2. CASE SCENARIO
⢠10 mo old male child admitted to KIMS in March 2020
ď Fever - 7days
ď Vomiting- 5 days
ď Excessive cry- 3days
⢠H/O Past Illness- H/o poor weight gain and non erupted teeth(+),No h/o
admission in hospital with diarrhoea,pneumonia or any other illness
3. ⢠Antenatal History- Normal,Non consanguineous marraige,No H/o fever in
mother,Antenatal USG of mother - Normal
⢠Natal History- First order child,Term,NVD,Birth weight-2.7KG
⢠Post Natal History- No h/o admission to NICU
⢠Immunization History- Immunised till age
⢠Devolopment History- Attained devolopmental milestones as per age
4. ⢠Dietary History- Exclusive breast feeding till 3 months of age followed by
which formula feeding was given.
⢠Weaning started at the age of 6months with semi-solid home made
foods(cereal based)
ď Calorie Gap- 400Kcal/kg/day
ď Protein Gap- 1.5g/kg/day
⢠Family History- Non consanguineous marraige,No h/o of any chronic or
genetic diseases in family members
⢠Socioeconomic History- Lower socioeconomic class
5. ⢠General Examination:-
- Child was consious but lethargic.
-Pallor(+)
- Vitals:- Temp-101F, HR-120/min, BP-112/70 mm Hg(>95th centile,95th
percentile- 102/54 mmHg),RR-27/min
- Anthropometry- Length-67cm(Less than 3rd percentile)
Weight- 5.2kg(Less than 3rd percentile)
HC- 42cm(Btw 3rd and 5th percentile)
Wt/L- below -3z score
MUAC-10cm(MUAC<11.5cm- Severe Acute Malnutrition)
6. -Head to Toe Examination-
Teeth - not erupted,
Head,hair,face,eyes,mouth,tongue,ears,nose,limbs,chest,abdomen,genitalia,spine,
skin and nails- Normal
- Systemic Examination-
CNS-
Higher mental function- Normal
Sensory system- Normal
Motor system- Muscle wasting(+) in bilateral upper and lower limbs
Reflexes- Normal
No Meningeal Signs
7. -Cardiovascular,Respiratory and Gastrointestinal system Examination- Normal
- Provisional Diagnosis- Severe Acute Malnutrition with Urinary Tract Infection
-Differential Diagnosis- Severe Acute Malnutrition with Enteric Fever,Malaria,Sepsis
10. Day 1
⢠Child was treated with IV Fluids and IV Ceftriaxone
⢠USG kidney, ureter and bladder(KUB) showed Bilateral Medullary
Nephrocalcinosis(NC)
⢠On detailed enquiry,documentation of Mega dose of Vitamin D, total amont
of vitamin D 8400,000 IU over 3 months (injection Vitamin D 600,000 I.M
weekly, 14doses) was seen.
12. ⢠Morning urine calcium/creatinine(Ca/cr) ratio- 2.33, suggestive of
hypercalciuria (N<0.8 in 6-12 months).
⢠X-ray wrist with elbow and Echocardiography- Normal
⢠Child was diagnosed as a case of Severe Acute Malnutrition with Urinary
Tract Infection with Vitamin D Intoxication with Medullary
Nephrocalcinosis
13. Treatment
⢠All medicine containing vitamin D and calcium was stopped
⢠Breast feeding was witheld temporarily with continuing oral feeding on
demand
⢠Intravenous Normal Saline(150 ml/kg/day)
⢠Oral furosemide(1 mg/kg/day) in 3 divided doses
⢠Oral nifedipine(0.25 mg/kg/day)
⢠During this treatment he was monitored regularly for improvements of
symptoms, intake/output chart and serum calcium level.
14. Day 2
⢠Repeat Investigation:-
-Repeat calcium level was 14.5 mg/dL
- Prednisolone @1mg/kg/day was added
15. Day 3
⢠Urine culture grown Citrobacter Freundi which was senstive to Amikacin
⢠Since the child was afebrile after staring IV Ceftriaxone,it was continued.
16. Day 4
⢠In view of persisting hypercalcemia(S.Calcium- 14.3mg/dl) ,Oral
alendronate was added in a dose of 5 mg/day
⢠Prednisolone was stopped
⢠Calcitonin was not given because of the parents refusal and risk of
tachyphylaxis.
17. Day 7
⢠Serum calcium dropped rapidly to 12 mg/dl and I.V Normal Saline
was discontinued.
⢠Feeding was started with proper dietary advice for Severe Acute
Malnutrition with calorie of 900Kcal/day and 16g/day protein.
⢠He required total 3 doses of oral alendronate
18. At the time of discharge:-
⢠Child was afebrile
⢠S. Calcium- 10.5mg/dl
⢠Child was on energy rich diet with total calorie intake of 900Kcal/day and
protein intake of 16g/day
⢠Oral Nifedipine was advised to continue till the follow up after 1 week.
⢠Parents were counselled regarding regular follow up, but due to pandemic
situation in region, they failed.
20. VITAMIN D INTOXICATION
⢠First reported in India in 2004 in AIIMS New Delhi
(Ref:- Acute Vitamin D Toxicity in an infant,The Japanese society for Pediatric
Endocrinology, 2004)
⢠Follow up of this case after 14 years showed persistent medullay
nephrocalcinosis.
⢠In a retrospective study of 152 children and adolescents,prophylactic bolus
administration of Vitamin D was the cause of nephrocalcinosis in 9% cases.
(Ref:- Nephrocalcinosis in children:a retrospective multi centre study, Acta
Pediatrica 2009)
21. - Etiology:-
ďź High doses of vitamin D given by health care providers
ďź Inappropriate administration of high doses in infants for complaints
such as delayed teething, âlate walkingâ, and âknock-kneed gaitâ.
-According to the AAP:-
ďź Serum levels above 100 ng/ml -Hypervitaminosis D
ďź Serum levels above 150 ng/ml- Vit D Intoxication(VDI)
22. Mechanism of Vitamin D Intoxication(VDI)
⢠Serious consequences due to the degree of hypercalcemia and subsequent
hypercalcuria/nephrocalcinosis.
⢠Active vitamin D is a potent stimulator of osteoclastogenesis resulting in
bone resorption
⢠Hypercalcemia predominantly results from bone resorption.
25. LABORATORY DIAGNOSIS
In patients with VDI:-
ďźHypercalcemia,
ďźNormal or high serum phosphorus levels,
ďźNormal or low levels of alkaline phosphatase,
ďźHigh levels of serum 25OHD,
ďźLow serum parathyroid hormone,
ďźHigh urine calcium/creatinine ratio
ďźMedullary nephrocalcinosis can be detected better in ultrasound scanning
26. Treatment
⢠Discontinuing intake
⢠Diet with low calcium and phosphorus content
⢠Intravenous (IV) hydration with Normal Saline
⢠Loop diuretics
⢠Glucocorticoids
⢠Calcitonin
⢠Bisphosphonates
⢠Hemodialysis
27.
28. Nephrocalcinosis
⢠Well known but rare complication of VDI which is usually irreversible
⢠Defined as generalized deposition of calcium salts(Calcium oxalate or
phosphate) in the kidney,predominantly in the interstitium.
⢠Usually involves renal medulla(>97%cases) and less commonly cortex.
29. ⢠Grading-
- I - Mild increase in echogenecity of medullary pyramids
-II - Mild diffuse increase in echogenecity of medullary pyramids without
accoustic shadowing
-III - Homogenous increase in echogenecity of medullary pyramids with
accoustic shadowing.
31. In a pediatric series of 40 patients from North India with NC:-
ďźRTA (50%),
ďźIdiopathic hypercalciuria (7.5%),
ďźPrimary hyperoxaluria (7.5%)
ďźVitamin D Intoxication (5%)
â˘In a series of 41 patients from Italy with NC :-,
ďźRenal tubulopathies (41%)
ďźVitamin D Intoxication (10%)
Ref:Etiology of ephrocalcinosis in northern Indian Children, Pediatric Nephrol 2007