Orthopedics

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Chapter 16

Orthopedics

Qusai Hammouri, MBBS, MD, and Joshua E. Hyman, MD

1. What are the components of the newborn orthopedic screening examination?

All newborn babies should be examined for evidence of hip dysplasia, spinal dysraphism, and lower and upper extremity deformities. ¹

2. How do you check for occult spinal dysraphism?

Any midline dimple (especially a deep or asymmetric pit), subcutaneous mass, hemangioma, nevus, tuft of hair, or areas of hypopigmentation or hyperpigmentation might indicate occult spinal dysraphism and a tethered cord. Coccygeal pits are generally benign. The presence of two or more midline skin lesions is the strongest predictor of spinal dysraphism. An ultrasound of the spine is indicated whenever occult spinal dysraphism is suspected. Magnetic resonance imaging is an alternative imaging study.

3. How do you check for extremity deformity?

Look at the extremities, and check for asymmetry or an abnormal appearance. Look at the baby when crying to determine if he or she moves all extremities. Gently examine the joints and their range of motion. Finally, stimulating the extremities should result in some kind of response, usually withdrawal. ²

4. A premature newborn infant receiving ventilator support in the NICU has decreased movement in the right lower extremity. What diagnostic tests may be appropriate?

Neonatal osteomyelitis or fracture need to be ruled out. Baseline laboratory testing should be considered (e.g., complete blood count and C-reactive protein) as part of the evaluation for possible joint infections, which are not uncommon in this setting. If an osteomyelitis is suspected, a blood culture should always be obtained. These tests may not be rewarding because infants may develop infection without abnormalities in laboratory values. Plain radiographs of the entire extremity should be obtained to help detect a subtle fracture that may not be apparent on clinical examination. Radiographs are often normal in the early phases of bone and joint infection. In this setting bone and joint infections most often involve more than one site. Therefore careful clinical assessment to detect subtle joint effusions or swelling over long bones is indicated. Often an ultrasound scan is helpful in confirming a joint effusion in the hip because overlying muscle may mask the usual clinical findings. A technetium-99 bone scan is very useful in detecting other sites of multicentric infection. ³

5. The initial evaluation of a first-born infant reveals multiple stiff joints in both the upper and lower extremities and thin, tapered, and “shiny” fingers. What is the main diagnostic consideration?

Arthrogryposis multiplex congenita is a clinical syndrome characterized by poor development of the joints in utero leading to multiple contractures. This does not appear to be a hereditary condition, and there is no increased risk in siblings of the same family. Many mothers report decreased fetal movement in utero. On clinical examination the limbs are usually symmetric. Joints may have either flexion or extension contractures. There is decreased active and passive motion of the affected joints. The normal skin creases are usually absent, and the skin is taut and glossy. Dimpling at the joints may be present. There is atrophy of the limbs. Often the hips are dislocated, and clubfoot (i.e., talipes equinovarus) or congenital vertical talus affects the feet. The upper extremities are usually internally rotated at the shoulder, with elbow flexion or extension contractures. There are often radial head dislocations. The forearms are pronated with adduction deformity of the thumbs. Delivery may be difficult as a consequence of the stiff elbow and knee joints. This may result in birth fractures of the humerus and the femur. General health is not affected by this syndrome, although patients often exhibit minor respiratory difficulties and failure to thrive as newborns. ⁴

6. What congenital spine malformation is associated with maternal insulin-dependent diabetes?

Caudal regression syndrome (also known as lumbosacral agenesis) is more common in women with insulin-dependent diabetes. It is characterized by an absence of variable amounts of the sacrum and lumbar spine and the associated neural elements. There may also be concomitant anomalies of the genitourinary and gastrointestinal tracts. The level of the lesion may vary, and this will influence the clinical picture. These lesions are classified into four types according to the Renshaw classification. Depending on the severity of the agenesis, the patient may have variable foot deformities and abnormalities of the hips and knees.

7. A newborn infant is noted to have external rotation of the lower extremities at rest, with little spontaneous movement and bilateral foot deformities. What radiographs should be ordered?

Both spine and pelvis radiographs should be ordered. The abnormalities described can result from anomalies of the spine or the lower extremities. ⁵

8. A newborn child is suspected of having a genetic skeletal dysplasia. What is the most critical orthopedic radiographic examination?

The most important radiograph is the lateral cervical spine. More than 150 distinct osteochondrodysplasias have been identified. Each has distinctive features, but many also have similar radiographic findings. One of the most common is agenesis or hypoplasia of the upper cervical spine elements. This can lead to instability and places the child at great risk of spinal cord injury during ordinary handling. Detection of cervical instability is mandatory to allow proper stabilization and protection. ⁶

9. What is developmental dysplasia of the hip (DDH)?

DDH is a maldevelopment of the hip joint characterized by a spectrum of pathology ranging from instability of the hip to irreducible dislocation. ⁷

10. What is congenital hip dislocation (CDH)?

CDH is an outdated term; DDH is preferred because it reflects the evolutionary nature of hip problems in infants in the first months of life. The overt pathologic process may not be present at birth, and periodic examination of the infant’s hip is recommended at each routine well-baby visit until the age of 1 year ( Fig. 16-1). ⁸

11. What are the four examinations that constitute a newborn hip evaluation?

The hip abduction, Ortolani, Barlow, and Galeazzi tests are recommended. ⁹

KEY POINTS: DEVELOPMENTAL DYSPLASIA OF THE HIP IN NEWBORNS

1. Every newborn should have a hip examination.

2. The examination consists of the Ortolani, Barlow, and Galeazzi maneuvers.

3. The three main risk factors for DDH are first-born status, female sex, and breech presentation.

12. How do you interpret the hip abduction exam?

Infants should have symmetric hip abduction. Having asymmetry in hip abduction could be a sign of a dislocated hip. ¹⁰

13. How do you perform an Ortolani exam?

It is performed with the child in the supine position. Beginning with the hips flexed 90 degrees and adducted to the midline, the examiner places the index finger on the greater trochanter and the thumb on the inside of the thigh, then gently abducts the hip and lifts up on the greater trochanter. If the hip is dislocated and reducible, a palpable sensation will be felt as the hip reduces into the acetabulum (known as an Ortolani-positive hip) ( Fig. 16-2). ¹¹

14. What does it mean to describe a hip as “Ortolani positive”?

The Ortolani examination is a reduction maneuver. Therefore an Ortolani-positive hip is a hip that is dislocated in its resting state and reducible with gentle manipulation. A simple way to remember this: Think of the O in Ortolani meaning that a hip is “out,” or dislocated, when you start the examination. ¹²

15. How do you perform a Barlow examination?

It is performed with the child supine on the examination table. The hip is flexed 90 degrees and adducted just beyond midline. Gentle downward pressure is then applied to the hip through the knee. The sensation of the femoral head sliding out of the acetabulum indicates a Barlow-positive hip. ¹³

16. What does it mean to describe a hip as “Barlow positive”?

The Barlow examination is a provocative maneuver. A Barlow-positive hip is normally reduced but can be subluxed. A normal hip will not subluxate and is Barlow negative. ¹⁴

17. How do you perform the Galeazzi examination?

It is performed with the child supine. The hips and knees are flexed such that the feet are lying flat on the table. The examiner then looks at the heights of the knees. If there is a difference, there may be a dislocated hip. ¹⁵

18. What does it mean to have a “Galeazzi-positive” hip?

The Galeazzi exam identifies apparent or real shortening of the femur. It could be due to DDH or other congenital anomalies. ¹⁶

19. What radiographic studies can you order if you suspect DDH?

Ultrasound of the hip is the study of choice for suspected DDH in neonates and infants younger than four months of age. In children of this age the ossific nucleus of the femoral head is completely cartilaginous and therefore will not be seen on x-ray. After the infant is four months of age, radiographs should be obtained. ¹⁷

20. What are the risk factors for DDH?

First-born female infants who present in the breech position and have a positive family history of DDH are at a significantly increased risk. A simple mnemonic: First, Female, Family, and Breech ¹⁸

21. What other conditions are associated with DDH?

Torticollis, congenital hyperextension of the knee, metatarsus adductus, and clubfoot are associated with DDH. ¹⁹

22. How is DDH treated in newborns?

In a newborn child DDH can be very effectively treated with dynamic splinting in a brace, such as a Pavlik harness. A child in a Pavlik harness will lie with her hips and knees flexed approximately 90 degrees and her hips abducted to 60 degrees. This position is quite comfortable and natural for the infant. In this position the femoral head is deeply seated within the acetabulum. The soft-tissue structures around the hip will then stabilize with the hip in this reduced position. ²⁰

23. What is clubfoot?

Clubfoot, (also called talipes equinovarus), is a congenital condition in which the foot points downward and inward. More specifically, the hindfoot is in equinus and varus and the forefoot is in adduction and supination. ²¹

KEY POINTS: CLUBFOOT

1. Most clubfeet can be treated effectively with manipulation and casting.

2. Treatment should begin as soon as possible after birth.

3. Clubfoot may be associated with other congenital conditions; therefore a thorough evaluation of the entire infant is necessary.

24. How common is clubfoot?

The incidence of clubfoot is 1.2 per 1000 live births, although this estimate varies with different ethnic subgroups, ranging from as high as 7 per 1000 in Hawaii to 0.87 in India. ²²

25. Is there a gender difference in the incidence of clubfoot?

Boys are affected nearly twice as often as girls, and 50% of the patients have bilateral involvement. ²³

26. What are the causes of clubfoot?

The etiology of clubfoot is unknown. It is seen in conjunction with cerebral palsy, myelomeningocele, arthrogryposis, and other neuromuscular conditions. Most often, however, it occurs as an isolated deformity in an otherwise healthy infant (i.e., it is idiopathic). ²⁴

27. What is the treatment for clubfoot?

The initial treatment for clubfoot is weekly manipulation and casting according to the Ponseti method. Approximately 6 to 10 casts are required. A brace is worn for 3 to 4 years to maintain the correct position. With this technique, approximately 80% to 90% of idiopathic clubfeet will be successfully treated. Those feet that cannot be corrected with this method will require surgical correction ( Fig. 16-3). ²⁵

28. When should clubfoot treatment be initiated?

As soon as the deformity is recognized, treatment should be started. This can frequently occur in the newborn nursery. ²⁶ ²⁷

29. What is Klippel-Feil syndrome?

A congenital condition characterized by the triad of a short neck, a low posterior hairline, and fusion of elements of the cervical spine. It results in decreased cervical spine motion. ²⁸ ²⁹

30. What is the general clinical significance of Klippel-Feil syndrome?

The cervical spine develops embryologically at the same time as the genitourinary and cardiovascular systems. As a result, patients with cervical spine anomalies may also have genitourinary and cardiovascular anomalies. In addition, other fusions and malformations of the spinal column may occur. There may also be abnormalities within the spinal cord, such as syringomyelia and cord tethering. ³⁰ ³¹

31. What does the evaluation of a child with Klippel–Feil syndrome entail?

These children must undergo an abdominal ultrasound scan to evaluate possible genitourinary anomalies. They should have a careful clinical cardiac examination. If the results of this examination are thought to be abnormal, an echocardiogram should be considered. Complete radiographs of the entire spinal column must be obtained to look for other vertebral anomalies. Finally, a thorough neurologic evaluation, including magnetic resonance imaging from the base of the brain to the cauda equina, should be performed. ³²

KEY POINTS: NEONATAL INFECTIONS

1. Newborn children with a bone or joint infection may present with pseudoparalysis of the affected extremity.

2. A fever is not a prerequisite for a bone or joint infection.

3. Treatment of joint infections requires aspiration and antibiotics.

32. What are the clinical findings of septic arthritis of the hip in the newborn?

The inability of the newborn to communicate makes this diagnosis quite difficult; however, there are some hallmark signs to be aware of. Affected children will appear lethargic and irritable. They will have difficulty feeding and will exhibit pseudoparalysis, or decreased movement, of the affected limb. A fever is not obligatory. The diagnosis is made by joint aspiration and microscopic examination of the fluid. ³³

33. What are the consequences of a missed joint infection?

Bacteria within the joint will lead to an inflammatory response by the host immune system. The enzymes released (e.g., collagenases, proteases, elastases) by both the leukocytes and bacterial cells cause cartilage damage. Initially, glycosaminoglycans are removed from the cartilage. Over time, there is eventual collagen destruction. This damage is irreversible. In addition, if sufficient pressure develops within the joint, blood flow to the epiphysis will be compromised and may lead to avascular necrosis. ³⁴

34. What are the most common bacterial agents in neonatal osteomyelitis?

Staphylococcus aureus; group B streptococci; and Escherichia coli, Klebsiella, Salmonella, and Pseudomonas species are the most common bacterial agents in neonatal osteomyelitis. As opposed to osteomyelitis with secondary spread to the joint space, isolated septic arthritis is extremely rare. Staphylococci are the most common organisms, but the clinician should always think of gonococci as well with early septic arthritis.

35. Which bone is most frequently fractured in newborns?

The clavicle is most frequently fractured in newborns. This injury, which stems from excessive traction during delivery, generally results in a greenstick fracture. This fracture usually heals quite nicely without any therapy, although the callus formation may be notable.

36. How long should fractures in neonates be immobilized?

Neonatal fractures generally heal more quickly than their counterparts in children or adults. Because of this, and because of the difficulty in casting neonates, some fractures that would be severely problematic in an adult are barely treated in a neonate. A clavicular fracture will heal within 3 weeks in a newborn infant, as opposed to 6 to 8 weeks in an adult, and does not need to be immobilized in most cases. Femoral fractures, common in premature infants with rickets, are usually well healed within 3 weeks, compared with the 6 to 10 weeks required in an older child or adult with this fracture. Femoral fractures usually are splinted or placed in a Pavlik harness to help healing, but not always if there is minimal displacement.

37. What are the features of constriction ring syndrome (i.e., Streeter dysplasia).

Constriction ring syndrome is a rare syndrome that is characterized by ringlike constriction bands around the upper and lower extremities or the trunk. The etiology is unknown, and it is not hereditary. The extent and depth of the rings vary. The bands may be subcutaneous or may extend down to bone. These bands may interfere with lymphatic and venous return, resulting in edema and enlargement of the distal part with decreased capillary refill. If there is great disruption to the local circulation, the part may undergo autoamputation in utero. Often there are other concomitant anomalies of the hand including syndactyly, acrodactyly, hypoplasia, camptodactyly, and symphalangia. Other associated anomalies include cleft palate and lip and talipes equinovarus deformity of the foot.

38. The foot of a newborn appears to be dorsiflexed such that the top of the foot lies directly against the anterior portion of the lower leg. What are the two diagnostic considerations, and how would you differentiate between the two?

Calcaneovalgus foot deformity is the most likely diagnosis. It is believed that there is no intrinsic problem with bone or joint development and that the deformity results from intrauterine positioning. The natural history of the untreated condition is one of spontaneous correction with no long-term sequelae. The second possibility is posteromedial bowing of the distal tibia. The foot is folded on the anterior surface of the leg, but the flexibility of the foot and ankle is normal. There is significant shortening of the affected side and decreased soft tissue. Because the physical findings may be difficult to distinguish from calcaneovalgus foot deformity in the newborn, anteroposterior and lateral radiographs of the leg should be obtained. The deformity improves with time, usually during the first 3 years of life. However, long-term orthopedic care is required because the affected limb always shows significant growth discrepancy and internal tibial torsion at maturity.

39. What are the orthopedic manifestations of thrombocytopenia with absent radius (TAR) syndrome?

TAR syndrome presents with several orthopedic findings. In the upper extremity there is bilateral absence of the radius, usually with all five fingers present. The thumbs may be hypoplastic. Abnormalities of the fingers may include absence of the middle phalanx of the fifth finger, clinodactyly, or partial syndactyly. In almost one half of the patients, shortening or bowing of the ulna with deficiency of the extensor tendons may occur. In addition, the humerus may be short or absent. In almost 40% of patients, there are associated lower extremity anomalies. These mainly involve the knee and include subluxation or dislocation of the patella and hypoplasia of the knee. The most common deformity of the lower extremities is genu varum with a flexion contracture and internal tibial torsion. These patients also may have hip dislocations, varus or valgus deformities of the hips, and shortening of the legs with hypoplastic or absent tibias or fibulas.

40. A newborn exhibits swelling over the midshaft of the right clavicle. What are the two most common diagnostic considerations?

Birth fractures of the clavicle are extremely common but most often are accompanied by pseudoparalysis of the extremity (caused by “splinting” from pain) for at least 3 to 5 days. There is pain with passive movement. Radiographs show the fracture, which usually heals with a massive callus. In the absence of pain, the clinician must consider congenital pseudarthrosis of the clavicle. The pseudarthrosis is fully present at birth. There is no history of birth injury or other trauma. The right clavicle is almost always affected. At the pseudarthrosis, the clavicular ends are enlarged, and there is painless motion between the two fragments. The etiology remains unknown, but several theories have been proposed, including exaggerated arterial pulsations and pressure on the clavicle by the subclavian artery that is normally more cranial on the right side. In bilateral cases it is thought that an abnormally high subclavian artery is present on both sides. With growth the deformity increases, and the overlying skin becomes thin and atrophic. The affected shoulder often droops, and there is asymmetry between the two shoulders. No functional impairment is noted. Treatment involves resection of the nonunion and internal fixation with bone grafting.

¹ Blasco PA. Pathology of cerebral palsy. In: Sussman MD, editor. The diplegic child. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1992. p. 3–20.

² Blasco PA. Pathology of cerebral palsy. In: Sussman MD, editor. The diplegic child. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1992. p. 3–20.

³ Shaw BA, Kasser JR. Acute septic arthritis in infancy and childhood. Clin Orthop Relat Res 1990;257:212–25.

⁴ Einhorn T. Orthopaedic Basic Science, Rosemont, IL: American Academy of Orthopaedic Surgery, 2006.
Morrissy R, Weinstein S, editors. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 293–296.

⁵ Einhorn T. Orthopaedic Basic Science, Rosemont, IL: American Academy of Orthopaedic Surgery, 2006.
Morrissy R, Weinstein S, editors. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 293–296.

⁶ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

⁷ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

⁸ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

⁹ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁰ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹¹ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹² Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹³ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁴ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–242.

¹⁵ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁶ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁷ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁸ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

¹⁹ Guille JT, Pizzutillo PD, MacEwen GD. Development dysplasia of the hip from birth to six months. J Am Acad Orthop Surg 2000;8:232–42.

²⁰ Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–30.

²¹ Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–30.

²² Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–130.

²³ Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–30.

²⁴ Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–30.

²⁵ Roye BD, Hyman JE, Roye DP Jr. Congenital idiopathic talipes equinovarus. Pediatr Rev 2004;25:124–130.

²⁶ Hyman JE, Roye DP Jr. Torticollis. In: Burg FD, Ingelfinger JR, Polin RA, Gershon AA, editors. Gellis and Kagan’s current pediatric therapy. Philadelphia: Saunders; 2002. p. 849–50.

²⁷ Einhorn T. Orthopaedic Basic Science, Rosemont, IL: American Academy of Orthopaedic Surgery, 2006.
Morrissy R, Weinstein S, editors. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 332.

²⁸ Hyman JE, Roye DP Jr. Torticollis. In: Burg FD, Ingelfinger JR, Polin RA, Gershon AA, editors. Gellis and Kagan’s current pediatric therapy. Philadelphia: Saunders; 2002. p. 849–50.

²⁹ Einhorn T. Orthopaedic Basic Science, Rosemont, IL: American Academy of Orthopaedic Surgery, 2006.
Morrissy R, Weinstein S, editors. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 889–891.

³⁰ Hyman JE, Roye DP Jr. Torticollis. In: Burg FD, Ingelfinger JR, Polin RA, Gershon AA, editors. Gellis and Kagan’s current pediatric therapy. Philadelphia: Saunders; 2002. p. 849–50.

³¹ Einhorn T. Orthopaedic Basic Science, Rosemont, IL: American Academy of Orthopaedic Surgery, 2006.
Morrissy R, Weinstein S, editors. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 889–891.

³² Shaw BA, Kasser JR. Acute septic arthritis in infancy and childhood. Clin Orthop Relat Res 1990;257:212–225.

³³ Shaw BA, Kasser JR. Acute septic arthritis in infancy and childhood. Clin Orthop Relat Res 1990;257:212–25.

³⁴ Shaw BA, Kasser JR. Acute septic arthritis in infancy and childhood. Clin Orthop Relat Res 1990;257:212–25.

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