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Rickets
and
Osteomalacia
DR SREERAJ S R
Physiotherapy for
Sreeraj S R
Definitions
RICKETS
o It is a metabolic disease of childhood in which, the osteoid,
the organic matrix of bone, fails to mineralize due to
interference with calcification mechanism.
OSTEOMALACIA
o It is the adult counterpart of rickets and is characterized by
failure of mineralization and an excess of osteoid due to an
interference with calcification mechanism.
2
Sreeraj S R
Role of Calcium
o Calcium serves a major structural role and remains
metabolically stable under normal circumstances.
o Calcified bone contains about 25% organic matrix (2-5% of
which are cells), 5% water and 70% inorganic mineral,
hydroxyapatite (Ca10 (PO4)6 (OH)2), the main mineral deposited on
the organic matrix as calcium.
o It has structural and metabolic importance.
3
Sreeraj S R
Calcium Metabolism
o Vitamin D, PTH, bile salts, calcitonin help in the absorption of
calcium from the upper small intestine, while the oxalates,
citrates, phosphates, phytic acids and fats impair absorption.
o Hormones, which help calcium to be deposited into the bone, are
estrogen, thyroxin, growth hormone and testosterone, while that
which remove the calcium from bone are glucocorticoids, thyroid
hormones, PTH and acidosis.
o Any upset in this delicate balance either results in increase or
decrease in serum calcium.
4
Sreeraj S R
Rickets: causes
1. Vitamin D deficiency:
• Reduced dietary intake
• Reduced amount of sunlight
• Pigmented skin.
2. Malabsorption due to:
• Celiac disease
• Hepatic osteodystrophy.
3. Renal disease:
• Glomerular failure
• Renal osteodystrophy.
4. Antiepileptic drugs favors formation of hepatic enzyme, which prevents conversion of
calciferol.
5
Sreeraj S R
Rickets: varieties
1. Type I: This is due to dietary deficiency or defects in
metabolism of vitamin D.
2. Type II: This is due to low serum phosphorus due to
dietary phosphate deficiency or defective tubular
resorption.
o Type I dietary deficiency of vitamin D is the most common
variety of rickets.
6
Sreeraj S R
Rickets: symptoms
• Delayed growth
• Delayed motor skills
• Pain in the spine, pelvis and legs
• Muscle weakness
7
Sreeraj S R
Rickets: signs
1. Frontal bossing
2. Dentition changes
3. Chovstek’s sign
4. Rickety rosary
5. Pigeon chest
6. Malabsorption
7. Aminoaciduria
8. Expanded wrist
9. Pelvis deformity
10.Genu valgum
11.Myopathy
12.Skin changes
8
Sreeraj S R
Frontal bossing
o Broadened forehead
o Skull squared (caput
quadratum)
o Frontal and parietal
bossing—seen after the
age of 6 months.
9
Sreeraj S R
Chovstek’s sign
o It is a clinical sign
of hypocalcemia which
consist of twitching of
muscles innervated by
facial nerve.
o It refers to an abnormal
reaction to the stimulation
of the facial nerve.
10
Sreeraj S R
Rickety rosary
o Enlargement of
costochondral junction.
11
Sreeraj S R
Pigeon chest
o due to prominent sternum.
12
Sreeraj S R
Narrow chest
o Costochondral dysplasia
(short rib size).
o Ribs cannot extend anteriorly,
resulting in anteroposterior
and lateral thoracic diameters
reduction (narrow chest).
o The highlights include alveolar
hypoventilation and lung
growth restriction.
o Also Jeunes Syndrome
13
Sreeraj S R
Harrison’s sulci
o Symmetrical horizontal
grooves above the costal
margin, along the line of
attachment of diaphragm.
o Due to diaphragmatic pull
on the soft ribs.
14
Sreeraj S R
Expanded wrist
o Enlargement of the
metaphyseal segments of
long bones like radius,
tibia, costochondral
junction, etc. seen in
children between 6 and 9
months of age.
15
Sreeraj S R
Skin changes & Genu valgum
16
Sreeraj S R
Pelvis deformity
17
Sreeraj S R
Rickets: X-ray findings
Characteristic Lovette and Jones radiological changes
o Delayed appearance of epiphysis and widening of the epiphyseal plates.
o Champagne glass appearance (widening and cupping of the distal ends of
long bones) also called‘trumpeting’.
o Space between diaphysis and epiphysis is increased.
o Deformity and bowing of the ends of long bones.
o Thickened epiphysis.
o Decreased density of cortex (rarefaction).
o Coarse trabecular pattern in bone.
18
Sreeraj S R
Rickets: Differential Diagnosis
o Acute poliomyélites
o Congenital syphilis
o Septic arthritis
o Infantile scurvy
o Renal tubular acidosis
o Malabsorption syndromes
o Prematurity
19
Sreeraj S R
Rickets: Treatment
o Medical treatment in the initial stages is a single oral dose of 6
lakh IU of vitamin D is given.
o A second same dose may be required after 3-4 weeks of
treatment if no sclerotic (healing sign) change is seen on the
radiograph at the metaphyseal side of the growth plate.
o A maintenance dose of 4,000 IU of vitamin D may be required if
the child responds to the above treatment regimen.
o Absolute and strict bed rest, rickets splints, etc. can help
prevention of deformity.
20
Sreeraj S R
Rickets: Treatment
o Correction by splints (Mermaid splint): This is mainly useful when
the disease is active, and the deformity is slight.
o It is very effective in children and in preventing deformities
concerning the lower limbs.
o However, it is slow and requires continual supervision.
o Correction by osteotomy is indicated when deformity is near the
joint and when the growth stops.
o It is done during III stage (Lovett’s) (nonunion follows if done
before).
21
Sreeraj S R
Rickets: Treatment
o There are no direct physical therapy interventions for Rickets or
Vitamin D deficiency.
o Patient will be referred to physical therapy for treatment of impairments
such as decline in muscle strength, decline in physical functioning, or
falls prevention.
o Physical therapists can take a team approach with medical
management through patient education on:
o Foods high in Vitamin D
o Importance of following medical recommendations
o Importance of proper sun exposure with risks of overexposure
22
Sreeraj S R
Rickets: Treatment
o Exercises while standing can help increase bone growth but
due to osteoporosis may also be at risk for fractures.
o Physical therapy can help to also reduce any bone or
muscle pain through stretching and strengthening exercises
as well as hands on manual techniques.
23
Sreeraj S R
Osteomalacia: Etiology
o Decreased vitamin D absorption from the intestine.
o Derangement of vitamin D and phosphorus metabolism
(hereditary or acquired).
24
Sreeraj S R
Osteomalacia: Clinical Features
o The patient complains of generalized skeletal pain and
muscle weakness.
o Other symptoms related to causative factors like dietary,
renal and GIT may be seen.
o The following deformities are encountered;
o scoliosis, kyphosis, coxa vara, protrusioacetabuli, thighs and
legs are bent, pelvis is trefoil, etc.
25
Sreeraj S R
Osteomalacia: Radiographs
o Radiographic features reveal generalized demineralization,
loss of transverse trabeculae, no subperiosteal resorption of
bone, etc.
o Presence of Looser’s zones is
quite characteristic of
osteomalacia.
26
Case courtesy of Radswiki, Radiopaedia.org, rID: 11585
Sreeraj S R
Osteomalacia: Radiographs
o Spine: The bodies of
spine are biconcave
and are called “codfish
spine”.
o Hip show
protrusioacetabuli and
triradiate pelvis.
27
https://assets.cureus.com/uploads/figure/file/
32017/fb167130288a11e8b9db9304fcf484ba-
Figure-12_Formatted_V1-PME.PNG
Case courtesy of Dr Dalia Ibrahim, Radiopaedia.org, rID: 58864
https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-
78522002000400007#:~:text=Protrusio%20acetabuli%20is%20a%20disease,and%20limited%20limb%20hip%20movement.
Sreeraj S R
Osteomalacia: Treatment
• Primary Prevention/Risk Reduction for Skeletal
Demineralization
• Pain
• Impaired Posture
• Impaired Muscle Performance
• Impaired joint Mobility
• Impaired balance
28
Sreeraj S R
Osteomalacia: Treatment
o Calcium is given at 0. Osteomalacia: Treatment
o 5-3 gm/day, vitamin D 10,000 IU/day, and high protein diet.
o The gastrointestinal tract errors are also corrected
simultaneously.
o Fifteen minutes of sunshine a day may be adequate.
29
Sreeraj S R
Osteomalacia: Treatment
o Physiotherapy plays an important role in a multidisciplinary
approach to treatment.
o Tailored exercise programs are important to ensure strengthening
of major muscle groups and improvement in ADL and social
activities.
o Weight bearing exercises should be encouraged such as walking
but not intensive or high impact exercises.
o A similar approach can be taken as to exercise programs
for osteoporosis.
30
Sreeraj S R
References
1. “Metabolic Disorders.” Textbook of Orthopedics, by John Ebnezar,
St. Louis, Jaypee Brothers Medical Publishers, 2010, pp. 527–539.
2. Tbilisi State Medical University. Rickets in children [Internet].
Slideshare.net. 2014 [cited 2020 Sep 13]. Available from:
https://www.slideshare.net/jinujvarghese/rickets-in-children-
42660531
3. Osteomalacia [Internet]. Physiopedia. 2019 [cited 2020 Sep 13].
Available from: https://www.physio-pedia.com/Osteomalacia
31

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Physiotherapy for Rickets and Osteomalacia

  • 2. Sreeraj S R Definitions RICKETS o It is a metabolic disease of childhood in which, the osteoid, the organic matrix of bone, fails to mineralize due to interference with calcification mechanism. OSTEOMALACIA o It is the adult counterpart of rickets and is characterized by failure of mineralization and an excess of osteoid due to an interference with calcification mechanism. 2
  • 3. Sreeraj S R Role of Calcium o Calcium serves a major structural role and remains metabolically stable under normal circumstances. o Calcified bone contains about 25% organic matrix (2-5% of which are cells), 5% water and 70% inorganic mineral, hydroxyapatite (Ca10 (PO4)6 (OH)2), the main mineral deposited on the organic matrix as calcium. o It has structural and metabolic importance. 3
  • 4. Sreeraj S R Calcium Metabolism o Vitamin D, PTH, bile salts, calcitonin help in the absorption of calcium from the upper small intestine, while the oxalates, citrates, phosphates, phytic acids and fats impair absorption. o Hormones, which help calcium to be deposited into the bone, are estrogen, thyroxin, growth hormone and testosterone, while that which remove the calcium from bone are glucocorticoids, thyroid hormones, PTH and acidosis. o Any upset in this delicate balance either results in increase or decrease in serum calcium. 4
  • 5. Sreeraj S R Rickets: causes 1. Vitamin D deficiency: • Reduced dietary intake • Reduced amount of sunlight • Pigmented skin. 2. Malabsorption due to: • Celiac disease • Hepatic osteodystrophy. 3. Renal disease: • Glomerular failure • Renal osteodystrophy. 4. Antiepileptic drugs favors formation of hepatic enzyme, which prevents conversion of calciferol. 5
  • 6. Sreeraj S R Rickets: varieties 1. Type I: This is due to dietary deficiency or defects in metabolism of vitamin D. 2. Type II: This is due to low serum phosphorus due to dietary phosphate deficiency or defective tubular resorption. o Type I dietary deficiency of vitamin D is the most common variety of rickets. 6
  • 7. Sreeraj S R Rickets: symptoms • Delayed growth • Delayed motor skills • Pain in the spine, pelvis and legs • Muscle weakness 7
  • 8. Sreeraj S R Rickets: signs 1. Frontal bossing 2. Dentition changes 3. Chovstek’s sign 4. Rickety rosary 5. Pigeon chest 6. Malabsorption 7. Aminoaciduria 8. Expanded wrist 9. Pelvis deformity 10.Genu valgum 11.Myopathy 12.Skin changes 8
  • 9. Sreeraj S R Frontal bossing o Broadened forehead o Skull squared (caput quadratum) o Frontal and parietal bossing—seen after the age of 6 months. 9
  • 10. Sreeraj S R Chovstek’s sign o It is a clinical sign of hypocalcemia which consist of twitching of muscles innervated by facial nerve. o It refers to an abnormal reaction to the stimulation of the facial nerve. 10
  • 11. Sreeraj S R Rickety rosary o Enlargement of costochondral junction. 11
  • 12. Sreeraj S R Pigeon chest o due to prominent sternum. 12
  • 13. Sreeraj S R Narrow chest o Costochondral dysplasia (short rib size). o Ribs cannot extend anteriorly, resulting in anteroposterior and lateral thoracic diameters reduction (narrow chest). o The highlights include alveolar hypoventilation and lung growth restriction. o Also Jeunes Syndrome 13
  • 14. Sreeraj S R Harrison’s sulci o Symmetrical horizontal grooves above the costal margin, along the line of attachment of diaphragm. o Due to diaphragmatic pull on the soft ribs. 14
  • 15. Sreeraj S R Expanded wrist o Enlargement of the metaphyseal segments of long bones like radius, tibia, costochondral junction, etc. seen in children between 6 and 9 months of age. 15
  • 16. Sreeraj S R Skin changes & Genu valgum 16
  • 17. Sreeraj S R Pelvis deformity 17
  • 18. Sreeraj S R Rickets: X-ray findings Characteristic Lovette and Jones radiological changes o Delayed appearance of epiphysis and widening of the epiphyseal plates. o Champagne glass appearance (widening and cupping of the distal ends of long bones) also called‘trumpeting’. o Space between diaphysis and epiphysis is increased. o Deformity and bowing of the ends of long bones. o Thickened epiphysis. o Decreased density of cortex (rarefaction). o Coarse trabecular pattern in bone. 18
  • 19. Sreeraj S R Rickets: Differential Diagnosis o Acute poliomyélites o Congenital syphilis o Septic arthritis o Infantile scurvy o Renal tubular acidosis o Malabsorption syndromes o Prematurity 19
  • 20. Sreeraj S R Rickets: Treatment o Medical treatment in the initial stages is a single oral dose of 6 lakh IU of vitamin D is given. o A second same dose may be required after 3-4 weeks of treatment if no sclerotic (healing sign) change is seen on the radiograph at the metaphyseal side of the growth plate. o A maintenance dose of 4,000 IU of vitamin D may be required if the child responds to the above treatment regimen. o Absolute and strict bed rest, rickets splints, etc. can help prevention of deformity. 20
  • 21. Sreeraj S R Rickets: Treatment o Correction by splints (Mermaid splint): This is mainly useful when the disease is active, and the deformity is slight. o It is very effective in children and in preventing deformities concerning the lower limbs. o However, it is slow and requires continual supervision. o Correction by osteotomy is indicated when deformity is near the joint and when the growth stops. o It is done during III stage (Lovett’s) (nonunion follows if done before). 21
  • 22. Sreeraj S R Rickets: Treatment o There are no direct physical therapy interventions for Rickets or Vitamin D deficiency. o Patient will be referred to physical therapy for treatment of impairments such as decline in muscle strength, decline in physical functioning, or falls prevention. o Physical therapists can take a team approach with medical management through patient education on: o Foods high in Vitamin D o Importance of following medical recommendations o Importance of proper sun exposure with risks of overexposure 22
  • 23. Sreeraj S R Rickets: Treatment o Exercises while standing can help increase bone growth but due to osteoporosis may also be at risk for fractures. o Physical therapy can help to also reduce any bone or muscle pain through stretching and strengthening exercises as well as hands on manual techniques. 23
  • 24. Sreeraj S R Osteomalacia: Etiology o Decreased vitamin D absorption from the intestine. o Derangement of vitamin D and phosphorus metabolism (hereditary or acquired). 24
  • 25. Sreeraj S R Osteomalacia: Clinical Features o The patient complains of generalized skeletal pain and muscle weakness. o Other symptoms related to causative factors like dietary, renal and GIT may be seen. o The following deformities are encountered; o scoliosis, kyphosis, coxa vara, protrusioacetabuli, thighs and legs are bent, pelvis is trefoil, etc. 25
  • 26. Sreeraj S R Osteomalacia: Radiographs o Radiographic features reveal generalized demineralization, loss of transverse trabeculae, no subperiosteal resorption of bone, etc. o Presence of Looser’s zones is quite characteristic of osteomalacia. 26 Case courtesy of Radswiki, Radiopaedia.org, rID: 11585
  • 27. Sreeraj S R Osteomalacia: Radiographs o Spine: The bodies of spine are biconcave and are called “codfish spine”. o Hip show protrusioacetabuli and triradiate pelvis. 27 https://assets.cureus.com/uploads/figure/file/ 32017/fb167130288a11e8b9db9304fcf484ba- Figure-12_Formatted_V1-PME.PNG Case courtesy of Dr Dalia Ibrahim, Radiopaedia.org, rID: 58864 https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413- 78522002000400007#:~:text=Protrusio%20acetabuli%20is%20a%20disease,and%20limited%20limb%20hip%20movement.
  • 28. Sreeraj S R Osteomalacia: Treatment • Primary Prevention/Risk Reduction for Skeletal Demineralization • Pain • Impaired Posture • Impaired Muscle Performance • Impaired joint Mobility • Impaired balance 28
  • 29. Sreeraj S R Osteomalacia: Treatment o Calcium is given at 0. Osteomalacia: Treatment o 5-3 gm/day, vitamin D 10,000 IU/day, and high protein diet. o The gastrointestinal tract errors are also corrected simultaneously. o Fifteen minutes of sunshine a day may be adequate. 29
  • 30. Sreeraj S R Osteomalacia: Treatment o Physiotherapy plays an important role in a multidisciplinary approach to treatment. o Tailored exercise programs are important to ensure strengthening of major muscle groups and improvement in ADL and social activities. o Weight bearing exercises should be encouraged such as walking but not intensive or high impact exercises. o A similar approach can be taken as to exercise programs for osteoporosis. 30
  • 31. Sreeraj S R References 1. “Metabolic Disorders.” Textbook of Orthopedics, by John Ebnezar, St. Louis, Jaypee Brothers Medical Publishers, 2010, pp. 527–539. 2. Tbilisi State Medical University. Rickets in children [Internet]. Slideshare.net. 2014 [cited 2020 Sep 13]. Available from: https://www.slideshare.net/jinujvarghese/rickets-in-children- 42660531 3. Osteomalacia [Internet]. Physiopedia. 2019 [cited 2020 Sep 13]. Available from: https://www.physio-pedia.com/Osteomalacia 31

Editor's Notes

  1. Celiac disease  is a chronic digestive disorder resulting from an immune reaction to gliadin, a gluten protein found in wheat, barley, rye, and sometimes oats. It involves inflammation and destruction of the inner lining of the small intestine and can lead to the malabsorption of minerals and nutrients. Hepatic osteodystrophy this term was used for metabolic bone disease seen in chronic liver disease patients. It is prevalent in other chronic liver diseases (CLD) also. It is an important complication of CLD since it can result in fragility fractures, which have a significant impact on morbidity, quality of life and even survival. Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood. It's common in people with kidney disease and affects most dialysis patients.
  2. Tubular resorption.: In renal physiology, reabsorption or tubular reabsorption is the process by which the nephron removes water and solutes from the tubular fluid and returns them to the circulating blood. Tubular reabsorption mechanisms in the nephrons of your kidneys return the water and solutes that you need back into your extracellular fluid and circulatory system. In addition to reabsorbing the substances that you need, your nephrons are able to secrete unwanted substances from your bloodstream into the filtrate. Together these processes complete the transformation of the glomerular filtrate into urine.