Muscle Injury: Pathophysiology, Diagnosis, and Treatment^[*]

Keywords

musculoskeletal system/physiopathology - musculoskeletal system/injury - musculoskeletal system/surgery - regeneration

Introduction

Muscle injuries are the most frequent cause of physical disability in sports practice. It is estimated that between 30 and 50% of all sports-associated injuries are caused by soft tissue injuries.[1] This incidence may be higher according to the sport. In athletics and soccer, ∼ 30 to 41% of all injuries are muscular,[2] [3] [4] while in weightlifting, muscle injuries account for up to 59%.[5]

Although nonsurgical treatment results in a good prognosis in most athletes with muscle injury, the consequences of treatment failure can be dramatic, postponing the return to physical activity for weeks or even months.[6] Knowledge of some basic principles of skeletal muscle regeneration and repair mechanisms can help prevent imminent dangers and accelerate the return to sport.

Anatomy and biomechanics

Muscle fibers usually originate in a bone or dense connective tissue and insert themselves into another bone through a tendon insertion.

There are muscles that go through one or more joints to generate movement. Muscles with tonic or postural function are usually uniarticular, wide, flat, with low contraction speed and with the ability to generate and maintain large contractile strength. They are usually located in the deepest compartments.

Biarticular muscles have greater contraction speed and ability to change length; however, they have less ability to withstand tension. They are usually located in surface compartments.

Regarding shape, the fusiform muscles allow a greater range of motion, while the feathered muscles have greater contractile strength.

Fiber length is an important determinant of the amount of contraction possible in muscles. Because muscle fibers usually have oblique distribution within a muscle belly, they are usually smaller than the total length of the muscle.

Mechanisms of injury

The cause of muscle injury can be considered indirect or direct.[7] Indirect injury is related to lack of contact. It may be of functional cause, due to mechanical overload or neurological injury,[8] or structural, which occurs when there is a partial or complete muscle rupture, such as the lesion in an eccentric concentration. Direct injury occurs at the contact site, which may cause a laceration or contusion. More than 90% of all sports-related injuries are bruises or stretches.[9] Muscle lacerations are the least frequent injuries in sports.

The tensil strength exerted on the muscle leads to an excessive stretching of myofibrils and, consequently, to a rupture near the myotendinous junction. Muscle stretches are typically observed in the superficial muscles that work crossing two joints, such as the recurrent femoral, semitendinous and gastrocnemius muscles.

Hamstrings, for example, show increased muscle tension as the hip and knee extend, either at the beginning of a sprint or of a kick, into a classic mechanism of muscle injury by eccentric contraction of a biarticulate muscle.[10]

Classification

Currently, there are several classification systems described for muscle injuries. In the last 10 years only, 5 different systems have been published.[11] Classically, the systems describe muscle injury at 3 different levels, mild, moderate and severe (or grade I, II and III) from imaging evaluation[12] [13] or from the clinical aspects revealed.[14] New systems stage the lesions in a more complex way,[8] [15] [16] using, in addition to the characteristics described above, aspects related to the etiology and anatomical location of the lesion. [Table 1] shows some of the current classification models.[11]

Table 1

1. Classifications based on clinical and imaging findings
Author	Description
Lopes, A. 1993.	Classification based on etiology and ultrasound findings Type I: muscle injury caused by extrinsic factors: muscle contusion Type II: muscle injury caused by intrinsic factors without muscle rupture Type III: muscle injury caused by intrinsic factors with muscle rupture
Verrall, J. 2003.	Clinical parameters				Image findings - MRI Classification of the lesion
	Beginning		Insidious	Abrupt
	Circumstance		Playing	Training	Positive		Negative
	Pain		(0–10) visual analog scale
Malliaropoulos, N. 2010.	Clinical Grade - ROM Deficit				Image findings (US)
	I		< 10th		Degree 0 to 3 (based on Peetrons)		Injury area:
	II		10th–19th				< 25%
	III		20th–29th				25–50%
	IV		> 30th				> 50%
Pollock, N.[15] (British athletics muscle injury classification)	Degree of injury			Description		MRI
	Grade 0: referred pain
	0a			Local pain		Normal
	0b			Generalized muscle pain		normal or with signs of delayed pain
	Grade 1: small muscle injuries (< 5 cm or < 10% of total muscle area)
	1a			Fascial pain		Intermuscular fluid
	1b			Muscle or JMT pain		Intermuscular fluid
	Grade 2: moderate muscle injuries (5–15 cm or 10–50% of total muscle area)
	2a			Fascial pain		high perspherical signal
	2b			Muscle or JMT pain		high signal in JMT
	2c			Tendon pain		high sign on tendon
	Grade 3: extensive muscle injuries (> 15 cm or > 50% of total muscle area)
	3a			Fascial pain		high perspherical signal
	3b			Muscle or JMT pain		high signal in JMT
	3c			Tendon pain		high sign on tendon
	Grade 4: complete muscle injuries
	4a			Fascial pain		high perspherical signal
	4b			Muscle or JMT pain		high signal in JMT
	4c			Tendon pain		high sign on tendon
Mueller-Wohlfahrt, H.[8] (The Munich consensus statment)	A. Indirect muscle injury
	Functional muscle injury Type 1: Overload-related muscle disorder  Type 1A: Fatigue-induced muscle disorder  Type 1B: Late-onset muscle pain (DMIT) Type 2: Neuromuscular disorder  Type 2A: Related to the spine  Type 2B: Related to muscles
	Structural muscle injury Type 3: Partial muscle injury  Type 3A: Minimal partial muscle injury  Type 3B: Moderate partial muscle injury Type 4: Injury (sub)total  Subtotal or complete muscle injury  Tendinous avulsion
	B. Direct muscle injury    Bruise  Laceration
Maffulli, N.[16]	- Direct muscle injury   Bruise  Laceration
	- Indirect muscle injury  Nonstructural muscle injury Type 1: Fatigue muscle injury  Type 1A: Fatigue-induced muscle disorder  Type 1B: Late-onset muscle pain (DMIT) Type 2: Neuromuscular disorder  Type 2A: Related to the spine  Type 2B: Related to muscles
	- Indirect muscle injury  Structural muscle injury Type 3: Partial muscle injury  Type 3A: Minimal partial muscle injury  Type 3B: Moderate partial muscle injury (< 50%) Type 4: Injury (sub)total  Subtotal or complete muscle injury  Tendinous avulsion Structural lesions can be proximal (P), middle (M), and distal (D)
Valle, X.[7]	Clinical findings
	Injury mechanism (M)		Location of the lesion (L)			Degree of injury (G)	Rescan number (R)
	T - Direct lesion of the hamstrings		P Lesion located in the proximal third of the muscle belly M Lesion located in the middle third of the muscular belly D Lesion located in the third of the muscular belly			0–3	0: 1st episode 1st reinjury 2: 2nd reinjury
	I - Indirect injury of the hamstrings, plus index s if it is by stretching (stretching), or index p if it is run.		P Lesion located in the proximal third of the muscle belly. The second letter is index p or d, describing whether the lesion is proximal or distal to JMT, respectively M Lesion located in the middle third of the muscle belly, plus the corresponding index D Lesion located in the middle third of the muscle belly, plus the corresponding index			0–3
	N - Negative MRI injury		N p Lesion in the proximal third N m Injury in the middle third N d Lesion in the distal third			0–3
	Magnetic resonance findings
	Grade 0		Negative MRI
	Grade 1		Hyperintense muscle fiber edema without intramuscular hemorrhage or change in architecture
	Grade 2		Hyperintense edema of muscle fiber and/or paratendon with minimal intramuscular hemorrhage without gaps or minimal alteration in muscle architecture.
	Grade 3		Any gap between muscle fibers in the craniocaudal or axial plane. Hyperintense focal defect with partial retraction of muscle fibers ± intermuscular hemorrhage.
	(r) code overwrite		Used when there is intratendinous injury or affecting JMT or intramuscular injury with retraction or loss of normal tension.
2. Classifications based on image findings
Pomeranz, S. 1993.	MRI assessment
	Muscle group involved		Injury area		Location		Superficial Involvement
	Semimembranosus		< 50%		Tendineous		Yes
	Semitendinosus		> 50%		JMT		No
	Femoris biceps		Total
	Femoris square
Takebayashi, S.[12]	US findings
	Type 1				Normal
	Type 2				Hyperecoic infiltration
	Type 3				Mass
	Type 4				Complete lesion (Infiltration + mass)
Peetrons, P.[13]	US findings
	Grade 0		Normal
	Grade 1		Hyperecoic area, < 15 mm on the longest axis; < 5% of muscle.
	Grade 2		5–50% of muscle. Partial muscle rupture.
	Grade 3		Complete muscle or fascia injury, with collection extravasation from the injured muscle.
Slavotinek, J. 2002.	MRI image of hamstring injury
	Affected muscle			Location		Total area of the lesion
	Femoris biceps			Proximal to short biceps head		0–100%
	Semitendinosus			Distal to short biceps head
	Semimembranosus
Bordalo-Rodrigues, M. 2005	MRI image of Proximal Rectus Femoris - anatomical location
	Avulsion injury of the apophysis Musculotendinous junction injury (JMT) Muscle contusion and laceration
Cohen, S. 2011.	MRI-based graduation system
	Item	Description		0 points	1 point	2 points	3 points
	1	N° of muscles involved		No	1	2	3
	2	Location		−	Proximal	Middle	Distal
	3	Insertion		No	−	Yes	−
	4	Total area of injury in % of the muscle involved		0%	25%	50%	≥ 75%
	5	Retraction		No	−	> 2 cm	−
	6	Longitudinal axis involvement		0 cm	1–5 cm	6–10 cm	> 10 cm
Chan, O. 2012	Graduation based on imaging findings and lesion site
	Degree		MRI		US		Local
	I (distension)		< 5% fiber rupture;		Normal; without distortion of architecture		. Proximal to JMT
	II (Partial loom)		< 5% fiber rupture; high intramuscular signal; edema and bleeding of the muscle or JMT extending to the fascial planes between the muscle groups		Discontinuity of muscle fibers		Muscle A. Proximal B. Medium C. Distal
	III (Complete loom)		Complete discontinuity of muscle fibers, hematoma, and muscle retraction		Comparable with MRI		Distal to JMT
Corazza, A. 2013.	Combined US-MRI assessment
	Degree	MRI			US
	0	No pathological findings			No pathological findings
	I	Muscle edema without tissue alteration			Altered echotexture at the site of pain, without rupture
	Ii	Partial muscle injury			Lesion with associated hematoma
	Iii	Complete muscle injury			Complete muscle injury
3. Classifications based on clinical findings
Bass, A. 1969.	Classifies muscle injuries by etiology and location
	Type	Etiology			Location
	I	Direct external contact			Intramuscular
	Ii	Twitch			Intermuscular
Wise, D. 1977	Classification based on cause, severity, and location of leg muscle injury
	Indirect lesions - inflammation
	Direct injuries - trauma
	Degree	Pain	Circumference difference	Arc of motion	During contraction
					Pain	Loss of strength	Function disorder
	I	Minimum;	< 6 mm	100%	Minimum	No	Moderate
	Ii	Substantial	6–12 mm	50%	Middle	Middle	Important
	Iii	Intractable	> 12 mm	<5 0%	Serious	almost total	Don't step

The classification proposed by Mueller-Wohlfarht et al.,[8] known as the Munich Consensus, and the system described by Mafulli et al.,[16] also consider etiological aspects. These classify muscle injury as direct, caused by contusion or laceration, and indirect, subclassified into functional (nonstructural) or structural.

The system described by Pollock et al.[15] (British athletics muscle injury classification) uses the anatomical location and extension of the lesion. It evaluates, through imaging, whether the damage is superficial (myofascial tissue), if it affects the myotendinous junction, or if there is a tendon injury.

The classification published by Valle et al.[7] seeks to group four characteristics of muscle injury into a system formed by the initials MLG-R, related to each letter as follows: mechanism of injury (M), location (L), degree of injury (G) and number of re-injuries (R).

The systems described above also consider clinical aspects, such as intensity, time of onset, and location of pain, to define the type of lesion and provide an adequate prognosis.

The classification of muscle injury in 3 levels is still well-known and used. It is usually based on clinical findings that are related to the extent of muscle tissue rupture, as described below.

Stretches and mild contusions (grade I) represent an injury of only a few muscle fibers with small edema and discomfort, accompanied by no or minimal loss of strength and movement restriction. It is not possible to palpate any muscle defect during muscle contraction. Although pain does not cause significant functional disability, maintenance of the athlete in activity is not recommended due to the high risk of increasing the extent of the injury.[4]

Moderate stretches and bruises (grade II) cause greater damage to the muscle, with evident loss of function (ability to contract). It is possible to palpate a small muscle defect, or gap, at the site of the lesion, and a slight local hematoma with eventual ecchymosis occurs within 2 to 3 days. The evolution to healing usually lasts from 2 to 3 weeks and, in ∼1 month, the patient can return to physical activity slowly and carefully.[14]

An injury extending throughout the transverse session of the muscle and resulting in virtually complete loss of muscle function and severe pain is determined as severe stretch or contusion (grade III). The failure in the muscle structure is evident, and the ecchymosis is usually extensive, often distant to the site of rupture. This type of injury requires intense rehabilitation and for long periods of up to 3 to 4 months. The patient may remain with some degree of pain for months after the occurrence and treatment of the lesion.[14]

Pathophysiology

Skeletal muscle healing follows a constant order, with no major changes depending on the cause (contusion, stretch or laceration).

Three phases were identified in this process: destruction, repair, and remodeling. The last two phases (repair and remodeling) overlap and are closely related.

Phase 1: destruction – characterized by rupture and subsequent necrosis of myofibrils, by the formation of hematoma in the space formed between the ruptured muscle, and by the proliferation of inflammatory cells.

Phase 2: repair and remodeling – consists of the phagocytosis of the necrotic tissue, the regeneration of myofibrils, and the concomitant production of connective scar tissue, as well as vascular neoformation and neural growth.

Phase 3: remodeling – maturation period of regenerated myofibrils, contraction and reorganization of scar tissue, and recovery of muscle functional capacity.

Since myofibrils are fusiform and very long, there is an imminent risk that the necrosis initiated at the site of the lesion extends throughout the length of the fiber. However, there is a specific structure, called a contraction band, which is a condensation of the cytoskeletal material that acts as an "antifire system".[17]

Once the destruction phase decreases, the present repair of muscle injury begins with two simultaneous and competitive processes: the regeneration of the myofibril route and the formation of the scar connective tissue. A balanced progression of these processes is a prerequisite for optimal recovery of contractile muscle function.[17]

Although myofibrils are generally considered nonlytic, the regenerative capacity of skeletal muscle is guaranteed by an intrinsic mechanism that restores the injured contractile tract. During embryonic development, an undifferentiated cell reserve pool called satellite cells is stored below the basal lamina of each myofibril. In response to the lesion, these cells first proliferate, then differentiate into myofibrils, and finally join each other to form multinucleated myobribules.[18]

Over time, the formed scar decreases in size, leading the edges of the lesion to a greater grip with each other. However, it is not known whether the transection of the myofibrils from the opposite sides of the scar will definitely merge with each other or if it will form a septum of connective tissue between them.[19]

Immediately after the muscle injury, the interval formed between the rupture of muscle fibers is filled by hematoma. From the 1^st day, inflammatory cells, including phagocytes, invade the hematoma and begin to organize the clot.[20]

Blood-derived fibrin and fibronectin intersperse to form granulation tissue, an initial frame and anchoring of the site for the recruited fibroblasts.[17] More importantly, this new formed fabric provides the property of initial tension to resist the contractions applied against it.

Approximately 10 days after the trauma, the maturation of the scar reaches a point in which it is no longer the most fragile site of the muscle injury.[21]

Although most skeletal muscle lesions heal without the formation of disabling fibrous scar tissue, fibroblast proliferation may be excessive, resulting in the formation of dense scar tissue within the muscle lesion.

A vital process for the regeneration of the injured muscle is the area of vascularization. Restoration of vascular supply is the first sign of regeneration and is a prerequisite for subsequent morphological and functional recoveries.[21]

Diagnosis

The diagnosis of muscle injury begins with a detailed clinical history of the trauma followed by a physical examination with inspection and palpation of the muscles involved, as well as function tests with and without external resistance.[23] The diagnosis is easy when a typical history of muscle contusion is accompanied by an evident edema or ecchymosis distal to the lesion.

Complementary exams

Imaging tests such as ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) provide useful information to verify and determine the lesion more accurately. New methods have been studied to detect physiological changes related to muscle injury, such as thermography.

Ultrasonography is traditionally considered the method of choice for initial evaluation of muscle injury. It is a relatively inexpensive and easily accessible imaging method. It is possible to dynamically evaluate muscle contraction and rupture. Renoux et al.[24] demonstrated a correlation between the severity of the acute muscle injury assessed by US with the time of return to sports activities. This examination presents the disadvantage of being examiner-dependent, having limited field of vision and reduced sensitivity for morphological evaluation.[25]

Computed tomography has already been shown to be able to identify changes related to muscle injuries, such as the presence of edema.[26] But the fact that CT generates radiation and produces a static image with little definition in relation to MRI[26] caused this evaluation method to be replaced.

Magnetic resonance imaging allows detailed evaluation of muscle morphology due to the ability to generate multiplanar and high-resolution soft tissue images.[25] It is the method of image evaluation used by many authors to define the classification of muscle injury.[8] [15] [16] The ability to differentiate ruptures and edemas and to perform calculation of the size of the hematoma proved to be useful in guiding the return time and the risk of re-injury in athletes.[27] In chronic lesions, it has the ability to show signs of tissue healing and fatty degeneration.[25] Advanced MRI techniques allow the evaluation of microstructure and muscle composition.[25]

Infrared medical thermography enables a noninvasive and nonradioactive assessment of body temperature. It allows the detection of physiological changes that mean increased risk of muscle injuries, such as inflammatory reactions by overload.[28] [29] Thermography does not show data from deep surfaces and should not be used as a single diagnostic tool. Its use has been shown to be effective in preventing muscle injuries, reducing the incidence of injuries in professional soccer players by > 60%.[30]

Treatment

The current principles of treatment of muscle injury are lacking in solid scientific foundations.

Early mobilization induces an increase in local vascularization in the lesion area, better regeneration of muscle fibers, and better parallelism between the orientation of regenerated myofibrils when compared with movement restriction.[31] However, reruptures at the original site of the trauma are common if active mobilization begins immediately after the injury.[33]

A short immobilization period with firm or similar adhesive bandage is recommended. This period of rest allows the scar tissue to reconnect to the muscle failure.[9]

The patient should use a pair of crutches for the most severe muscle injuries of the lower limbs, especially in the initial 3 to 7 days.

Acute phase

Immediate treatment for skeletal muscle injury or any soft tissue injury is known as the Protection, Rest, Ice, Compression, and Elevation (PRICE) principle. The justification for using the PRICE principle is because it is very practical, since the five measures cry out to minimize bleeding from the site of the injury.[23] Some authors advocate the use of the POLICE protocol, which presents as the main innovation the orientation for the optimized use of the injured limb in the acute phase, avoiding the adverse effects of long periods of rest.[33]

Putting the injured limb at rest soon after the trauma prevents a late muscle retraction or the formation of a larger muscle gap by reducing the size of the hematoma and, subsequently, the size of the scar connective tissue. Regarding the use of ice, it was shown that the early use of cryotherapy is associated with a significantly smaller hematoma in the gap of ruptured muscle fibers, with lower inflammation,[34] and with accelerated regeneration.[35]

The combination of ice application and compression in shifts of 15 to 20 minutes, repeated within intervals of between 30 and 60 minutes is recommended, since this type of protocol results in a decrease in 3° to 7°C of intramuscular temperature and in a 50% reduction of intramuscular blood flow.[37]

Finally, the elevation of the limb above the level of the heart results in decreased hydrostatic pressure, reducing the accumulation of fluid in the interstitial space.

Medication

There are few controlled studies using non-hormonal anti-inflammatory drugs (NHAIDs) or glucocorticoids in the treatment of muscle injuries in humans. O'Grady et al.[37] reported that the use of anti-inflammatory drugs in the treatment of in situ necrosis, the mildest type of muscle injury, in the short term, results in a transient improvement in the recovery of exercise-induced muscle injury. Despite the lack of evidence, the effects of NHAIDs have been well-documented. Järvinen[19] argued that short-term use in the early stages of recovery decreased the cellular inflammatory reaction without side effects on the healing process, on the tensil strength, or on the ability to contract muscle.

Furthermore, INAD does not delay the abilities activated by satellite cells in the proliferation or in the formation of myotubules.[38] However, chronic use seems to be harmful in the model of eccentric contraction in stretch lesions, as discussed by Mishra et al.[39]

Regarding the use of glucocorticoids, delays in the elimination of hematoma and necrotic tissue were reported, as well as delay in the regeneration process and reduction of the biomechanical strength of the injured muscle.[40]

Acute postphase treatment

1. Isometric training (muscle contraction in which the muscle length remains constant and tension changes) can be started without the use of weights and, later, with the addition of them. Special attention should be taken to ensure that all isometric exercises are performed painlessly.

2. Isotonic training (muscle contraction in which the muscle size changes and tension is maintained) can be initiated when isometric training is performed painlessly with resisted loads.

3. Isokinetic exercise with minimum load can be initiated once the two previous exercises are performed painlessly.

Local application of heat or “contrast therapy” (hot and cold) can be of value, accompanied by careful passive and active stretching of the affected muscle. It is emphasized that any rehabilitation activity should be initiated with the proper heating of the injured muscle.[41]

Another reason for stretching is to distend the mature scar tissue during the phase when it is still plastic. Pain-free scar stretches can be acquired by gradual stretches, starting with shifts of 10 to 15 seconds and then progressing to periods of up to 1 minute.

However, if the symptoms caused by the lesion do not improve in between 3 and 5 days after the trauma, the possibility of an intramuscular hematoma or of extensively injured tissue that will require special attention should be considered. Puncture or aspiration of the hematoma may be necessary.

Ultrasound

Therapeutic US is diffusely recommended and used in the treatment of muscle injury; some authors argue that there is vague scientific evidence of its effectiveness.[42] The fact that US produces micromassages by high frequency waves apparently makes it work for pain relief. Engelmann et al.[43] showed a reduction in inflammatory activity with the use of pulsed US. Ultrasound may also be useful for the performance of therapeutic procedures and in the surgical treatment of muscle injuries.[44] [45]

Surgical treatment

There are precise indications in which surgical intervention is required. These indications include patients with large intramuscular hematomas, complete lesions or ruptures (grade III) with little or no associated agonist musculature, and partial lesions in which more than half of the muscle is ruptured.[46] [47]

Surgical intervention can also be considered if the patient complains of persistent pain when stretching for > 4 to 6 months, particularly if there is an extension deficit. In this case, scar injuries should be suspected, restricting muscle movement at the site of the injury.

After surgical repair, the muscle should be protected by an elastic bandage around the limb to promote relative immobility and compression. Naturally, the duration of immobilization depends on the severity of the trauma. Patients with complete rupture of the quadriceps or of the gastrocnemius muscle are instructed not to load the limb for at least 4 weeks.

If the gap or muscle failure is exceptionally wide, the denervated part can generate a permanent neurological deficit and consequent muscle atrophy.[21] Surgical repair in these circumstances increases the chance of reinnervation, and the development of thick scar tissue can be avoided.

New perspectives

The therapeutic use of growth factors and gene therapy, alone or in combination, and the application of stem cells provide the latest and most promising existing therapeutic options. However, there is currently a need for greater scientific validation for its intensification in the treatment of skeletal muscle injuries.

Growth factors and cytokines are potent mitogenic activators for numerous cells, including myogenic precursor cells (MPCs) during the regeneration of injured muscle cells.[48] Therefore, they are promising therapeutic options to aid in the recovery of skeletal muscles.

In relation to stem cells, it has recently been shown that, in response to the injury, not only tissue-specific cells, but also nonmuscle stem cells participate in the repair process.[49]

The first steps of gene therapy have already been taken. Successful studies have shown good results of the use of stem cells in muscle tissue in the treatment of muscular dystrophy, of cardiac muscle injuries, and of urinary incontinence.[10] [50] Future studies will demonstrate in which sphere gene therapy can fulfill the current expectations regarding the treatment of muscle trauma scans.

Clinical Presentation

Quadriceps muscle injury

Distal quadriceps injury is an unusual lesion, occurring more frequently in individuals > 40 years old.[51] The injury may occur due to direct trauma, but it is classically reported as a forced eccentric contraction in a position of slight flexion of the lower limb in an attempt to regain balance at the time of a fall.

Spontaneous ruptures and bilateral ruptures have been described in athletes with systemic metabolic disorders and steroid use.[51]

The diagnosis of rupture is based on clinical findings. The patient typically presents, after a fall with flexed knees, acute pain above the patella and the inability to remain in the orthostatic position without assistance.

During physical examination, the patient is not able to actively extend the knee and, often, there is a palpable interval above the patella, known as the "groove sign" or gap test. Patients can actively flex the knee and have total passive knee flexion and extension.

Plain radiography is an inexpensive tool for the diagnosis of breakage. Although it does not show a specific alteration of the lesion, it shows indirect signs of rupture. Soft tissue edema, joint effusion, calcifications, shadow of quadriceps rupture, and low patella are all indirect signs seen on plain radiography.[53]

Ultrasound is another inexpensive method for diagnosing muscle injury. Magnetic resonance imaging is particularly useful for better visualization, accuracy of lesion location and extent, and anatomical details for preoperative programming.

For complete muscle ruptures, the treatment is surgical. Early surgical treatment in these cases is associated with better functional results.[54] The delay in surgical repair is associated with a period of prolonged physiotherapy, with inadequate flexion, and with loss of total knee extension.[54] After surgical repair, patients have the knee immobilized for 4 to 6 weeks.

Injury of the hamstring muscles

The hamstring muscles are the least elongated of the lower limb and, for this reason, more easily injured during eccentric muscle contraction.

The severity of the injury is usually neglected, especially in the acute phase.

Hamstring stretching is the most common lesion in athletes.[55]

The diagnosis of the lesion is usually made from a high rate of clinical suspicion and careful clinical examination. Magnetic resonance imaging is valuable for differentiating between a complete or incomplete lesion and for treatment planning.

Complete rupture of the hamstring muscles proximally in their origin is rare. The conduction of the case varies between conservative treatment with an immobilizer in flexion and surgical repair in a second moment. Although surgical repair in a second moment may show good results, early repair allows for faster functional rehabilitation and avoids the potential neurological symptom of gluteal sciatica.

Adductor muscle injury

The adductor muscle group acts in conjunction with the low abdominal muscles to stabilize the pelvis during activities involving the lower limbs. Athletes who participate in activities that require repetitive kicks, starts, or frequent changes of direction have a higher incidence of chronic pain in the topography of the adductors.[5]

There is evidence that athletes with imbalance between the adductor musculature and the abdominal wall are more likely to acquire pubalgia during the season.[57] Weakness of the adductor muscles and decreased amplitude of hip movement are also related to pubalgia.[58]

Patients typically present with a sore groin area or medial pain in the thigh and may or may not report a triggering factor. On physical examination, pain is presented on palpation with focal edema along the adductor muscles and decreased muscle strength and pain in resistance exercise of hip adduction.

The diagnosis can be made with the findings of the physical examination. However, contrast-enhanced MRI may be useful to confirm the diagnosis or to make the differential diagnosis between pubic osteitis and sports hernia.[59]

The initial treatment is conservative. Infiltration of the long adductor entese may be useful for refractory treatment. In cases of acute rupture, open surgical repair with anchor placement and suture has been described with good results.[60]

Patients may resume the sport after returning to the previous pattern of strengthening and range of motion of the hip and resolution of pain. Due to the predisposition of the adductor injury to be caused by muscle imbalance, attention should be paid to strengthening the musculature to prevent further injuries.

Injury of gastrocnemius muscles

Like the hamstring and quadriceps muscles, the gastrocnemius is prone to injury because it crosses two joints.

The medial head of the gastrocnemius is more commonly injured than the lateral head, since it is more active.[61] Deep vein thrombosis may be associated with or be a differential diagnosis of calf pain, as well as thrombophlebitis.[62]

The term tennis leg has been used to describe calf pain and injury. The term is attributed to the movement of the serve in tennis, in which there is a complete extension of the knee associated with an abrupt dorsiflexion of the ankle, causing maximum stretching of the calf. However, this injury has also been described in young athletes during periods of strenuous exercises such as basketball, running, and bodybuilding.[63]

The onset of pain is sudden, with focal edema and ecmosis of the calf. Classically, tennis leg is referred to as a lesion of the distal myotendinous junction, although proximal injury may occur.

Because of the superficial nature of the lesion, US evaluation is reliable, makes it possible to easily exclude the presence of deep vein thrombosis, and provides aspiration of image-guided liquid collections.

The treatment of most gastrocnemius lesions is conservative. Occasionally, surgery should be performed to drain hematomas, to repair a grade III lesion, or to perform compartmental decompression in cases of compartment syndrome.

Pectoral muscle snare injury

The pectoralis major (PM) muscle presents a complex anatomy. The tendon is bilaminar (anterior and posterior layers) and the muscular belly is composed of the clavicular head and of the sternal head, divided into 7 segments.[65]

Cases of PM muscle injury have become more common in recent years. The main reason is the increase in the practice of weightlifting. The most common mechanism is indirect injury during the eccentric phase in weightlifting in supine.[65] This injury is also frequent in sports such as gymnastics, Greco-Roman wrestling, and windsurfing.[66]

Loss of upper limb adduction strength leads to the need for surgical treatment, both for acute (up to 3 weeks) and chronic (after 3 weeks) lesions. Treatment in the acute phase is usually repair near the humeral insertion. In chronic lesions, reconstruction of the PM tendon with the use of flexor tendons may be necessary.[66]

Minor pectoral muscle injuries are rare, and are often confused with PM injury. Conservative treatment was effective in the few reported cases of this type of lesion.[67]

Distal lesion of the brachial biceps muscle

The brachial biceps muscle is composed of the long head, which originates in the supraglenoidal tubercle and acts on the supination, and of the short head, which originates from the coracoid process and presents a greater performance in elbow flexion. The distal insertion is in the radial tuberosity.[68]

Distal rupture is uncommon, occurring in 10% of all lesions of the biceps. It happens mainly in the dominant limb, in male patients. The mechanism is eccentric contraction during elbow extension.[9]

Biomechanical studies show reduced supination strength and resistance and a lower loss of elbow flexion strength. Conservative treatment is usually indicated for sedentary or low-demand patients.[68] Surgical treatment is performed by reinsertion into the radial tuberosity with the use of cortical buttons, anchors, interference screw, or transosseous suture.[68]

Final Considerations

Understanding the pathophysiological mechanisms that regulate muscle repair and its adaptation to physical training are essential for the professional who proposes to treat these patients. They are the basis for the development of means of injury prevention and for the proper treatment and rehabilitation of installed injuries.

Regarding the appropriate time of return to training specific to the sport, the decision can be based on two simple and inexpensive measures: the ability to lengthen the injured muscle as much as the healthy contralateral side, and absence of pain in the injured muscle in basic movements.

When the patient refers to reaching this point in recovery, permission to gradually start the exercises specific to the sport is guaranteed. However, it should always be emphasized that the final phase of rehabilitation should be carried out under the supervision of a qualified professional.

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