Neonatal hypercalcemia

[Guest sameera_reddy]

How is neonatal hypercalcemia >17 managed in a term LGA perinatal asphyxia child aged 25 days ?.Is Ethidronate routinely used after normal saline and frusemide infusions.Opinions on using sc calcitonin. Child is on full feeds.He had elevated blood pressures with LVH in 2nd week of life managed with frusemide infusions.

[Francesco Cardona]

Do you mean 17mg/dl of total calcium? That corresponds to about 4.25mmol/l in SI units. Do you have any indication on the cause of hypercalcemia? How is the babies kidney function? Is calcium excretion in urine high or low? Any clinical symptoms (vomiting, polyuria or dehydration, irritability?

We rarely see hypercalcemia in our neonates, so I have no experience about calcitonin. I remember using Etidronate once.

[Guest sameera_reddy]

Baby's renal functions are normal. Parathormone and Vit D levels are low normal.During the initial days baby had very bad subacute fat necrosis/sclerema which we are supposing to be the cause. Baby is sucking well at breast, fair activity levels with no hypertension now

[ftandoi]

I remember of a case of fat necrosis that we succesfully treated with furosemide.

[Urban Rosenqvist]

This is an interesting topic for me.  

We´ve just had two cases of fat necrosis with following hypercalcemia in the last 2 months. 

 

One baby had birth asphyxia 41+2, APGAR 0,2,2 (HIE I/II) and was cooled.

The other baby was not so ill but had reduced peripheral circulation the first hours of life (a risk factor) due to PPHN which resolved quickly on oxygen treatment. 

 

The latter one developed subcutanoeus fat necrosis in about a week after birth and also more necrosis after a month. 

In this patient hypercalcemia was no more than 3,0 mmol/l (2,2-2,7) and we noted no symptoms of hypercalcemia. 

 

The former baby was in pain and tender to touch and was treated with morphine and paracetamol with some success.

This baby had a higher calcium with calcium above 3 during a couple of weeks, up to 3,51 mol/l. 
 

Searching for information on this topic yields no conclusive recommendation.

I´ve also talked to colleagues and the opinions vary enormously - from: "Do nothing, we have never monitored calcium in these babies and we´ve never seen any pathology because of it", to "monitor and treat!" 

 

Some studies states that fat necrosis itself is a self resolving harmelss condition but the effects of hypercalcemia can be dangerous and a cause of for example nefrocalcinosis and even death (cardiac arrythmias).

 

We have just kept on monitoring the well baby with the lower calciums levels without any intervention. 

 

The baby with the higher calcium was constantly irritable despite pain management so we suspected that these symptoms were rather caused by the hypercalcemia (which can cause irritability) than actual pain from subcutaneous necrosis. .

After discussing this with an endocrine specialist we started NaCl infusion, after a while we also added oral frusemide.

We also changed the babies formula to Locasol which is low calcium/low vitamin D formula and we postponed supplementation with vitamin D (which every child in Sweden gets).  

 

This had an effect (though not immidiate) lowering s-calcium.

With the hypercalcemia resolving the baby was happier and less irritable so it seemed that the symptoms had been caused by the hyperclalcemia.  

Our next step would have been oral prednisone 1mg/kg/day but s-calcium is returning to normal so the only treatment now is Locasol and no vitamin D for another 3-4 weeks. 

[Dinesh N Patel]

What about nutritional manage ment in this patient?

[Dinesh N Patel]

Incaseof prolongedNBM without supliment of phosphatecan ecause hypercalcemiaasparental phosphorous iis not avaible in india

[Guest mmerocru]

This is an interesting topic for me.  

We´ve just had two cases of fat necrosis with following hypercalcemia in the last 2 months. 

 

One baby had birth asphyxia 41+2, APGAR 0,2,2 (HIE I/II) and was cooled.

The other baby was not so ill but had reduced peripheral circulation the first hours of life (a risk factor) due to PPHN which resolved quickly on oxygen treatment. 

 

The latter one developed subcutanoeus fat necrosis in about a week after birth and also more necrosis after a month. 

In this patient hypercalcemia was no more than 3,0 mmol/l (2,2-2,7) and we noted no symptoms of hypercalcemia. 

 

The former baby was in pain and tender to touch and was treated with morphine and paracetamol with some success.

This baby had a higher calcium with calcium above 3 during a couple of weeks, up to 3,51 mol/l. 

 

Searching for information on this topic yields no conclusive recommendation.

I´ve also talked to colleagues and the opinions vary enormously - from: "Do nothing, we have never monitored calcium in these babies and we´ve never seen any pathology because of it", to "monitor and treat!" 

 

Some studies states that fat necrosis itself is a self resolving harmelss condition but the effects of hypercalcemia can be dangerous and a cause of for example nefrocalcinosis and even death (cardiac arrythmias).

 

We have just kept on monitoring the well baby with the lower calciums levels without any intervention. 

 

The baby with the higher calcium was constantly irritable despite pain management so we suspected that these symptoms were rather caused by the hypercalcemia (which can cause irritability) than actual pain from subcutaneous necrosis. .

After discussing this with an endocrine specialist we started NaCl infusion, after a while we also added oral frusemide.

We also changed the babies formula to Locasol which is low calcium/low vitamin D formula and we postponed supplementation with vitamin D (which every child in Sweden gets).  

 

This had an effect (though not immidiate) lowering s-calcium.

With the hypercalcemia resolving the baby was happier and less irritable so it seemed that the symptoms had been caused by the hyperclalcemia.  

Our next step would have been oral prednisone 1mg/kg/day but s-calcium is returning to normal so the only treatment now is Locasol and no vitamin D for another 3-4 weeks. 

Think about lesions due to hypotermia in your cooled baby.

[Guest mmerocru]

Think about lesions due to hypotermia in your cooled baby.

Total body cooling: skin and

renal complications

Subcutaneous fat necrosis (SFN) is a rare, self-limiting panniculitis

mostly reported in infancy and childhood. Newborns

and infants have a greater saturated to unsaturated fats ratio

in their subcutaneous fat compared with older children and

adults, causing an increased tendency to crystallise with cold

stress.1

A full-term baby suffering hypoxic ischaemic encephalopathy

(HIE) and treated with total body hypothermia is reported.

SFN was fi rst noted on physical examination at 35 h of life,

presenting with a very painful erythema on the upper back

area and evolving into fi rm erythematous nodules within a

few days (fi gure 1). A spontaneous skin recovery was observed

in the following weeks.

Hypercalcaemia is the most commonly recognised metabolic

complication of SFN.1 2 During the hospital stay calcium

plasma levels were normal. Despite weekly blood analysis after

discharge, the baby was evaluated in the emergency paediatric

department at 6 weeks of age with vomit and weight loss.

Severe hypercalcaemia (17 mg/dl) was observed. Abdominal

ultrasound scan showed hyperechoic foci involving all pyramids

in both kidneys, with normal appearance of the cortex,

consistent with nephrocalcinosis (fi gure 2).

Total body cooling has recently become a widely available

therapy for HIE3 4 but it is likely to increase the risk of SFN.5

Thus, neonatologists should be aware of these potentially

emerging complications.

Monica Fumagalli,1 Luca A Ramenghi,1 Silvia Pisoni,1

Irene Borzani,2 Fabio Mosca1

1NICU, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Università degli

Studi di Milano, Milan, Italy

2Institute of Pediatrics-Pediatric Radiology Unit, Fondazione IRCCS Ca’ Granda

Ospedale Maggiore Policlinico, Milan, Italy

Correspondence to Dr Monica Fumagalli, NICU, Fondazione IRCCS Ca’ Granda

Ospedale Maggiore Policlinico, Università degli Studi di Milano, Via Commenda 12,

20122 Milan, Italy; monica.fumagalli@mangiagalli.it

Competing interests None.

Patient consent Obtained.

Provenance and peer review Not commissioned; externally peer reviewed.

Accepted 12 March 2011

Published Online First 16 May 2011

Arch Dis Child Fetal Neonatal Ed 2011;96:F377. doi:10.1136/adc.2010.207886