Vitamin D deficiency remains the most common cause of Osteomalacia & rickets.
My first presentation prepared by me as a first year family medicine board resident. đ
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Osteomalacia & Rickets
1. Osteomalacia and
Rickets
Family Medicine Residency Program
Supervised by: Assistant Prof. D.Ali Shakir, Dr.Lara Abbas
Prepared by: Dr.Shajwan Hdayat Dara
27 Mar.2023
2. Introduction:
⢠Osteomalacia is a disorder of deficient mineralization of newly formed
osteoid at sites of bone turnover and manifestations are more subtle
& frequently overlooked.
⢠Rickets is a disorder of defective mineralization of both cartilaginous
growth plate & bone causing characteristic deformities.
⢠Both can occur together in children (open growth plate), but only
Osteomalacia occurs in adults (fused growth plate).
3. Pathophysiology:
⢠Normal bone mineralization :
1. Availability of sufficient Ca & phosphorus.
2. Presence of normal bone collagen.
3. Absence of inhibitors of mineralization.
4. Adequate amount of alkaline phosphatase activity.
*any defect in these requirements are the cause of most forms of Osteomalacia &
rickets.
9. Epidemiology:
⢠Nutritional Rickets continues to be an evolving & multifactorial
problem worldwide.
⢠About 25% of women in US have 25-OHD level <25 ng/ml & 8% below
12 ng/ml.
⢠Osteomalacia & rickets must be excluded before administration of
antiresorptive drugs used for postmenopausal osteoporosis.
⢠Recent migration to Europe & US has been accompanied by
resurgence of deficiency diseases especially vit D def.
*Goldman-Cecil medicine textbook, 26th ed.
10. Clinical manifestations of Osteomalacia:
⢠Depending of extent of mineralization delay, overt Osteomalacia may take
many years to develop.
⢠Symptoms may be insidious in onset & present radiologically as osteopenia.
⢠Most common Sx: pelvis & leg pain, muscle weakness & bone tenderness.
⢠The pain is dull, poorly localized aggreviated by sudden movements & weight
bearing resulting in a âwaddling gaitâ made worse by proximal muscle
weakness.
⢠Patients may complain that they can only climb stairs by pulling themselves up
with hand rail or rise from a chair or toilet by using their hands to push off.
⢠So decrease in strength is far greater than muscle wasting.
11. Clinical manifestations cont.
⢠Fracture with little or no trauma (ribs, vertebrae & long bones).
⢠Paresthesias, muscle cramp, seizurs & +ve Chvostekâs sign (severe hypocalcemia).
⢠Spinal, thoracic & pelvic deformity (severe long standing Osteomalacia)
⢠In XLH: +ve FH, short stature & lower leg deformity.
12. Clinical manifestations of Rickets:
⢠Most common during first 2 yr of life & may become evident only after several
months of a vit D-deficient diet.
⢠Skeletal findings Initially manifest at distal forearm, knees & costochondral
junctions (sites of rapid bone growth with greatest demand for Ca & P).
⢠Extraskeletal findings: dental hypoplasia in calcipenic rickets, dental abscesses
in hereditary phosphopenic rickets.
13.
14. Radiographic findings:
⢠Radiological abnormalities in Osteomalacia are
less striking than in rickets & may be subtle or
absent.
⢠Presence of bilaterally symmetrical, thin (2-
3mm) radiolucent bands known as
pseudofractures found perpendicular to
cortical margins of ribs, pubic & ischial rami,
neck of femur, metatarsals & scapulae is
generally considered to be pathognomonic of
Osteomalacia.
19. Diagnosis of Osteomalacia:
⢠A delay in diagnosis is commonly reported because clinicians consider
other differentials prior to confirmation of Osteomalacia including
OA, osteoporosis, paget disease, CA, malabsorption, IBS, depression..
⢠History: it should be suspected in cases of bone pain associated with
GI malabsorption, CKD or Chronic liver disease. Onset, dietary habits,
sun exposure, surgical procedures, drug hx.
⢠Radiologic findings: to distinguish Osteomalacia from multiple
myeloma or paget disease.
20. Diagnosis of Osteomalacia cont:
⢠Histomorphometric assessment:
⢠transiliac crest bone biopsy using double tetracycline labelling is most
accurate way to dx Osteomalacia. However itâs infrequently
performed clinically because itâs invasive & dx can usually be made
from combination of clinical, lab & radiologic findings.
⢠indicated when in doubt or the cause is not determined by
noninvasive testing eg. Rare disorders as axial Osteomalacia or
fibrogenesis imperfecta.
21. Diagnosis of Osteomalacia cont:
⢠Bone Mineral Density:
⢠several studies have shown markedly reduced spine, hip & forearm
BMD as measured by DEXA in pt with vit-D deficient Osteomalacia.
⢠However, BMD is not required for Dx of ostemalacia & unable to
differentiate it from osteoporosis.
28. Treatment & prognosis:
⢠Rx is directed at reversal of underlying disorder & correction of
mineral deficiencies. Response to appropriate Rx is usually excellent.
⢠Improvements in bone pain & muscle weakness usually occur within
2-3 mo & healing of skeletal lesions within 6-18 mo.
⢠Bone density improvement from Rx may continue for up to a year.
⢠Depending on the quantity of excess osteoid, repeat BMD may show
as much as 20% gains at lumbar spine & total proximal femur.
29. Treatment & prognosis cont:
⢠However, BMD at radial diaphysis may not improve due to irreversible
loss of cortical bone resulting from prolonged secondary
hyperparathyroidism.
⢠Presence of decreased bone volume in addition to excess osteoid,
skeletal recovery may be incomplete resulting in residual osteoporosis.
⢠However, caution must be considered before adding antiresorptive agent
& wait for normalization of Ca, Pi & alkaline phosphatase.
30.
31.
32.
33. Treatment of Vit-D deficiency in Rickets:
â˘Daily therapy â The most widely used Rx consists of daily replacement
doses of vitD2 or vitD3. The following dosing is recommended for children
without underlying defects in intestinal absorptive function:
⢠â˘Infants <1 mo â 1000 IU daily for up to three months, followed by
maintenance dosing of 400 IU daily.
⢠â˘Infants 1 to 12 mo â 1000 to 2000 IU daily for up to three months, followed by
maintenance dosing of 400 IU daily.
⢠â˘Children 1 to 12 yr â 2000 to 6000 IU daily for three months, followed by
maintenance dosing of 600 IU daily.
⢠â˘Children âĽ12 yr â 6000 IU daily for three months, followed by maintenance
dosing of 600 IU daily.
34. Treatment of Vit-D deficiency in Rickets:
â˘Stoss therapy â An alternative Rx protocol which consists of a
high dose of vitamin D given on a single day. The Global Consensus
prefers daily therapy rather than stoss therapy, but recognizes that it is
sometimes more practical & provides the following dosing using
oral vitamin D3 & not vitD2:
⢠â˘Infants <3 moâ Stoss therapy not recommended
⢠â˘Infants 3 to 12 moâ A single dose of 50,000 IU
⢠â˘Children 1 to 12 yr â A single dose of 150,000 IU
⢠â˘Children ⼠12 yr â A single dose of 300,000 IU
35. Monitoring of VitD Therapy:
Serum Ca, Pi, alkaline phosphatase & urinary Ca:cr ratio should be measured 4
weeks after the start of therapy.
⢠They become normalized except urinary Ca:Cr ratio may still be low.
⢠These tests should be repeated monthly until doses are adjusted downward to
a typical daily replacement amount.
⢠This typically occurs by three months of therapy, at which time radiographs can
be obtained to document the healing of rachitic lesions.
⢠Monitoring is also important to ensure that no toxicity has occurred.
36. Treatment of calcium deficiency rickets:
⢠It can be treated by ensuring a daily intake of 1000 mg of calcium and
maintenance of vitamin D intake at the recommended daily value.
37. Prevention:
⢠High risk populations (eg. Dark skinned, immigrants) require lifelong
supplementation & food fortification with vitD or Ca.
⢠Optimal vitD supplementation isnât clear but most bone & mineral problems are
avoided by 50,000 IU cholecalciferol given once monthly. Except in pt with celiac
disease, gastric operation or bypass for obesity who often require much larger
amounts.
⢠VitD is recommended for all breast-fed infants as 400 IU/d started soon after
birth& given until the infant is taking >1000 IU of formula or vitD-fortified milk
(for age>1 yr).