Lower torso ischemia and reperfusion leads to both local and remote tissue injuries. The purpose of this study was to assess the role of complement in mediating the local and remote microvascular permeability after bilateral hind limb tourniquet ischemia. Four hours of ischemia and 4 hours of reperfusion produced an increased skeletal muscle permeability index (muscle/blood 125I albumin ratio) of 2.90 +/- 0.35 compared with the index in nonischemic muscle of 0.25 +/- 0.02 (p < 0.01). Muscle wet-to-dry-weight ratio increased from 3.93 +/- 0.04 in sham to 5.55 +/- 0.09 in ischemic muscle (p < 0.0001). Lung permeability rose at 4 hours as indicated by the increased bronchoalveolar lavage (BAL)/blood 125I albumin ratio 4.36 +/- 0.41 x 10(-3) versus sham 2.64 +/- 0.28 x 10(-3) (p < 0.05) and neutrophil sequestration 0.28 +/- 0.02 U/g myeloperoxidase (MPO) versus sham 0.14 +/- 0.02 U/g (p < 0.001). Serum lytic activity of the classical but not the alternate complement pathway was reduced. The soluble complement receptor (sCR1) was used to inhibit complement activity and attenuated the increase in the permeability index after reperfusion in ischemic muscle 1.11 +/- 0.08 (p < 0.01) and reduced the lung BAL/blood 125I albumin ratio to sham levels 2.46 +/- 0.39 x 10(-3) (p < 0.05) at 6 mg/animal, without reducing the lung neutrophil sequestration, 0.24 +/- 0.02 U/g. The authors conclude that complement activation occurred during tourniquet ischemia and mediated permeability changes in the ischemic muscle and the lungs during reperfusion.

Background: Sodium imbalances are among the most common electrolyte abnormalities encountered in the acute care setting. The syndrome of inappropriate anti-diuretic hormone (SIADH) and cerebral salt wasting (CSW) are characterized by hyponatremia and can be difficult to differentiate. Failure to accurately diagnose these conditions and implement the correct treatment results in an increased mortality risk, a longer length of stay in the hospital, and an increase in the cost of hospitalization. Objective: The purpose of this review is to summarize the key diagnostic findings in each disorder and to review the use of the fractional excretion of uric acid (FeUA) and the fractional excretion of phosphate as additional diagnostic measures to differentiate between SIADH and CSW. Observation: Publications from MEDLINE, CINAHL, and Google Scholar from 2009 through 2017 were reviewed. Articles were included if original data was presented and diagnosed either SIADH or CSW. Articles were excluded if they did not discuss diagnostic measures or were review articles. Results: Thirteen out of 51 publications met the inclusion criteria; four (31%) were clinical trials, seven (54%) were case reports, one (7.5%) was a prospective study and one (7.5%) was a retrospective-observational study. The populations studied, the etiologies causing hyponatremia, and diagnostic criteria used to distinguish between SIADH and CSW varied. Conclusion and Relevance: There is a need for consistent diagnostic criteria for SIADH and CSW. Based on current evidence, the use of FeUA and the fractional excretion of phosphate have consistently and accurately differentiated between SIADH and CSW.