The treatment of malignant endobronchial obstruction with laser ablation.

BACKGROUND: We compared a new endoscopic treatment for malignant endobronchial obstruction known as photodynamic therapy (PDT) with the more established therapy of neodymium: yttrium-aluminum garnet laser (Nd:YAG) therapy. METHODS: A retrospective review was conducted of the medical records at our institution from 1988 to 1999 of patients treated for bronchial obstruction by thermal laser vaporization (Nd:YAG) or by PDT using the tunable dye laser in combination with a light-sensitive dye (PDT). The Nd:YAG procedure vaporized the obstructing neoplasm, whereas the PDT procedure photoablated the obstruction. Thirty-day mortality and morbidity rates were analyzed for both treatment groups using chi-square analysis. RESULTS: Of the 102 patients who were suitable for review, 83 received treatment with the Nd:YAG laser and 19 patients received treatment with PDT. Morbidity rates were comparable in both groups (22% for Nd:YAG vs 31% for PDT; P > .05). Equally common complications in both groups were respiratory failure and hypoxemia. Five Nd:YAG patients (6%) died within 30 days after treatment (3 of respiratory failure, 2 of massive hemoptysis), whereas 2 patients (10%) in the PDT group (1 of massive hemoptysis, 1 of acute myocardial infarction) died (P > . 05). CONCLUSIONS: PDT and Nd:YAG have similar mortality and morbidity rates. In our experience, PDT is a better choice for the treatment of malignant bronchial obstruction because it is technically easier, potentially safer, and does not require general anesthesia.

Constitutive and stimulated expression of ICAM-1 protein on pulmonary endothelial cells in vivo.

The expression of intercellular adhesion molecule-1 (ICAM-1) on pulmonary endothelial cells after stimulus and subsequent binding of neutrophils is a first step leading to lung injury. A similar process may dictate the binding of tumor cells to the pulmonary endothelium during metastasis. We report the development of a new technique that allowed us to monitor the location and relative expression of ICAM-1 levels on the luminal surface of the pulmonary microvasculature in vivo. This technique uses intravital microscopy together with a two-step labeling procedure involving fluorescent microspheres. Constitutive expression of ICAM-1 was not detectable to a significant level by our model, but expression was observed after upregulation by the systemic administration of TNF alpha. Sprague-Dawley rats were injected with 0-5.0 micrograms/kg TNF alpha and ICAM-1 expression was monitored through 24 hr. ICAM-1 expression was related to both the dose of TNF alpha administered and the time elapsed between injection of TNF alpha and observation. Injection of 5 micrograms/kg TNF alpha caused upregulation of ICAM-1 protein expression from 0.30 +/- 2.76 binding events/175,000 microns2 to 62.6 +/- 5.48 through 4 hr observation, after which levels returned to near baseline within 24 hr. The delay required for maximal expression is likely related to the time required for the cell to respond to the stimulus and generate ICAM-1 protein. Reductions in the relative numbers of ICAM-1 protein expressed between 4 and 24 hr in vivo are likely a result of protein turnover after the initial stimulus.