Health Awareness blog

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 .

Hypertensive disorder affected about 6 to 8% of pregnancies and it is the leading cause of maternal and neonatal mortality in the United States. In Malaysia, the rate is quite high when it is reported that hypertensive disease in pregnancy has contributed almost 14% of maternal death.

Hypertension is a systolic blood pressure at 140mmHg and above or a diastolic blood pressure above > 90mmHg.The hypertension can be classified into several categories as follows:

Source: Coppage, K.H. and Sibai, B.M. Hypertension Emergencies. In Foley, M.R.., Strong T.H.J and Garite, T.J. editors. Obstetric Intensive Care Manual 2^nd edition. Mc Graw-Hill Medical Publishing; 2004.p. 5 1-65

Gestational hypertension is defined by the elevation of blood pressure during the second half of pregnancy or beyond 6 weeks postpartum. It happens without the presence of symptoms and proteinuria. It can be divided into mild or severe gestational hypertension depending on the degree of the blood pressure.

Chronic hypertension occurred when the patient is diagnosed with hypertension at earlier stage (the onset before 20 weeks gestation) or even before the pregnancy itself. It is also considered chronic hypertension if the hypertension persists longer than six weeks post partum. In this case, thorough investigation and examination should be done to this patient to look for causes of hypertension. We need to rule out hyperlipidaemia, connective tissue disease or phaemochromocytoma (particularly in young patients). We can only conclude it as essential hypertension if all investigations come back negative. Essential hypertension is commoner in older multips and may present before the pregnancy. Those women with this disease are more likely to develop preeclampsia if we compare with those who are normotensive.

Ideally, hypertensive disorder in pregnancy should be managed by an obstetrician. However, primary care practice has its own approach and definitely playing a major role in preventing, detecting, monitoring and managing this disease and its complication till certain extent. This includes both during preconceptional and antenatal stage. During pre pregnancy stage, women with known chronic hypertension and currently on antihypertensive agents should be change to methyldopa and labetalol. Methyldopa is a centrally acting antihypertensive agent and is limited to be use during pregnancy in view of its side effects. Atenolol (a beta blocker) is not recommended because it has shown to lead to fetal growth restriction. Angiotensin converting enzymes inhibitor (ACEI) and angiotensin receptor blocker (ARB) is contraindicated for use in pregnancy in view of its potential to increase fetal and neonatal mortality hence should be avoided during preconceptional stage. For acute severe hypertension, parenteral hydralazine should not be the drug of choice in view of its potential of more maternal and perinatal adverse effects in comparison with other type of drugs particularly intravenous labetalol, oral or sublingual nifedipine. Nifedipine is a calcium channel blocker and is known to be very effective in lowering the blood pressure.  Intravenous labetalol has fewer side effects on maternal hypotension, fewer placental abruptions and fewer low apgar score of the fetus. Sublingual nifedipine is phased out in view of it may cause sudden drop of blood pressure. Furthermore, it may lead to placenta hypoperfusion which later will compromise the fetus outcome.

Women who delivered low birth weight babies were 5 times more likely to have had pregnancy induced hypertension compared to mother who delivered normal weight babies. As addition, women with a history or experience in hypertension in pregnancy had significantly increased risk of hypertension, myocardial infarction and ischemic heart disease later in life.

References:

1.  Coppage, K.H. and Sibai, B.M. Hypertension Emergencies. In Foley, M.R.., Strong T.H.J and Garite, T.J. editors. Obstetric Intensive Care Manual 2^nd edition. Mc Graw-Hill Medical Publishing; 2004.p. 5 1-65
2. Seely, E.W. Hypertension in Pregnancy: A Potential Window into Long Term Cardiovascular Risk in Women; 1999
3. Minister of Health. Training Manual on Hypertensive Disorder in Pregnancy. National Technical Committee Confidential Enquiries into Maternal Deaths. 2000
4. Collier, J., Longmore, M. and Brown, T.D. Oxford Handbook of Clinical Specialties, Oxford University Press;  2001.
5. Clinical Practice Guidelines Management of Hypertension. 3^rd edition. Ministry of Health Malaysia, Academy of Medicine of Malaysia and Malaysian Society of Hypertension; 2008.
6. Magee, L.A., Onstein, M.P. and Dadelszen, P.V. Management of Hypertension in pregnancy. British Medical Journal. 1999; 318 (7194): 1332-1336
7. Hannaford P., Perry and Hirsch S. Cardiovascular Sequelae of Toxemia of Pregnancy. Heart, 1997; 77: 154-158.
8. Rahman, L.A., Hairi, N.N., and Salleh (2008), association between Pregnancy Induced Hypertension and Low Birth Weight; A population based Control Case Study, Asia Pacific Journal of Public Health. 2008; 20 (2):152-158.