**4. Classification**

Many classifications of muscle injuries have been performed in according with anatomical location, pathophysiological characteristics, clinical and radiological features (Tol et al., 2013) (Chan, N. Maffulli et al classification 2012) (The Munich Consensus Statement ). Depending on the muscular structures involved, muscle injuries are distinguished in intramuscular, myofascial, myofascial/perifascial and musculo-tendinous.

The **intramuscular** hematoma is characterized by the integrity of epimysium and by blood extravasation into the body of the muscle affected by the trauma. This causes an increasing of the intramuscular pressure with consequent compression of the capillary bed, which contrasts the bleeding; therefore clinical signs and symptoms remain localized. Since the presence of blood flow may cause an increase in the osmotic gradient, the swelling may increase more than 48 hours after the traumatic event. This change of the osmotic gradient causes a passage of the

The size of the effusion can be more or less conspicuous depending on the athlete's muscle status of contraction and on the athlete's characteristics of vascularization and coagulation characteristics.

Antitrombine III or C protein or S protein deficit, or quantitative abnormalities in Leiden V or VIII or IX factors or anti-coagulants therapies or massive anti-inflammatory drugs use . External

Many classifications of muscle injuries have been performed in according with anatomical location, pathophysiological characteristics, clinical and radiological features (Tol et al., 2013) (Chan, N. Maffulli et al classification 2012**. )** (The Munich Consensus Statement ). Depending on the muscular structures involved, muscle injuries are distinguished in intramuscular, myofascial,

We will only classify hematomas on the basis of their localization in intramuscular, intermuscular

Very influent in the severity of hematoma are inherited abnormalities of coagulation like

condition like a delayed or insufficient compression is important as well.

**4. CLASSIFICATION** 

myofascial/perifascial and musculo-tendinous**.**

treatment in superficial or deep. (Fig. 2)

tissues while, in a relaxed muscle, the structural damage and the consequent hematoma, generally occur in depth, nearest the bone. The severity of the lesion depends on the site of impact, the activation status of the muscles involved, the age of the patient, and the presence

**Figure 1.** Hamstring subcutaneous hematoma occurred in consequence to a muscle rupture after a sudden eccentric

The size of the effusion can be more or less conspicuous depending on the athlete's muscle status of contraction and on the athlete's characteristics of vascularization and coagulation. Very influent in the severity of hematoma are inherited abnormalities of coagulation like Antitrombine III or C protein or S protein deficit, or quantitative abnormalities in Leiden V or VIII or IX factors or anti-coagulants therapies or massive anti-inflammatory drugs use. External

Many classifications of muscle injuries have been performed in according with anatomical location, pathophysiological characteristics, clinical and radiological features (Tol et al., 2013) (Chan, N. Maffulli et al classification 2012) (The Munich Consensus Statement ). Depending on the muscular structures involved, muscle injuries are distinguished in intramuscular,

The **intramuscular** hematoma is characterized by the integrity of epimysium and by blood extravasation into the body of the muscle affected by the trauma. This causes an increasing of the intramuscular pressure with consequent compression of the capillary bed, which contrasts the bleeding; therefore clinical signs and symptoms remain localized. Since the presence of blood flow may cause an increase in the osmotic gradient, the swelling may increase more than 48 hours after the traumatic event. This change of the osmotic gradient causes a passage of the

condition like a delayed or insufficient compression is important as well.

myofascial, myofascial/perifascial and musculo-tendinous.

of fatigue.

204 Muscle Injuries in Sport Medicine

contraction

**4. Classification**

**Figure 2.** From Orthopaedic Sports Medicine: Principles and Practice Delee, Jesse C. M.D.; Drez, David Jr. Saunders Company, 1994 **Figure 2.** From Orthopaedic Sports Medicine: Principles and Practice Delee, Jesse C. M.D.; Drez, David Jr. Saunders Company, 1994

interstitial fluid through the muscle fascia, in order to balance the same osmotic gradient. This fact causes a further increase in the swelling of the injured muscle up to the limits of extensi‐ bility of the muscle fascia or the muscle itself. The main symptoms related to the onset of an intramuscular hematoma consists of pain, especially during the first 72 hours after the trauma and, after a few days, involve a decreased contractility and muscle functionality and extensi‐ bility. The prognosis for intramuscular hematomas is worse than for intermuscular hemato‐ mas, and experts' opinions suggest treating these with drainage in order to avoid potential post-traumatic myositis ossificans or fibrosis. The **intramuscular** hematoma is characterized by the integrity of epimysium and by blood extravasation into the body of the muscle affected by the trauma. This causes an increasing of the intramuscular pressure with consequent compression of the capillary bed, which contrasts the bleeding; therefore clinical signs and symptoms remain localized. Since the presence of blood flow may cause an increase in the osmotic gradient, the swelling may increase more than 48 hours after the traumatic event. This change of the osmotic gradient causes a passage of the interstitial fluid through the muscle fascia, in order to balance the same osmotic gradient. This fact causes a further increase in the swelling of the injured muscle up to the limits of extensibility of the muscle fascia or the muscle itself. The main symptoms related to the onset of an intramuscular hematoma consists of pain, especially during the first 72 hours after the trauma and, after a few days, involve a decreased contractility and muscle functionality and extensibility. The prognosis for

Although **intermuscular** hematomas appear initially more dramatic due to the resultant bruising and swelling, intramuscular hematomas are considered a more serious condition because the intact fascia creates an increasing of muscle pressure. 2

In intermuscular hematoma the muscle fascia looks damaged thereby allowing the extrava‐ sation of blood flow between muscles and fascia. This causes the formation of a more or less wide livid and swelling area. Contrary to the intramuscular hematoma, the intermuscular hematoma causes a painful symptoms limited to the first 24 hours post-trauma.

Finally in case of a **mixed** hematoma, after a first stage characterized by a temporary pressure increasing due to an extravasation, a rapid decrease in blood pressure can be observed. The swelling due to a blood extravasation appears usually after 24-48 hours, but after a sudden increase in pressure and swelling, the symptoms decrease and functional recovery is fairly rapid with an usually complete healing.

The knowledge of skeletal muscle regeneration principles and healing processes can help in respecting the timing for return to competitions (Klein, 1990).

Muscle repair is a multistep process which includes myofibers degeneration, regeneration and remodeling by acute inflammatory response (Clever JL, Sakai Y, Wang RA, Schneider DB 2010).

family of proteins controls the transcription of important muscle-specific proteins such as

The Treatment of Muscle Hematomas http://dx.doi.org/10.5772/56903 207

The MGF mechano-growth factor isoform appears to work by activating satellite cells MGF expresses the level of mechanical stress in muscles and other tissues and could have a impor‐

We extend these new findings to clinical practice to propose an evidence-based approach for the diagnosis and optimal treatment of skeletal muscle hematomas. Optimal treatment of skeletal muscle injuries start with the right diagnosis (Jarvinen et al., 2005). The clinical diagnosis of a surface hematoma is rather easy thanks to the detection of a bruised area of variable extension depending on the extent of the trauma, contextual to swelling and loss of muscle function. On the other hand, the clinical diagnosis of a deep hematoma may be much more complicated. In this case, the clinical diagnosis must necessarily be supported by the imaging consisting of ultrasonography and / or MR. However, the formulation of a precise and definitive diagnosis in case of an intramuscular hematoma, becomes possible only after 12-72 hours from the detrimental event, since the formation of the hematoma may also appear over three days after the trauma, thereby preventing a possible early diagnosis. A more detailed characterization of the injury can be made using imaging (ultrasound or MRI) repeated at second, seventh and fifteenth day, and certainly at the time of going back to aerobic

A decrease in swelling, a reduction in pain, in the appearance of an area in the first 24 hours post-traumatic and a recovery of muscle function, are indicators of a favorable prognosis. On the contrary, an increase or a persistent swelling after 48-72 hours, an increase in pain, a decrease of peripheral pulses, a prolonged or progressive limitation of joint caused by pain or muscle weakness, a numbness and a sense of / or paresthesia below the area of injury, are all

In any case, there is a better prognosis in the case of intermuscular compared intramuscular hematoma In case of intermuscular hematoma is possible an early mobilization and the patient returns to the sport activity between 1 and 10 weeks. On the contrary, the intramuscular hematoma, especially if is extended, requires greater caution in order to avoid the worrying complications, the myositis ossificans or the fibrosis. For this reason, in the case of intramus‐ cular hematoma, return to sport activity is generally not possible before a period of 10-20 weeks

The evaluation of the longitudinal size (measured in mm) is a more important severity predictor than the cross section of the lesion and the entity of the hematoma. Ultrasonography,

myosin heavy chain and muscle creatine kinase.

**5. Clinical examination and prognosis**

and anaerobic work (Nanni and Roi, 2013).

negative prognostic factors.

(Ryan, 1999).

**6. Imaging**

tant role in muscle growth and repair.

The phases of **inflammation** are, in order: organization of the hematoma, necrosis and finally, degeneration of muscle fibers with diapedesis1 of macrophages and phagocytosis of necrotic material Anti-inflammatory drugs which target cyclooxygenase-2 are found able of hindering the skeletal muscle repair process. Muscle regeneration phase can be aided by growth factors, including insulin-like growth factor-1 and nerve growth factor, but these factors are typically short-lived, and thus more effective methods of healing are needed. Skeletal muscle injuries are repaired by muscle cells, myoblasts in condition of oxygenation. The stem cells repair the tissue with paracrine effects, leading to neovascularization of injured site. The *Gharaibeh B'*Group of University of Pittsburgh has found that factor invoked in paracrine action is Angiotensin II, the hormone of blood pressure control.The "LOSARTAN", a drug receptor blocker, in fact reduces fibrotic tissue formation and improves repair of murine injured muscle( Gharaibeh et al. 2012)Other authors hypothesized that a combination of platelet-rich plasma (PRP) injection and oral administration of LOSARTAN, as antifibrotic agent, could enhance muscle healing by stimulating muscle regeneration and angiogenesis and by pre‐ venting fibrosis in contusion-injured skeletal muscle Terada et al., 2013.

The stage of **regeneration** includes all final phases of the healing process: the production of connective tissue scar and neoangiogenesis, phases very important for the restoration of the muscle visco-elastic properties. The low neovascularization would cause fibrosis, due to local ischemia and low O2 tension. So, in this phase, it's important the utilization of physical therapies which cause vasodilatation and neovascularization.

The regeneration process requires the activation of a myogenic stem cells population,, which give rise to proliferating myoblasts. Today we know that repair of muscle takes place with the increase of protein synthesis and activation of satellite cells (stem cells) The satellite cells are quiescent myogenic precursor cells located between the basal membrane and the sarcolemma of myofiber. The adaptation of skeletal muscles to altered use is governed by three major processes: satellite (stem) cell activity, gene transcription, and protein translation. A defect in any of these processes could interfere with muscle maintenance and regeneration. (Shefer G 2012).

In the **remodeling** phase we can observe the "restitutio funtio lesa".

Myoblasts differentiate and unite together into regenerated myofibers. During the final stages of muscle repair, myofibers remodel to produce mature muscle fibers and recover the con‐ tractile capacity of the injured muscle (Mayssa et al 2012)

In response to stimuli such as injury or exercise, satellite cells become activated and express myogenic regulatory factors (MRFs, transcription factors of the myogenic lineage including Myf5, MyoD, myogenin, and Mrf4) that proliferate and differentiate into myofibers. The MRF

<sup>1</sup> Passage of corpuscular elements of the blood through the capillary walls, typical of inflammatory states.

family of proteins controls the transcription of important muscle-specific proteins such as myosin heavy chain and muscle creatine kinase.

The MGF mechano-growth factor isoform appears to work by activating satellite cells MGF expresses the level of mechanical stress in muscles and other tissues and could have a impor‐ tant role in muscle growth and repair.
