ConclusionsIntravenous fluid therapy is a medicine like insulin, chemotherapy or antibiotics. Prescribing fluids should fit the child’s history and condition, consider the right dose at the right rate as well as the electrolyte levels and other laboratory variables. It is unlikely that a single type of fluid will be suitable for all pediatric patients. “Balanced” salt crystalloids, although more expensive, should be preferred for volume resuscitation, maintenance and perioperatively. Lactated Ringer appears unsuitable for patients at risk for brain edema and for those with overt or latent chloride-deficiency. Finally, in pediatrics there is a need for new fluids to be developed on the basis of a better understanding of the physiology and to be tested in well-designed trials.
Guidelines on the diagnosis and management of urinary tract infections in childhood do not address the issue of abnormalities in Na(+), K(+), Cl(-) and acid-base balance. We have conducted a narrative review of the literature with the aim to describe the underlying mechanisms of these abnormalities and to suggest therapeutic maneuvers. Abnormalities in Na(+), K(+), Cl(-) and acid-base balance are common in newborns and infants and uncommon in children of more than 3 years of age. Such abnormalities may result from factitious laboratory results, from signs and symptoms (such as excessive sweating, poor fluid intake, vomiting and passage of loose stools) of the infection itself, from a renal dysfunction, from improper parenteral fluid management or from the prescribed antimicrobials. In addition, two transient renal tubular dysfunctions may occur in infants with infectious renal parenchymal involvement: a reduced capacity to concentrate urine and pseudohypoaldosteronism secondary to renal tubular unresponsiveness to aldosterone that presents with hyponatremia, hyperkalemia and acidosis. In addition to antimicrobials, volume resuscitation with an isotonic solution is required in these children. In secondary pseudohypoaldosteronism, isotonic solutions (such as 0.9 % saline or lactated Ringer) correct not only the volume depletion but also the hyperkalemia and acidosis. In conclusion, our review suggests that in infants with infectious renal parenchymal involvement, non-renal and renal causes concur to cause fluid volume depletion and abnormalities in electrolyte and acid-base balance, most frequently hyponatremia.
Hypotonic hyponatremia, a serious and recognized complication of any intracranial disorder, results from extra-cellular fluid volume depletion, inappropriate anti-diuresis or renal salt-wasting. The putative mechanisms by which intracranial disorders might lead to renal salt-wasting are either a disrupted neural input to the kidney or the elaboration of a circulating natriuretic factor. The key to diagnosis of renal salt-wasting lies in the assessment of extra-cellular volume status: the central venous pressure is currently considered the yardstick for measuring fluid volume status in subjects with intracranial disorders and hyponatremia. Approximately 110 cases have been reported so far in subjects ≤18 years of age (male: 63%; female: 37%): intracranial surgery, meningo-encephalitis (most frequently tuberculous) or head injury were the most common underlying disorders. Volume and sodium repletion are the goals of treatment, and this can be performed using some combination of isotonic saline, hypertonic saline, and mineralocorticoids (fludrocortisone). It is worthy of a mention, however, that some authorities contend that cerebral salt wasting syndrome does not exist, since this diagnosis requires evidence of a reduced arterial blood volume, a concept but not a measurable variable.
Aim Intramuscular or, more rarely, local drug injection is occasionally followed by immediate local pain, livedoid skin lesions and, some days later, the development of ischemic lesions. This very uncommon but potentially severe reaction, termed Nicolau syndrome, is traditionally associated with bismuth and β‐lactam antimicrobials. The aim of this report was to review the literature associating Nicolau syndrome with the administration of non‐steroidal anti‐inflammatory drugs. Methods The National Library, Excerpta Medica, Web of Science and Cochrane library databases were used. Results Sixty‐two cases (40 females and 22 males aged from 13 to 81, median 57 years) of Nicolau syndrome were published after 1992. Fifty‐three cases occurred after diclofenac. The remaining nine cases were associated with ketoprofen (N = 2), ketorolac (N = 2), phenylbutazone (N = 2), etofenamate (N = 1), ibuprofen (N = 1) and piroxicam (N = 1). Conclusion Although Nicolau syndrome is extremely uncommon, physicians must be aware of this complication after intramuscular administration of non‐steroidal anti‐inflammatory drugs and should avoid unnecessary injections.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.