Emergency Medicine: Theory and Practice in China (1998 Volume)

Author: Chief Editor: Yan Bo et al
Publisher:
Publish Date: 1998-05-01
Features: Introduction This volume is compiled based on the theoretical and practical issues of emergency medicine in China, incorporating expert lectures from renowned emergency medicine specialists in China, as well as outstanding research papers, academic discussion papers, and research highlights recommended by provinces, municipalities, autonomous regions, and medical institutions nationwide for the current year. The volume brings together experts, scholars, and clinical healthcare workers from 30 provinces, municipalities, and autonomous regions, with the aim of addressing and resolving practical clinical problems. It is divided into 20 chapters, covering multiple organ dysfunction syndrome and failure, cardiac and respiratory arrest with cardiopulmonary resuscitation, shock, water, electrolyte, and acid-base imbalance disorders, acute abdominal pain, pre-hospital emergency care, internal medicine, surgery, obstetrics, pediatrics, emergency care in dentistry, ophthalmology, otolaryngology, infectious disease emergencies, poisoning emergencies, disaster medicine, emergency medicine diagnostic techniques, emergency techniques, integrated traditional Chinese and Western medicine, emergency medicine nursing, pharmaceutical research, drugs and clinical practice, and practical and theoretical issues of emergency medical systems and hospital management. In terms of content, the volume closely integrates theory and practice, focusing on solving practical problems based on clinical needs. Due to the varying conditions of hospitals and emergency centers (stations) across China, we have included both high-standard diagnostic and treatment methods and experiences from medical universities, as well as the experiences and lessons learned from grassroots healthcare workers utilizing local hospitals or health clinics for on-site emergency care and transport. This volume emphasizes urgent clinical diagnostic and treatment issues, highlighting the importance of practicality, the integration of theory with practice, and a balance between popularization and advancement. It serves as an excellent reference for emergency medicine specialists, attending physicians, and senior medical students. Excerpt: 3.1 The precise meaning of multiple organ dysfunction syndrome (MODS) – Definition – MODS is a sequential failure of multiple organ systems following acute severe infection or trauma. It must be distinguished from chronic diseases that lead to multiple organ failures over a long period, such as rheumatic heart disease, where cardiac failure is followed by liver and kidney failure, even though three organ systems are involved, this is not MODS but rather a complication of heart disease. Do not confuse them. 3.2 During severe infection or trauma, two major physiological changes occur in the body: impaired oxygen delivery and a significant increase in cytokine activity. This triggers acute respiratory distress syndrome (ARDS), leading to sequential multiple organ dysfunction syndrome. The mortality rate is very high. 3.3 Clinical recognition and emphasis on MODS began in the mid-1970s. Many issues related to pathogenesis, pathophysiology, and treatment have not yet reached consensus. Some experts even question the name of this critical illness. For example, in the past three years, some have proposed naming it "multiple organ dysfunction syndrome (MODS)." We believe there is no need to change it. For individual organ failure, such as heart failure, names such as "incomplete cardiac compensation" and "cardiac insufficiency" have been used. In the end, "heart failure" is still the most appropriate term. The same applies to "renal failure." 3.4 Severe acute abdominal pain can lead to the destruction of the intestinal barrier, i.e., impaired immunity. Additionally, other pathophysiological changes can cause severe systemic infection. These can trigger ARDS and subsequently MODS. For example, severe pancreatitis can directly cause hypoxemia and ARDS, ultimately leading to MODS. Conclusion To date, most scholars agree that severe infection and trauma are two major causes of ARDS. The main pathways leading to ARDS are impaired oxygen delivery and immune system damage. Acute severe pancreatitis can directly trigger ARDS due to subclinical disseminated intravascular coagulation and hypoxemia, leading to MODS. Acute intestinal infections, trauma, and obstruction can cause severe bloodstream infections and impair immune function, also triggering ARDS and MODS. Mortality rates are significantly higher. Therefore, when treating acute abdominal pain, no should be underestimated, as it may transform a relatively simple case into a complex critical illness. Ischemia/Reperfusion Injury – A New Frontier in Critical Care Basic and Clinical Research Jiang Jian1 In the past decade, emergency critical care medicine has advanced rapidly, particularly in critical care monitoring, diagnostic methods, and rescue measures, achieving remarkable progress. The establishment and development of intensive care units (ICUs) are clear indicators of this progress. The success rate of critical care rescue and prognosis have also improved. However, it is undeniable that many critical illnesses, such as severe infections, hemorrhagic shock, multiple traumas, adult respiratory distress syndrome, multiple organ dysfunction syndrome, and cardiac arrest, still face challenges in rescue. For example, high doses of antibiotics cannot control sepsis; restoring blood volume and using pressor drugs cannot reverse shock, or blood pressure may temporarily recover but the condition may worsen; cardiac arrest or severe trauma cardiopulmonary resuscitation may fail to achieve brain resuscitation, ultimately leading to death or a persistent vegetative state. The reasons are clearly complex, with some indeed due to severe conditions that are irreversible. However, there are also cases where a lack of sufficient understanding of the condition and its pathogenesis leads to the failure to take effective measures, allowing the condition to continue to develop and worsen. In recent years, research and progress in the mechanism of ischemia/reperfusion injury (I/R) have received widespread attention and have provided us with many insights. For diseases caused by various etiologies, it is not only necessary to recognize their primary damage and understand the uniqueness of each disease but also to emphasize the study of their secondary damage, recognizing the body's (host) chain reaction to pathogenic factors, which has universal significance, i.e., general patterns. Extensive basic and clinical research on I/R injury has provided new clues and hope for further understanding the pathogenesis of critical illnesses, improving treatment, and enhancing prognosis. 1. Ischemia/Reperfusion Injury 1.1 Introduction Ischemia can cause cellular damage or death, and the targeted treatment is to rapidly restore blood supply. After the establishment of coronary care units (CCUs), the mortality rate of acute myocardial infarction has decreased, and prognosis has improved, which is related to restoring coronary perfusion, salvaging ischemic myocardium, reducing the size of myocardial infarction, and controlling arrhythmias. However, with the simultaneous development of animal experiments and clinical research, tissue ischemia can also cause reperfusion injury after restoration of blood flow. As early as 1960, experiments found that temporarily ligating a branch of the dog's coronary artery (＞20min) and then restoring blood flow resulted in more severe myocardial necrosis compared to permanent ligation of the coronary artery branch. Moreover, more deaths due to ventricular fibrillation were observed [1]. Increasingly, experimental and clinical studies have shown that I/R injury can affect all organ systems in the body. I/R injury in the intestines and liver can cause multiple organ damage and failure in the liver, lungs, heart, and intestines [2, 3]; hemorrhagic shock can lead to microcirculatory failure and bacterial translocation [4, 5]; myocardial I/R can cause heart failure, myocardial "stunning," and arrhythmias [6, 8]; and renal failure after kidney transplantation are all associated with I/R-induced systemic inflammatory responses. I/R stimulation first leads to the expression of inflammatory mediators, activating polymorphonuclear neutrophils (PMNs) and vascular endothelial cells; activated PMNs adhere intermittently and roll over endothelial cells via L-Selectin and P-Selectin; PMNs' CD11/CD18 react with endothelial ICAM-1, causing firm adhesion between PMNs and endothelial cells; under the action of vascular extravasating chemokines, PMNs migrate extravasally; during migration, PMNs release proteases, toxic oxygen reaction products, etc., leading to tissue damage. (See Figure 1) 1.2 Systemic Inflammatory Response Syndrome (SIRS) The inflammatory response to severe sepsis is similar to I/R in many ways. Through the activation of the white blood cell system (PMNs, lymphocytes, monocytes), the direct action of bacterial toxins, and arachidonic acid metabolism, many inflammatory mediators and cytotoxins are released, leading to increased capillary permeability, platelet adhesion, fibrin deposition, PMN extravasation and degranulation, increased toxic oxygen reaction products, and ultimately tissue damage. (See Figure 2) Cell infection can cause irreversible damage and death of tissue cells, while post-infection sepsis, through a series of inflammatory responses in the body (even in the absence of cells), can also cause tissue cell damage and death. Antibiotics play a decisive role in controlling infection but have no therapeutic effect on post-infection sepsis. The inflammatory response to sepsis can continue to exist and develop. This damage caused by the body's (host) chain reaction to severe infection or non-severe trauma leads to the emergence of a new concept of disease, i.e., systemic or systemic inflammatory response syndrome [10–12]. Through this definition, our understanding of the disease has deepened. That is to say, any pathogenic factor, as long as it has sufficient intensity, not only can cause primary damage to the body's tissues but can also produce secondary damage by triggering the body's (host) chain reaction.