Despite the significant development and advancement in antibiotic therapy, life-threatening complication of infective diseases cause hundreds of thousands of deaths world. This paper updates some of the issues regarding the etiology and treatment of abdominal sepsis and summaries the latest guidelines as recommended by the Intra-abdominal Infection (IAI) Consensus (2017). Prognostic scores are currently used to assess the course of peritonitis. Irrespective of the initial cause, there are several measures universally accepted as contributing to an improved survival rate, with the early recognition of IAI being the critical matter in this respect. Immediate correction of fluid balance should be undertaken with the use of vasoactive agents being prescribed, if necessary, to augment and assist fluid resuscitation. The WISS study showed that mortality was significantly affected by sepsis irrespective of any medical and surgical measures. A significant issue is the prevalence of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae in the clinical setting, and the reported prevalence of ESBLs intra-abdominal infections has steadily increased in Asia. Europe, Latin America, Middle East, North America, and South Pacific. Abdominal cavity pathology is second only to sepsis occurring in a pulmonary site. Following IAI (2017) guidelines, antibiotic therapy should be initiated as soon as possible after a diagnosis has been verified.

Background: Despite recent advancements in antibiotic therapy and the progress made in critical care and modern diagnostic methods, acute mediastinitis continues to be a severe condition. Diagnosis and treatment: Acute mediastinitis can occur in the context of cardio-thoracic surgery, oesophageal perforations and oropharyngeal infections condition. Forty-five percent of oesophageal perforations occurs during simple endoscopy. Spontaneous perforation (Boerhaave syndrome) accounts for 15% of perforations, and twelve percent are due to the ingestion of foreign bodies. Other causes include blind or penetrating trauma, and circa 9% to intraoperative lesions. CT scan is the standard investigation that reveals direct signs of mediastinitis. The oral administration of contrast substances can underscore the level of oesophageal perforation. Conservative treatment is the first-choice treatment and surgical treatment is reserved only for specific situations. The principles of surgical treatment consist of drainage, primary suture, oesophageal exclusion with or without the application of oesophagectomy, endoscopic vacuum wound assisted therapy of the perforation and associated paraoesophageal mediastinal drainage and endoscopic stenting associated with drainage. Conclusions: The lowest mortality rate is recorded in patients with perforations diagnosed less than twenty-four hours after the onset of symptoms. Surgical treatment remains the gold standard especially in cases of thoracic and abdominal perforations while further investigations are mandatory before endoscopic stenting is carried out.

Background: Atherosclerosis is a progressive disease that results from endothelial dysfunction, inflammatory arterial wall disorder and the formation of the atheromatous plaque. This results in carotid artery stenosis and is responsible for atherothrombotic stroke and ischemic injury. Low-grade plaque inflammation determines biological stability and lesion progression. Methods: Sixty-seven cases with active perilesional inflammatory cell infiltrate were selected from a larger cohort of patients undergoing carotid endarterectomy. CD68+, iNOS2+ and Arg1+ macrophages and CD31+ endothelial cells were quantified around the atheroma lipid core using digital morphometry, and expression levels were correlated with determinants of instability: ulceration, thrombosis, plaque hemorrhage, calcification patterns and neovessel formation. Results: Patients with intraplaque hemorrhage had greater CD68+ macrophage infiltration (p = 0.003). In 12 cases where iNOS2 predominated over Arg1 positivity, the occurrence of atherothrombotic events was significantly more frequent (p = 0.046). CD31 expression, representing neovessel formation, correlated positively with atherothrombosis (p = 0.020). Conclusions: Intraplaque hemorrhage is often described against the background of an intense inflammatory cell infiltrate. Atherothrombosis is associated with the presence of neovessels and pro-inflammatory macrophages expressing iNOS2. Modulating macrophage polarization may be a successful therapeutic approach to prevent plaque destabilization.

Background: severe carotid artery stenosis is a major cause of ischemic stroke and consequent neurological deficits. The most important steps of atherosclerotic plaque development, leading to carotid stenosis, are well-known; however, their exact timeline and intricate causal relationships need to be more characterized. Methods: in a cohort of 119 patients, who underwent carotid endarterectomy, we studied the histological correlations between arterial calcification patterns and localization, the presence of the inflammatory infiltrate and osteopontin expression, with ulceration, thrombosis, and intra-plaque hemorrhage, as direct signs of vulnerability. Results: in patients with an inflammatory infiltrate, aphasia was more prevalent, and microcalcification, superficial calcification, and high-grade osteopontin expression were characteristic. Higher osteopontin expression was also correlated with the presence of a lipid core. Inflammation and microcalcification were significantly associated with plaque ulceration in logistic regression models; furthermore, ulceration and the inflammatory infiltrate were significant determinants of atherothrombosis. Conclusion: our results bring histological evidence for the critically important role of microcalcification and inflammatory cell invasion in the formation and destabilization of advanced carotid plaques. In addition, as a calcification organizer, high-grade osteopontin expression is associated with ulceration, the presence of a large lipid core, and may also have an intrinsic role in plaque progression.

Background: This study aimed to identify early postoperative complications after carotid endarterectomy and the factors that may influence their occurrence. Methods: This was an observational, analytical, prospective study conducted over a period of 3 years in 2 university hospitals in Târgu Mureș, Romania. One hundred nineteen patients who underwent carotid endarterectomy for severe carotid stenosis were included. Statistical analysis was used to identify the independent factors with a direct influence on the acute complications in the first 48 h after carotid endarterectomy. Results: We followed up on the acute postoperative complications occurring in the first 2 days after surgery. These were represented by a limited number of neurological complications and major neck hematomas. Among all comorbidities and risk factors, only advanced coronary artery disease (p = 0.05) and smoking (p = 0.03) were independent factors that directly influenced the occurrence of major neck hematomas. Operative time exceeding the median time of 90 minutes increased the risk of neurological complications (p = 0.02). The risk of major neck hematomas was also increased by preoperative treatment with anticoagulants (p = 0.01) and anticoagulants associated with antiplatelet therapy (p = 0.009). Conclusions: This study has identified factors such as advanced coronary artery disease, smoking, operative time, and anticoagulant therapy that may be independently associated with an increased risk of acute postoperative complications after carotid endarterectomy.