Pathophysiology of acute pancreatitis
Pathophysiology of acute pancreatitis
复制标题
急性胰腺炎的病理生理学
DOI：
10.1007/bf01657986
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发表时间：
1981
影响因子：
2.6
通讯作者：
J. Trapnell
中科院分区：
文献类型：
--
作者：
J. Trapnell
急性胰腺炎的局部实质损害已被公认多年。这种损伤导致细胞外液大量渗漏，从而导致严重的血容量不足。它还产生疼痛，这是该疾病的主要临床特征。最近，自动消化过程已被确认为在腺体内和周围产生许多成分的“肉汤”，其具有血管活性和组织破坏性，并进而产生全身变化。这些变化会影响整个身体，并可能导致多器官损伤。凝血机制，心脏的行动，外周阻力，肝功能，以及肺，肾，脑和内分泌稳态机制都受到影响，这些模式及其临床意义进行了审查。当这种多系统衰竭以最常见的形式发生时，病人最好被描述为处于“酶休克”状态。这一假说不仅具有学术意义，它还提供了一个工作概念，为更科学地治疗急性胰腺炎奠定了基础。
Local parenchymal damage in acute pancreatitis has been well recognized for many years. This damage leads to a considerable leak of extracellular fluid and so to gross hypovolemia. It also produces the pain that is a major clinical feature of the disease. More recently, the autodigestive process has been recognized to generate, within and around the gland, a “broth” of many components that is vasoactive and tissue destructive and which, in turn, produces systemic changes. These changes affect the whole body and may lead to multiorgan damage. The coagulation mechanism, heart action, peripheral resistance, liver function, as well as the lungs, kidneys, brain, and endocrine homeostatic mechanism are all affected; these patterns and their clinical implications are reviewed. When this multisystem failure occurs in its severest form, the patient may best be described as in a state of “enzymic shock.” This hypothesis is not just of academic interest; it provides a working concept upon which to base a more scientific treatment of acute pancreatitis.