Hypernatremia and intravenous fluid resuscitation in collapsed ultramarathon runners.

OBJECTIVE: To determine if a return to normonatremia is required for symptomatology to resolve in collapsed hypernatremic runners and if intravenous (IV) administration of an isotonic solution would adversely affect serum sodium concentration ([Na+]) in collapsed normonatremic runners. DESIGN: Observational study. SETTING: 2006 Comrades Marathon. PARTICIPANTS: 103 collapsed runners. MAIN OUTCOME MEASURE: Final serum [Na] upon discharge. RESULTS: 58% of all collapsed runners were hypernatremic. Hypernatremic runners reported significantly more vomiting than normonatremic runners (79 versus 34%; P < 0.001). A significant decrease in serum [Na] in hypernatremic collapsed runners occurred after the IV administration of either 1 L of 0.45% normal saline (150.5 +/- 3.5 versus 148.0 +/- 4.6; P < 0.05) or Ringers lactate solution (147.7 +/- 2.2 versus 146.2 +/- 2.1; P < 0.05). One liter of IV fluid administration caused an increase in plasma volume that was not significantly different between (1) hypernatremic runners receiving a hypotonic solution (13.5 +/- 12.7%) and (2) normonatremic runners receiving an isotonic solution (15.6 +/- 11.3%). The final serum [Na+] of hypernatremic runners was above the range for normonatremia upon discharge (>145 mmol/L). CONCLUSIONS: A return to normonatremia was not required for hypernatremic runners to "recover" and be discharged from the medical tent. Vomiting either aggravated and/or facilitated the development of hypernatremia. IV administration of 1 L of either (1) a hypotonic solution to hypernatremic runners or (2) an isotonic solution to both normonatremic and hypernatremic runners did not produce any adverse biochemical or cardiovascular changes and can therefore be considered a safe and effective treatment for collapsed runners if used in this context.

Lethal non-rhizomelic dysplasia epiphysealis punctata.

We describe two new cases of a rare form of lethal chondrodysplasia punctata (so-called X-linked dominant, non-rhizomelic form), a condition characterized by widespread multicentric stippled calcifications of the cartilaginous parts of the long bones, spine, ribs and flat bones. The mother of one of the patients had bone dysplasia consistent with the X-linked dominant form of chondrodysplasia punctata. We suggest that a skeletal survey, including lateral view of the spine, together with biochemical studies of peroxisomal status are indicated in all newborns with severe, unusual forms of chondrodysplasia punctata. In this way, accurate categorization of the lethal, non-rhizomelic types of this condition will be facilitated.