Abe Fingerhut, Ari Leppäniemi, Raul Coimbra, Andrew B. Peitzman, Thomas M. Scalea and Eric J. Voiglio (eds.)Emergency Surgery Course (ESC®) Manual10.1007/978-3-319-21338-5_4

4. Pathophysiology

Ari Leppäniemi¹

(1)

Chief of Emergency Surgery, Meilahti Hospital, University of Helsinki, Helsinki, Finland

Ari Leppäniemi

Email: Ari.Leppaniemi@hus.fi

4.1 Introduction

4.2 Hemorrhage

4.3 Contamination

4.4 Obstruction

4.5 Ischemia

4.6 Toxic Injury

4.7 Abdominal Compartment Syndrome (ACS)

4.8 Summary

Bibliography

Objectives

Characterize the pathophysiological processes in abdominal emergencies.
Categorize these processes into corresponding groups.
Outline the systemic and local consequences of these processes.
Link the consequences into the development of symptoms and signs.
Describe the primary aim of therapy in different pathophysiological conditions.

4.1 Introduction

Acute disease processes in the abdomen, whatever the cause, manifest in the vast majority of cases in a limited number of ways. These manifestations can be grouped according to the principal pathophysiological process and used as a guiding principle toward both diagnosis and therapy. Regardless of the organ or organ system involved, the clinical presentation of a specific pathological process in the abdomen is constant. Knowing the usual presentation of a disease, i.e., appendicitis, ruptured ectopic pregnancy, pelvic inflammatory disease, etc., allows early diagnosis, expeditious formulation of the principal goal of treatment, as well as understanding the natural course of the process if not interrupted by intervention that in most cases is surgical.

4.2 Hemorrhage

Acute extravasation of blood can:

Occur freely into the abdominal cavity (e.g., ruptured ectopic pregnancy or liver adenoma)
Be contained and confined to the retroperitoneal space (ruptured abdominal aortic aneurysm) or specific pathological cavity (bleeding pancreatic pseudocyst)
Bleed into a hollow organ such as the gastrointestinal (bleeding peptic ulcer), biliary, or urinary tract (renal tumor).

Depending on the amount of blood extravasated and speed of extravasation, the symptoms are dominated either by local irritation or compression caused by the blood and blood clot or by systemic manifestations of acute hypovolemia that, if untreated, can result in exsanguination of the patient.

If the bleeding stops spontaneously, the extravasated blood or clot can cause delayed problems in form of:

Compression on adjacent organs
Obstruction of hollow organs (urinary bladder tamponade)
Infected hematoma and subsequent abscess formation
Recurrent bleeding (at high risk if the underlying pathological process is not treated)

The main aim of treatment is to stop the bleeding, utilizing one or more of the following interventions:

Operation
Endoscopic procedure
Interventional radiology (angioembolization)

The urgency of treatment depends on the rate of bleeding. Hypovolemic shock is corrected with intravenous volume expansion avoiding complete normotension in uncontrolled hemorrhage, thus reducing the rate of bleeding and decreasing the risk of recurrent bleeding after spontaneous hemostasis. Extravasated blood is replaced with blood transfusion including clotting factors to maximize the chance of hemostasis that in most cases requires mechanical intervention to seal off the bleeding vessel.

4.3 Contamination

The sources of bacterial contamination in the abdominal cavity include:

Perforation of a hollow organ containing normal bacteria flora, such as the gastrointestinal tract (most common source of contamination)
Bacterial translocation through gangrenous intestine (gangrenous appendicitis, ischemic or gangrenous loop of bowel) or other hollow organ wall (gangrenous cholecystitis)
Previously contained abscess perforating into the free intraperitoneal space

Whether caused by translocation or frank perforation, the bacterial contamination will induce both a local and systemic inflammatory response.

Depending on the size and location of the perforation and the ability of the adjacent organs and the greater omentum to seal off the perforation, the condition can progress to:

Generalized secondary peritonitis
Walled-off inflammatory process followed either by resolution or formation of a mature abscess

Occasionally, the bacterial contamination is preceded by chemical contamination (e.g., perforated peptic ulcer) causing the initial reaction and symptoms, and the effects of bacterial contamination will manifest within the next few hours.

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