Approach to hip pain (Stewart)
Osteomyelitis
Infectious osteomyelitis results from hematogenous spread or direct invasion of pathogens into the bone. In some cases, the osteomyelitis may be precipitated by trauma. The infectious agents responsible are similar to those described for septic arthritis. Children who have osteomyelitis typically present with fever and localized pain. Careful examination may reveal erythema, swelling, pinpoint tenderness of the affected bone, or decreased ROM due to muscle splinting. When the lower extremities are involved, children often limp. The bones involved most commonly are the femur, followed by the tibia, humerus, fibula, radius, calcaneus, and ilium. Osteomyelitis requires prompt treatment with appropriate antibiotics, administered intravenously initially, followed by an oral course (4 to 6 wk total duration). The response to treatment is determined by clinical improvement as well as by normalization of inflammatory markers. Most patients have a good prognosis, but complications include recurrence, chronic osteomyelitis, and growth abnormalities (eg, leg length discrepancy). To achieve a favorable outcome, the clinician must verify patient compliance in completing the full course of antibiotics.
OM in children v. adults
Kids have better overall prognosis
Hip pain - physical exam
Log roll test: Patient's leg is extended and relaxed on examination table as the examiner internally and externally rotates the leg (log roll). Antalgic Gait: Minimized stance phase on the affected side secondary to pain that produces a limping gait Trendelenberg Gait: Torso shifts over the affected hip to compensate for muscular weakness on the affected side antalgic = limpy gait trendelenberg = muscle weakness, gluteal muscles, lean over to side to maintain center of gravity
Diagnosis and treatment of septic arthritis?
Septic arthritis requires prompt treatment with antibiotics. Empiric antibiotic therapy should be administered intravenously and changed to more specific therapy once the pathogen has been identified and antibiotic sensitivities have been determined. With clinical improvement, antibiotics can be changed to the oral route for 3 additional weeks of therapy. When the hip, shoulder, or knee is involved, assessment and additional management by orthopedic surgeons may be necessary. Joint drainage can be beneficial to reduce intra-articular pressure and to remove bacterial debris, inflammatory cytokines, enzymes, adhesions, and necrotic tissue that can contribute to damage of the affected joint. Drainage is performed by using closed needle aspiration, arthroscopy, or open surgical drainage, which always is used to manage septic arthritis of the hip. The outcome of septic arthritis depends on the timing of diagnosis, initiation of antibiotics, adequacy of drainage, virulence of the pathogen, and host factors. The single most important prognostic factor for a good outcome is early treatment. Favorable outcomes are associated with treatment that was initiated within 4 days of symptom onset; poor functional outcomes are associated with a delay of 5 or more days before treatment is begun. Prompt recognition and initiation of therapy along with assurance of patient compliance with the antibiotic course are essential in preventing the severe joint destruction seen in septic arthritis (Fig. 1) as well as associated deformities, decreased ROM, leg length discrepancies, and disabilities.
Septic arthritis
Septic arthritis typically presents as an acute monoarthritis, with erythema, warmth, swelling, and intense pain on passive movement. The pain can be so severe that it causes a pseudoparalysis of the involved limb. The joint involved most commonly is the knee, but other joints, including the hip, ankle, wrist, elbow, shoulder, and small joints, can be affected. It is important to know that signs of erythema and warmth do not occur in children whose hips are involved. Fever is present in up to 70% of cases and may be accompanied by chills. The definitive diagnostic test for septic arthritis is aspiration of the joint and analysis of the synovial fluid. The synovial fluid characteristically is cloudy or turbid, has a very high white blood cell (WBC) (predominantly neutrophils), and is positive on Gram stain in approximately 50% of cases. Culture of the synovial fluid is positive in up to 70% of cases, with a corresponding positive blood culture in 40% to 50%. Specific media may be needed to isolate and identify potential pathogens in the synovial fluid (eg, N gonorrhoeae in adolescents). The peripheral WBC count is elevated (predominance of neutrophils), along with the markers of inflammation (eg, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]). When compared with ESR, CRP has been found to be more accurate, especially as a negative predictor of disease. Imaging studies are not diagnostic for septic arthritis but are helpful in supporting a clinical suspicion of the disease. Radiologic manifestations may not be apparent until 10 days into the illness and can include osteopenia, marked joint space loss, and soft-tissue swelling. Ultrasonography is useful in detecting joint effusions. *acute, monoarticular* - may not see erythema/warmth in hip b/c of deep joint
Hip pain history - where does it hurt?
The C Sign: The classic complaint of patients with hip pathology is "groin pain." However, the author has identified a common characteristic sign of patients presenting with hip disorders. The patient will cup their hand above the greater trochanter when describing deep interior hip pain. The hand forms a C and thus this has been termed the "C-sign". Because of the position of the hand, this sign can be misinterpreted as indicating lateral pathology such as the iliotibial band or trochanteric bursitis, but quite characteristically, the patient is describing deep interior hip pain. *groin pain*, C-sign = hip pain
Meralgia paresthetica
The lateral femoral cutaneous nerve, a pure sensory nerve, is susceptible to compression as it courses from the lumbosacral plexus, through the abdominal cavity, under the inguinal ligament, and into the subcutaneous tissue of the thigh. The majority of meralgia paresthetica cases result from entrapment of the lateral femoral cutaneous nerve as it passes under the inguinal ligament. The most frequent associated conditions are obesity, diabetes mellitus, and older age paresthetica is the term used to describe the clinical syndrome of pain, dysesthesia, or both in the anterolateral thigh associated with compression of the nerve. Burning pain, paresthesia (numbness and tingling), and hypesthesia (diminished sensation) over the upper outer thigh is the classic presentation of meralgia paresthetica. The onset of pain is typically subacute. Sensory loss is quite discrete, and it is often possible to clearly demarcate the area of numbness. The patient often rubs the outer thigh when describing the symptoms. Neurologic symptoms are restricted to sensory changes since the lateral femoral cutaneous nerve does not contain motor fibers.
Osteonecrosis overview
The most common presenting symptom of osteonecrosis is pain. Groin pain is most common in patients with femoral head disease, followed by thigh and buttock pain. Weight bearing or motion-induced pain is found in most cases. Rest pain occurs in approximately two-thirds of patients, and night pain occurs in one-third. Although rare, pain in multiple joints suggests a multifocal process. The evaluation for suspected osteonecrosis of the femoral head should begin with anterior-posterior and frog-leg lateral films. Lateral films are necessary to evaluate the superior portion of the femoral head in which subchondral abnormalities are often seen. The plain radiograph can remain normal for months after symptoms of osteonecrosis begin; the earliest findings are mild density changes, followed by sclerosis and cysts as the disease progresses. The pathognomonic crescent sign (subchondral radiolucency) is evidence of subchondral collapse. Later stages reveal loss of sphericity or collapse of the femoral head. Ultimately, joint-space narrowing and degenerative changes in the acetabulum are visible. Imaging: MRI is the most sensitive test X-ray insensitive in early phases may show collapsed bone in late phases Bone scan no uptake in early stages increased uptake in later stages *anterior groin pain*
Galeazzi test
With the infant lying supine on a firm surface, such as an examination table, and the hips and knees flexed 90 degrees, a unilateral dislocated hip usually demonstrates a positive Galeazzi sign, that is, the knee on the side of the dislocated hip appears lower than that of the other side. Some unstable hips may have a negative Galeazzi sign.
Legg-Calve Perthes disease (LCP)
male predominance, uncommon
How do you manage femoral neck fractures?
management: repair quickly (surgery or external repair depending on risks, age) + comorbidities up to 50% of elderly will die within 2 yrs of femoral neck fracture
Greater trochanter bursitis
pretty intense, lateral hip pain
LCP pathophysiology
self-limited condition...will fix itself without treatment in 2-3 yrs
Slipped capital femoral epiphysis (SCFE)
*obese + prepubertal males*
LCP history and PE
*painless limp*
Sacroiliac joint dysfunction
FABER - Flexes, Abducts, Externally Rotates, Extends, this test may also reproduce pain in the groin area or the lumbar spine. The location of pain with the test can further localize the area of involvement. Pain with a FABERE maneuver in the absence of pain with passive hip joint motion suggests SI joint pathology.
DDH treatment
Infants (newborn to 2 weeks old) who have a positive finding on an Ortolani or Barlow examination should be referred urgently (within 1-2 weeks) to an orthopedist comfortable with the management of DDH. Infants age 2 weeks who have equivocal findings may undergo ultrasonography or be evaluated by an orthopedist to confirm whether or not a dislocated hip is present. Pavlik harness
Case 10 redo answer
E. osteonecrosis - note steroid use
Developmental dysplasia of the hip
A number of risk factors for DDH have been reported, but three primary factors have been supported consistently in the literature. Being female presents the greatest risk for DDH, an association thought to be due to increased sensitivity to maternal estrogen and relaxin, yielding increased joint laxity and abnormal motion during fetal development. Breech position during the last trimester presents a similar risk, whereas genetic factors (often identified through family history) also play a role. The acetabulum and femoral head evolve from the same mesenchymal tissue during the first trimester; but formation of a concentric hip joint relies on contact between the femoral head and acetabulum during growth. As a result, factors beyond genetics that disrupt joint motion or position may result in abnormal development. This disruption may occur in utero, as with breech positioning or female gender, as well as after birth. One area of concern is infant positioning, either with swaddling or placing children on a papoose board with the hips extended. Instead, infants should be swaddled with the legs left free or the hips in a flexed and abducted position. Early detection is essential because restoration of the normal relationship between the femoral head and acetabulum increases the likelihood of normal development during remaining growth. Dislocated hips that remain dislocated carry a poor prognosis, as do unstable hips, which may progress to acetabular dysplasia or subsequent dislocation. An unfavorable outcome is especially noteworthy in regard to premature infants, whose hips may be overlooked amid other health issues resulting in a late presentation.
Osteonecrosis
A variety of traumatic and atraumatic factors contribute to the etiology of osteonecrosis. A definitive etiologic role has been established for some of these factors but not for the majority, which are considered associated risk factors. Use of glucocorticoids and excessive alcohol intake are associated with more than 80 percent of atraumatic cases. The pathogenesis of osteonecrosis is an area of controversy. Most experts believe that it is the result of the combined effects of genetic predisposition, metabolic factors, and local factors affecting blood supply, such as vascular damage, increased intraosseous pressure, and mechanical stresses. It probably begins by an interruption of the blood circulation within the bone; subsequently, the adjacent area becomes hyperemic, resulting in demineralization, in trabecular thinning, and, later, in collapse.
Case 2 answer
A. Px should immediately be placed in a non-weight bearing state
Case 5 answer
A. Staph aureus
Case 4 answer
A. This is a self limited and benign condition that will resole with time and conservative management
Case 10 answer
A. Yes - joint replacements only last ~10 years, good for 70 yo maybe not for 50 yo
Transient (toxic) synovitis
Boys ages 3 to 8 years (typically 4 y) are affected most commonly, presenting with a sudden onset of a painful hip or, less commonly, complaints of discomfort in the knee. However, the pain is not as pronounced as that seen in children who have septic arthritis or osteomyelitis. Most patients are afebrile or have only a low-grade fever. The child otherwise appears well and is capable of ambulating, but usually with a limp. When the hip is involved, the limb usually is held in a position of flexion and external rotation. Mildly restricted ROM of the joint is demonstrated on physical examination. Transient synovitis is diagnosed following the exclusion of other disorders, especially septic arthritis and osteomyelitis. The WBC count tends to be normal, but the markers of inflammation can be mildly elevated. Imaging studies often show evidence of a joint effusion. A recent algorithm developed to help differentiate septic arthritis from transient synovitis of the hip showed four clinical predictors associated more highly with septic arthritis: history of fever, inability to bear weight, ESR greater than 40 mm/h, and WBC count greater than 12103/mcL (12109/L). Unlike septic arthritis, transient synovitis is self limited and is managed with conservative measures such as bed rest and anti-inflammatory medications. *less than 5 yo, WBC < 12,000*
Case 8 answer
C. Greater trochanteric bursitis
Case 1 answer
C. Urgent orthopedic consultation should be ordered for the infant
Case 11 answer
C. high risk
Femoral neck fractures
Common fracture in elderly; mortality rate of 20% Epidemiology: most common in osteoporotic females; 4:1 female to male ratio; 300,000/yr. in US Mechanism: minor trauma, falls; may occur spontaneously in the absence of trauma Presentation: Symptoms severe hip and groin pain aggravated by movement. unable to move the hip may have history of other osteoporotic fractures vertebral compression fracture Colle's fracture Physical exam limb shortened, abducted and externally rotated Evaluation: Radiographs Treatment Initial Treatment IV analgesia for pain managment Operative ORIF with parallel pinning of femoral neck indicated in younger patients hip arthroplasty indicated in displaced fractures in elderly Prognosis, Prevention, and Complications: DVT and PE a complications of recumbency and immobilization needs prophylactic anticoagulation Pneumonia a complications of recumbency and immobilization Avascular necrosis (AVN) and nonunion displaced femoral neck fractures associated with avascular necrosis (AVN) and nonunion subcapital fracture places MFCA at risk has risk of AVN intracapsular, disrupts retinacular arteries from MCFA pertrochanteric fracture no risk of AVN extracapsular, does not disrupt blood supply to femoral head
Case 13 answer
D. MRI of lumbar spine - spinal stenosis
Case 7 answer
D. Pediatric patients are more likely to develop disease from acute hematogenous spread than through contiguous spread - A-C, peds patients are easier to treat, less likely to develop chronic infection, prompt Ax initiation is warranted
Case 9 answer
D. counseling on the disease pathology and lifestyle modification - A could be diagnostic, but not needed
Case 3 answer
D. higher risk for developing OA
Case 12 answer
D. squaring of the vertebral bodies of the lumbar spine
Lumbar spinal stenosis
Narrowing of central or lateral lumbar spinal canal caused by degenerative joint disease; leads to compression of nerve roots Epidemiology middle-aged or elderly Presentation Symptoms back pain and referred buttock pain neurogenic claudication pain worse with extension (walking downhill, standing upright) pain relieved with flexion at hips and bending forward (sitting, leaning over shopping cart) leg pain (often unilateral) weakness bladder disturbances recurrent UTI present in up to 10% due to autonomic sphincter dysfunction cauda equina syndrome (rare) Physical Exam Kemp sign unilateral radicular pain from foraminal stenosis made worse by extension of back Straight leg raise (nerve root tension sign) is usually negative Valsalva test does not worsen pain (pain is worse in the case of herniated disc) Differential Important to differentiate symptoms of neurogenic claudication from vascular claudication flexion improves symptoms in neurogenic claudication because this posture increases the limited area available for the neural elements in the spinal canal and foramen Imaging Radiographs standing AP and lateral may show disk space narrowing, osteophyte formation facet hypertrophy degenerative spondylolithesis CT myelogram will show spinal stenosis useful in patients that can not have an MRI MRI show spinal stenosis Treatment Nonoperative NSAIDS, physical therapy NSAIDS, physical therapy (abdominal muscle strengthening) weight loss and bracing steroid injections (epidural and transforaminal) for advanced symptoms Operative surgical laminectomy may achieve short term success but many patients have recurrence *exacerbated by down-hill activities or lumbar extension* pseudoclaudication - resting --> pain to get better (due to spine, not vasculature)
Greater trochanter bursitis PE
Pain over the lateral aspect of the greater trochanter. Associated with: female runners running on banked surfaces Mechanism: repetitive trauma caused by iliotibial band tracking over trochanteric bursa irritates the bursa, causing inflammation Imaging: Radiographs will be unremarkable; diagnosis is made on clinical grounds Treatment: NSAIDS, stretching, PT, corticosteroid injections
