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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.amjsurg.2005.08.022 Byline: Vered Avidan (a), Moshe Hersch (b), Yaron Armon (a), Ram Spira (a), Dvora Aharoni (c), Petachia Reissman (a), William P. Schecter (a)(d) Keywords: Blast injury; Acute lung injury; Barotrauma; Explosions Abstract: Blast lung injury (BLI) is a major cause of morbidity after terrorist bomb attacks (TBAs) and is seen with increasing frequency worldwide. Yet, many surgeons and intensivists have little experience treating BLI. Jerusalem sustained 31 TBAs since 1983, resulting in a local expertise in treating BLI. Author Affiliation: (a) Department of Surgery, Sharee Zedek Medical Center, Jerusalem, Israel (b) Department of Anesthesiology and Intensive Care, Sharee Zedek Medical Center, Jerusalem, Israel (c) Department of Radiology, Sharee Zedek Medical Center, Jerusalem, Israel (d) Department of Surgery, University of California, San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, 3A33, San Francisco, CA 94110, USA Article History: Received 8 April 2005; Revised 8 August 2005

Forty six people were injured by a large explosive charge detonated in a Jerusalem bus. Four were killed instantaneously and 22 needed hospital care. We describe our experience in five patients with blast lung injury (BLI), all of whom survived in spite of severe respiratory failure requiring mechanical ventilation. Disseminated intravascular clotting (DIC) developed in three of the five patients and significant hypopotassemia ranging from 2.2 to 2.9 mEq/L in four. These two complications have not been previously described in association with BLI. Both DIC and hypopotassemia responded to replacement therapy. Vigorous treatment of respiratory failure, early recognition, and prompt correction of hemostatic and electrolyte abnormalities may have contributed to the avoidance of fatalities among the five patients with severe blast injury.

The potential for significant interaction between PEEP and the peripheral microcirculations is not as well appreciated as are its central circulatory effects. Therefore, we studied the effects of PEEP, 15 mm Hg, on microvascular fluid flux in the hindlimb of ten mature sheep. Changes in prefemoral lymph flow ( Q˙l) and in lymph to plasma [L/P] total protein (TP) ratios were measured following the application of PEEP for 2 h, before and during hyperdynamic sepsis. Sepsis was induced by cecal ligation and perforation (CLP). Although the onset of sepsis was not associated with an increase in prefemoral Q˙l, the [L/P] ratio of iodinated 125I human serum albumin (125I-HSA) was significantly greater 72 h after CLP than during the nonseptic baseline study. Histologic examination of gastrocnemicus muscle also demonstrated an increase in protein-rich interstitial edema during the septic studies. During the 2 h of PEEP, prefemoral Q˙lincreased equally (p<0.05) in three study periods: (1) baseline nonseptic, Δ Q˙l=+1.2±1.4 ml/h; (2) septic period 1, 24 to 48 h after CLP, Δ Q˙l=+ 1.3±L2 ml/h; and, (3) septic period 2, 72 h after CLP, Δ Q˙l=1.0±0.6 ml/h. Calculated microvascular hydrostatic pressures also rose significantly during PEEP therapy in all three study periods. We conclude that PEEP, 15 mm Hg, increased hindlimb microvascular fluid flux and may thereby increase interstitial fluid content in tissues drained by the prefemoral lymph node. These effects of PEEP were not aggravated by hyperdynamic sepsis, despite a presumed increase in systemic microvascular permeability at this time.