Nephro

1. BASIC PRINCIPLES OF
CLASSIFICATION AND
CLINICS OF RICKETS
NAME : Mina Tara , Saman Sohail
GROUP : 01
SEMESTER : 06
SUBJECT : EARLY CHILDHOOD DISEASES

2. Rickets is defective mineralization of bones
before epiphyseal closure in infants due to
deficiency or impaired metabolism of vitamin D
phosphorus or calcium, potentially leading to
fractures and deformity. Rickets leads to
softening and weakening of the bones and is seen
most commonly in children 6-24 months of age.
WHAT IS RICKETS?

4. CLASSIFICATION AND CLINICS OF
RICKETS
By severity: mild, moderate, severe
By period: initial, advanced, recovery,
residual
By clinical course: acute,
subacute,recurrent

5. Mild : small changes of nervous system,
changes of one part of the skeleton;
Moderate : changes of all organs and
systems, changes of two parts of the
skeleton;
Severe : damaging function of all organs and
systems, changes of three parts of the
skeleton;
BY SEVERITY

6. Initial stage
Usually begin at 3 months old
Symptoms: mental psychiatric symptoms
Irritability, sleepless,
Laboratory findings: Serum Ca, P normal or
decreased slightly, ALP normal or elevated slightly,
25(OH)D3 decreased
X-ray changes: normal or slightly changed
BY PERIODS

7. Advanced stage
On the base of early rickets, osseous changes
become marked and motor development becomes
delayed.
 Osseous changes:
1) Head: craniotabes, frontal bossing, boxlike
appearance of skull, delayed closure of anterior
fontanelle
2) Teeth: delayed dentition with abnormal order,
defects
3) Chest: rachitic rosary, Harrison’s groove, pigeon
chest, funnel-shaped chest, flaring of ribs

8. 4) Spinal column: scoliosis, kyphosis,
lordosis
5) Extremities: bowlegs, knock knee,
greenstick fracture
6) Rachitic dwarfism
 Muscular system: potbelly, late in
standing and walking
 Motor development: delayed
 Other nervous and mental symptoms

9. Laboratory findings:
Serum Ca and P decreased ALP elevated
X-ray changes:
Wrist is the best site for watching the changes
Widening of the epiphyseal cartilage
Blurring of the cup-shape metaphysis of long
bone.

10. Nutritional Rickets
Nutritional rickets results from inadequate sunlight
exposure or inadequate intake of dietary vitamin D,
calcium, or phosphorus.

11. Vitamin D dependent
Type I is secondary to a defect in the gene that codes
for the production of renal 25(OH)D3-1-alpha-
hydroxylase.
Type II is a rare autosomal disorder caused by
mutations in the vitamin D receptor. Type II does not
respond to vitamin D treatment; elevated levels of
circulating calcitriol differentiate this type from type I.

12. Vitamin D resistant
Familial (X-linked ) hypophosphataemic
rickets – renal tubular defect in phosphate
transport.
Fanconi syndrome (renal loss of phosphate)

13. A two – month – old infant was admitted in emergency room due to
recurrent seizures from 3 days ago. In the last day convulsions
repeated every one hour. Initial Laboratory study revealed a serum
total calcium 5.7 mg/dl (8.5-10.5), albumin 3.5 gram/dl, and ALP 1270
IU (180-1200). After calcium administration, serum calcium changed
to 8.3 mg/dl after 48 hours, and then 10000 IU vitamin D daily for 6
weeks continued. In outpatients follow up he was found to be a well
developed and well nourished normal baby

14. This case presents a scenario of a two-month-old infant with recurrent seizures and hypocalcemia,
likely due to vitamin D deficiency rickets. Here's a breakdown:Diagnosis:The initial presentation
with recurrent seizures, low serum calcium (5.7 mg/dl), and elevated alkaline phosphatase (ALP)
levels suggests hypocalcemia.The normal albumin level indicates that corrected calcium is still low,
confirming hypocalcemia.The elevated ALP suggests bone turnover and possible rickets.Treatment
with calcium administration resulted in an increase in serum calcium to 8.3 mg/dl after 48 hours,
supporting the diagnosis of hypocalcemia.Subsequent treatment with high-dose vitamin D (10000 IU
daily for 6 weeks) aims to correct the underlying vitamin D deficiency, a common cause of
hypocalcemia and rickets in infants.Management:Calcium administration initially helps stabilize
the infant's serum calcium levels.High-dose vitamin D supplementation addresses the underlying
vitamin D deficiency, aiming to promote calcium absorption and prevent further episodes of
hypocalcemia and seizures.Outpatient follow-up confirms the effectiveness of treatment, with the
infant showing normal development and nutrition, indicating successful management of the
underlying condition.Prognosis:With appropriate treatment, including calcium administration and
vitamin D supplementation, the infant's condition improves, as evidenced by the resolution of
seizures and normalization of serum calcium levels.Long-term prognosis is good, but regular
monitoring of serum calcium and vitamin D levels, as well as continued vitamin D supplementation
and dietary modifications, may be necessary to prevent recurrence of hypocalcemia and ensure
optimal bone health and development.