{
 "topic": "Rickets",
 "slug": "rickets",
 "category_id": 14938,
 "passage_count": 14,
 "source_chars": 11986,
 "enough_material": true,
 "references": [
  {
   "title": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024",
   "author": null,
   "pages": [
    517,
    518,
    519,
    523,
    526
   ]
  },
  {
   "title": "Algorithms in Pediatrics",
   "author": null,
   "pages": [
    488
   ]
  },
  {
   "title": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "author": null,
   "pages": []
  },
  {
   "title": "MedStudy Pediatrics Core 11th Edition 2024-2025",
   "author": null,
   "pages": [
    632
   ]
  },
  {
   "title": "Pediatrics for Practitioner (Sharad Thora)",
   "author": null,
   "pages": [
    299
   ]
  },
  {
   "title": "Cover",
   "author": "Vitalsource Download",
   "pages": [
    8229
   ]
  },
  {
   "title": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition",
   "author": "Hay, William W., Levin, Myron J., Deterding, Robin R., Abzug, Mark J.",
   "pages": [
    1067
   ]
  }
 ],
 "passages": [
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 518",
   "text": "## ~~Table 69.3 Clinical Features of Rickets~~ GENERAL Failure to thrive (malnutrition) Listlessness Protruding abdomen Muscle weakness (especially proximal) Hypocalcemic dilated cardiomyopathy Fractures (pathologic, minimal trauma) Increased intracranial pressure HEAD Craniotabes Frontal bossing Delayed fontanel closure (usually closed by 2 yr) Delayed dentition No incisors by age 10 mo No molars by age 18 mo Caries Craniosynostosis CHEST Rachitic rosary Harrison groove Respiratory infections and atelectasis* BACK Scoliosis Kyphosis Lordosis EXTREMITIES Enlargement of wrists and ankles Valgus or varus deformities Windswept deformity (valgus deformity of one leg with varus deformity of other leg) Anterior bowing of tibia and femur Coxa vara Leg pain HYPOCALCEMIC SYMPTOMS[\u2020] Tetany Seizures Stridor caused by laryngeal spasm *These features are most frequently associated with the vitamin D deficiency disorders."
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 517",
   "text": "Rickets is principally caused by vitamin D deficiency. Although largely corrected through public health measures that provided children with adequate vitamin D, rickets remains a persistent problem in developed countries, especially in children with restrictive diets (autism) or elimination diets (fear of allergies). It remains a significant problem in developing countries and may be secondary to nutritional vitamin D deficiency and inadequate intake of calcium (Table 69.1). ## **Etiology** There are many causes of rickets, including vitamin D disorders, calcium deficiency, phosphorus deficiency, and distal renal tubular acidosis (Table 69.2). ## **Clinical Manifestations**"
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 519",
   "text": "## **Diagnosis** The diagnosis of rickets is based on the presence of classic radiographic abnormalities. It is supported by physical examination findings, history, and laboratory results consistent with a specific etiology (Table 69.4). ## **Clinical Evaluation** Because the majority of children with rickets have a nutritional deficiency, the initial evaluation should focus on a **dietary history** , ![](/tmp/pdf-images/pdf-0519-12.png) Fig. 69.3 Windswept deformity of the legs in an older child with rickets. _(From Rickets and osteomalacia. In Hochberg MC, Silman AJ, Smolen JS, et al., eds. Rheumatology, 4th ed. London: Mosby; 2008: Fig 192- 6.)_"
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 523",
   "text": "Rickets secondary to inadequate dietary calcium is a significant problem in some countries in Africa, although there are cases in other regions of the world, including industrialized countries. Because breast milk and formula are excellent sources of calcium, this form of rickets develops after children have been weaned from breast milk or formula and is more likely to occur in children who are weaned early. Rickets develops because the diet has low calcium content, typically <200 mg/day if <12 months old or <300 mg/day if >12 months old. The child has minimal intake of dairy products or other sources of calcium. In addition, because of reliance on grains and green leafy vegetables, the diet may be high in phytate, oxalate, and phosphate, which decrease absorption of dietary calcium. In industrialized countries, rickets caused by calcium deficiency can occur in children who consume an unconventional diet. Examples include children with milk allergy who have low dietary calcium and children who transition"
  },
  {
   "source": "Algorithms in Pediatrics, p. 488",
   "text": "![](/tmp/pdf-images/pdf-0488-03.png) _S Thangavelu, M Vijayakumar_ ## **IntroductIon** Rickets is caused by defective mineralization of growing bones resulting in bony deformities. Vitamin D deficiency is the most common cause of rickets. Rickets, like illness can occur in wide variety of other disorders like renal tubular disorders, chronic liver disease, and some metabolic disorders. Clinical appearance is similar, but after biochemical evaluation, one can differentiate one from the other."
  },
  {
   "source": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "text": "Clinical Considerations Clinical Recognition Children with rickets may come to medical attention because of specific physical abnormalities (bowed legs), limb pain and swelling, seizures, failure to thrive (renal tubular acidosis), biochemical abnormalities (hypocalcemia), radiographic findings (broadened, frayed metaphysis), or during the evaluation of a fracture. Triage Rickets should be considered in patients with nonspecific bony complaints. Initial Assessment/H&P A thorough social and dietary history is helpful in delineating the probable cause of the rickets and in sparing the patient an extensive and expensive evaluation. A family history may be useful in identifying the 1-alpha-hydroxylase deficiency or renal phosphate wasting. If the child has previously been treated with vitamin D, the reported response to that treatment may be helpful in identifying the likely site of defect."
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 526",
   "text": "Chapter 69 u Vitamin D Deficiency (Rickets) and Excess 479 birthweight and younger gestational age. Rickets occurs because unsupplemented breast milk and standard infant formula do not contain enough calcium and phosphorus to supply the needs of the premature infant. Other risk factors include cholestatic jaundice, a complicated neonatal course, prolonged use of parenteral nutrition, the use of soy formula, and medications such as diuretics and corticosteroids. weekly measurements of calcium, phosphorus, and ALP. Periodic measurement of the serum bicarbonate concentration is also important because metabolic acidosis causes dissolution of bone. At least one screening radiograph for rickets at 6- 8 weeks of age is appropriate in infants who are at high risk for it; additional films may be indicated in high- risk infants. ## **Prevention** ## **Clinical Manifestations**"
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 526",
   "text": "Rickets of prematurity occurs 1- 4 months after birth. Infants can have nontraumatic fractures, especially of the legs, arms, and ribs. Most fractures are not suspected clinically. Because fractures and softening of the ribs lead to decreased chest compliance, some infants have respiratory distress from atelectasis and poor ventilation. This rachitic respiratory distress usually develops >5 weeks after birth, distinguishing it from the early- onset respiratory disease of premature infants. These infants have poor linear growth, with negative effects on growth persisting beyond 1 year of age. An additional long- term effect is enamel hypoplasia. Poor bone mineralization can contribute to dolichocephaly. There may be classic rachitic findings, such as frontal bossing, rachitic rosary (see Fig. 69.1), craniotabes, and widened wrists and ankles (see Table 69.3). Most infants with rickets of prematurity have no clinical manifestations, and the diagnosis is based on radiographic and laboratory findings."
  },
  {
   "source": "MedStudy Pediatrics Core 11th Edition 2024-2025, p. 632",
   "text": "Itis the result of an abnormality in calcium, phosphorus, or vitamin D metabolism. Rickets results in secondary hyper- parathyroidism, except for hypophosphatemic rickets. Table 1. Type of Rickets Calcium Phosphorus Vitamin Mild \u201cNilow \u2014\u2014\u2014Nilow deficiency Moderate NI, low Low Severe Low Low FARR \u2014sCSN'sCVery low Deficiency of: 25-hydroxylase NI Low FHR = familial hypophosphatemic rickets NI= normal Patients with rickets present with a history of irritability, weakness, fractures, and growth restriction. On exam, an infant with advanced rick- ets presents with frontal bossing, craniotabes, wid- ened sutures, nodules on the ribs (a.k.a. \u201crachitic rosary\u201d), and flared wrists. The older child presents with flared wrists or ankles, genu valgum, or genu varum (Figure 15-25). The diagnosis is made by Figure 15-25: Bowing of the lab and x-ray. All patients _!egs in a child with rickets with rickets have an abnor- mality in their calcium and/or phosphorus, and all have"
  },
  {
   "source": "Pediatrics for Practitioner (Sharad Thora), p. 299",
   "text": "## **Key Messages** - Rickettsial infections are prevalent in various parts of India - These are one of the most difficult infections to diagnose in their early course and high index of suspicion is the key to early diagnosis - Fever, rash, headache, myalgia, lymphadenopathy and eschar are various clinical features of these infections - Epidemiological features and history of exposure to vector are crucial for diagnosis - Therapy is easy and affordable with dramatic results and needs to be started on clinical suspicion, as there is no specific test for early diagnosis - Doxycycline is the drug of choice and it can be used safely even in children below 8 years of age ## **Suggested Reading** 1. Porter RS, Kaplan JL, Homeier BP (Eds). Merck Manual. Hoboken, New Jersey: Wiley Publication; 2011. 2. Rathi N, Rathi A. Rickettsial infections: Indian perspective, Indian Pediatr. 2010;47(2):157-64. ## **Recurrent Wheezing in Childhood** 41 _Somu Sivabalan_ ## **Introduction**"
  },
  {
   "source": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "text": "The clinical findings in rickets may vary considerably, depending on the underlying disorder, the duration of the problem, and the child\u2019s age. Most features are related to skeletal deformity, skeletal pain, slippage of epiphyses, bony fractures, and growth disturbances. Muscular weakness, hypotonia, and lethargy are often noted. Failure of calcification affects those parts of the skeleton that are growing most rapidly or that are under stress. For example, the skull grows rapidly in the perinatal period; therefore, craniotabes is a manifestation of congenital rickets. However, the upper limbs and rib cage grow rapidly during the first year of life, and abnormalities at these sites are more common at this age (i.e., rachitic rosary, flaring of the wrist). Bowing of the legs is unlikely to be noted until the child is ambulatory. Dental eruption may be delayed, and enamel defects are common. Management/Diagnostic Testing"
  },
  {
   "source": "Cover, p. 8229",
   "text": "**Clinical Features** Clinical presentation of rickets may vary depending on etiology and severity. Clinical presentation may also include widened wrists and ankles since cartilage and osteoid continue to expand even with decreased mineralization; hence, the growth plate thickens and increases in circumference. Newborns and preambulatory infants with rickets may present with fractures, hypocalcemia, bowing of the forearms, craniotabes that are still present after a few months of age (weakness of the cranial bones detected by applying pressure over the occiput or parietal bones), frontal bossing, delayed closure of the cranial fontanelles, and diffuse demineralization. In children, skeletal abnormalities include genu varum or valgum, enlarged wrists and ankles due to widening of the growth plate, rachitic rosary (prominence of the costochondral junctions), and Harrison groove (indentation of the lower anterior thoracic wall during inspiration due to weakening of the ribs). Other clinical manifestations"
  },
  {
   "source": "Cover, p. 8229",
   "text": "Rickets is characterized radiographically by cupping, splaying, and fraying of the metaphyses of the long bones, bowing of the long bones, cortical narrowing, stress fracture lines, and diffuse demineralization. ## **Prematurity/Low Birth Weight** Compared to older infants and children, all neonates have higher requirements of calcium and phosphorous for adequate mineralization and skeletal growth. Preterm infants and low-birth-weight infants, especially those less than 27 weeks of gestation or with a low birth weight of less than 1500 g, have a higher risk of rickets compared to term infants since the transfer of calcium and phosphorous from mother to fetus peaks in the third trimester as this is the stage of maximum skeletal growth and deposition of minerals. Calcium and phosphorous are"
  },
  {
   "source": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition, p. 1067",
   "text": "Rickets describes characteristic clinical and bony radiologic features associated with hypophosphatemia (see Chapter 11). Vitamin D deficiency, caused by lack of sunlight exposure or dietary deficiency, is the most common cause of rickets. Recently, high rates of occult vitamin D deficiency have formed the basis for the 2008 recommendation by the American Academy of Pediatrics that breast-fed infants receive vitamin D supplementation of at least 400 IU/day. See Table 34\u20135 for features of other causes of rickets. Familial hypophosphatemic rickets occurs due to abnormal renal phosphate loss related to abnormal fibroblast growth factor 23 (FGF23) regulation. ## \u00bb **Clinical Findings** ## **A. Symptoms and Signs**"
  }
 ]
}