Osteopenia of Prematurity

 Osteopenia of Prematurity

Osteopenia of Prematurity

Osteopenia of prematurity is the decrease in the amount of calcium and phosphorus in bones which makes the bones weak and brittle resulting into broken bones.

Prematurity affects bone mineralization and bone growth—thus the condition osteopenia of prematurity;

Normal bone is formed by the deposition of minerals, predominantly calcium (Ca+2) and phosphorus (P), onto an organic matrix (osteoid) secreted by the osteoblasts. Osteoclasts play an important role in bone resorption and remodeling.

Osteopenia of prematurity is principally a result of inadequate calcium intake to meet bone growth demands.

Causes

  •  Lack of vitamin D (vitamin D helps in absorption of calcium from intestines and kidneys) by the mother during pregnancy which has to be transferred from the mother to the fetus.
  • Prematurity these neonates lose much more phosphorous in their urine than babies that are born full-term
  •  Liver problems which may lead to deficiency of vitamin D e.g
    cholestasis(obstruction of bile flow).

Signs and symptom

Clinically, osteopenia manifests between 6 and 12 weeks of age and is usually asymptomatic; however, severe manifestations may include the following:

Severe manifestations

    1. Poor weight gain and growth failure.

    2. Rickets-like findings may include growth retardation, frontal bossing,  and epiphyseal widening.

    3. Fractures may manifest as pain on handling.

    4. Respiratory difficulties or failure to wean off ventilator support due to poor chest wall compliance.

Consequences of osteopenia. Osteopenia can result in myopia of prematurity due to alterations in the shape of the skull. In childhood, infants remain thinner and shorter with a decreased total BMC(Bone Marrow Concentration) and density. Increased urinary calcium excretion has also been reported.

  • Decreased movements
  • Swelling of the arm or legs due to unknown fractures.

Pathophysiology

  • Bone mineralization begins during embryonic phase of human development, but the large part of this process occurs in the third trimester of gestation, during this period .
  •  The most of placental transfer of calcium and phosphorous  occurs in the third trimester at  the 34th  week of gestation .when 80% of the mineral content is stored.
  •  By the 28th week of gestation mineral accumulation is about 60mg/day then  increases  to more 300mg /day between 35-38th week .
  • The osteoblast produce the  organic bone matrix for deposition of calcium and phosphate  with a progressively expansion of bone volume through an increase in trabecular thickness. This This activity is thought  to be important for bone development and it helps the baby to grow,  If this doesn’t occur the child develops osteopenia of prematurity. Which leads to fractures of long bones including ribs resulting into respiratory insufficiency.
  • A premature infant may not receive the proper amount of calcium and phosphorus needed to form strong bones.
  • Premature babies lose much more phosphorus in their urine and they have limited physical activities  which lead to weak bones.

Risk Factors

Fetal and neonatal causes

    1. Prematurity and birthweight. Preterm birth results in Calcium and Phosphorus deficiency. The frequency of osteopenia is inversely related to gestational age and birthweight. Both conditions predispose these infants to mineral deficiencies in the face of increased nutritional and growth requirements.

    2. Feeding practices. Delayed enteral feeding, prolonged use of parenteral nutrition, use of unfortified human milk, enteral feeding restrictions, and malabsorption states can result in mineral deficiencies.

    3. Human milk is low in Phosphorus, and donor milk content is even lower compared with preterm maternal milk. Prolonged use can result in low serum phosphate levels and decreased incorporation into the organic bone matrix. Unfortified human milk cannot match the mineral accretion that can be achieved across the placenta.

    4. Drugs. Corticosteroids, furosemide, and methylxanthines are commonly used in preterm infants and cause mobilization of Calcium from the bone, resulting in decreased bone mineral content.

    5. Lack of mechanical stimulation. Bone growth requires mechanical stimulation that is interrupted by preterm birth, illness, sedation, and paralysis. Neurologically impaired infants with spina bifida  have limited mobility and poor bone growth.

    6. Vitamin D.  Postnatal vitamin D deficiency may occur in breast-fed infants without fortification due to low levels (25–50 IU/L) in breast milk. Other causes of vitamin D deficiency in preterm infants include the following:

      1. Renal (osteodystrophy) disorders.

      2. Drugs such as phenytoin and phenobarbital increase vitamin D metabolism.

    7. Aluminum contamination of parenteral nutrition.

    8. Malabsorption of vitamin D and Ca+2 can occur in infants with prolonged cholestasis and short gut syndrome.

  1. Maternal factors

    1. Maternal deficiency of vitamin D results in low fetal levels. 

    2. Maternal smoking, thin body habitus, low Calcium intake, and increased physical activity in the third trimester result in a decreased Calcium in the fetus.

    3. Exposure to high doses of magnesium in utero, preeclampsia, chorioamnionitis, and placental infections are associated with osteopenia.

    4. Higher incidence of postnatal rickets is seen in infants with intrauterine growth restriction (chronic damage to the placenta may alter phosphate transport).

    5. Increased maternal parity and boys have higher incidence.

    6. Placental hormones including estrogen and parathyroid hormone (PTH) and PTH-related protein also play a role.

Predisposing factors

  • Prematurity ;Gestation period of less than 30 weeks
  • Chronic use of medication that increase mineral excretion e.g diuretics ,theophylline.
  • Vitamin D deficiency.
  • Low parathyroid hormone during pregnancy which suppresses the fetal calcium and phosphorous levels.
  • A less effective intake  of calcium and phosphorous occurs in infants with Poor tolerance to Enteral feeds with low mineral content who require total parenteral nutrition.
  • Common neonatal morbidities like sepsis, acidosis, necrotizing enterocolitis can impair bone remodeling by reducing osteoclast  activity, decreasing calcium absorption and increasing calcium renal excretion.
  • Paralysis may increase calcium renal excretion.
  • Short gut syndrome(malabsorption of vitamin D and calcium

Diagnosis and Investigations

Radiographs. Most commonly, osteopenia is recognized on radiographs, which are often subjective.

Calcium levels may remain normal until late in the course.

Phosphorous. Serum phosphate levels are low (<3 mg/dL). 

Ultrasound.  Ultrasound offers several advantages, including easy accessibility and lack of exposure to ionizing radiation. It uses peripheral sites such as the calcaneus and tibia. It measures both qualitative and quantitative bone properties, such as bone mineralization and cortical thickness, respectively, in addition to bone mass (osteopenia), elasticity, and microarchitecture.

Dual-energy x-ray absorptiometry (DEXA). DEXA is the gold standard used to assess both bone size and bone mineral status and can predict risk of fractures in newborn infants. However, limitations in its use and interpretation of data preclude wide clinical application.

Management

Aims

  1. To  restore normal calcium and phosphorus in the body
  2. To prevent further complications or disease progress

Admission

The child is admitted to pediatric ward in case the child is referred from outside the hospital.

Assessment 

  • A demographic data of patient is taken which includes name, age, sex, etc 
  • A detailed medical and obstetric  history,prenata and natal data,birth weight, APGAR score at birth history are taken
  • Physical examination is done from head to toe putting more emphasis on bone formation to notify any abnormalities. 

Immediate care

  • Baby is put in a comfortable, warm bed to prevent hypothermia.
  • Analgesics like paracetamol 2.5mg 8hourly for three days are administered to relieve pain which may be due to unknown fractures.
  • In case of fractures immobilisation is done which helps to maintain the bone in position.
  • Meanwhile the doctor is called who will come and perform a quick assessment and order for investigastions which will help him make a diagnosis depending on the results.

Investigations will include: 

  • Blood to detect calcium and phosphorus levels and a protein called alkaline phosphate.
  • Ultra sound to rule out fractures.
  • X-rays to rule out the extent of fractures.

TREATMENT

  • The following treatment is administered to the patient as prescribed by the doctor.
  •  Calcium 1.25mmol/kg /dose added to iv fluids  like normal saline and ringers lactate given until the condition is stable.
  • Iv Phosphorus 1mmol/kg/dose  added to iv fluids until the condition stabilizes.
  • Vitamin D supplements are given to children with liver problems.

Nursing interventions

  • Ensure the baby is warm and comfortable.
  • Monitoring of vital observations i.e. TPR 
  • Ensure the patient is getting a diet rich in calcium and phosphorus. By feeding the baby with fortified milk
  • Physical exercises by the physiotherapists are encouraged
  • Ensure the baby is getting adequate rest and sleep by providing a conducive environment.
  • Psychological care is done to the mother to allay the anxiety
  • Both environmental and personal hygiene is promoted to prevent cross infection.
  • Administration of medicine to the patient as prescribed by the doctor.
  • Weekly monitoring of urine calcium, phosphorus.
  • When the patient improves  discharge is considered.

Advise on discharge

  • Mother is advised to continue feeding the baby on a diet containing calcium and phosphorus.
  • Mother is also advised to handle the baby gently since there is a risk of broken bones.
  • A return date is given to help in the follow up and to know the prognosis of the disease 
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