The hip joint is a synovial joint formed between the head of the femur and the acetabulum of the innominate bone. The head of the femur is slightly more than half a sphere and faces anteriorly, superiorly and medially to articulate with the acetabulum forming a ball-and-socket joint. This articulation offers great stability and provides sufficient mobility for gait. The close packed position of the hip joint is full extension, with a degree of abduction and medial rotation (Hartley 1995, Standring 2009).

The acetabulum is deepened by the fibrocartilaginous acetabular labrum and all articular surfaces are covered by articular cartilage. The fibrous capsule, lined with synovium, surrounds most of the neck of the femur, attaching above to the acetabular rim, below to the intertrochanteric line anteriorly and 1 cm above the inter-trochanteric crest posteriorly. Both the joint capsule and the articular cartilage tend to be thicker anterosuperiorly, which is the region of most stress in weight-bearing. Synovial plicae (folds or reflections of the synovial membrane) have been identified by Fu et al (1997), found mainly on the external surface of the lower medial part of the acetabular labrum (labral plicae) but also at the base of the ligament of the head of the femur and on the base of the femoral neck. The labral plicae may potentially be a source of pain if injured or thickened since, in the normal state, these have been seen to slip between the articular surfaces of the femoral head and acetabulum during medial rotation and to return to their original position during lateral rotation.

Three ligaments reinforce the articular capsule and control movement. All three are taut in extension and relaxed in flexion. The iliofemoral ligament has strong medial and lateral bands which form a Y-shape, passing from the anterior inferior iliac spine to the intertrochanteric line. The pubofemoral ligament passes from the superior pubic ramus to blend distally with the capsule and the medial border of the iliofemoral ligament. The ischiofemoral ligament passes from the ischium and winds superiorly and laterally to the upper part of the femoral neck, blending with the capsule of the hip joint and supporting it posteriorly.

The psoas bursa (L2–L3; Cyriax 1982) is 5–7 cm long and 2–4 cm wide in its normal collapsed state (Underwood et al 1988, Toohey et al 1990, Flanagan et al 1995, Zimmermann et al 1995). In 15% of cadaveric specimens, the psoas bursa was seen to communicate with the hip joint via an aperture between the iliofemoral and pubofemoral ligaments (Flanagan et al 1995). It may be a simple bursa or multiloculated with well-defined thin walls (Meaney et al 1992).

The psoas bursa lies beneath the musculotendinous junction of the iliopsoas muscle and the front of the capsule of the hip joint (Fig. 10.1). It cushions the ilio-psoas tendon as it winds round the front of the hip joint to its posteromedial insertion on the lesser trochanter. It is related anteromedially to the femoral artery and anteriorly to the femoral nerve (Canoso 1981). Its point of location is just distal to the midpoint of the inguinal ligament, deep to the femoral artery.

The gluteal bursa (L4–L5; Cyriax & Cyriax 1993) is not a single entity, but for clinical purposes is considered to be so. At least four separate bursae lie between the different planes of the gluteal muscles as they attach to or pass over the greater trochanter, collectively forming the gluteal bursa.

Two bursae are associated with gluteus maximus: a large trochanteric bursa (Fig. 10.2), separating it from the lateral aspect of the greater trochanter, and a gluteofemoral bursa, lying between it and vastus lateralis (Standring 2009). The trochanteric bursa of gluteus medius lies between its tendon and the anterosuperior aspect of the greater trochanter. The trochanteric bursa of gluteus minimus separates its insertion from the medial part of the greater trochanter (Standring 2009). One further bursa may be present, the ischial bursa, lying between the ischial tuberosity and the lower part of gluteus maximus.

Anterior muscles are flexors of the hip, although they may also assist other hip movements. Some pass over the knee where they also have an effect. Resisted flexion of the hip tests mainly psoas major; with the knee flexed it is also testing rectus femoris.

Psoas major (ventral rami L1–L3) has its origin from the lumbar spine. It descends to pass under the centre of the inguinal ligament receiving the fibres of iliacus on its lateral side. The iliopsoas tendon crosses the front of the hip joint where it is cushioned by the underlying psoas bursa. The combined tendon winds posteriorly to insert into the lesser trochanter of the femur.

Sartorius (femoral nerve L2–L3) passes from the anterior superior iliac spine to cross the thigh medially, inserting into the upper medial aspect of the tibia. It marks the lateral border of the femoral triangle.

Rectus femoris (femoral nerve L2–L4) is part of the quadriceps mechanism and has its main effect at the knee. However, its origin above the hip makes it a two-joint muscle and it also acts as a powerful hip flexor, being most efficient when the knee is flexed (Kapandji 1987). It has two heads of origin: a straight head from the anterior inferior iliac spine and a reflected head from just above the acetabular rim. It joins the rest of the quadriceps to insert into the patellar tendon.

Posterior muscles are extensors of the hip. Gluteus maximus acts principally as a hip extensor while the hamstrings assist hip extension, but their main effect is in flexing the knee. Since the hamstring muscles run over two joints, their efficiency in extending the hip increases if the knee is locked into extension (Kapandji 1987).

Gluteus maximus (inferior gluteal nerve L5, S1–S2) is the largest and most superficial of the gluteal muscles. It passes from behind the posterior gluteal line on the blade of the ilium to the iliotibial tract and upper femur. The large trochanteric bursa separates the insertion of gluteus maximus from the lateral aspect of the greater trochanter.

Biceps femoris (sciatic nerve L5, S1–S2) is the lateral hamstring with two heads of origin. A long head arises from an inferomedial facet on the ischial tuberosity (which it shares with semitendinosus) and a short head from the lateral lip of the linea aspera. Its fibres converge into a fusiform muscle belly and its tendon of insertion attaches to the head of the fibula.

Semitendinosus and semimembranosus are the medial hamstrings. Semitendinosus (sciatic nerve L5, S1–S2) takes origin from the inferomedial facet on the ischial tuberosity. Its muscle belly ends in the middle of the thigh and its long tendon of insertion lies on semimembranosus before winding around to the medial aspect of the upper tibia. Semimembranosus (sciatic nerve L5, S1–S2) takes origin from the superolateral facet on the ischial tuberosity and has its main insertion onto the posterior aspect of the medial tibial condyle into the tuberculum tendinis.

Functionally, the small, deep muscles of the hip are responsible for lateral rotation.

Piriformis (L5, S1–S2) originates in the pelvis, exiting through the greater sciatic foramen to attach to the upper border of the greater trochanter.

Obturator externus (posterior branch of the obturator nerve L3–L4) and obturator internus (nerve to obturator internus L5, S1) pass posteriorly to the hip joint and insert into the medial surface of the greater trochanter and trochanteric fossa.

Gemelli (L5, S1) pass from the ischial spine and ischial tuberosity to the medial aspect of the greater trochanter.

Quadratus femoris (nerve to quadratus femoris L5, S1) passes from the ischial tuberosity to the quadrate tubercle in the middle of the trochanteric crest.

Lateral muscles are abductors and lateral rotators. Gluteus medius is the main hip abductor while medius and minimus together are responsible for maintaining the position of the opposite side of the pelvis in single-leg stance. Weakness of the hip abductors produces a positive Trendelenburg sign. Tensor fascia lata and the anterior fibres of gluteus medius and minimus also produce medial rotation and flexion because they lie anterior to the frontal plane of the hip joint. Lying posteriorly, some fibres of gluteus medius and minimus are responsible for lateral rotation and extension (Kapandji 1987).

Gluteus medius (superior gluteal nerve L5, S1) is partially overlapped by maximus and lies in a slightly deeper plane. It originates from the blade of the ilium between posterior and anterior gluteal lines and inserts into the lateral aspect of the greater trochanter.

Gluteus minimus (superior gluteal nerve L5, S1) is the deepest gluteal muscle and arises between the anterior and inferior gluteal lines, inserting into the medial part of the anterior trochanteric surface.

Tensor fascia lata (superior gluteal nerve L4–L5) arises from the anterior 5 cm of the outer lip of the iliac crest and the anterior superior iliac spine. It passes downwards and laterally to insert into the anterior border of the ilio-tibial tract.

The adductor muscles originate in the pelvis and pass to the medial aspect of the thigh.

Functionally, the medial muscles are responsible for adduction of the hip. Medial rotation at the hip is a secondary function of gluteus medius, minimus and tensor fascia lata; adductor magnus, longus and pectineus may also contribute to this movement.

Gracilis (obturator nerve L2–L3) is the most medial hip adductor. It passes from the lower half of the body of the pubis, the inferior pubic ramus and the adjacent ischial ramus, to run vertically downwards to just below the medial tibial condyle.

Pectineus (femoral nerve L2–L3) passes from the pecten pubis running posterolaterally to a line joining the lesser trochanter to the linea aspera.

Adductor longus (obturator nerve L2–L4) is the most superficial adductor. It passes from the body of the pubis, in the angle between the crest and the symphysis pubis, to descend posterolaterally to the middle third of the linea aspera.

Adductor brevis (obturator nerve L3) lies deep to adductor longus, passing from the lower aspect of the body of the pubis and the inferior pubic ramus to its attachment on the femur, between the lesser trochanter and the linea aspera.

Adductor magnus (upper fibres, obturator nerve; lower fibres, tibial branch of the sciatic nerve, L2–L4) is the largest and deepest adductor muscle. It is considered to have two separate portions, one an adductor portion and the other a hamstring portion, each with its own separate nerve supply. It takes origin from the inferior pubic ramus, the adjacent ischial ramus and the infero-lateral aspect of the ischial tuberosity. Its upper fibres pass mainly horizontally to the linea aspera of the femur and form the adductor part of the muscle. Its lower fibres pass more vertically to the adductor tubercle on the medial femoral condyle and form the hamstring part.

Palpate the iliac crest, which should be obvious in most people as no muscles attach to its superior border. The highest point of the crest lies just posterior to the midpoint and gives an approximate indication of the level of the spinous process of L4.

Palpate the anterior superior iliac spine which is sub-cutaneous and located at the anterior end of the iliac crest. It marks the lateral attachment of the inguinal ligament and the origin of the sartorius muscle.

Palpate the posterior superior iliac spine which is situated at the posterior end of the iliac crest. It is not as readily palpable as the anterior spine, but lies under a dimple in the upper buttock, approximately 4 cm lateral to the spinous process of S2. It gives attachment to the sacro-tuberous ligament. Imagine a line drawn from the posterior superior iliac spine to the spinous process of S2; this line crosses the centre of the sacroiliac joint and gives an indication of the joint’s position.

Consider the position of the anterior and posterior inferior iliac spines which lie below the superior spines and are not as readily palpable. The anterior inferior spine gives origin superiorly to the long head of rectus femoris and inferiorly to part of the iliofemoral ligament.

Locate the position of the pubic tubercle at the medial end of the inguinal crease, lying at the same level as the top of the greater trochanter. It marks the medial attachment of the inguinal ligament.

Palpate the bony ischial tuberosity, which lies in the buttock approximately 5 cm lateral to the midline just above the gluteal fold. In the sitting position, body weight is supported by the ischial tuberosities. Each is most easily palpated with the patient in side-lying and the hip placed in flexion, to bring the ischial tuberosity out from under the bulk of gluteus maximus.

In side-lying palpate the greater trochanter, which is a large quadrangular bony prominence situated at the upper lateral shaft of the femur, approximately one hand’s breadth below the iliac crest. Grasp the greater trochanter with your thumb, index and middle fingers (Fig. 10.3), lifting the leg passively into abduction to relax the iliotibial tract. The greater trochanter will be a useful bony landmark for some of the injection techniques around the hip.

Consider the position of the femoral triangle on the anterior thigh (Fig. 10.4). Place the leg into the FABER position – a combination of Flexion, ABduction and External (lateral) Rotation of the hip – to give you an indication of the borders of the triangle. The inguinal ligament forms the base of the triangle, sartorius its lateral border and adductor longus its medial border. Iliopsoas and pectineus lie in the floor of the femoral triangle.

Consider the position of the lateral femoral cutaneous nerve of the thigh (L2–L3) as it passes under or through the inguinal ligament, just medial to the anterior superior iliac spine. It may be compressed here, causing a condition called meralgia paraesthetica, which produces paraesthesia and pain in the nerve’s distribution on the lateral side of the thigh. It is found in obese patients and those who wear tight-fitting clothes or belts (Adkins & Figler 2000).

Palpate for the femoral artery which passes down through the middle of the triangle with the femoral vein situated medially and the femoral nerve laterally. You will locate a strong pulse just distal to the midpoint of the inguinal ligament.

Locating the femoral pulse will prove a useful landmark for the structures passing deep to it. From superficial to deep these are the iliopsoas tendon, which is en route to its insertion into the lesser trochanter, the psoas bursa, and the hip joint.

Consider the position of the sciatic nerve in the buttock (Fig. 10.5). You can locate its approximate position by marking a point midway between the posterior superior iliac spine and the greater trochanter, which identifies the position of the nerve as it leaves the pelvis via the greater sciatic foramen, emerging under piriformis. Join this to another mark at a point just medial to the midpoint between the greater trochanter and the ischial tuberosity. This indicates the position of the nerve as it continues to exit the buttock under the lower border of gluteus maximus (Standring 2009).

Place the leg into the FABER position to identify the thick, cordlike tendon of adductor longus. Palpate this tendon to appreciate its width and depth.

A general observation is made of the patient’s face and overall posture, but particular attention is paid to the gait. Since the function of the hip joint is to support body weight, lesions involving the joint mechanics tend to cause alterations in the gait pattern. An uneven stride will indicate restricted movement, as found in arthritis, or may be due to pain on weight-bearing. Excessive lateral rotation on walking may indicate a slipped epiphysis in the young or may be present with pain or advanced capsular contracture in the elderly, indicating an arthrosis with a marked capsular pattern. A Trendelenburg gait will indicate weak abductor muscles.

Pain in the hip joint region may originate in the lumbar spine and a detailed history will help to eliminate a lesion in the area.

The age, occupation, sports, hobbies and lifestyle of the patient may alert the examiner to the possible cause of the lesion.

The age of the patient is relevant to conditions at the hip. Degenerative osteoarthrosis typically presents in the middle to older age group, although it is not uncommon to find it in younger athletes, especially road runners. Muscle lesions and bursitis affect the middle age group, while loose bodies can present as a complication of osteo-arthrosis in the older group or as osteochondritis dissecans in adolescents.

Children can develop hip problems which if misdiagnosed can be potentially serious, and an orthopaedic opinion should always be sought. ‘Irritable hip’ is a non-specific diagnosis for groin pain, limited movement and a limp. Perthes’ disease affects boys aged 3–10 and is an osteochondritis of the femoral epiphysis. Slipped epiphysis is either sudden or gradual slipping of the superior epiphyseal plate which may produce a lateral rotation deformity. It tends to occur in overweight adolescents (10–16) and is more common in boys, who present with pain on exercise. Transient synovitis is of unknown aetiology and affects children under 10 years with an acute onset (Gough-Palmer & McHugh 2007). Juvenile chronic arthritis usually begins in other joints, but it can also affect the hip joints. Emms et al (2002) remind us that, although it is well known that knee pain in children may be referred from the hip, it must not be forgotten that hip pathology may masquerade as knee pain in adult patients as well.

Excessive muscle contraction, as involved in explosive sports changing rapidly from running to jumping (hurdling, etc.), can lead to avulsion fractures and chronic apophysitis in adolescents, most commonly at the origin of the long head of rectus femoris at the anterior inferior iliac spine (Brukner & Khan 2007).

Occupation, sports, hobbies and lifestyle will certainly indicate the aggravating factors of the condition and allow the clinician to formulate a programme of treatment and advice, tailored to the patient’s individual needs.

Specific sports-related conditions should be considered. Stress fracture of the femoral neck may be encountered in young adults who are involved in endurance and high-intensity sports; initially anterior hip pain occurs late into the sporting activity but progresses to limit activity, occurring during any weight-bearing episode and even at rest. It should also be suspected in women with the female athletic triad of amenorrhoea, eating disorder and osteo-porosis. Diagnosis is essential to prevent progression to avascular necrosis of the femoral head (O’Kane 1999, Adkins & Figler 2000).

Osteitis pubis, a poorly understood pathological condition involving the pubic bone and symphysis pubis, presents with groin pain which may be bilateral. The symptoms may be aggravated by exercise, twisting, turning and kicking. Pain is provoked by resisted adduction (the ‘squeeze test’) which is usually accompanied by weakness, and there is tenderness to palpation over the pubic tubercles and symphysis pubis (Brukner & Khan 2007). The so-called ‘sports hernias’ should also be considered as a cause of anterior hip pain. These are thought to be responsible for activity-related hip pain, particularly in football, rugby and ice hockey players (O’Kane 1999). Inguinal hernia presents as a lump in the groin that goes away when the patient lies down. The lump reappears or increases on coughing and is not usually painful (Jenkins & O’Dwyer 2008). ‘Gilmore’s groin’ is not a hernia but should be considered in the differential diagnosis of groin pain, particularly in the sporting male. It is a disruption of the external oblique aponeurosis causing dilatation of the superficial inguinal ring, torn conjoined tendon and dehiscence between the inguinal ligament and the torn conjoined tendon (Williams & Foster 1995, Tibor & Sekiya 2008) (see p. 272).

The site and spread of pain may be local, indicating a superficial or less irritable lesion such as a muscle strain, or diffuse, indicating a larger lesion or gross inflammation.

Referred pain may originate from the lumbar spine. The sensory nerve supply to the hip joint is mainly through the femoral nerve L2–L3; therefore the joint itself refers pain into these dermatomes depending on the size of the lesion. Part of the L2 and L3 dermatomes covers the upper buttock and a hip lesion may present as low back pain only. Lesher et al (2008) looked at pain referral patterns arising from the hip joint. Of the 51 patients assessed, 55% of patients had referral to the groin and 57% to the thigh; 22% experienced pain in the lower limb distal to the knee, and occasionally to the foot, but the most common area for referral was buttock pain, experienced by 71% of patients. The most common referral combination was buttock pain with thigh referral, which occurred in 20% of subjects. This pattern of referral is similar to both the lumbar spine and sacroiliac joint and differential diagnosis can be difficult on the basis of pain referral alone. Other factors from the history and the objective examination will help towards clinical diagnosis and it is not unusual for the initial diagnosis to be modified following consideration of treatment outcomes.

Groin pain or pain referred to the knee in the child or adolescent without obvious cause must be considered serious and a specialist opinion sought for the possibility of the conditions mentioned above.

The onset of the symptoms may be gradual or sudden.

In osteoarthrosis the pain has a gradual onset, initially during weight-bearing activities, progressing to hip pain without weight-bearing, and present at rest (Cailliet 1990). A history of previous trauma such as fracture, which alters joint biomechanics, can predispose the joint to degenerative changes.

Relatively minor trauma can fracture the pelvis in the elderly, producing severe pain of sudden onset. Loose bodies present suddenly, as do traumatic muscular lesions. Muscles around the hip joint can be easily strained, since many are two-joint muscles, and a sudden explosive contraction such as that seen in sprinting may produce overstretching (Hartley 1995). Overuse or repetitive movements may produce chronic contractile lesions or bursitis.

The duration of symptoms indicates the stage of the lesion in the inflammatory process. Degenerative osteo-arthrosis will present a typical history of gradually worsening episodes of pain. Bursitis tends to give a gradual onset of aching pain and therefore is often present for many months before the patient seeks treatment. A severe pain which gradually increases in intensity, and remains so, is indicative of a serious lesion. This, coupled with other findings in the history, may be indicative of the ‘sign of the buttock’ (see p. 274).

The symptoms and behaviour need to be considered. The behaviour of the pain gives an indication of the nature of the lesion. For example, osteoarthrosis at the hip joint may be aggravated by activity or weight-bearing, or inflamed bursae and muscle sprains are worse with use and eased by rest.

The other symptoms described by the patient may give essential clues to diagnosis. Bursae produce pain on activities which squeeze or compress them, e.g. lying on the side or sitting. Loose bodies tend to produce twinging pain and a sensation of giving way on weight-bearing. Similar symptoms may be associated with labral tears or anterior acetabular chondral defects where clicking or locking may also be present (Neumann et al 2007). Arthritis tends to produce morning pain and stiffness due to accumulation of intracapsular swelling overnight (Hartley 1995). Degenerative osteoarthrosis, in its early stage, often produces night pain. Unrelenting pain should be considered serious, especially if the patient is unwell with a fever, night sweats and rigors.

To determine if the pain is coming from the lumbar spine, the patient is questioned about the presence of paraesthesia and pain produced by a cough or sneeze.

An indication of past medical history, other joint involvement and medications may give a clue to diagnosis and will establish whether contraindications to treatment techniques exist. Patients should be asked about any unexpected recent weight loss, indicative of more serious lesions, such as secondary deposits which are common in the hip and pelvis (Paice 1995). Differential diagnosis should also consider the exclusion of hip pain associated with pathology of the abdominal and pelvic organs as well as femoral or inguinal hernias. In addition to past medical history, establish any ongoing conditions and treatment. Explore other previous or current musculoskeletal problems with previous episodes of the current complaint, any treatment given and the outcome of treatment.

An inspection of the general posture in weight-bearing will indicate any bony deformity. Look for general postural asymmetry which may be relevant, the position of the buttock creases, posterior superior iliac spines, anterior superior iliac spines, level of the iliac crests, any leg length discrepancy and the position of the feet.

Colour changes and swelling are not expected at the hip because it is such a deep joint, but they may be associated with trauma, bruising and abrasions. If redness and swelling are present in the buttock area without a history of trauma, the ‘sign of the buttock’ (see p. 274) may be suspected.

Muscle wasting may be seen in the glutei associated with a lumbar lesion, or in the quadriceps associated with degenerative osteoarthrosis of the hip or a lumbar lesion.

Before any movements are performed, the state at rest is established to provide a baseline for subsequent comparison.

The suggested sequence for the objective examination will now be given, followed by a commentary including the reasoning in performing the movements and the significance of the possible findings. Comparison should always be made with the other side.

The routine for the examination of the hip is conducted in the above order as it allows all tests in each position of standing, supine and prone to be completed.

The lumbar spine is first assessed by the four active movements. If active lumbar extension reproduces the pain, it should be repeated with the hip joint eliminated by placing it into flexion with the foot up on a stool. If extension is still painful, the lesion lies in the lumbar spine and a more thorough investigation of this must then be made. The straight leg raise and femoral stretch tests are applied within the examination sequence to test for neural involvement. The straight leg raise does stretch the hamstrings, which needs to be considered within clinical reasoning, and is part of an accessory test to look for serious pathology in the hip or pelvis (see below).

Tests for sacroiliac joint involvement may also be included at this stage, as indicated by the history, and are described in Chapter 14.

The passive hip movements test the inert structures for pain, range of movement and end-feel. Limited movement may be typical of the capsular pattern of limitation due to arthritis. Normally, passive flexion has a ‘soft’ end-feel while passive medial rotation, lateral rotation and extension have an ‘elastic’ end-feel. It is not possible to appreciate the end-feel of the capsule on passive abduction and adduction as the tension in the overlying soft tissue structures provides the end of range of these movements before the capsule can be stressed. Abduction may still be limited as part of the capsular pattern nonetheless. A bursitis or a loose body in the joint produces a non-capsular pattern of movement.

The resisted movements test the contractile structures for pain and power. At the hip, muscle lesions are commonly found in the adductors, quadriceps and hamstrings, but positive resisted tests may also be an accessory sign in bursitis. Resisted flexion tests mainly psoas, but since the knee is flexed it also tests rectus femoris. Resisted abduction tests mainly gluteus medius, while resisted adduction tests the adductor muscles, particularly adductor longus. Resisted extension tests mainly gluteus maximus, but since the knee is extended, this also tests the hamstrings. Resisted rotation tests the medial and lateral rotators of the hip, resisted knee flexion tests the hamstring muscles and resisted knee extension tests the quadriceps muscle group.

Accessory tests can be applied if indicated. Combined hip flexion and adduction can be applied to compress the psoas bursa to confirm its diagnosis, and a straight leg raise can be included if the ‘sign of the buttock’ is suspected as an indicator of serious pathology in the hip or pelvis (see p. 274).

This is usually the initial phase of diagnosis of the condition. At this stage, the key findings are as follows:

The principle of treatment, applied during this early stage, is to stretch the capsular adhesions using a Grade B capsular stretching technique in conjunction with heat applied to the joint. The aim of treatment is to relieve pain, allowing a greater range of pain-free movement to be established.

Here the patient’s symptoms and signs indicate a progression of the disease. Pain may be present at rest as well as exacerbated by weight-bearing activities. On examination, a moderate to severe capsular pattern is found and the limited movements have a ‘hard’ end-feel. Capsular stretching may no longer provide benefit and the treatment of choice in the short term may be injection.

A lateral approach is advocated for reasons of safety. Leopold et al (2001) conducted a study of 30 cadaver hips to test the hypothesis that, using anatomical landmarks, the anterior and lateral injection approaches to the hip joint result in reproducibly correct intra-articular needle placement and avoid important periarticular neurovascular structures. The success rate of intra-articular injection was 60% using the anterior approach and 80% using the lateral approach. During the anterior approach the needle passed significantly closer to neurovascular structures than the lateral approach, which was never within 25 mm of any such structures. The study concluded that the lateral approach under fluoroscopy or ultrasound would be the safest and most effective method for injecting the hip joint. It is certainly becoming common practice to perform hip injections with image guidance to ensure intra-articular placement (Robinson et al 2007).

A minimum dose 40 mg of triamcinolone acetonide is recommended but support for a larger dose of 80 mg is provided by a study conducted by Robinson et al (2007) who compared the outcome of infiltration with 40 mg and 80 mg methylprednisolone, using fluoroscopic guidance and an anterior approach. For the 40 mg dose there was statistical improvement in pain and stiffness, but not disability, at week 6 and only the improvement in stiffness remained at 12 weeks. For the 80 mg dose, there was significant improvement in pain, stiffness and disability at week 6 that was maintained at 12 weeks.

Injection of the hip joint

Suggested needle size: 20G × 3½ in (0.9 × 90 mm) spinal needle

Dose: 40–80 mg triamcinolone acetonide in a total volume of 5–6 mL

Position the patient in side-lying with the painful leg uppermost and supported in a neutral position on a pillow. Locate the greater trochanter by grasping it between thumb, index and middle fingers; the index finger should be resting on the top of the trochanter. To test you are in the correct position, move the leg passively into some abduction (Fig. 10.35), to relax the iliotibial tract, and you should feel your index finger sink in over the top of the trochanter.

The capsule of the hip joint almost completely surrounds the neck of the femur. By inserting the needle just above the index finger, i.e. above the greater trochanter, and aiming vertically downward towards the neck of the femur, the needle should be intracapsular once you gently make contact with bone (Fig. 10.36). You will feel a resistance as the needle pierces first the fascia lata, then the capsule before reaching bone (Fig. 10.37). Deliver the injection as a bolus. The patient is advised to maintain a period of relative rest for approximately 2 weeks following injection.

Controversy exists concerning repeated steroid injections into weight-bearing joints and the risk of steroid arthropathy (Cameron 1995). Therefore, as a general precaution, repeated corticosteroid injections into the hip joint have not been recommended and it has been advised that no more than two a year should be given without monitoring the degenerative condition of the joint with X-ray investigation. Raynauld et al (2003) conducted a study on repeated injections into the knee joint and established no harmful effects (see Ch. 11), although reassurance for hip injections on the basis of this study cannot be assumed.

Kaspar & de Van de Beer (2005) conducted a retrospective study of 40 patients who had had injections prior to hip arthroplasty and 40 who had not. The hip injections had all been given under sterile theatre conditions with the same dosages of corticosteroid and local anaesthetic but the study found a significantly increased rate of postoperative infection in those hips that had had previous injection. No firm explanation could be given and there was no mention of the length of time after the injection that the hip replacements took place. The outcome of the study does beg for further research to be conducted since, as the authors suggest, previous injection into the hip joint could be considered to be a contraindication to arthroplastic procedures. In contrast to this finding, a similar study to establish the influence of corticosteroid injections on the incidence of infection following total knee arthroplasty found no link between previous injection and subsequent postoperative infection (Horne et al 2008) (see Ch. 11). Further studies are needed to clarify whether previous corticosteroid injection should provide a bar to subsequent replacement surgery. Clinicians should seek the opinion of their local hip surgeons prior to injecting the hip.

Conservative management no longer controls the patient’s pain and functional disability may now be serious. Surgery is probably indicated, but there are no agreed criteria or guidelines for electing to perform hip surgery (Dieppe 1995). Pain, age and disability, as well as psychological factors, should all be taken into consideration by the patient and surgeon. Hip resurfacing restores the normal anatomy and biomechanics of the hip joint and provides proximal femoral anatomy and loading to near normal. It allows greater activity levels and tends to be preferred by the younger, fitter population (Heilpern et al 2008).

Injection may be given for pain relief during this stage, as described above.

This may affect the hip joint and symptomatic relief may be gained from intra-articular injection, given as described above.

A loose body in the hip joint causes twinges of pain felt in the groin or radiating down the front of the leg. These twinges may be associated with a momentary sensation of locking or giving way and an inability to weight-bear. This history suggests a loose body in the joint which periodically becomes impacted between the joint surfaces. The loose body may be associated with the rare condition osteochondritis dissecans in adolescents, but most commonly occurs secondary to the onset of degenerative osteoarthrosis at the joint (Cyriax & Cyriax 1993, Saotome et al 2006, Tibor & Sekiya 2008). Loose bodies associated with arthrosis can be chondral, osteochondral or osseous. They can increase in size and progressively worsen the damage to the joint surfaces as well as the clinical symptoms (Bianchi & Martinoli 1999). To avoid this they should be removed arthroscopically (Tibor & Sekiya 2008).

Differential diagnosis should exclude labral tears which are found in the young adult. Labral pathology is often associated with traumatic incidents which may be minor twisting, repetitive flexion or hyperextension injuries. Pain is usually felt in the groin with clicking, locking and/or giving way (O’Kane 1999, Hickman & Peters 2001, Neumann et al 2007). A short stance phase in gait may be evident, or a Trendelenburg gait, and impingement tests, combining forced flexion, adduction and medial rotation, or flexion, abduction with lateral rotation, may reproduce pain (Martin et al 2008, Tibor & Sekiya 2008). There may also be pain at the extremes of movement. Magnetic resonance imaging (MRI) can be used to confirm the tear (Bharam 2006). However, in looking at the diagnostic accuracy of clinical examination in determining intra-articular pain for potential hip arthroscopy candidates, Martin et al (2008) found that even if a labral tear is present on MRI it may not be responsible for the patient’s symptoms and the whole clinical presentation should therefore be considered.

Capsular laxity is an emerging and controversial concept. The laxity may result from acute dislocation or without specific trauma and can occur as a consequence of overuse or repeated axial loading, e.g. in golfers. It may be a cause of anterior hip pain (Tibor & Sekiya 2008).

Signs of a loose body consist of a non-capsular pattern, commonly with pain at the end of range of full passive hip flexion and lateral rotation. If the range of movement demonstrates limitation, a springy end-feel may be appreciated. The principle of treatment applied is to reduce the loose body using strong traction together with Grade A mobilization. If successful, the loose body will be moved to a position within the joint where it no longer causes these typical symptoms.

Two mobilization techniques will be described (Cyriax 1984, Cyriax & Cyriax 1993).

Psoas, trochanteric or occasionally ischial bursitis may be a cause of pain at the hip, although these conditions are difficult to diagnose definitively and may be overlooked. They present a muddled clinical picture and may be misdiagnosed as a tendinopathy. However, because of the close anatomical relationship of bursae to tendons, bursitis may coexist with tendinopathy.

The patient commonly presents with a gradual onset of pain, often with no obvious cause. Although it is possible to induce a bursitis by direct trauma, it is usually the result of overuse activity, with the pain increased by activity and better for rest.

On examination, a muddled clinical picture emerges of a non-capsular pattern with some resisted tests and some passive tests reproducing the pain. This may mimic that of tendinopathy. Tendinopathy usually produces a predictable clinical picture of pain on the appropriate resisted test and pain on passive stretching in the opposite direction. In contrast, a bursitis may produce pain when passively squeezed under a contracted muscle or tendon and thus this muddle emerges.

The sign of the buttock is pain produced on straight leg raise which increases on flexing the knee and hip (Cyriax & Cyriax 1993, Hattam & Smeatham 2010). An empty end-feel is appreciated as more range of movement is available, but any attempt to produce more hip flexion is abruptly stopped by voluntary muscle spasm and the patient puts out the hand to stop the movement.

A positive sign indicates a major lesion in the buttock or hip region. The history will usually reveal an unwell patient, who looks ill and may have a fever with night sweats and rigors. The pain may be unrelenting in the buttock, hip or leg. It is not eased by rest and therefore night pain is a feature.

On examination, a non-capsular pattern of movement at the hip, and often the lumbar spine, is discovered. Pain may be increased by lumbar flexion and resisted tests at the hip, but the cardinal feature of this condition is the positive sign of the buttock.

Possible causes of the sign of the buttock are neoplasm of the upper femur or ilium, fracture of the sacrum, ischiorectal abscess, sepsis, either septic bursitis or arthritis, or osteomyelitis of the upper femur (Cyriax & Cyriax 1993). Urgent medical attention and further investigation are required.

The hamstrings act to extend the hip and flex the knee and commonly present as strained, perhaps due to their relative weakness in comparison to the quadriceps (Sutton 1984). As two-joint muscles, they are susceptible to injury, because there is a greater potential for overuse. Injury can occur at the tendinous origin at the ischial tuberosity, within the muscle belly, or at the musculotendinous junction.

The onset is usually sudden, e.g. on a sudden stretch or a rapid contraction against resistance such as the ballistic action of sprinting, which produces acute pain, further increased by activity, swelling and bruising. The vulnerable phase in the running cycle appears to be at the end of the swing phase, where peak muscle lengths occur, and the beginning of the stance phase. Biceps is more susceptible as its peak length exceeds that of the medial hamstrings (Hunter & Speed 2007).

Symptoms may include stiffness, muscle cramps and spasms in the posterior aspect of the distal thigh or weak knee flexion. Patients with a complete distal hamstring tear may also report a sensation of instability at the knee and diagnostic imaging may be required as an adjunct to clinical examination to aid decision-making in the management of more severe lesions (Lempainen et al 2007).

Precipitating factors have been put forward as altered posture, poor condition, inadequate warm-up and fatigue (Sutton 1984, Worrell 1994). In exploring various established and speculative management approaches, Hoskins & Pollard (2005) were unable to find conclusive evidence for a wider range of specific factors leading to hamstring injury, namely muscle strength and balance, warm-up, fatigue, flexibility, body mechanics, sports-specific activities, psychosocial factors or running technique. Hunter & Speed (2007) reviewed this list of possible factors and also looked at age and previous injury. From their own review they found that only age and previous injury had confident support as risk factors.

Croisier et al (2008) have since looked at the role of muscle imbalance in hamstring injury. Pre-season isokinetic concentric and eccentric testing was performed on 687 professional soccer players to monitor strength imbalances. Follow-up was obtained in 462 players within whom 35 hamstring injuries were recorded and it was demonstrated that players with untreated muscle imbalances were four to five times more likely to sustain a hamstring injury than those recorded as normal.

The patient may report tightness or pain in the posterior thigh some time before the acute onset. Gradual onset due to overuse is possible and injuries may occur in dancers following sustained stretching at warm-up, whilst dancing, or during cool-down (Askling et al 2006). Askling et al observed 18 sprinters and 15 dancers and noted that, although injuries of sudden onset were functionally worse initially, they tended to return to pre-injury levels more quickly than the slower onset injuries, with an average of 16 weeks for the former group and 50 weeks for the latter. Re-injury is relatively common at 12–17% and Askling et al implicate early or over-zealous stretching as a contributing factor.

Chronic hamstring strain is more commonly the result of a previous acute episode which may have healed during a period of relative immobilization. Consequent tightness or shortening of the muscle belly makes it vulnerable to repeated injury. Koulouris et al (2007) conducted a study to identify whether any MRI-identifiable parameters could be predictive of athletes at risk of sustaining a recurrent hamstring injury within the same playing season. The only statistically significant risk factor for recurrent hamstring strain was a history of anterior cruciate ligament injury. However, it was noted that reinjured muscles presented with an increased length of tear and of the imaged parameters the measured length of the strain had the strongest correlation with a repeat strain.

On examination the patient has pain on resisted knee flexion and pain on passive straight leg raising. In most clinic situations, testing for hamstring strain is conducted statically in a non-weight-bearing position. In reality the hamstrings function, and are most often injured, in dynamic weight-bearing situations. This is an important point to remember for full rehabilitation of any muscle lesion in the region.

Palpation reveals the site of the lesion, with muscle belly strains commonly occurring deeply in the mid-thigh region. Chronic overuse strain occurs at the origin from the ischial tuberosity. Treatment of the origin may be by deep transverse frictions or injection.

The mechanism of injury of the quadriceps is similar to that of the hamstrings and the principles of treatment and rehabilitation can be applied in much the same way. The patient presents with anterior thigh pain, pain on resisted knee extension and pain on resisted hip flexion (if rectus femoris is involved). As a two-joint muscle, rectus femoris is the most susceptible to injury. Palpation reveals the site of the lesion, which may be within the tendon of rectus femoris from the anterior inferior iliac spine, or in the belly of the muscle, usually mid-thigh (see Ch. 11).

Adductor longus is the most common adductor muscle to be strained at the hip. It is sometimes known as a ‘rider’s strain’ due to overuse of adductor longus in working a horse while riding.

The patient has groin or medial thigh pain, often presenting as a dull ache, with pain on resisted adduction and passive abduction (Tibor & Sekiya 2008). The lesion is in one of two sites: either the origin from the pubis or the musculotendinous junction. Treatment of the origin is by either transverse frictions or injection. The musculotendinous junction usually responds well to transverse frictions and injection is not usually necessary.