Skeletal Imaging of Nutritional Disorders in Children

Imaging of skeleton plays a major role in the diagnosis of nutritional disorders in children. The disorders can be


Introduction
Despite governmental and nongovernmental service programs in improving pediatric nutrition with supplementary foods, it is not uncommon to see children with nutritional deficiency disorders. Most of them reflect upon the musculoskeletal system. The major deficiency disorders include nutritional rickets, scurvy, osteoporosis, hypoprotenemia and anemias. The conventional radiological appearances are classical and very rarely are it needed to have advanced imaging methods. However, quantitative computed tomography (CT), dual-energy photon absorptiometry, and dualenergy x-ray absorptiometry, which are reliable measurement methods to assess the degree of osteoporosis. Rarely this is used in pedeatric practice. The conventional radiological characteristics are described in detail supported by illustrations. The differential diagnosis and their varied radiological appearances are mentioned. Rickets can be encountered in neonatal, childhood and adolescents.
The toxic disorders include hypervitaminosis A and D. Other causes include plumbism, hypercalcemia, steroids, heparin over use, antiepiliptic drugs and flurosis.

Pathophysiology of Rickets
The deposition of mineral in cartilage needs adequate amounts of both calcium and phosphorous. If these are deficient failure of new bone mineralization takes place. The resorption of unmineralized osteoid is less due to inhibition of osteoclastic resorption of matrix. As a result the skeleton becomes soft resulting in deformities in fractures. In rickets normal amount of bone has rarely adequate time to accumulate and hence the patient has both osteoporosis and osteomalacia. Osteoid excess in the growing cartilage results in widening of growth plate. During the process of healing the islands of unremodelled cartilage remain in the metaphyseal zone resulting in patches, resulting in lytic appearances on radiography.
An age old disorder principally affects the growing cartilage and bone. This is equivalent to osteomalacia in adults [1][2][3][4][5]. The etiological and metabolic factors of rickets include the following (Table 1) There are three types of rickets related to vitamin D,

2) Vitamin D Dependant and
3) Vitamin D Resistant. Radiological findings of nutritional rickets are listed in (Table 2).  The most severely affected long bones include distal femur, the proximal tibia, distal radius, ulna and proximal end of the humerus which are actively growing ends of the bones. In long-standing rickets, bowing of weight bearing bones and increased incidence of fractures for which surgical correction may be required [6].

Rickets (Radiological findings)
Radiological findings of the Skull and Spine are included in Table  3. These are less severe as compared with growing long bones.

Neonatal Rickets
In first 2 years of life, incidence of Rickets is 5 to 20%. Neonatal rickets is believed to be of multifactorial origin. Major contributing factors are related to nutrition, immaturity of enzyme systems & iatrogenic/ metabolic factors. Premature infants of low birth weight are primarily affected. Bony changes appear around 2 months of age. The most frequent causes of Rickets in patients under 6 months of age also include conditions like Biliary Atresia ( Figure 1).   In young children and adolescents, characteristic radiological appearances are noted on conventional films. These include osteoporosis, metaphyseal cupping and ground glass appearance of growing and weight bearing bones (Figure 2a

Healing Rickets
With Vitamin D and calcium treatment, regression of radiological findings is noted. During healing, radiolucent bands at metaphyses of long bones become sclerotic. Cupping of metaphyses become clearly prominent. As healing progresses remodelling of bowing deformities occur. In skull, characteristic bossing of frontal & parietal bones becomes apparent (Figure 4a-4d). There may be with premature closure of sutures.

Sequelae Post-Rickets
Complete healing and restoration of normal structures occurs in nutritional rickets. However distortion/sclerosis of spongiosa in affected segment may occur after healing & may remain visible for several years. Cortical thickening of segments of bone involved during active stage also may persist. Angular deformities secondary to pathological fractures result in deformities like knock-knee, bow leg and sabre shin ( Figure 5).  Signs of healing are listed in Table 4.

Signs of healing
Reappearance of dense zone of provisional calcification -first sign of healing Increase in cupping of healing metaphysis

Recalcification of subperiosteal osteoid
Sharply defined epiphyseal ossification centres.  Radiological findings of nutritional rickets are almost the same in other forms of rickets. In the Differential diagnosis, Hypophospatasia (low serum alkaline phosphatase) and metaphyseal chondrodyplasia (type schmid). Hypophospatasia may be encountered in neonates, children, adolescents and adults. Radiographics manifestations are different according to ages [7]. Deep cupping with irregularity of metaphyses is a common finding in children, simulating healing rickets ( Figure 6). Metaphyseal chondrodysplasia is a rare genetic abnormality with no Vitamin D abnormality. There is generalized symmetric disturbance of enchondral bone formation. Radiologically, the metaphysic are well mineralized and may have increased density with irregular margins, simulating healing rickets7. Serum calcium, phosphorus and alkaline phosphatase are normal (Figure 7).

Scurvy
Scurvy, which in infants is also known as Barlow disease, is a disorder caused by dietary lack of vitamin C and characterised by increased bleeding tendency and impaired collagen synthesis 6/9 Nov Tech Nutri Food Sci Volume 1 -Issue 1 resulting in osteoporosis and impaired wound healing. Today, scurvy is very rare due to consumption of qualitative foods in pregnant mothers as well as in infants. The radiographic features are listed in Table 5 [1,3,4,7].     On occasion, a combination of vitamin deficiencies may be encountered, in which case both rachitic and scorbutic findings may be noted on radiographs.
Generally, conventional radiographs are enough and advanced imaging such as CT and MRI are superfluous. However, MRI may depict better pictures and show marrow changes ( Figure 8). In the differential diagnosis, non accidental injury in children may be considered. In non accidental injuries, multiple fractures occurring at different times are noted. Bucket handle fracture is a common finding [1]. Elicitation of history is essential (Figure 9). Osteoporosis in children: Unlike in adults primary osteoporosis in children is very rare. Osteoporosis is a metabolic disorder. The bones become weak and hence break easily. Juvenile osteoporosis may be primary or secondary; the cause of primary is unknown and is called idiopathic juvenile osteoporosis. Radiological findings include lucency of the bones with pathological fractures [8,9]. However, it is too late to diagnose and grade osteopenia by conventional radiology (Figure 10). In adults, bone mineral density (BMD) is measured by dual energy bone absorptiometry. This is not very reliable in children. There is another kind of osteoporosis of the vertebrae associated with Schmorl's nodes and kyphosis called Schuermann's disease (Figure 11a-11b). It is very rare but uneducated mothers may go on giving high doses of Vitamin A. Radiological findings include coned epiphysis with triangular notching of metaphysic (Figure 12a). Periosteal reactions are also noted along ulna and 5th metatarsal bones Table 5: The radiographic features.  simulating Caffey's infantile hyperostosis [1,9,10] (Figure 12b).

Hypervitaminosis D
This is also rare but often seen with overdose of Vitamin D in treating rickets [11]. Radiologically dense metaphyses are noted with osteoporosis of rest of bones (Figure 13a & 13b).

Plumbism
Lead toxicity leads to plumbism, where the children suck the Chinese matel toys which are lead coated. Radiographic features of lead toxicity in children include, bands of increased density at the metaphyses, can affect any metaphysis [12]. Involvement of proximal fibula and distal ulnar metaphysis is highly suggestive (Figure 14ab). Occasionally a bone in a bone appearance may be seen.

Fluorosis
FLUORIDE EXCESS by 1.8 PPM for a length of time in endemic areas may produce changes in pediatric skeleton. The radiological findings include increased sclerosis of bones, rickets and stress lines in the growing bones [13] (Figure 15).

Steroids
Use of steroid medications is not uncommon in pediatric practice. The radiological findings include: osteoporosis, avascular necrosis, stress fractures and infarcts of bone. The vertebral end plates show concavity resembling fish mouth vertebrae ( Figure  16). In advanced cases, vertebral fractures are noted [14].

Antiepileptic drugs
Antiepileptic drugs such as dilantin sodium may produce rachitic changes due to induced microsomal P-450enz and decreased Vitamin D. Radiological findings for similar to those noted in nutritional rickets.
Starvation and Anorexia nervosa: In these disorders osteoporosis is noted with bone marrow changes [15] (Figure 17).

Summary
Nutritional disorders include nutritional deficiencies as well as hyperdoses of vitamins and minerals. The major deficiencies include lack of vitamin D and C. The radiological characteristics are described with illustrations. Similarly, toxicities such as