Oedema and Infarction Overview

Oedema

• Oedema signifies increased fluid in interstitial tissue spaces
• Categorized based on pathophysiological mechanisms:
  • Increased hydrostatic pressure (e.g., deep vein thrombosis (DVT), congestive heart failure)
  • Reduced plasma oncotic pressure (e.g., nephrotic syndrome, cirrhosis)
  • Lymphatic obstruction (e.g., cancer, parasitic infections)
  • Sodium retention (e.g., kidney failure)
  • Inflammation

Morphology of Oedema

• Microscopically, oedema manifests as subtle cell swelling and separation of extracellular matrix elements.
• Oedema is easily identified macroscopically.
  • Subcutaneous oedema: finger pressure creates a pitting depression.
  • Periorbital oedema: swelling around the eyes.
  • Pulmonary oedema: lungs are significantly heavier, sectioning reveals frothy, blood-tinged fluid.
  • Brain oedema: brain appears swollen, with narrowed sulci and distended gyri.

Infarction

• An infarct is an area of ischemic necrosis due to blood supply blockage.
• Almost all infarcts (99%) are caused by thrombotic or embolic events involving arterial occlusion.
• Other causes include:
  • Local vasospasm
  • Extrinsic vessel compression (e.g., tumors)
• Infarcts are often wedge-shaped. If the base is a serosal surface (tissue lining body cavities like the lungs), sometimes an overlying fibrinous exudate is present. The lateral margins can reflect the pattern of vascular supply.
• Initially, infarcts are poorly defined and mildly hemorrhagic. Over time, margins become better defined, and eventually, the area is replaced by scar tissue.
• Different infarcts may be characterized based on colour (red vs. white) or presence of infection (septic vs. bland).

Morphology of Infarcts

• Wedge-shaped, with the base on the periphery and the apex towards the hilus (often showing the point of blockage in the tissue).
• Replaced by scar tissue; depressed on surface.

Classification of Infarcts

• Colour: Red (hemorrhagic) or white (anemic). Hemorrhagic infarcts occur with venous blockage, areas with dual blood circulation or reperfusion, or in organs with sluggish venous outflow. Anemic infarcts occur with arterial blockages in solid organs, with end arteries, where the tissue limits the amount of hemorrhage from neighbouring tissues.
• Infection: Septic (infected) or bland (not infected)

Septic Infarcts

• Develop when embolization of bacteria from a heart valve occurs, or when microbes seed a necrotic area.
• Converted to an abscess in these circumstances.

Histology of Infarcts

• The dominant characteristic of an infarct is ischemic coagulative necrosis.
• Most infarcts are ultimately replaced by scar tissue.
• The brain is an exception; ischemic injury often results in liquefactive necrosis in the central nervous system.

Shock

• Shock, or cardiovascular collapse, often results in potentially lethal clinical events.
• Causes often include hemorrhage, extensive trauma/burns, massive myocardial infarction, or massive pulmonary embolism.
• Can result from microbial sepsis.
• Shock characterizes systemic hypoperfusion (reduced blood flow to tissues) due to blood volume loss.
• Ultimately resulting in hypotension (low blood pressure), tissue perfusion impairment and cellular hypoxia, which often leads to organ failure.

Types of Shock

• Cardiogenic: myocardial pump failure
  • Intrinsic myocardial damage (infarct)
  • Ventricular arrhythmias
  • Extrinsic compression (e.g., cardiac tamponade)
  • Outflow obstruction (e.g., pulmonary embolism)
• Hypovolemic: blood or plasma volume loss (hemorrhage, fluid loss, trauma)
• Septic: systemic microbial infection
  • Most often from gram-negative bacteria (endotoxin production)
  • Occurs when bacteria invade bloodstream.
• Neurogenic: loss of vascular tone (anesthesia, spinal injury)
• Anaphylactic: hypersensitivity response. Leading to systemic vasodilation and increased vascular permeability. Characterized by blood pooling in peripheral vessels

Morphology of Shock

• Cellular and tissue changes from shock are related to hypoxic/ischemic injury.
• Changes can occur in any tissue. For example:
  • Heart: focal or widespread coagulation necrosis
  • Kidneys: extensive tubular ischemic injury (acute tubular necrosis)
  • Gastrointestinal tract: patchy mucosal hemorrhage and necrosis
  • Lungs: diffuse alveolar damage (shock lung)
  • Liver: fatty changes; central hemorrhagic necrosis.

This quiz covers key concepts related to oedema and infarction, including their pathophysiology and morphological characteristics. Learn about the different types of oedema, their causes, and how they can be identified both microscopically and macroscopically. Explore the implications of these conditions in the context of medical health.