Page 147 - Textbook of Pathology, 6th Edition

form of injury, the blood flow may be re-established in 3-5 These features, thus, elicit the classical signs of inflam- 131
seconds while with more severe injury the vasoconstriction mation—redness, heat, swelling and pain.
may last for about 5 minutes.
2. Next follows persistent progressive vasodilatation which Altered Vascular Permeability
involves mainly the arterioles, but to a lesser extent, affects PATHOGENESIS. In and around the inflamed tissue, there
other components of the microcirculation like venules and is accumulation of oedema fluid in the interstitial compart- CHAPTER 6
capillaries. This change is obvious within half an hour of ment which comes from blood plasma by its escape through
injury. Vasodilatation results in increased blood volume in the endothelial wall of peripheral vascular bed. In the initial
microvascular bed of the area, which is responsible for stage, the escape of fluid is due to vasodilatation and
redness and warmth at the site of acute inflammation. consequent elevation in hydrostatic pressure. This is
3. Progressive vasodilatation, in turn, may elevate the local transudate in nature. But subsequently, the characteristic
hydrostatic pressure resulting in transudation of fluid into inflammatory oedema, exudate, appears by increased
the extracellular space. This is responsible for swelling at vascular permeability of microcirculation. The differences
the local site of acute inflammation. between transudate and exudate, are already summarised
4. Slowing or stasis of microcirculation follows which in Table 4.1 (see page 96).
causes increased concentration of red cells, and thus, raised The appearance of inflammatory oedema due to increased
blood viscosity. vascular permeability of microvascular bed is explained on Inflammation and Healing
the basis of Starling’s hypothesis. In normal circumstances,
5. Stasis or slowing is followed by leucocytic margination
or peripheral orientation of leucocytes (mainly neutrophils) the fluid balance is maintained by two opposing sets of forces:
along the vascular endothelium. The leucocytes stick to the i) Forces that cause outward movement of fluid from
vascular endothelium briefly, and then move and migrate microcirculation are intravascular hydrostatic pressure and
through the gaps between the endothelial cells into the colloid osmotic pressure of interstitial fluid.
extravascular space. This process is known as emigration ii) Forces that cause inward movement of interstitial fluid
(discussed later in detail). into circulation are intravascular colloid osmotic pressure and
The features of haemodynamic changes in inflammation hydrostatic pressure of interstitial fluid.
are best demonstrated by the Lewis experiment. Lewis Whatever little fluid is left in the interstitial compartment
induced the changes in the skin of inner aspect of forearm is drained away by lymphatics and, thus, no oedema results
by firm stroking with a blunt point. The reaction so elicited normally (Fig. 6.2,A). However, in inflamed tissues, the
is known as triple response or red line response consisting of endothelial lining of microvasculature becomes more leaky.
the following (Fig. 6.1): Consequently, intravascular colloid osmotic pressure
i) Red line appears within a few seconds following stroking decreases and osmotic pressure of the interstitial fluid
and is due to local vasodilatation of capillaries and increases resulting in excessive outward flow of fluid into
venules. the interstitial compartment which is exudative inflammatory
ii) Flare is the bright reddish appearance or flush surroun- oedema (Fig. 6.2,B).
ding the red line and results from vasodilatation of the MECHANISMS OF INCREASED VASCULAR PERME-
adjacent arterioles. ABILITY. In acute inflammation, normally non-permeable
iii) Wheal is the swelling or oedema of the surrounding skin endothelial layer of microvasculature becomes leaky. This is
occurring due to transudation of fluid into the extra- explained by one or more of the following mechanisms which
vascular space. are diagrammatically illustrated in Fig. 6.3.

Figure 6.1 A, ‘Triple response’ elicited by firm stroking of skin of forearm with a pencil. B, Diagrammatic view of microscopic features of triple
response of the skin.