Nirav Shastri, MD

A 10-year-old boy injured his left elbow during football practice. He subsequently had pain with normal range of motion of the elbow. He had minimal tenderness over his olecranon but no joint swelling, bruising, or palpable mass. He denied tingling or numbness of his fingers. His left shoulder and wrist showed no signs of injury. Distal neurovascular status was normal.

) radiographs of the left arm revealed a beaklike projection of the distal humerus. There was no fracture or dislocation.

A supracondylar process is a bony spur that arises from the surface of the anteromedial humerus, typically 5 to 7 cm above the medial epicondyle. It protrudes about 2 cm and points down toward the elbow joint.

 This is unlike an osteochondroma, which points up away from the joint. The anomaly occurs in about 0.3% to 2.7% of the population.

 The incidence is increased within families and in patients with Cornelia de Lange syndrome.

The bony projection is a developmental variation located in the area of the supracondyloid foramen, which while present in most mammals is absent in most humans. A fibrous band, known as the ligament of Struthers, extends from the supracondylar process to the medial epicondyle.

 The supracondylar process and the ligament of Struthers create a fibro-osseous tunnel that may cause compression of the median nerve, and more rarely the ulnar nerve, called supracondylar process syndrome.

The supracondylar process is usually asymptomatic and is often found incidentally on radiographic examination after an injury, as in this patient. In rare cases, pain (usually in the elbow and forearm), paresthesias in the hand and fingers, subjective weakness of the associated extremity, and a palpable mass or swelling over the distal medial portion of the upper arm have been reported.

 The pain and paresthesias usually worsen with elbow extension and hand pronation. Symptoms may be of insidious onset or associated with traumatic injury, such as fracture.

Conservative treatment of symptomatic patients includes rest, avoidance of exacerbating positions, analgesics, and an upper extremity sling. Operative resection of the process provides definitive cure.

 Rarely, regrowth of the process may occur.

This patient's elbow pain was related to the injury not the spur and was treated symptomatically.

1. Kolb LW, Moore RD. Fractures of the supracondylar process of the humerus. Report of two cases. 

2. Rau R, Subrahmaniam D. Supracondylar process. 

3. Subasi M, Kesemenli C, Necmioglu S, et al. Supracondylar process of the humerus. 

4. Curtis JA, O'Hara AE, Carpenter GG. Spurs of the mandible and supracondylar process of the humerus in Cornelia de Lange syndrome. 

5. Bilecenoglu B, Uz A, Karalezli N. Possible anatomic structures causing entrapment neuropathies of the median nerve: an anatomic study. 

6. Tsai P, Steinberg DR. Median and radial nerve compression about the elbow. 

Articles

A 10-year-old boy injured his left elbow during football practice. He subsequently had pain with normal range of motion of the elbow.

Supracondylar Process

For the past few weeks, a 10-year-old boy had a pruritic abdominal rash that had not responded to over-the-counter topical medications. The rash had appeared around the time he started wearing a new belt (shown). The child was otherwise healthy. There was a family history of asthma.

 Allergic contact dermatitis from the nickel in the child's belt buckle and the buttons on his pants was diagnosed. Nickel is the most common cause of metal sensitivity.

 The average prevalence of nickel allergy is almost 9% in the general population.

 Skin contact with nickel results when sweat or friction causes the metal to leach out of buttons, zippers, belt buckles, and jewelry. Patch testing is generally not needed to confirm the diagnosis.

The only definitive treatment is avoidance of the allergen, in this case, the belt buckle and buttons. Placing tape or clear nail polish on small metallic objects, such as buttons, can prevent contact. Inexpensive home kits are available to test metallic objects for nickel content. Use of cool compresses and antihistaminies can relieve associated symptoms. Potent topical corticosteroids are also effective for treating small areas of moderate contact dermatitis. Topical immunomodulators have been used as second-line therapy. Oral corticosteroids are usually indicated when more than 10% of the body surface area is involved.

This patient was treated with topical triamcinolone and oral diphenhydramine. The rash resolved about 2 weeks after he discontinued wearing the belt.

Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence.

 2nd ed. Philadelphia: WB Saunders; 1993:68-77. 
    

 Thyssen JP, Linneberg A, MennÃ© T, Johansen JD. The epidemiology of contact allergy in the general population-prevalence and main findings. 

 Bruckner AL, Weston WL. Allergic contact dermatitis in children: a practical approach to management. 

Nickel Dermatitis

FigureThis blanching, erythematous, maculopapular, confluent rash on the shins of an 8-year-old girl began as a few red spots 2 weeks earlier and had progressively worsened and become painful. A week before presentation, the child had been treated for pharyngitis. She had full range of motion in both legs without joint pain or swelling. 

 Results of a complete blood cell count (CBC), measurements of electrolyte concentrations, and urinalysis were normal. A rapid streptococcal test result was negative. The C-reactive protein level was elevated at 3.3 mg/L (normal, less than 1 mg/L); the erythrocyte sedimentation rate was 58 mm/h (normal, 4 to 20 mm/h).

 Erythema nodosum (EN) was diagnosed. This disorder is the most common inflammation of subcutaneous fat.1 Miescher granuloma-a small, well-defined, nodular aggregation of histiocytes arranged radially around a variably shaped central cleft-is its histopathological hallmark.

 Between 1 and 5 persons per 100,000 are affected; the peak incidence is between 20 and 30 years of age. The male-to-female ratio is 1:1 in children but 1:2 in adults. 

The rash may be preceded by a 1- to 3-week prodrome of weight loss, malaise, low-grade fever, cough, and arthralgia with or without arthritis.

 The eruption usually presents as symmetrical, tender, erythematous, warm nodules with raised plaques.

 Pretibial involvement is most common; however, the extensor surfaces of the forearms, thighs, and trunk can also be affected.

 The history helps guide the evaluation, which may include CBC, sedimentation rate, antistreptolysin O titer, urinalysis, throat culture, intradermal tuberculin test, and chest radiography to exclude an underlying cause. EN is associated with infections (?-hemolytic streptococcal infection, 

infection, tuberculosis, and leprosy), drugs (antibiotics and hormonal contraceptives), chronic inflammatory diseases (sarcoidosis, Behet syndrome, and inflammatory bowel disease), and malignancy (lymphoma and leukemia).3 The frequency of EN in different diseases varies with the population studied. The likely cause in this patient was streptococcal pharyngitis. 

The nodules of EN are self-limited and heal without scarring. The goal of treatment is to manage any underlying condition. Bed rest, elevation, compressive bandages, NSAIDs and corticosteroids, and avoidance of contact irritation can relieve symptoms.

Schwartz RA, Nervi SJ. Erythema nodosum: a sign of systemic disease. Am    Fam Physician. 2007;75:695-700. 
    

Requena L, Requena C. Erythema nodosum. Dermatology Online Journal,    Volume 8, Number 1. http://dermatology.cdlib.org/DOJvol8num1/reviews/    enodosum/requena.html. Accessed May 6, 2008. 
    

Moraes AJ, Soares PM, Zapata AL, et al. Panniculitis in childhood and adolescence.    Pediatr Int. 2006;48:48-53.    

Erythema Nodosum

FigureSeven days after birth, a baby boy was brought for evaluation of a "diaper rash." The eruption began 2 days earlier as a few vesicles and progressed to large blisters. Some of the lesions had burst. There was no history of fever. The infant was born at term via normal vaginal delivery. He was breast-feeding adequately. The mother tested negative for group B 

 infection. She had no history suggestive of mastitis. There was no family history of skin infection. 

Multiple tender flaccid bullae (about 2 mm to 2 cm) were present on the perineum. There was no associated discharge. The ruptured blisters had marked erythema in the center and a scaly rim at the periphery. The Nikolsky sign could not be elicited. The infant was afebrile. The remainder of the examination findings were normal.

Bullous impetigo (BI) was diagnosed. This common, highly contagious, superficial blistering skin infection is now recognized as a localized form of staphylococcal scalded skin syndrome (SSSS), or Ritter disease.

 The Table lists the differences between the 2 conditions.

 (most commonly phage type II) or, rarely, by group A ?-hemolytic 

. Culture helps identify the cause, which in this patient was methicillin-sensitive 

 may be isolated. Results of antistreptolysin O and streptozyme tests may be positive but are rarely performed.

; up to 50% of the general population are nasal carriers of this bacteria.

 is commonly found on the skin, around the eyes, umbilicus, perineum, wound sites, circumcision wounds, and umbilical stumps.

 was isolated in 72% of 2482 skin and soft tissue infections in children.

 Predisposing factors for staphylococcal infection include immunodeficiency, diabetes, chronic granulomatous disease, skin breakdown (surgery, insect bites, varicella, herpes simplex), burns, and foreign substances (sutures, shunts, intravascular catheters).

BI begins as a single red macule or papule that quickly becomes a vesicle. The vesicle rapidly enlarges into flaccid bullae with sharp margins without surrounding erythema. The bullae may rupture, ooze, and leave yellow crusts. The rash spreads by autoinoculation. A pathognomonic finding is a collarette of scale around the blister roof at the periphery of ruptured lesions.

 Moist, intertriginous areas, such as the diaper area, axillae, and neck folds, are commonly affected. The lesions may be mistaken for child abuse (eg, localized disease may mimic cigarette burns and more extensive infection may resemble scald injuries).

Systemic symptoms are uncommon. Most cases are self-limited and resolve without scarring within several weeks.

Medical treatment of neonates who have BI consists of parenteral antistaphylococcal antibiotics. Control of pain, temperature, and hydration is essential. Coverage for secondary Gram-negative infection is recommended in severe cases. Exfoliation usually continues for 24 to 48 hours after starting antibiotics.

This patient responded well to treatment with intravenous clindamycin and was discharged after 72 hours.

Cole C, Gazewood J. Diagnosis and treatment of impetigo. 

Ladhani S, Garbash M. Staphylococcal skin infection in children-rational drug therapy recommendations. 

Darmstadt GL. Oral antibiotic therapy for uncomplicated bacterial skin infections in children. 

Koning S, Verhagan AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. 

Sandhu K, Kanwar AJ. Generalized bullous impetigo in a neonate. 

Stanley JR, Amagai M. Pemphigus, bullous impetigo and the staphylococcal scalded skin syndrome. 

Hanakawa Y, Schechter NM, Lin C, et al. Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome. 

Bullous Impetigo in a Neonate

Three-year-old boy limping on right foot after an unwitnessed fall from trampoline the day before. Pain controlled with ibuprofen. No history of chronic diseases or routine medication use.

Swelling and mild tenderness over the dorsum of the right foot and anterolateral ankle. Patient able to bear weight but limps on the right side and refrains from bearing weight on the right foot. No distal neurovascular deficit. Range of motion of foot and ankle reduced because of pain. No signs of external injuries, such as abrasions or bruises. Physical findings otherwise normal. 

The x-ray films show sclerosis of the proximal cuboid bone (arrows), suggestive of cuboid compression fracture.

 A compression fracture does not have a piece of displaced bone or a break in the bone, such as Colles fracture. Cuboid compression fractures are uncommon, and there are limited reports about the condition in children. The fracture was first described by Hermel and Gershon-Cohen

 in 1953; such fractures tend to affect children between ages 1 and 6 years.

The fracture is a result of a fall from a height. Rarely, the cause may be direct trauma, which is usually associated with other injuries.

A fall from a height produces heel-to-toe compression of the lateral column of the foot either alone or with abduction force at the tarsometatarsal joint. This is called the "nutcracker theory," which describes the compression of the cuboid bone between the calcaneus and the bases of the fourth and fifth metatarsals, when the forefoot is fixed and the weight of the body is transmitted through the foot in plantar flexion.

A fall while riding a horse can produce a cuboid fracture, usually in association with other midfoot injuries. In this setting, the stirrup acts as a fulcrum and the forefoot is forcefully hyperabducted, trapped between the horse and the ground.

Patients who have a systemic or genetic condition associated with osteoporosis (such as corticosteroid-dependent asthma or osteogenesis imperfecta) are at increased risk for cuboid compression fracture. These patients may present with foot pain or limping without an obvious history of trauma.

Preschool children with a cuboid compression fracture may limp and refrain from bearing weight on the affected foot, especially on the lateral side of the foot. Older children may complain of foot pain at the site of the cuboid bone. Tenderness over the cuboid bone can be elicited or a nutcracker maneuver may be performed. In this test, the calcaneus is stabilized and the forefoot is abducted. This compresses the cuboid bone between the calcaneus and the base of the fourth and fifth metatarsals: if the bone is fractured, the maneuver will cause pain.

Diagnosis is usually made with plain x-ray films, which show sclerosis or cortical irregularity of the proximal or distal cuboid bone.

A bone scan may be helpful in a symptomatic patient with normal radiographic findings. 

 CT can be used in patients with a history of significant trauma or with suspected multiple foot injuries, such as those associated with a fall from a horse.

 Ultrasonograms show step-like discontinuity of the cuboid bone.

A sagittal MRI scan may show a marked linear hypointense signal.

Neither ultrasonography nor MRI is routinely necessary.

Patients with non displaced cuboid compression fractures need immediate immobilization and a short leg walking cast for 2 to 3 weeks.

The fracture should be asymptomatic within 4 to 5 weeks with this treatment-as was the case in this patient. Those who are observed-whose foot is not immobilized-take longer (about 7 to 8 weeks) to become symptom-free.

 Displaced cuboid compression fractures are best managed surgically with bone grafting. Conservative treatment for such fractures results in poor functional outcome.

 Hermel MB, Gershon-Cohen J. The nutcracker fracture of the cuboid by indirect    violence. Radiology. 1953;60:850-854.

. Senaran H, Mason D, De Pellegrin M. Cuboid fractures in preschool children.    J Pediatr Orthop. 2006;26:741-744. 

     Ceroni D, De Rosa V, De Coulon G, Kaelin A. Cuboid nutcracker fracture due    to horseback riding in children: case series and review of the literature. J Pediatr    Orthop. 2007;27:557-561. 

     Holbein O, Bauer G, Kinzl L. Fracture of the cuboid in children: case report    and review of the literature. J Pediatr Orthop. 1998;18:466-468.

Englaro EE, Gelfand MJ, Paltiel HJ. Bone scintigraphy in preschool children    with lower extremity pain of unknown origin. J Nucl Med. 1992;33:351-354. 

     Enns P, Pavlidis T, Stahl JP, et al. Sonographic detection of an isolated cuboid    bone fracture not visualized on plain radiographs. J Clin Ultrasound. 2004;32:    154-157.

 Stalder H, Zanetti M. Stress fracture of the cuboid in an 8-year-old boy: a characteristic    magnetic resonance imaging diagnosis. Arch Orthop Trauma Surg.    2000;120:233-235.    

Three-year-old boy limping on right foot after an unwitnessed fall from trampoline the day before. Pain controlled with ibuprofen. No history of chronic diseases or routine medication use. 

Cuboid Compression Fracture 

A 4-year-old US-born Hispanic boy presented with penile discharge and painful urination. His mother reported that he had no fever, trauma, history of masturbation, or recent travel history. She did not suspect any abuse. There had been no similar complaints in the past.

The child had mild purulent discharge at the external urethral meatus; erythema of the glans penis; and minimal swelling of the prepuce, which could not be retracted. There were no other abnormal physical findings. The patient was able to pass urine normally. Results of urinalysis by dipstick were normal.

The clinical diagnosis was acute balanoposthitis. In one US study, the third most common reason for post-neonatal circumcision was recurrent balanoposthitis (in 23% of cases). The most common reasons were concomitant surgery (in 27% of cases) and parental choice (in 39%).

 An Australian study found phimosis, acute balanoposthitis, and balanitis xerotica obliterans to be the most common medical indications for circumcision at all ages.

Inadequate hygiene is the most common cause of nonspecific acute balanoposthitis, which usually occurs in boys aged 2 to 5 years.

 Irritation from soaps, bubble baths, laundry detergent, and antistatic sheets have also been implicated. Other causes include trauma from masturbation and zip-fastener injuries.

Infection is a relatively uncommon cause of acute balanoposthitis in children. 

is the most frequently identified pathogen, although it is an innocent saprophyte in most cases. 

Streptococcus pyogenes, Staphylococcus aureus, Neisseria gonorrhoeae, Chlamydia trachomatis,

 and anaerobes are the usual bacterial pathogens in children in this country.

 Viral and protozoal infections are reported causes in third world countries.

 infection because of the increased incidence of perineal carriage in patients with streptococcal pharyngitis.

Balanitis xerotica obliterans is a rare cause of acute balanoposthitis in children.

 This condition manifests as whitish plaques on the surface of glans and prepuce, usually around the corona and up to the external meatus; the foreskin is thickened, fibrous, and nonretractable.

Clinical features of nonspecific acute balanoposthitis include pain, erythema, and swelling of the glans penis and prepuce.

 In most cases, there is little or no discharge. Acute balanoposthitis caused by 

 presents with pain, intense redness, and a moist exudate under the prepuce and on the glans.

 True urethral discharge, suggestive of sexually transmitted disease, is seen after milking the length of the urethra starting from the base of the penis.

In most prepubertal patients with acute balanoposthitis, diagnostic testing is unnecessary. In patients with discharge, a rapid group A b-hemolytic 

Treatment of nonspecific acute balanoposthitis includes a sitz bath, gentle cleaning of the preputial sulcus, and application of a low-potency corticosteroid cream.

 Children with recalcitrant, recurrent (more than 2 episodes), or an initial acute balanoposthitis that causes pathological phimosis may require circumcision.

Educating parents on foreskin care can help prevent recurrence. Prognosis is good for patients with nonspecific or streptococcal acute balanoposthitis. In some patients, recurrence may be related to a persistent underlying cause, such as diabetes or atopy.

 Wiswell TE, Tencer HL, Welch CA, Chamberlain JL. Circumcision in children beyond the neonatal period. 

 Spilsbury K, Semmens JB, Wisniewski ZS, Holman CD. Circumcision for phimosis and other medical indications in western Australian boys. 

 Schwartz RH, Rushton HG. Acute balanoposthitis in young boys. 

Vohra S, Badlani G. Balanitis and balanoposthitis. 

 Orden B, Martin R, Franco A, et al. Balanitis caused by group A beta-hemolytic streptococci. 

 Kyriazi NC, Costenbader CL. Group A beta-hemolytic streptococcal balanitis: it may be more common than you think. 

 Edwards S. Balanitis and balanoposthitis: a review. 

 Mogielnicki NP, Schwartzman JD, Elliott JA. Perineal group A strepococcal disease in a pediatric practice. 

 Birley HD, Walker MM, Luzzi GA, et al. Clinical features and management of recurrent balanitis; association with atopy and genital washing. 