Soft-tissue injury: pathophysiology
The effective treatment of fractures depends upon good softtissue management. Fractures with a soft-tissue injury must be considered as surgical emergencies. They need a sophisticated management protocol and an excellent grading system to achieve the goal of uncomplicated healing with complete restitution of function.
Open fractures and fractures with severe, closed soft-tissue damage are often associated with polytrauma. Life-saving treatment must always take priority and the surgeon must consider both the local injury and the whole patient. Evaluation of the fracture must determine the extent of the softtissue injury, which will be a key factor in management. The surgeon needs to be familiar with the pathophysiology of a soft-tissue injury and the timing, risks, and benefits of the different treatment options.
|Pathophysiology and biomechanics|
The condition of the wound after injury is determined by the following factors:
- type of insult and area of contact (blunt, penetrating, crushed, etc);
- force applied;
- direction of force;
- area(s) of body affected;
- wound contamination;
- general physical condition of the patient.
A combination of these factors will produce different types of wounds.
Types of wounds
Wounds do not only differ in their shape, but also in the type of treatment required and the prognosis for healing . All injuries cause bleeding and tissue destruction. This activates humoral and cellular mechanisms to stop bleeding and resist infection. The sequential healing process starts immediately after trauma and can be divided into three phases:
- exudative or inflammatory phase;
- proliferative phase;
- reparative phase.
|Pathophysiological responses in healing|
In the inflammatory phase, there is a massively increased interaction between leukocytes and the injured microvascular endothelium. Trauma exposes subendothelial collagen structures, leading to the aggregation of thrombocytes. These release serotonin, adrenaline, and thromboxane-A, causing vasoconstriction and producing cytokines such as platelet derived growth factor (PDGF) and transforming growth factor (TGF-β) that have a strong chemotactic and mitogenic effect on macrophages, polymorphonuclear neutrophils, lymphocytes, and fibroblasts. Vasoconstriction and thrombocyte aggregation contribute to the clotting and are an important part of the coagulation process to stop bleeding. As a side effect the damaged tissue is underperfused, leading to hypoxia and acidosis. The first cells to move from the small vessels into the damaged tissue are polymorphonuclear neutrophils (PMN) and macrophages. PMN are mobilized rapidly and produce an extremely vigorous initial response. The main function of the macrophages is the removal of necrotic tissue and microorganisms (phagocytosis and secretion of proteases) and the production and secretion of cytokines (PDGF: mitogenic and chemotactic; TNF-α: proinflammatory and angiogenic; β-FGF, EGF, PDGF, and TGF-β: mitogenic ).
Macrophages are responsible for the cytokine-induced early activation of immunocompetent cells, the inhibition and destruction of bacteria, and the removal of cell debris from the damaged tissue. However, the capacity of the macrophages for phagocytosis is limited. If their capacity is overloaded by an excessive amount of necrotic tissue, this will decrease the antimicrobial activities of the mononuclear phagocytes. Since these phagocytic activities are associated with superoxide production and high oxygen consumption, areas of hypoxia and avascular areas are especially threatened by infection. Thus, the pathophysiological rationale for performing radical surgical debridement of dead tissue is to support the phagocytic process of the macrophages [3, 4].
Chemotactic substances, such as kallikrein, improve vascular permeability and exudation by releasing the nanopeptide bradykinin that belongs to the α2-globulin fraction. Prostaglandins, originating from tissue debris, stimulate the release of histamine from mast cells and cause local hyperemia, which is necessary for the metabolic processes of wound healing. In addition, highly reactive oxygen and hydroxyl radicals are released during the peroxidation of membrane lipids , which cause a further destabilization of the cell membranes. These mechanisms result in an impairment of capillary endothelial permeability, which again promotes hypoxia and acidosis in the damaged areas. The infiltrating granulocytes and macrophages with their capacity to resist infection and to engulf cell debris and bacteria (physiological wound debridement) play a key role in the inflammatory response of traumatized tissue and therefore have a decisive effect on the subsequent reparative processes .
Proliferative and reparative phases
The proliferative phase begins when fibroblasts, followed by endothelial cells, migrate into the area of the wound and proliferate there. This is stimulated by mitogenic growth factors. These cells have a series of growth factor receptors on their surfaces and, by paracrine and autocrine processes, release several cytokines and synthesize the structural proteins of the extracellular matrix (collagen). Fibronectins—proteins detached from the surface of the fibroblasts by hydrolases—facilitate the bonding of type I collagen to α1-chains. This is an important prerequisite for progressive, reparative cell proliferation.
There is a smooth transition to the reparative phase and, simultaneously, the proliferating endothelial cells form ingrowing capillaries, the typical characteristic of granulation tissue. At the end of the reparative phase, water content is reduced and the collagen initially formed is replaced by crosslinked collagen type III. Fibrosis and scarring follow. The role of the growth factors in scar formation remains unclear, but it seems that TGF-β plays a decisive role [6, 7].
|Timing of surgery|
The timing of fracture surgery.
|Details of injury||Time of primary surgery||Procedure of primary surgery||Time of early reconstruction surgery||Definitive reconstruction surgery|
|Hemodynamically unstable||Immediate||Damage-control surgery|
|5–10 days “window of opportunity”||After 3 weeks|
ISS < 25
|Immediate||Early total care||-||-|
|Type I–IIIA||< 6 hours||Definitive fracture fixation||24–72 hours|
Debridement and soft-tissue coverage
|After 6–20 weeks|
Bone graft and softtissue management
|Type IIIB and IIIC||< 6 hours||Definitive fracture fixation or local damage control||24–72 hours|
Debridement and soft tissue cover and definitive fracture fixation
|Good soft tissues||1-3 days||Definitive fracture fixation||-||-|
|Poor soft tissues||< 24 hours||Local damage control, spanning external fixator||-||After 10–14 days|
Definitive fracture fixation
|Unstable fracture dislocation|
|Good soft tissues||Early||Definitive fracture fixation||-||-|
|Poor soft tissues||Immediate||Local damage control, spanning external fixator||-||After 10–14 days|
Definitive fracture fixation