ABSTRACT
INTRODUCTION: While acute appendicitis is a common surgical problem, the simultaneous occurrence of appendicitis and an infected iliac artery pseudoaneurysm is exceedingly rare. We report the successful treatment of an infected right external iliac artery pseudo aneurysm in the 1setting of acute appendicitis. PRESENTATION OF CASE: The patient is an 83-year-old male who presents with severe sepsis, right lower quadrant and right leg pain. Additional past medical history is significant for rectal cancer status post resection and radiation therapy in 1997. Computed tomography (CT) on admission revealed a right iliopsoas muscle abscess, an inflamed Appendix and a pseudo aneurysm arising from the right external iliac artery. After consultations by multiple specialties, the plan was to proceed with percutaneous drainage of the abscess, antibiotic therapy and subsequent repair of the pseudoaneurysm. CT guided drainage of the iliopsoas abscess was performed with return of hemorrhagic fluid. Due to the concern of contained pseudoaneurysm rupture, the patient was taken for expedited repair. Due to the patient's frailty and hostile abdomen, we performed embolization of the right external iliac artery pseudoaneurysm with Amplatzer I plugs (St. Jude Medical, St. Paul MN) and left common femoral to right superficial femoral bypass with cryopreserved cadaveric femoral vein. Following pseudoaneurysm exclusion, continued percutaneous drainage and antibiotic therapy, the patient has done well with no further evidence of infection. CONCLUSION: Repair of infected pseudo aneurysms can prove challenging. Ongoing infection, a hostile surgical abdomen and patient frailty further complicates the treatment of these patients. This case displays a minimally invasive approach to this rare but morbid condition.
ABSTRACT
We tested if vagus nerve stimulation (VNS) would prevent gut injury, mesenteric lymph toxicity, and systemic multiple organ dysfunction syndrome following trauma-hemorrhagic shock (T/HS). Four groups of experiments were performed. The first tested whether VNS (5 V for 10 min) would protect against T/HS-induced increases in gut and lung permeability as well as neutrophil priming. In the second experiment, mesenteric lymph was collected from rats subjected to T/HS or trauma-sham shock with or without VNS and then injected into naive mice to assess its biologic activity. Lung permeability, neutrophil priming, and red blood cell deformability were measured. Next, the role of the spleen in VNS-mediated protection was tested by measuring gut and lung injury in splenectomized rats subjected to sham or actual VNS. Lastly, the ability of nicotine to replicate the gut-protective effect of VNS was tested. Vagus nerve stimulation protected against T/HS-induced gut injury, lung injury, and neutrophil priming (P < 0.05). Not only did VNS limit organ injury after T/HS, but in contrast to the mesenteric lymph collected from the sham-VNS T/HS rats, the mesenteric lymph from the VNS T/HS rats did not cause lung injury, neutrophil priming, or loss of red blood cell deformability (P < 0.05) when injected into naive mice. Removal of the spleen did not prevent the protective effects of VNS on gut or lung injury after T/HS. Similar to VNS, the administration of nicotine also protected the gut from injury after T/HS. Vagus nerve stimulation prevents T/HS-induced gut injury, lung injury, neutrophil priming, and the production of biologically active mesenteric lymph. This protective effect of VNS was not dependent on the spleen but appeared to involve a cholinergic nicotinic receptor, because its beneficial effects could be replicated with nicotine.
