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Objectives: Immediate recognition of salt toxicity and aggressive resuscitative measures are critical in the treatment of this lethal poisoning. Despite heroic measures, pediatric deaths due to salt toxicity still occur from irreversible neurological damage. The objective of this article is to review the relevant literature and offer a therapeutic algorithm for the management of pediatric patients presenting with salt toxicity., Methods: A literature search for cases of salt toxicity was conducted. Articles in English that were available electronically through PubMed and Google Scholar were reviewed., Results: Nineteen cases and case series of salt toxicity were located using our search strategy. Salt poisoning has a distinct pathophysiology compared with hypernatremia, most notable for the lack of formation of idiogenic osmoles., Conclusions: The approach to treatment differs between salt toxicity and hypernatremia, focusing on rapid correction of serum osmolality rather than gradual normalization of serum sodium concentrations. Consultation of nephrology and child protection services are strongly recommended in the comprehensive treatment approach.

Background/objectives: There is an increasing public health concern regarding high salt intake, which is generally between 9 and 12 g per day, and much higher than the 5 g recommended by World Health Organization. Several relevant sectors of the food industry are engaged in salt reduction, but it is a challenge to reduce salt in products without compromising on taste, shelf-life or expense for consumers. The objective was to develop globally applicable salt reduction criteria as guidance for product reformulation., Subjects/methods: Two sets of product group-specific sodium criteria were developed to reduce salt levels in foods to help consumers reduce their intake towards an interim intake goal of 6 g/day, and—on the longer term—5 g/day. Data modelling using survey data from the United States, United Kingdom and Netherlands was performed to assess the potential impact on population salt intake of cross-industry food product reformulation towards these criteria., Results: Modelling with 6 and 5 g/day criteria resulted in estimated reductions in population salt intake of 25 and 30% for the three countries, respectively, the latter representing an absolute decrease in the median salt intake of 1.8-2.2 g/day., Conclusions: The sodium criteria described in this paper can serve as guidance for salt reduction in foods. However, to enable achieving an intake of 5 g/day, salt reduction should not be limited to product reformulation. A multi-stakeholder approach is needed to make consumers aware of the need to reduce their salt intake. Nevertheless, dietary impact modelling shows that product reformulation by food industry has the potential to contribute substantially to salt-intake reduction.

Background: Acute iodine excess in newborns can cause hypothyroidism, but there are limited data on the effects of iodine excess on thyroid function in older infants. The aim of this study was to measure the effects of chronic excess iodine intake on thyroid function in 6-24-month-old infants., Methods: In this cross-sectional study, infants (n=696) in eastern Nepal were studied. Spot urine samples, venous blood samples, and household salt samples were collected, and urinary iodine concentration (UIC), serum free thyroxine (fT4), thyrotropin (TSH), thyroglobulin (Tg), and titrated household salt iodine concentration (SIC) were measured. Daily iodine intake was calculated from UIC based on estimates of urine volume at this age., Results: Median (25th-75th percentile) household SIC was 89 (70-149) ppm, while national legislation stipulates a fortification level of 50 ppm. Median UIC was 407 (312-491) μg/L; 76% of infants had a UIC >300 μg/L, suggesting iodine excess. Calculated mean iodine intake in 12-24-month-old infants was 220 μg/day, exceeding the recommended safe upper limit for iodine at this age (200 μg/day). Among the infants, 15.8% had an elevated Tg, 7.4% had subclinical hypothyroidism, but <1% had overt hypothyroidism. UIC was not a significant predictor of thyroid function, thyroid hormones, or Tg., Conclusion: In 6-24-month-old infants exposed to excessive iodine intake, ∼7% have subclinical hypothyroidism but <1% have overt hypothyroidism. These findings suggest the thyroid in late infancy is already able to adapt to high iodine intakes and, in most cases, maintain euthyroidism.

Objective: We investigated the mechanism of antihypertensive effects of sodium alginate oligosaccharides, which are enzymatic products of high-molecular-weight natural alginate from seaweeds, in Dahl salt-sensitive (Dahl S) rats., Materials and Methods: Dahl S rats fed a high-salt (4% NaCl) diet were subcutaneously administered sodium alginate oligosaccharides (60 mg/day using a continuous osmotic mini-pump) for 14 days. Systolic blood pressure (SBP) was measured using the tail-cuff method, and we determined the influence of the alginate treatment on the metabolism of sodium by measuring sodium excretions in the feces and urine., Results: SBP increased in an age-dependent manner in the untreated Dahl S rats. Sodium alginate oligosaccharide treatment via the subcutaneous route almost completely abolished salt-induced hypertension in Dahl S rats fed a high-salt diet. The level of fecal or urinary sodium excretion did not significantly change during the treatment period with the alginate oligosaccharides. The reduction in SBP rapidly recovered after cessation of the treatment. Moreover, the level of urinary protein excretion was lower in the treated Dahl S rats than in the untreated rats during the experimental period., Conclusions: Our results suggest that sodium alginate oligosaccharides attenuate salt-induced hypertension in Dahl S rats not through reducing salt absorption, but probably through a direct action on vascular vessels.

Objective: We aimed to review the English and Chinese literature on Pa Ping and to confirm by personal interview the story of how its pathogenesis was uncovered., Background: In 1930, Dr. Alexander Stewart Allen noticed a pattern of illness arising in the region of Kiating, China. Area residents began presenting to local hospitals with nausea, vomiting, and diarrhea, and what emerged was a clinical picture of a gradual ascending paralysis that could result in death, termed Pa Ping. All 3 patients observed by Dr. Allen were male, had no family history of the disease, and had recently eaten before the onset of paralysis. Pa Ping developed in Dr. Allen himself, but he survived., Methods: Medical literature was reviewed for primary sources. Interviews of living descendants and friends of the doctors in China and North America were conducted and information was corroborated by written records., Results: Dr. Huang, with the National Central University College of Medicine, noticed a striking similarity between Pa Ping and familial periodic paralysis in 12 patients and reported 2 patients with Pa Ping treated with potassium citrate who experienced a reversal of the paralysis. Dr. K.T. Du analyzed meals of patients with Pa Ping seen by Dr. Zhe Tung and found barium in concentrations as high as 25.7%. This finding was confirmed by administering barium chloride to animals, which recapitulated the human syndrome., Conclusions: Although Dr. Huang had correctly noticed an underlying potassium depletion in patients with Pa Ping, the observations of Dr. Zhe Tung and Dr. K.T. Du ultimately established barium-induced hypokalemia as the underlying cause.

Although a plethora of reports on life-threatening complications of salt emesis has been published since the early 1960s, salt is still used to induce emesis in cases of intoxication in the clinical as well as in the domestic setting. We report three cases of fatal hypernatremia after salt was used as an emetic. All fatalities were subjected to medico-legal autopsy at the Institute of Legal Medicine in Hamburg, Germany. In all cases, symptoms of cerebral damage such as seizures, fever and somnolence developed within hours after salt ingestion. All individuals were admitted to hospital before their deaths. Here, severe hypernatremia (up to 245 mmol/l) was detected, and all patients died under the clinical picture of cerebral edema despite intensive medical treatment. At autopsy, unspecific signs of a central regulatory failure were present. Histology revealed crenated red blood cells and few venous microthrombi in internal organs. Neuropathological investigations yielded no specific results but confirmed fatal cerebral edema and excluded other cerebral causes of death. Viewing the results of clinical and post-mortem investigations together, death could clearly be attributed to excessive salt intake in all cases.

Fatal hypernatremia due to soy sauce ingestion is rare. We describe a 65-year-old woman who became unresponsive after ingesting 1150 ml of soy sauce. Her initial blood sodium concentration was 176 mEq/l. She was treated successfully with acute hemodialysis and her serum sodium concentration decreased to 146 mEq/l without any significant neurologic complication. We recommend hemodialysis is the best approach to correct severe hypernatremia.

Hypernatremia is a common electrolyte abnormality, but it is rarely attributable to excess sodium. Hypernatremia due to exogenous salt intake, caused either by accidental ingestion or as a form of child abuse, is rare, difficult to manage and results in high mortality. Although hypernatremia is easily recognized by laboratory tests, its etiology is often difficult to determine. A surprisingly small amount of salt intake can result in a fatal outcome. We report two cases of severe salt intoxication in two girls, aged 20 and 7 months, who presented with severe hypernatremia. Both had seizures after accidental salt ingestion. In the first case, salt instead of sugar was inadvertently added to two yoghurts, leading to hypernatremia and convulsions. In the second case, a mistake in the preparation of salt-saturated water as an oral rehydration solution provoked seizures, coagulopathy and longitudinal venous sinus thrombosis. Both cases developed encephalic death. We discuss the clinical course and the difficulties in the treatment of these cases in the context of the available literature.