Restoring patency of long-term central venous access devices.

More patients are receiving extended and complex infusion therapies, so there is an increased need for long-term central venous access and the placement of "permanent" central venous access devices (CVADs). CVADs may be necessary for home parenteral nutrition and chronic intravenous antibiotics, chemotherapy, analgesia, and hydration therapies. The use of these catheters for multiple therapies increases the potential for catheter occlusion. Occlusions may be secondary to thrombosis, lipid deposits, or the precipitation of medications or minerals and electrolytes. Various pharmacologic agents have been used to restore patency of occluded CVADs. These agents include thrombolytics, ethyl alcohol, hydrochloric acid, and sodium bicarbonate. A thorough evaluation of the CVAD and the therapies administered via this catheter is necessary to select the most appropriate pharmacologic agent to restore catheter patency.

Chromium deficiency after long-term total parenteral nutrition.

A 63-year-old female developed unexplained hyperglycemia and glycosuria during administration of a total parenteral nutrition regimen on which she had been stable for several months. Because the patient had no history of diabetes or evidence of an infection, chromium deficiency was considered. Plasma chromium level was 0.1 microgram/dl (laboratory reference interval: 1.8-3.8 micrograms/dl). Fourteen days of supplemental intravenous chromium chloride (200 micrograms/day) allowed complete withdrawal of exogenous insulin with no further hyperglycemia or glycosuria. Correction of unexplained glucose intolerance following vigorous chromium supplementation indicates that the patient had chromium deficiency. Subsequent plasma chromium levels remained unchanged, possibly reflecting the sensitivity limits of the assay that was used, the uncertainty that exists regarding appropriate reference intervals for this element, and the fact that plasma levels do not always correlate with total body stores. The patient did not manifest peripheral neuropathy, which was present in one of the two previously reported cases, nor encephalopathy, which was reported in the other. We conclude that this patient developed chromium deficiency as a result of inadequate administration of chromium in the parenteral formula (6 micrograms/day) plus excessive enteric losses, and she presented with glucose intolerance as the only clinical manifestation of the deficiency. Caution should be exercised when interpreting plasma chromium in patients with suspected deficiency.