Soft Tissue Healing

Original Editor - Bo Hellinckx

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The Healing Process

The healing process after a muscle injury:

This classification is based on a treatment protocol of “Clanton et al.”  (Level of evidence: 3B) But is not indifferent from other classifications. It is possible that some phases overlap, dependable on the individual response to healing and the type of injury. Not every patient undergoes all phases to achieve a full rehabilitation.

1. PHASE 1: Acute phase: ( 1 to 7 days)
In this phase treatment exists out of the RICE-method. This method exists of Rest, Ice, Compression and Elevation. The main goal of this method is to minimize inflammation and pain. During the treatment with ice, a flexion and extension exercises are important but must be pain free (to prevent further injury).

2. PHASE 2: Subacute phase: (Day 3 to < 3 weeks)
This phase starts when signs of inflammation begin to reduce. Inflammation signs are heat, swelling, redness and pain. Muscle action is important to prevent muscle atrophy. When the patient has a full range of motion without any pain during this movement, concentric strength exercises can be done. When there is pain, the intensity must be immediately decreased.

3. PHASE 3: Remodeling phase: ( 1 to 6 weeks )
In this phase, the patient can begin with stretching exercises to avoid a decrease in flexibility of the hamstrings. Eccentric strengthening exercises can also be done in this stage. These exercises are heavier than concentric exercises. Therefore it is important that the muscle is already regenerated because otherwise, reinjury is possible.

4. PHASE 4: Functional phase: ( 2 weeks to 6 months)
The main goal in this stage is to return to sport without a reinjury. To accomplish this goal, the patients need to increase their strength, endurance, speed, agility, flexibility and proprioception until the normal values of patient. Sport specific activities are the best indicators for a patient who returns to his sport.

5. PHASE 5: Return to competition phase: ( 3 weeks to 6 months)
When a patient returns to the competition, it is important that he can avoid a reinjury. Only when the patient has a full range of motion, strength, coordination and psychological readiness, he is allowed to return to competition. A study reveals that a program consisting of progressive agility a trunk stabilization is effective in promoting return to sports and in preventing for reinjury. This program turned out to be less risky for acute reinjury than isolated stretching and strengthening exercises.

Inflammatory phase

The acute inflammatory response is of relatively brief duration and involves activities that generate exudates- plasma like fluid that exudes out of tissue or its capillaries and is composed of protein and granular leukocytes (white blood cells).

In the Chronic inflammatory response is of prolonged duration and involves the presence of nongranular leukocytes and the production of scar tissue.

The acute phase involves three mechanisms that act to stop blood loss from the wound:

1). Local vasoconstriction occurs, lasting a few seconds to as long as 10 min. Larger vessels constrict due to neurotransmitters and capillaries and smaller arterioles and venules constrict due to the influence of serotonin and catecholamines released from platelets. The resulting reduction in the volume of blood flow in the region promotes increased blood viscosity or resistance to the flow, which further reduces blood loss at the injury site.

2). The platelet reaction provokes clotting as individual cells irreversibly combine with each other and with fibrin to form a mechanical plug that occludes the end of a ruptured blood vessel. The platelets also produce an array of chemical mediators in the inflammatory phase: serotonin, adrenaline, noradrenaline, and histamine. Also ATP is use for energy in the healing process.

3). Fibrinogen molecules are converted into fibrin for clot formation through two different pathways. Following vasoconstriction, vasodilation is brought on by a local axon reflex and the complement and kinin cascades, approximately 20 proteins that normally circulate in the blood in inactive form become active to promote variety of activities essential for healing. Phagocytosis- is the activation of neutrophils and macrophages to rid the injured site debris and infectious agents. As the blood flows to the injured area slows, these cells are redistributed to the periphery, where they begin to adhere to the endothelial lining. Mast cells and basophils are also stimulated to release histamine, further promoting vasodilatation. Bradykinin also promotes vasodilation and increase blood vessel wall permeability, contributing to the formation of tissue exudates.

Approximately 1 hour postinjury, swelling, or edema, occurs as the vascular walls become more permeable and increased pressure within the vessels forces a plasma exudate out into the interstitial tissues. These only happen for a few minutes in cases of mild trauma, with a return to normal permeability in 20-30 minutes.

More severe traumas can results in a prolonged state of increased permeability, and sometimes result in delayed onset of increased permeability, with swelling not apparent until some time has elapsed since the original injury.
Mast cells are connective tissue cells that carry heparin, which prolongs clotting and histamine. Platelets and basophil leukocytes also transport histamine, which serves as a vasodilator and increases blood vessel permeability.

Bradykinin, a major plasma protease present during inflammation, increases vessel permeability and stimulates nerve endings to cause pain.

Maturation and remodeling(WEEKS TO MONTHS)

The ultimate endpoint following remodeling depends on the tissue type. In non-CNS tissue that undergoes primary healing, very little remodeling occurs because of the lack of ECM produced during repair. Secondary healing, in contrast, involves fiber alignment and contraction to reduce the wound size and to reestablish tissue strength. Complete recovery of original tissue strength is rarely obtained in secondary healing because repaired tissue remains less organized than noninjured tissue, which results in scar formation. Collagen-rich scars are characterized morphologically by a lack of specific organization of cellular and matrix elements that comprise the surrounding uninjured tissue. In CNS tissue where there is no repair or regeneration of injured neurons, there is also relatively little reestablishment of structural integrity in the region. Instead, during CNS remodeling, the glial scar around the lesion becomes denser as astrocytic processes become more intertwined and more or less isolates but does not repair the injured region.

Non-CNS Remodeling

Primary

Partial-Thickness Cutaneous Tissue Remodeling

Stabilized Bone Remodeling

PNS Remodeling

secondary

Full-Thickness Cutaneous Tissue Remodeling

Unstabilized Bone Remodeling

CNS Remodeling

Remodeling in the CNS is limited. Because of the need to protect the CNS from the body’s robust inflammatory responses, reactive astrocytic processes become further intertwined, forming a dense sheath around the wound site .