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Multisystem organ failure (MSOF) is the major cause of late death following trauma. The gut is hypothesized to be the source of an ongoing systemic inflammatory response that drives MSOF. It has also been suggested that while a single physiologic insult might not reliably cause MSOF, the addition of a delayed second stress will. This is known as the "two-hit" theory. The purpose of this study was to investigate the two-hit theory by observing the hemodynamic and bacteriologic response to a second stress in a subacute pig model of hemorrhagic and endotoxic shock. Swine (n = 18, 30-40 kg) were fed an antibiotic-free diet for 14 days. During instrumentation and experimentation on days 1 and 3, all animals were anesthetized (ketamine, isofluorane). On day 1, all animals had placement of central venous and arterial catheters, a portal venous catheter, and superior mesenteric artery flow probe. Group E (n = 6) underwent instrumentation on day 1, then infusion of endotoxin (25 mcg/kg E. coli lipopolysaccharide) on day 3. Group HE (n = 7) underwent instrumentation then hemorrhagic shock (mean arterial pressure = 40 mm Hg for 4 hours) on day 1, then infusion of endotoxin on day 3. Group H (n = 5) were instrumented and hemorrhaged on day 1, and underwent anesthesia only on Day 3. Between periods of anesthesia the animals were allowed food and water ad lib and systemic blood was sampled for culture every 12 hours. On day 5, the animals were euthanized prior to organ sampling for bacterial culture. One animal from group HE died during endotoxic shock on day 3.(ABSTRACT TRUNCATED AT 250 WORDS)

A 54 year-old man had symptoms of acute right hemispheric cerebral ischemia. He was initially considered for participation in a trial of early thrombolysis in stroke, but an innominate artery embolus was found with no apparent arterial source. The embolus was removed by means of a combined brachial and carotid bifurcation approach to protect the cerebral vasculature from embolic fragmentation during extraction. Further investigation revealed deep venous thrombosis, evidence of pulmonary emboli, and a patent foramen ovale, supporting a diagnosis of paradoxic embolus. Additional treatment included anticoagulation and placement of an inferior vena caval filter. The unusual condition of paradoxic embolus is reviewed, and the management of this patient is discussed.

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