Traumatic intercostal arterial bleeding controlled with a novel surgical technique: a case report

<p>Abstract</p> <p>Introduction</p> <p>A blunt thoracic trauma may cause arterial bleeding requiring operative treatment or endovascular embolization or endovascular aortic stenting. A novel damage control technique to stop such bleeding is presented.</p> <p>Case presentation</p> <p>We present the case of an 82-year-old Caucasian man who experienced rib fractures I-VII on the left side and bleeding from damaged intercostal arteries after a blunt thoracic trauma. Emergency thoracotomy was performed.</p> <p>Conclusions</p> <p>Effective hemostasis was achieved by using a rolled surgical swab and inserting it against the chest wall next to the aorta with sutures pulled through the intercostal muscles and then sutured to the back side of the patient. The patient died four days after the surgery due to a head injury sustained in the car crash.</p

Analysis of cytokine immune response profile in response to inflammatory stimuli in mice with genetic defects in fetal and adult hemoglobin chain expression.

Injections of a crude fetal sheep liver extract (FSLE) containing fetal hemoglobin, MPLA, and glutathione (GSSH) reversed cytokine changes in aged mice. To investigate the role of fetal hemoglobin we derived mice with homzygous deletions for either of the two major βchains, Hgbβ &lt;sub&gt;ma&lt;/sub&gt; KO or Hgbβ &lt;sub&gt;mi&lt;/sub&gt; KO. Hgbβ &lt;sub&gt;mi&lt;/sub&gt; is the most prominent fetal Hgbβ chain, with Hgbβ &lt;sub&gt;ma&lt;/sub&gt; more prominent in adult mice. Mice lacking another fetal Hgb chain, HgbεKO, died in utero. CHO cells transfected with cloned Hgb chains were used to produce proteins for preparation of rabbit heteroantibodes. Splenocytes from Hgbβ &lt;sub&gt;ma&lt;/sub&gt; KO mice stimulated in vitro with Conconavalin A showed a higher IL-2:IL-4 ratio than cells from Hgbβ &lt;sub&gt;mi&lt;/sub&gt; KO mice. Following immunization in vivo with ovalbumin in alum, Hgbβ &lt;sub&gt;ma&lt;/sub&gt; KO mice produced less IgE than Hgbβ &lt;sub&gt;mi&lt;/sub&gt; KO mice, suggesting that in the absence of Hgbβ &lt;sub&gt;mi&lt;/sub&gt; KO mice had a predeliction to heightened allergic-type responses. Using CHO cells transfected with cloned Hgb chains, we found that only the fetal Hgb chain, Hgbε, was secreted at high levels. Secretion of Hgbβ &lt;sub&gt;ma&lt;/sub&gt; or Hgbβ &lt;sub&gt;mi&lt;/sub&gt; chains was seen only after genetic mutation to introduce the two N-linked glycosylation sites present in Hgbε, but absent in the Hgbβ chains. We speculated that a previously unanticipated biological function of a naturally secreted fetal Hgb chain may be partly responsible for the effects reported following injection of animals with fetal, not adult, Hgb. Mice receiving injections of rabbit anti-Hgbε but not either anti-Hgbβ &lt;sub&gt;ma&lt;/sub&gt; or anti-Hgbβ &lt;sub&gt;mi&lt;/sub&gt; from day 14 gestation also showed a bias towards the higher IL-2:IL-4 ratios seen in Hgbβ &lt;sub&gt;mi&lt;/sub&gt; KO mice