Fatal microvascular pulmonary emboli from precipitation of a total nutrient admixture solution.

BACKGROUND: Paroxysmal respiratory failure and death occurred in two young adult females with pelvic infections. Autopsy revealed an amorphous material containing calcium obstructing the pulmonary microvasculature of each patient. Both patients received an identical total nutrient admixture (TNA) solution before their deaths. METHODS: Infusion of TNA into an animal model was undertaken in an effort to reproduce the clinical effect. Laboratory investigation was also performed to isolate a precipitate and identify the factors contributing to precipitation. RESULTS: A nonvisible precipitate containing calcium, phosphorus, and organic material was isolated from the TNA solution. Infusion of the formulation into healthy pigs resulted in sudden death within 4 hours. Alteration of the amino acid component, mix sequence, agitation technique, and mixing container influenced precipitate formation. CONCLUSION: Pulmonary embolization of a precipitate containing calcium phosphate resulted in the death of two patients. The pH of the amino acid component, transient elevation of calcium and phosphorus concentrations during mixing, and the lack of agitation during automated preparation of the formulation were identified as the etiologic factors producing the fatal precipitate.

Eosinophilic panniculitis.

Eosinophillic panniculitis is a poorly defined entity with variable clinical features. We report a case of rapidly enlarging, asymptomatic subcutaneous scalp nodules in a 6-year-old black boy with atopic dermatitis. The nodules resolved spontaneously over two to three days. Biopsy specimens were remarkable for eosinophilic panniculitis without evidence of epidermal change or vasculitis. We believe that this is the youngest reported patient with this disorder.

The in vitro effect on T cell function of soluble IL-2Ralpha from advanced ovarian cancer ascites.

Activated T cells not only secrete interleukin-2 (IL-2) and express cell surface interleukin 2 receptor alpha (IL-2R alpha), but also shed IL-2R alpha. This soluble receptor is a truncated form of the membrane-bound p55 receptor with a similar binding affinity. It has been proposed that soluble IL-2R alpha (sIL-2R alpha) could negatively modulate local immune response. High levels of sIL-2R alpha have been found in the serum and ascites of ovarian cancer patients. The purpose of this investigation is to determine the amount of in vitro T cell inhibition seen in ovarian cancer ascites that is attributable to high levels of sIL-2R alpha. Purified sIL-2R alpha at levels up to 100,000 pg/ml was placed in lymphocyte proliferation assays. Soluble IL-2R alpha was removed from the ascites of three patients with advanced ovarian cancer. Lymphocyte proliferation assays utilizing phytohemaglutin (PHA) stimulation were carried out with this ascites. Untreated ascites from each patient served as control. Addition of purified sIL-2R alpha to lymphocyte proliferation assays failed to demonstrate significant lymphocyte suppression. Addition of ascites to the lymphocyte assays resulted in up to an 80% decrease in lymphocyte proliferation. Neutralization of ascites sIL-2R alpha as well as removal of sIL-2R alpha via a protein G column failed to reverse any of the observed lymphocyte suppression. We conclude that although sIL2R alpha is elevated in ascites of patients with ovarian cancer, it does not account for the profound ascites-induced T cell suppression observed in vitro.