Health Awareness blog

Chronic lung disease (CLD) is also known as bronchopulmonary dysplasia (BPD). It is defined as oxygen dependency at 28 days with the present of clinical evidence of respiratory distress together with abnormal chest radiograph. The infants may require oxygen supplement after 28^th day of life in order to keep partial O2 50mmHg. Chest X ray showing diffuse abnormalities characteristic of BPD. CLD arise as a consequence of the treatment of preterm and term infants that has suffered with primary respiratory disease. Commonly, it affects preterm infants born with hyaline membrane disease or infants with respiratory distress syndrome (RDS).

It is important to ensure that oxygen saturation is normal by obtained adequate oxygen therapy. SPO2 of 93-95% in older infants is optimal. Nutrition is vital aspect to ensure normal growth of these babies. Steroids have shown to have limited values in weaning the child from ventilation support or reducing the oxygen need. Therefore, postnatal steroids should be wisely reserved for those cases that are at risk of dying de to chronic lung disease. This child also should fully immunized to make sure that hey have enough protection from infection. A course of 5 injections of palivizumab should be given to all infants with CLD to reduce the risk of RSV infections. Palivizumab is a humanized monoclonal antibody which prevents entry of RSV (respiratory syncytial virus) into host cells. Vaccination for influenza is highly recommended.

In term of prognosis, most babies with chronic lung disease will eventually outgrow their disease. Some will outgrow the illness while they are still admitted in NICU. However, there are few long term complications of CLD that should be considered. During adolescence, the main airway changes are includes airway obstruction, lung hyper reactivity and inflation. There is evidence that this will increase risk for chronic obstructive pulmonary disease (COPD) for this group of patient later in their life.

References:

1. Beattie, J. and Carachi, R. Practical paediatrics problems. London.Hodder Arnold; 2005.

2. Ferri, F.F. Ferri’s clinical advisor instant diagnosis and treatment. Philadelphia: Mosby Elsevier; 2008.

3. Guidelines Global Initiative for Chronic Obstructive Lung Disease. 2009. Available online at: http://www.goldcopd.com/

Retinopathy of prematurity was previously known as ‘retrolental fibroplasia’ (RLF). Approximately 50,000 children worldwide are blind from ROP and the incidence is increasing at developing countries. It is caused by disorganized growth of retinal blood vessels and affects premature infants. It is found that prematurity was the main risk factor and also there is a significant association between gestational age, birth weight, oxygen therapy and blood transfusion. ROP consist of 5 stages (stage I to stage IV).

Stage I is the mild form of ROP, consist of mildly abnormal blood vessel growth. Majority of the child that develops stage I will eventually recovered and develop normal vision without any treatment. The disease usually resolves without further progression and the prognosis is good. Stage II consists of moderately abnormal blood vessels growth. This stage also has a good prognosis where usually no treatment is needed and the disease usually resolves on its own without become worsening in condition. The child will eventually develop normal vision.  Then, Stage III refers to severely abnormal blood vessel growth. The abnormal growth occurs toward the center of the eye instead of following the normal growth pattern along the surface of the retina. In terms of prognosis, some infants will improve without any treatment and eventually able to have normal vision like other kids. However, in some infants especially when he/she has a certain degree of stage III and ‘plus disease’, treatment is recommended to prevent retinal detachment. At this point, the treatment usually ensure good outcome. “Plus disease” means the blood vessels of the retina has become enlarged and twisted. These indicate the worsening of the ROP. For, Stage IV and stage V is already considered severe. Stage IV referred to partially detached retina. It occurs by the traction from the scar that produced by bleeding. In other words the abnormal vessels pull the retina away from the eye wall. Stage V is very severe defined by complete detached of retina. This is the end stage of the disease. The prognosis is poor, without treatment, the baby may have severe visual impairment. Blindness won’t be rare.

Risk factors for ROP are low birth weight, shortened gestation, exposure to prolong ventilation or oxygen and respiratory distress syndrome ROP affects over 20% of infants weighing less than 1500gram. Sepsis or infection at neonatal stage (in preemies) also may contribute to ROP. Furthermore, ROP is significantly associated with smaller, more immature and also sicker neonates.

There are some short term complications of ROP like retinal detachment,  blindness and low vision. The patient (when they grow up later) may also have myopia or hypermetropia. Myopia is short sightedness and far more common compared to hypermetropian or far sightedness.

Regardless the gestational age at birth, if ROP is going to occur, it will occur between 34 and 40 weeks after conception. That is why the newborn at risk should be sent for screening at this stage. The laser treatment is applied to the retina anterior to the vascular shunt that does not yet have a blood supply. The means of this treatment is to prevent retinal detachment. This is based on the idea abnormal vessels should be eliminated before they progress and lay down enough scar tissue that will cause traction of the wall of the eye. There are some other options of treatments include cryopexy, sclera buckle and vitrectomy.

References:

1.   Gilbert, C. Retinopathy of prematurity: A global perspective of the epidemics, population of babies at risk and implications for control. Early Human Development, 2008 February . 84 (2) : 77-8.

2.   Wheatley, CM., Dickson, JL., Mackey, DA., Craig JE. and Sale, MM. Retinopathy of prematurity: recent advances in our understanding. British Journal of Ophthalmology, 2002. 86:  696-700.

3.   Darlow,BA., Hutchinson, JL., Henderson-smart, DJ. Donoghue, DA,  Simpson, JM., Evans, NJ. Neonatal prenatal factors for severe retinopathy of prematurity of among very preterm infants of the Australian and New Zealand network. Pediatrics. 2005 April.  115 (4): 990-996.

4.      Karkhaneh, R,  Mousavi, SZ, Riazi-Esfahani, M, Ebrahimzadeh, SA., Roohipoor, R., Kadivar, M. Ghalichi, L, Mohammadi, SF. and Mansouri, MR. Incidence and risk factors of retinopathy prematurity in a tertiary eye hospital in Tehran. British Journal of Ophtalmology.  2008. 92: 1446-1449.

5.      Strobel, S,  Marks, S,  Smith,PK., El Habbal, MH. and Spitz, L. The great Ormond Street colour handbook of paediatrics and child health, London: Manson Publishing; 2007.

6.      Chye, JK.,  Lim, CT.,  Leong, HK. and Wong, PK. Retinopathy of prematurity in very low birth weight infants. Annals Academy  Medicine of  Singapore. 1999. 28: 193-198 .