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Compendium May 2013 (Vol 35, No 5)

Iliopsoas Muscle Injury in Dogs

by Quentin Cabon, DMV, IPSAV, Christian Bolliger, Dr.med.vet, DACVS, DECVS


    The iliopsoas muscle is formed by the psoas major and iliacus muscles. Due to its length and diameter, the iliopsoas muscle is an important flexor and stabilizer of the hip joint and the vertebral column. Traumatic acute and chronic myopathies of the iliopsoas muscle are commonly diagnosed by digital palpation during the orthopedic examination. Clinical presentations range from gait abnormalities, lameness, and decreased hip joint extension to irreversible fibrotic contracture of the muscle. Rehabilitation of canine patients has to consider the inciting cause, the severity of pathology, and the presence of muscular imbalances.

    Contrary to human literature, few veterinary articles have been published about traumatic iliopsoas muscle pathology.1–6 This is likely due to failure to diagnose the condition and the presence of concomitant orthopedic problems.5 In our experience, repetitive microtrauma of the iliopsoas muscle in association with other orthopedic or neurologic pathologies is the most common clinical presentation.

    Understanding applied anatomy is critical in diagnosing muscular problems in canine patients (BOX 1; BOX 2FIGURE 1FIGURE 2).

    Pathophysiology of Muscular Injuries

    Muscular injuries are usually classified as contusions (blunt trauma), strains (indirect injuries), vascular compromise, or lacerations (sharp injuries).6,7 Due to its profound and protected location, the iliopsoas muscle is more likely to be affected by strain injuries. Muscle strain injuries are common in humans and dogs and result from excessive stretch or stretch while the muscle is activated (i.e., eccentric contraction).5,8 When the muscle tears, the damage is usually localized close to the muscle-tendon junction or the origin of the tendon and less commonly in the muscle belly.5–7

    In veterinary medicine, strain injuries are classified as follows6,9,10:

    • Stage I (mild strain): myositis and bruising but architecture intact

    • Stage II (moderate strain): myositis and some tearing of the fascial sheath

    • Stage III (severe strain): tearing of the fascial sheath, muscle fiber disruption, and hematoma formation

    Chronic muscular injuries include repetitive strain injuries and/or myofascial pain syndrome and contractures, which are not well described by this structural classification system. In our experience, chronic repetitive microtrauma of the iliopsoas muscle is more common in dogs.

    Acute Muscular Strain Injuries

    Acute muscular strain injuries are caused by an explosive motion such as turning or twisting during a jump, fall or slip. Muscles are particularly vulnerable during an eccentric contraction, when the intramuscular forces are greatest and fewer muscle fibers are activated.8,11

    Typical anamnesis in conjunction with pain, swelling, loss of function, and hematoma formation can help to confirm the diagnosis of muscular injury.12 However, owners often do not appreciate the occurrence of a traumatic event, resulting in an inaccurate history.

    Sporting and working dogs may be particularly at risk for acute, traumatic muscle strains. Insufficient muscle conditioning, such as weak core stabilizers and imbalances between muscular agonists and antagonists, can increase the risk of a muscular stretch injury. Further predisposing factors include inflexibility of the affected muscles, inadequate warm-up, and, particularly, muscle fatigue.

    The mildest form of strain injury includes the so-called delayed-onset muscle soreness (DOMS) after repeated powerful muscle contractions. The site of maximal damage appears to be the Z-band of the sarcomere, where thick filaments are anchored. The Z-band disruption causes muscle cell damage with calcium influx and initiates an inflammatory response. The muscle swelling causes soreness and stiffness.13 This stage may be difficult to recognize unless it affects a performance dog. With appropriate rest, complete recovery usually occurs within a few days.

    More severe strain injuries (stages II and III) are characterized by rupture of muscle bundles. As long as the muscle fascia remains intact, bleeding remains intramuscular, but with a concurrent fascial tear, bleeding expands into the intermuscular space. The most severe injury is a complete muscle tear with total loss of function.

    Following strain injury, scar tissue formation competes with and protects regeneration of muscle fibers. Resting satellite cells in the extracellular matrix are stimulated to proliferate and to differentiate into myoblasts, which then fuse to form multinucleated myotubuli.14 Although fibroplasia from scar tissue provides some stabilization of the wound, it also creates a barrier for the newly formed myofibrils.14,15

    Chronic Muscular Strain Injuries

    More common, but also more subtle, are chronic muscular strain injuries. We see many dogs with lower back pain or hip or stifle pathologies that express a pronounced pain reaction upon direct palpation of the iliopsoas muscle ventral to the ilium or at its insertion point on the lesser trochanter. Protecting a painful joint by limiting its range of motion, the iliopsoas muscle fatigues, leading to local ischemia, acidosis, and swelling. The resulting exhaustion of ATP leads to a long-lasting muscle contracture. In people, it is hypothesized that during muscle fatigue, muscle spindle activity increases (excitatory signal) and Golgi tendon organ activity decreases (inhibitory signal), leading to increased muscle membrane excitability that can result in cramps.16

    Repetitive strain injuries and muscle fatigue can both initiate the same vicious cycle of inflammation and fibroplasia resulting in pain, muscle shortening, and adhesions. These chronic local muscle injuries are also called myofascial trigger points and can be palpated in more superficially located muscles as dense, hard, painful knots.17 If a muscle remains shortened over a longer period of time, distensibility is progressively lost, leading to irreversible muscle contracture. The formation of an insertion tendinopathy at the level of the lesser trochanter is also more frequently associated with repetitive strain injuries.

    Clinical Presentation

    The lameness or gait abnormalities associated with an iliopsoas muscle injury vary and can be acute or chronic, unilateral or bilateral.2,3,17–21 A reduction in hip extension resulting in a shortened stride is characteristic. An improvement with time is often observed, especially with acute stage I strains.5,6 Affected dogs can be any size or age and of either sex. Typically, iliopsoas myositis is distinctly painful, particularly if the femoral nerve becomes compressed inside the swollen or fibrosed muscle belly (FIGURE 3FIGURE 4).20–22 It is not uncommon that pain in the iliopsoas muscle secondary to another pathology exceeds that of the primary orthopedic problem. In certain cases, the pain originating from the iliopsoas muscle may persist due to insufficient rehabilitation, causing continuous strain on a weakened muscle even after resolution of the inciting cause.

    Direct palpation of the iliopsoas muscle and its insertion point is highly sensitive in localizing the source of pain and is accentuated with the hip joint in extension and the femur internally rotated (BOX 3).5 If hip joint pathology is the cause of pain during extension, simultaneous palpation of a normal iliopsoas muscle will not aggravate the animal’s response.

    Other muscle groups can be affected simultaneously, including the pectineus, gracilis, and semitendinosus muscles.5 Iliopsoas myositis is often associated with other neurologic or orthopedic problems, which must be diagnosed and treated concurrently.

    Decreased hip extension is commonly observed and is the result of pain-induced muscular spasm and shortening or fibrosis with advanced chronic lesions.2,3,20,23 A fibrotic iliopsoas muscle can be palpated as a distinct rigid band ventral to the ilium in the groin, preventing full extension of the hip joint.5,20

    A femoral neuropathy has also been described, caused by the close anatomic relation of the femoral nerve and the iliopsoas muscle (FIGURE 3FIGURE 4). Clinical signs include decreases in patellar reflex and conscious proprioception, hindlimb weakness, and quadriceps femoris muscle atrophy.18–21 Rarely, loss of cutaneous nociception can be detected on the medial aspect of the hindlimb.18

    Transient increase in muscle enzyme activity is common with, but not specific for, an individual muscle group.13

    Diagnostic Imaging

    Radiographic examination of the affected hindlimb allows visualization of lesser trochanter avulsion or dystrophic calcification at the insertion of the iliopsoas muscle as well as the diagnosis of other orthopedic problems (FIGURE 5).19 Dystrophic calcification does not necessarily mean active disease.

    Ultrasonography is commonly used to examine traumatized muscles as it is widely available, cost-effective, and noninvasive.24–26 Repeated evaluations during the recovery period are easily performed. However, the results of the examination are highly operator dependent.27,28 Normal muscle tissue appears as homogeneous hypoechoic parenchyma with multiple hyperechoic regions or lines, according to the section chosen.18,26 Acute strains are characterized by muscle swelling and hypoechogenic zones caused by edema, inflammation, or hemorrhage, whereas chronic lesions are hyperechogenic from fibrosis or ectopic mineralization (FIGURE 6).1,18,19,26

    Magnetic resonance imaging (MRI) is the best imaging modality for detecting musculotendinous lesions.27–29 During MRI, normal muscle tissue produces a homogeneous, hypointense signal in T1 and T2 sequences (FIGURE 7).28 Myositis generates a hyperintense signal in the T2 sequence, which is considered the best sequence to visualize muscular lesions.28,29 Intravenous injection of gadolinium as a contrast agent can amplify lesions during T1 sequence acquisition (FIGURE 7).

    Although definitive diagnosis of muscle lesions would require histopathologic examination, orthopedic examination in conjunction with advanced imaging allows an accurate diagnosis most of the time, limiting the need for more invasive procedures.


    Muscle injuries follow three partially overlapping phases of healing (BOX 4). The initial treatment is described by the acronym RICE (rest, ice, compression, elevation). Ice can be applied to the groin area and is beneficial during the first 72 hours following an injury. Reported local effects of cryotherapy include vasoconstriction and reduction in edema formation, hemorrhage, histamine release, local metabolism, muscle spindle activity, nerve conduction velocity, pain, and spasticity.30

    Due to the deeper location of the iliopsoas muscle, the effect of cold application diminishes rapidly between the skin level and underlying muscle.

    Rest forms the cornerstone of all treatments, although the anatomic location of the iliopsoas muscle prevents complete immobilization. Immobilization following a muscle injury reduces intramuscular bleeding and scar volume and allows some maturation and stabilization of the granulation tissue. In human athletes, strict immobilization during the first 4 to 6 days is recommended.12

    During the inflammatory phase, NSAIDs decrease inflammation and pain and are given usually for a period of 5 to 10 days.5,31 Clinically, NSAIDs help to achieve faster normal muscle activity, but in two experimental animal studies, histologic healing was delayed.32,33

    In chronic muscular strain injuries, the inflammatory reaction is not a main feature and, therefore, NSAIDs are less effective unless concurrent orthopedic problems exist. Methocarbamol, a centrally acting muscle relaxant, has been associated with better recovery in people, decreasing muscular spasticity and pain. In dogs, a dose of 40 to 60 mg/kg body weight three times per day on day 1, followed by 20 to 40 mg/kg three times per day for another 5 to 10 days has been recommended.5

    In some patients, additional pain relief may be necessary and can be provided in the form of an oral or transcutaneous opioid.

    Local treatment with platelet-enriched plasma (PEP) is under investigation in humans with promising results, although no standard protocol exists yet.34 PEP provides a high concentration of cytokines and growth factors locally, which can enhance recruitment of satellite cells and amplify the healing stimulus.34–36

    During the proliferating phase, vascular ingrowth, regeneration of muscle fibers, and cell orientation are improved when physiologic tension and load are applied (BOX 4).12 Regeneration of muscle fibers starts early, between 3 and 5 days after injury, and peaks during the second week.7 The time for transition between immobilization and mobilization has to be individually determined, based on the severity and chronicity of the muscular lesion and clinical signs. In humans, it has been reported that mobilization should begin between 5 and 10 days after trauma to maximize vascularization and muscle fiber orientation.12

    Under ideal conditions, the tensile strength of the scar tissue reaches values similar to or greater than those of the surrounding muscle tissue 10 days after the trauma.12

    Manual therapy, including range-of-motion exercises, stretching, and massage, forms the mainstay of rehabilitation. These passive exercises must be adjusted to the individual patient to avoid acute pain and worsening of clinical signs.37,38 Involving owners in therapy by teaching them proper techniques provides continuous and intensive rehabilitation. Early mobilization is started with passive flexion and extension of the hip joint in combination with stretching of the iliopsoas muscle. Range-of-motion exercises can limit fibrosis and adhesions and enhance blood and lymphatic flow and are performed three to six times daily for 10 to 30 repetitions.37,38

    Stretching is one of the most important manipulations of physical therapy. Restoring normal muscle length and distensibility breaks the vicious cycle of spastic shortening and modulates alignment of the repair tissues. Keeping the hip joint in extension for 30 to 60 seconds at a time up to three times a day for two to five repetitions is a practical recommendation in dogs.37,38

    Massages (rubbing, kneading, friction, or tapping) are easy to employ and useful to break the self-perpetuating cycle of muscle spasm leading to muscle shortening, which is a source of pain.38 The physiologic properties stem from reflex and mechanical effects. A practical recommendation for localized massage is approximately 10 minutes per day.38

    Other physical modalities employed in muscle injuries include superficial heat from hot packs and deep heat from ultrasound. Heat increases collagen extensibility, blood flow, pain threshold, macrophage activity, nerve conduction velocity, and enzyme activity and decreases muscle spasm. Shock-wave therapy and low-dose laser applications may also be helpful in some individuals.39

    Conservative treatment requires a progressive plan adapted to the patient. During muscular conditioning, the development of general muscular strength and neuromuscular coordination precedes the work-specific adaptations. Improving core stability is the mainstay of any rehabilitation program.

    Physical therapy is highly effective when initiated early. A study conducted on 25 dogs with iliopsoas injury demonstrated that dogs recovered completely with conservative treatment when lesions were present for <1 month.2 Shortening the recovery period, insufficient muscular conditioning, and neglecting the initiating cause of the injury pose a risk for reinjury and chronic muscular damage.5

    Surgical Therapy

    Surgical treatment is rarely necessary in acute iliopsoas injuries.5,17,19 Indications include chronic or recurrent lesions unresponsive to conventional therapy and fibrotic contracture of the iliopsoas muscle.20–22 Tenotomy of the iliopsoas muscle tendon through a ventral or craniolateral approach provides rapid pain relief and restoration of range of motion in the hip joint.19–23 The attachment to the iliacus muscle preserves core stability to a large degree. The outcome (pain relief and range of motion) is good if surgery is combined with physical therapy and the initiating factors are controlled (FIGURE 8). However, some decrease in performance should be anticipated in athletic dogs.


    Iliopsoas strain injuries are underdiagnosed in dogs. Primary traumatic lesions associated with an intensive sporting activity or accident seem to be less commonly presented to a veterinarian than secondary lesions associated with concomitant orthopedic problems such as hip dysplasia or cranial cruciate ligament rupture. Problems related to the iliopsoas muscle are readily diagnosed during a general orthopedic examination. Advanced imaging modalities help to confirm the diagnosis and detect associated pathologies.

    Conservative treatment, including rest, medical treatment, physical therapy, and muscular reconditioning, is successful in most patients, particularly if no other orthopedic or neurologic problems are present. Surgical treatment can be considered in cases unresponsive to conservative treatment.

    Downloadable PDF

    NOTE: CE Test Question #10 originally contained more than one correct response. This error was corrected on January 13, 2014.

    1. Breur GJ, Blevins WE. Traumatic injury of the iliopsoas muscle. Proc ACVS Congr 1994:421-422.

    2. Breur GJ, Blevins WE. Traumatic injury of the iliopsoas muscle in 25 dogs. Proc 5th ECVS Congr 1996:262.

    3. Breur GJ, Blevins WE. Traumatic injury of the iliopsoas muscle in three dogs. J Am Vet Med Assoc 1997;210(11):1631-1634.

    4. Pluhar GE. Diagnosis and treatment of iliopsoas injuries. Proc ACVS Congr 2005:343-345.

    5. Nielsen C, Pluhar GE. Diagnosis and treatment of hind limb muscle strain injuries in 22 dogs. Vet Comp Orthop Traumatol 2005;18:247-253.

    6. Carmichael S, Marshall W. Muscle and tendon disorders. In: Tobias KM, Johnston SA, eds. Veterinary Surgery: Small Animal. St. Louis, MO: Elsevier; 2012:1127-1134.

    7.Taylor R. Introduction to the normal musculoskeletal system. In: Bojrab MJ, ed. Disease Mechanisms in Small Animal Surgery. 2nd ed. Philadelphia: Lea & Febiger; 1993:1083-1088.

    8. Garrett W. Muscle strain injuries. Am J Sports Med 1994;24(6):2-8.

    9. König HE, Liebich HG. Veterinary Anatomy of Domestic Mammals: Textbook And Colour Atlas. 3rd ed. Stuttgart: Schattauer; 2001:247-250.

    10. Piermattei DL, Flo GL, DeCamp CE. Handbook of Small Animal Orthopedics and Fracture Repair. St. Louis, MO: Elsevier; 2006:216-232.

    11. Kirkendall DT, Garrett WE. Clinical perspectives regarding eccentric muscle injury. Clin Orthop Relat Res 2002;43:81-89.

    12. Kieb M, Lorbach O, Engelhard M. Muscle injuries: diagnostics and treatments. Orthopäde 2010;39:1098-1107.

    13. Armstrong RB. Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Med Sci Sports Exerc 1984;Dec;16(6):529-538.

    14. Morgan JE, Partridge TA. Muscle satellite cells. Int J Biochem Cell Biol2003;35(8):1151-1156.

    15. Winkler T, Von Roth P, Matziolis G, et al. Time course of skeletal muscle regeneration after severe trauma. Acta Orthopaedica 2011;82(1):102-111.

    16 .Schwellnus MP, Derman EW, Noakes TD. Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis. J Sports Sci 1997;15(3):277-285.

    17. Janssens LA. Trigger points in 48 dogs with myofascial pain syndromes. Vet Surg 1991;20(4):274-278.

    18. Rossmeisl JH, Rohleder JJ, Hancock R, Lanz OI. Computed tomography features of suspected traumatic injury to the iliopsoas and pelvic limb musculature of a dog. Vet Radiol 2004;45(5):388-392.

    19. Vidoni B, Henninger W, Lorinson D. Traumatic avulsion fracture of the lesser trochanter in a dog. Vet Comp Orthop Traumatol 2005;18:105-109.

    20. Stepnik MW, Olby N, Thompson RR, Marcellin-Little DJ. Femoral neuropathy in a dog with iliopsoas muscle injury. Vet Surg 2006;35:186-190.

    21. Ragetly GR, Griffon DJ, Johnson AL, et al. Bilateral iliopsoas muscle contracture and spinous process impingement in a German shepherd dog. Vet Surg2009;38:946-953.

    22. Adrega Da Silva C, Bernard F, Bardet JF, et al. Fibrotic myopathy of the iliopsoas muscle in a dog. Vet Comp Orthop Traumatol 2009;22:238-242.

    23. BallinariU, Montavon PM, Huber E, Weiss R. Pectineus myectomy, tenotomy of the iliopsoas and neurectomy of the joint capsule as symptomatic therapy for coxarthrosis of the dog. Schweiz Arch Tierheilkd 1995;137(6):251-257.

    24. Kramer M, Gerwing M, Hach V, Schimke E. Sonography of the musculoskeletal system in dogs and cats. Vet Radiol 1997;38(2):139-149.

    25. Cannon MS, Puchalski SM. Ultrasonographic evaluation of normal canine iliopsoas muscle. Vet Radiol 2008;49(4):378-382.

    26. Dennis R, Kirberger RM, Barr F, Wrigley RH. Handbook of small Animal Radiology and Ultrasound. 2nd edition. Edinburgh; Churchill Livingstone Elsevier 2010: 337.

    27. Daly BD, McPhillips M, Leung AW, et al. Ultrasound, computed tomography and magnetic resonance in the investigation of iliopsoas compartment disease. Australas Radiol 1992;36:294-299.

    28. El-Khoury GY, Brandser EA, Kathol MH, et al. Imaging of muscle injuries. Skeletal Radiol 1996;25:3-11.

    29. Gavin PR. MRI of musculotendinous injuries. Proc 13th ESVOT Congr 2006:45.

    30. Steiss JE, Levine D. Physical agent modalities. Vet Clin North Am Small Anim Pract 2005;35:1317-1333.

    31. Piras A. Muscle and tendon injuries and diagnosis, treatment and prognosis. Proc 13th ESVOT Congr 2006:121-127.

    32. Almekinders LC, Gilbert JA. Healing of experimental muscle strains and the effects of nonsteroidal anti-inflammatory medication. Am J Sports Med 1986;14:303-308.

    33. Obremsky WT, Seaber AV, Ribbeck BM, Garrett WE. Biomechanical and histologic assessment of a controlled muscle strain injury treated with piroxicam. Am J Sports Med 1994; 22: 558-561.

    34. MazzoccaAD, McCarthy MB, Chowaniec DM, et al. The positive effects of different platelet-rich plasma methods on human muscle, bone, and tendon cells. Am J Sports Med 2012;40(8):1742-1749.

    35. Wright-CarpenterT, Opolon P, Appell HJ, et al. Treatment of muscle injuries by local administration of autologous conditioned serum: animal experiments using a muscle contusion model. Int J Sports Med 2004;25(8):582-587.

    36. Huang S, Wang Z.Influence of platelet-rich plasma on proliferation and osteogenic differentiation of skeletal muscle satellite cells: an in vitro study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;110(4):453-462.

    37. Millis DL, Lewelling A, Hamilton S. Range-of-motion and stretching exercises. In: Millis DL, Levine D, Taylor RA, eds. Canine Rehabilitation and Physical Therapy. St. Louis, MO: Saunders; 2004:228-243.

    38. Bockstahler B, Millis D, Levine D, Mlacnik E. Physiotherapy—what and how. In: Levine D, Millis D, eds. Essential Facts of Physiotherapy in Dogs and Cats. Babenhausen: BE VetVerlag; 2004:46-58.

    39. Millis DL, Francis D, Adamson C. Emerging modalities in veterinary rehabilitation. Vet Clin North Am Small Anim Pract 2005;35:1335-1355.

    References »

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