Download Clinical management of muscle strains and tears

Clinical management of muscle strains and tears
Published on Physicians Practice (http://www.physicianspractice.com)
Clinical management of muscle strains and tears
November 02, 2008
By Michele Pescasio, MD [1] and Robert A. Pedowitz, MD, PhD [2]
Muscle strains are most common in the hamstring, gastrocnemius, soleus, and quadriceps strains,
as well as the lumbar and thigh adductor. This image-rich review covers imaging, treatment, and
prevention.
Muscle strains and tears are injuries to a muscle or tendon that occur when the muscle is stretched
too far too fast. These injuries are common in athletes, especially hamstring, gastrocnemius and
soleus, quadriceps, lumbar, and adductor strains; complete tears are less common. Most patients
with strains present after an acute onset of pain during activity. Physical examination may reveal
local swelling or ecchymosis; palpation usually reveals localized tenderness over the myotendinous
junction. Radiographs may demonstrate soft tissue swelling; MRI is occasionally helpful for local
injury. Acute management generally includes rest, ice, compression, elevation, and use of NSAIDs.
An exercise program should be instituted. Flexible, strong, and warmed-up muscles are the key to
strain rehabilitation and injury prevention. (J Musculoskel Med. 2008;25:526-532)
Skeletal muscle injuries are found frequently in all types of athletes, young and old, recreational and
professional. This category of injury may include strains, tears, delayed onset muscle soreness, and
contusions. Here we focus on strains and tears.
A muscle strain is a common injury to a muscle or tendon that occurs when a muscle is stretched
excessively. The most common type of strain injuries is hamstring strains, followed by
gastrocnemius and soleus strains, quadriceps strains, lumbar strains, and thigh adductor strains.
Complete muscle tears are seen less frequently.
Most athletes can return to their sports activities after appropriate diagnosis and treatment of
muscle strain injuries. Prevention of reinjury is the major goal after treatment because reinjury is
common; hamstring reinjury rates range from 12% to 31%.1 In this article, we discuss the anatomy
and pathophysiology of strain injury, the biology of the muscle healing process, the clinical diagnosis
of strains and tears, and various treatment and prevention strategies.
Anatomy and pathophysiology
Muscle groups are composed of tendon-muscle-tendon units that span one or more joints.
Contractions of muscle groups induce and control joint motions. For example, the hamstring muscles
(semimembranosus, semitendinosus, and biceps femoris) run from the pelvis and femur to the back
and side of the knee; with their attached bones, they make up contractile units that stabilize the
knee and hip and allow their motion (Figure 1). Injury occurs at the weakest part of the unit.
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Clinical management of muscle strains and tears
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Figure 1 – The most frequently strained muscle group is the hamstring,which consists of the
semimembranosus, semitendinosus, and biceps femoris muscles.The hamstring is more susceptible
to strain injury because it crosses more than 1 joint. A muscle tear of the long head of the biceps
femoris is illustrated.
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Clinical management of muscle strains and tears
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Figure 2 – Shown
here on a T2-weighted MRI scan is a complete tear of the distal end of the long head of the biceps
femoris (arrow) with retraction.
Figure 3 – A severe strain of
the long head of the triceps is demonstrated here by the increased signal intensity on the MRI scan
(arrow).
At the microscopic level, skeletal muscle is composed of contractile and connective tissue elements.
Actin and myosin myofilaments constitute the sarcomeric units of muscle fibers, which are
surrounded by endomysium and arranged in bundles. Satellite cells surround the muscle fibers;
these stem cells are important for tissue regeneration after injury. Muscle bundles are surrounded by
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Clinical management of muscle strains and tears
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perimysium and then by epimysium. Greater degrees of muscle injury tend to involve larger
amounts of connective tissue disruption.
Muscle stretch is resisted by interaction between the contractile units and the surrounding
connective tissues. As stretch moves beyond the physiological range, resistance shifts progressively
from the contractile elements to the connective tissues.
The most common site of strain injury is the myotendinous junction, a region of highly folded
basement membranes between the end of the muscle fiber and the tendon. These involutions
maximize surface area for force transmission. However, the transition from compliant muscle fibers
to relatively noncompliant tendon probably accounts for the unique vulnerability of the
myotendinous junction.
Of note, the myotendinous junction usually spans a large surface area of the muscle belly (as
opposed to the sharp demarcation often depicted in schematic diagrams). For example, the proximal
and distal myotendinous junctions of the hamstrings actually overlap on the posterior and anterior
surfaces of the muscle. This anatomical detail explains why, on clinical evaluation, strain injuries
occurring at the myotendinous junction produce swelling, ecchymosis, and tenderness over a
surprisingly large surface area.
Muscle contractions are categorized according to the sarcomeric length changes that occur during
muscle activation. Isometric contractions involve muscle tension but no muscle shortening or
lengthening. Concentric contractions involve muscle shortening; tension tends to be proportional to
the force induced by the contractile elements. Eccentric contractions occur during muscle
lengthening (resistance to stretch). The magnitude of contractile effort and the velocity of
lengthening affect eccentric contractions; the resultant forces are large.
Most muscle strains and tears occur during eccentric contraction. Muscles that cross 2 joints (eg,
hamstrings, gastrocnemius) are particularly vulnerable to stretch injury, because these muscles are
affected by the simultaneous angular positions and angular velocities of adjacent joints.
Fiber type and, thereby, muscle fiber composition also affect susceptibility to muscle strain injury.
Type I fibers generally are slow-twitch, oxidative fibers that have low glycogen levels and large
numbers of mitochondria; they are fatigue-resistant. Type II fibers generally are faster-twitch and
have variable oxidative dependencies. Type IIB fibers (fast, glycolytic) appear to be specifically
vulnerable to muscle stretch injury.
Muscle activation alone usually is insufficient to cause significant strain injury in a healthy
musculotendinous unit. Disruption at the myotendinous junction typically requires stretch beyond a
threshold length of the entire musculotendinous unit.This pathogenic stretch can be passive or
active; however, multiple animal studies have demonstrated that overt tissue failure tends to be
length-dependent.2 The major difference between active and passive stretch injury is the larger
energy force absorbed by the muscle group during active stretch before tissue failure.
A consistent sequence of events occurs after muscle fiber injury.3 The first phase involves acute
inflammation, which is maximal in the first 24 to 48 hours after injury. The next phase involves
removal of detritus, satellite cell activation, and subsequent fiber regeneration; this phase can last
as long as 6 to 8 weeks after injury. The final phase involves tissue remodeling. It is important to
recognize that complete tissue recovery involves delicate and finely coordinated elements of cellular
and metabolic inflammatory reactions.
Clinical evaluation of muscle injury
Specific physical features may contribute to muscle strains and tears, such as bone structure,
muscle-tendon imbalance, and growth spurts. Other causes include training errors and poor
biomechanics. These injuries generally occur at 2 distinct times: at the beginning of an exercise
program because of deconditioning and at the peak of training when the athlete is striving for
improvement.
Most patients present with muscle strain injuries after an acute onset of pain during activity. A
thorough history is needed to distinguish among acute, chronic, and "acute on chronic" injuries. The
mechanism of injury may help predict the diagnosis. Always inquire about previous muscle strains or
prodromal muscle soreness, which may influence both treatment and avoidance strategies.
Physical examination may reveal localized swelling, ecchymosis, or both. This may evolve over the
course of several days. Palpation usually reveals tenderness over the myotendinous junction. A
palpable defect may indicate a significant partial tear or a complete rupture. Active and passive
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range of motion usually is painful and limited.
Always include a neurovascular examination and a comparative evaluation of the opposite
extremity. Compartment syndrome (a surgical emergency) is quite rare in this setting, but it can
occur. Hallmark features include swelling, pain with passive stretch, and increased intramuscular
pressure.
The differential diagnosis of muscle strains is broad. It should include tendon tears, tendinitis, stress
fracture, muscle contusion, hematoma, avulsion fracture and, rarely, intramuscular infection.
Imaging techniques
Radiographs should be obtained initially, especially in adolescent athletes. They may demonstrate
only soft tissue swelling, but they also may reveal more. Fracture, avulsion fracture, and severe
underlying pathology can be ruled out with simple radiographs.
Ultrasonography is becoming a first-line technique in detecting superficial muscle strains and tears,
especially proximal myotendinous junction tears. Distal myotendinous junction tendon tears rarely
require ultrasonography for diagnosis. Diagnosis of these strains/tears is based on a good history
and physical examination.
The ultrasonographic appearance of a muscle strain or tear ranges from an ill-defined hyperechoic
area in less severe injuries to a hypoechoic area surrounded by a hyperechoic halo resulting from
blood infiltration of the surrounding muscle.4 Ultrasonography also may be used for guidance of
hematoma drainage in acute injuries.
The benefits of ultrasonography include easy accessibility and low cost, and it is noninvasive. It can
confirm a clinical diagnosis, assess the extent of damage, and reveal a tear not suspected clinically.4
Ultrasonography also can be used to verify healing, which allows patients earlier return to sports
activity. Disadvantages include a lack of operator experience, a slow learning curve, and potentially
limited reimbursement because of the newer application of this technology.
MRI may be a more sensitive measure because of sonographer experience. It may be helpful if the
diagnosis is unclear, if physical examination findings are out of proportion to the mechanism of injury
or objective findings, or if it is important to quantify injury severity in a high-level athlete (Figures 2
and 3). Hematoma and interstitial edema are well visualized on T2- weighted images. MRI also may
be helpful in the evaluation of complete tears with tendon retraction for surgical decision making.
Classification schemes are described for muscle strain injuries, but injury classification usually does
little to change treatment decisions.5 From a practical perspective, injuries may be described as
mild, moderate, or severe (complete tear). This assessment is based on the amount of fiber injury,
which may be estimated from the degree of swelling, pain, and fiber discontinuity. MRI is somewhat
useful in this regard.The greatest value of injury classification is estimation of the anticipated time to
return to sports activity. Disadvantages of MRI are lack of accessibility, prolonged examination time,
and high cost.
Treatment
The mnemonic RICE is still the mainstay of acute management of muscle strain injuries; rest, ice,
compression, and elevation all help decrease swelling and pain. Control and resolution of swelling
and recovery of range of motion are the 2 major goals. An appropriate rest interval should allow for
healing and recovery of muscle function, which has been shown to decrease sharply in the first few
days after acute strain injury in animal models.6
Cryotherapy is an important part of initial treatment, although the basic science of cold therapy is
not well delineated. Cryotherapy is thought to work by decreasing local blood flow by means of
vasoconstriction, thereby decreasing edema formation. Cold treatment probably also disrupts the
pain cycle through counterstimulation or modulation of pain impulse transmission. Regardless,
cryotherapy is inexpensive, readily available, easy to apply, and relatively safe.
NSAIDs, another mainstay of muscle strain treatment, work to block prostaglandin formation and
decrease pain associated with the inflammatory response. Although they are used commonly, some
controversy exists over their long-term use. Mishra and associates7 evaluated rabbit muscle function
after exercise-induced injury with 6 days of flurbiprofen or placebo administration. Contractile,
histological, and structural analyses demonstrated greater functional recovery at 3 and 7 days in the
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Clinical management of muscle strains and tears
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NSAID-treated group but decreased force production at 28 days after injury. Short-term benefit also
was noted by Obremsky and coworkers8 up to 7 days after strain injury with piroxicam treatment in
rabbits.
The cyclooxygenase (COX) enzymes have been shown to play a role in satellite cell proliferation,
fusion, and differentiation; COX-2 inhibition has been linked to a decreased satellite cell proliferation
in rats.9 Recall that satellite cell activation is necessary for repair of a muscle strain. A recent study
conducted by Mackey and associates10 on the effects of treatment with indomethacin, a nonselective
COX inhibitor, in endurance runners showed inhibition of satellite cell proliferation after a 36-km run.
Selective COX-2 inhibitor human studies have yet to be performed, but there is evidence that these
agents may be counterproductive in repair of muscle injury because COX-2 plays a role in satellite
cell proliferation.
Although it is likely that early NSAID treatment may be beneficial for decreasing the acute pain and
inflammation after muscle strain, prolonged treatment (weeks to months) may have some mild
adverse effect on muscle recovery.11 These medications have major value in facilitating
rehabilitation through their analgesic qualities, but analgesia also may be achieved with other types
of medications.
Prolonged immobilization after strain injury should be avoided because of the potential for
permanent stiffness. However, a short period of immobilization after severe strain injury may be
reasonable for pain relief and for protection during the initial phases of the healing response. In a
study of rat gastrocnemius injury, Jrvinen and Lehto12 noted some improvement in the orientation of
muscle fiber regeneration with less scar formation after a short period of immobilization followed by
mobilization.
An exercise program should be instituted as soon as the patient's pain and swelling subside to
progressively recover range of motion, strength, endurance and, ultimately, normal athletic skills.
Supervision of this program by a physical therapist or athletic trainer is reasonable after significant
muscle strain injury. Some physicians suggest return to sports activity when there is 80% return of
strength compared with the noninjured side.
Surgery may be indicated in the rare instance of a complete tear with significant retraction of the
muscle from the tendon. However, repair is quite difficult; muscle fibers do not hold sutures reliably.
Prevention
Recurrence of injury is very common without appropriate rehabilitation; return to activity before full
recovery in sports such as running and tennis often results in recurrence. Steps should be taken to
prevent recurrence, as well as identify those at risk for a first-time muscle strain injury.
Strength imbalance is thought to be one of the factors contributing to muscle strain injury. In a study
comparing muscle strain injuries in professional soccer players with strength imbalance with those
without imbalance, the risk of injury was significantly higher in players with the imbalance.13
Preseason screening for strength imbalance may be a valuable tool; intervention would be indicated
for the players found to have a strength imbalance.
In addition to strength imbalance, muscle atrophy is another factor to consider in older persons who
are living more active lifestyles and participating in sports activities. A study conducted by Kubo and
colleagues14 found that older persons have lesser force generation capabilities and tendon
extensibilities of knee extensors and plantar flexors. These weaknesses in strength and flexibility
should be addressed to help prevent strain injuries.
A study on the effects of a 6-week intervention program involving in vivo lengthening contractions in
young and old rats was performed, comparing differences in force deficit and muscle fiber breakage
rates.15 After the 6-week program, no differences were found between the young and old rats.This
result shows that some of the age-related weaknesses that contribute to muscle strains may be able
to be managed with intervention.
Although controversial, stretching before physical activity can help prevent muscle strain injury.
Hartig and Henderson16 studied effects of a stretching program in military basic training.The control
company proceeded through normal basic training; the intervention company added 3 hamstring
stretching sessions to the program. In the intervention group, hamstring flexibility increased and the
frequency of injuries was significantly lower than in the control group (16.7% vs 29.1%).
Appropriate warm-up activity also should be a part of strain injury prevention, because warm
muscles are more flexible and failure- resistant.17 In summary, flexible, strong, and warmed-up
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Clinical management of muscle strains and tears
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muscles are the goals of strain injury rehabilitation, as well as injury prevention.18,19
References:
References
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2. Garrett WE Jr. Muscle strain injuries. Am J Sports Med. 1996;24(suppl 6):S2-S8.
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Prevention, Treatment. 2nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2001:839-888.
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after controlled strain injury. Am J Sports Med. 1987;15:9-14.
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controlled muscle strain injury treated with piroxicam. Am J Sports Med. 1994;22:558-561.
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differentiation, and fusion. Muscle Nerve. 2004;30:497-500.
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exerciseinduced myogenic precursor cell responses in humans. J Appl Physiol. 2007;103:425-431.
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process following muscle injuries. Sports Med. 1993;15:78-89.
13. Croisier JL, Ganteaume S, Binet J, et al. Strength imbalances and prevention of hamstring injury
in professional soccer players: a prospective study. Am J Sports Med. 2008;36:1469-1475.
14. Kubo K, Ishida Y, Komuro T, et al. Age-related differences in the force generation capabilities and
tendon extensibilities of knee extensors and plantar flexors in men. J Gerontol A Biol Sci Med
Sci. 2007;62:1252-1258.
15. Lynch GS, Faulkner JA, Brooks SV. Force deficits and breakage rates after single lengthening
contractions of single fast fibers from unconditioned and conditioned muscles of young and old rats.
Am J Physiol Cell Physiol. 2008;295:C249-C256.
16. Hartig DE, Henderson JM. Increasing hamstring flexibility decreases lower extremity overuse
injuries in military basic trainees. Am J Sports Med. 1999;27:173-176.
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Clinical management of muscle strains and tears
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19. Brothers A, Alamin T, Pedowitz R. Basic clinical management of muscle strains and tears. J
Musculoskel Med. 2003;20:303-307.
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[1] http://www.physicianspractice.com/authors/michele-pescasio-md
[2] http://www.physicianspractice.com/authors/robert-pedowitz-md-phd
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