Acute Necrotizing Pancreatitis Post-Pancreatoduodenectomy
Savio George Barreto, Shailesh V. Shrikhande in Dilemmas in Abdominal Surgery, 2020
Postpancreatectomy acute pancreatitis has a pathophysiological course similar to acute pancreatitis due to gallstones or heavy alcohol consumption. The manifestation of Postpancreatectomy acute pancreatitis in the immediate postoperative period ranges from self-resolving inflammation to fulminant acute pancreatitis with multiple organ dysfunction syndrome and pancreatic necrosis. Post-pancreatoduodenectomy acute pancreatitis may be caused by duct obstruction during placement of sutures for the pancreaticojejunal anastomosis and/or due to local pancreatic ischemia caused by factors related to anatomical features, vascularization, and intraoperative hemodynamics. In post-pancreatoduodenectomy necrotizing pancreatitis, the treatment approach is guided by clinical signs and laboratory findings. In the case of the patient presented in the Case Scenario, the remnant pancreas post-pancreatoduodenectomy was soft. In patients with a soft pancreas and a non-dilated pancreatic duct, there is a significant risk of post-pancreatoduodenectomy acute pancreatitis and sepsis. Serum and drain amylase/lipase are helpful in determining patients at risk and in guiding a decision for re-exploratory laparotomy versus conservative treatment.
Septic Shock
Samuel M. Galvagno in Emergency Pathophysiology, 2003
Septic shock is a disease process characterized by a persistent, hyperdynamic, hypermetabolic state progressing to a gradual functional deterioration of multiple organs.1 Shock in general is a syndrome of generalized metabolic failure resulting from inadequate tissue perfusion; in septic shock, inadequate perfusion results from sepsis, bacteremia, or endotoxins. An estimated 400,000 cases occur each year worldwide with 100,000 cases treated in the United States anually.1 Septic shock is associated with an extremely high mortality: 30% in uncomplicated cases and over 80% in cases associated with multiple organ dysfunction syndrome.1,2 SEPSIS, SIRS, SEPTIC SHOCK It is often the case that the prehospital provider does not know whether septic shock, sepsis, or bacteremia is present until after definitive laboratory studies are performed. Since prompt recognition is always necessary to maximize survival, prehospital providers should be well-versed in the nomenclature pertaining to sepsis and related disorders. In an effort to mitigate the confusion regarding sepsis and associated syndromes, the Society of Critical Care Medicine Consensus Conference Committee and the American College of Chest Physicians revised the clinical categorization of sepsis to include SIRS, sepsis, and the varying degrees of septic shock.2 The revised definitions are explained in Figure 19-1.
Hypoxia Reperfusion Injury and Adhesion Molecules
Victor R. Preedy in Adhesion Molecules, 2010
Hypoxia reperfusion (HR) injury has been recognized to play a key role in the pathogenesis of many kinds of organ dysfunction. Ischaemia occurs in various clinical conditions such as myocardial infarction, stroke, peripheral vascular disease and hypovolumeic shock. It is important to restore the blood supply of the ischaemic organ, but sometimes reperfusion itself can cause tissue injury in excess of that caused by ischaemia alone. Reperfusion of ischaemic tissues is associated with microvascular dysfunction, manifested by enhanced leukocyte plugging in capillaries, and the migration of leukocytes into intrestisuum. Activated endothelial cells and leukocytes in all segments lead to the production and release of infl ammatory mediators (e.g., platelet-activating factor, tumour necrosis factor) and upregulate the expression of adhesion molecules that promote leukocyteendothelial cell adhesion. Once leukocytes reach the extravascular space, they exacerbate tissue injury by releasing oxygen free radicals and other destructive enzymes. Th e production of adhesion molecules in endothelium and leukocytes is regulated by a family of protein kinases, which are important signalling pathways during HR injury. Th e protein kinases initiate several interconnected intracellular enzyme reactions. Th e infl ammatory mediators released as a consequence of reperfusion also appear to activate endothelial cells in remote organs that are not exposed to the initial ischaemic insult. Th is distant response to HR can result in severe generalized infl ammatory response and can result in multiple organ dysfunction syndrome.
Optimal course of treatment in acute cardiogenic shock complicating myocardial infarction
Published in Expert Review of Cardiovascular Therapy, 2018
Sebastian Nuding, Karl Werdan, Roland Prondzinsky
ABSTRACT Introduction: About 5% of patients with myocardial infarction suffer from cardiogenic shock as a complication, with a mortality of ≥30%. Primary percutaneous coronary intervention as soon as possible is the most successful therapeutic approach. Prognosis depends not only on the extent of infarction, but also – and even more – on organ hypoperfusion with consequent development of multiple organ dysfunction syndrome. Areas covered: This review covers diagnostic, monitoring and treatment concepts relevant for caring patients with cardiogenic shock complicating myocardial infarction. All major clinical trials have been selected for review of the recent data. Expert commentary: For optimal care, not only primary percutaneous intervention of the occluded coronary artery is necessary, but also best intensive care medicine avoiding the development of multiple organ dysfunction syndrome and finally death. On contrary, intra-aortic balloon pump – though used for decades – is unable to reduce mortality of patients with cardiogenic shock complicating myocardial infarction.
Role of CCR2 and IL-8 in acute lung injury: a new mechanism and therapeutic target
Published in Expert Review of Respiratory Medicine, 2011
Yao Shen, Diane Wang, Xiangdong Wang
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe inflammatory lung diseases associated with very high mortality, and are the most common and earliest organ dysfunctions in the development of multiple organ dysfunction syndrome. The NIH estimates that more than 4.5 million people suffer from ALI/ARDS per year. Although the American–European Consensus Conference definition has been widely used for approximately 40 years, it still has some limitations that may impact on the conduct of clinical research and management of patients with ALI/ARDS. This article will focus on the role of CC chemokine receptor 2 and IL-8 in the pathogenesis and resolution in ALI/ARDS.
Mortality rate and pattern following carbamate methomyl poisoning. Comparison with organophosphate poisoning of comparable toxicity
Published in Clinical Toxicology, 2011
Byung Kook Lee, Kyung Woon Jeung, Hyoung Youn Lee, Yong Hun Jung
Context. Methomyl is a widely used carbamate insecticide. It is known that mortality rate is generally low in carbamate poisoning, but fatalities from methomyl poisoning have been reported. Nevertheless, there is no reported comparative outcome of methomyl and organophosphate poisoning of comparable toxicity concerning mortality rate and mortality pattern. Objective. This study aims to compare the mortality rate and pattern following methomyl poisoning with those after organophosphate poisoning of comparable toxicity. Material and methods. A retrospective study was conducted on patients with cholinesterase inhibitor poisoning admitted to our institution. Among a diverse group of cholinesterase inhibitors, we included patients who presented after ingesting methomyl or World Health Organisation hazard Class I organophosphate compounds. Patients were divided into two groups; the methomyl group and the Class I organophosphate group. Results. The methomyl group consisted of 17 patients, and the Class I organophosphate group consisted of 42 patients. Seven patients (41.2%) in the methomyl group presented with cardiac arrest, while none presented with cardiac arrest in the Class I organophosphate group (p < 0.001). In the methomyl group, patients who had not experienced cardiac arrest at presentation survived to discharge from hospital. Among the seven patients who presented with cardiac arrest, three died from multiple organ dysfunction syndrome after resuscitation from cardiac arrest. In the Class I organophosphate group, four patients died from pneumonia and complicating acute respiratory distress syndrome. Therefore, the mortality rate was 17.6% in the methomyl group and 9.5% in the Class I organophosphate group (p = 0.399). Conclusion. The mortality rate of methomyl poisoning was comparable to that of World Health Organisation Class I organophosphate poisoning. All died patients in the methomyl group experienced cardiac arrest, and died from multiple organ dysfunction syndrome after resuscitation from cardiac arrest.
Related Knowledge Centers
- Inflammation
- Systemic Inflammatory Response Syndrome
- Medicine
- Septic Shock
- Sepsis
- Homeostasis
- Organ