The use of pair and group work:

The outcome of preterm babies depends to a large extent on the types and severity of morbidities experienced particularly in the first two weeks following

delivery. Some of these problems are related to homeostatic adjustment while others are a consequence of their anatomic and physiologic immaturity. These problems include:

Temperature Regulation

The preterm baby is predisposed to hypothermia and sub-normal temperature.

11- 13 Some of the reasons advanced for these include their large body surface area (BSA) to weight ratio which is more than 3 times that of the adult and reduced insulation due to a thinner layer of subcutaneous fat. ^11-13 Thus, they are prone to excessive heat loss. Paucity of brown fat on its own part will reduce ability to generate heat.^{11- 13}

Respiratory Problems

The preterm infant, especially that less than 34 weeks gestation, experience a lot of respiratory problems as a result of his immaturity.^11-13 Respiratory distress syndrome remains a major cause of both mortality and morbidity in these infants. It is a consequence of deficiency of surfactant leading to abnormal surface property of the lungs manifesting soon after birth with progressive tachypnoea, grunting, intercostal recession and subcostal retraction and cyanosis associated with typical chest radiographs showing reduced lung volume, diffuse microatelectasis and air bronchogram.⁸² Management is based on surfactant replacement, increased inspired oxygen concentration with or without constant positive airway pressure (CPAP).⁸² Cardiovascular Problems

With their increased risk of respiratory problems and thus hypoxia and acidosis, the preterm baby is at an increased risk of left to right shunting of blood

through a patent ductus arteriosus (PDA) and foramen ovale¹². PDA increases mortality in patients with RDS and is a risk factor for necrotizing enterocolitis and intraventricular haemorrhage⁸².

Gastrointestinal Tract

The preterm baby, especially one less than 32 weeks gestation, is at an increased risk of gastro-oesophageal reflux, regurgitation, vomiting and aspiration of feeds.^12,13 Necrotizing enterocolitis (NEC) is a major cause of mortality among these infants after the first week of life. It is said to account for 15% of all deaths in the NICU and 40% of infants that develop NEC die.⁸² Its aetiology is unknown but it has been widely speculated that the aetiology is related to ischaemia of the gut with local necrosis of the luminal mucosa and secondary invasion of the wall of the gut by bacterial and/or viral organisms.⁸² Complications include perforation of the gut, short gut syndrome, stricture with difficulty in feeding and poor weight gain.⁸² Risk factors include LBW with increased incidence with decreasing gestational age.⁸² Others include RDS, polycythaemia, and use of umbilical arterial catheters, SPA, apnoea, PDA and hypertonic enteral feeds.⁸² Some centres have reported epidemics of NEC related to outbreaks of certain organisms both bacteria (Eschericia coli and Clostridium difficile) and viruses (corona virus).^83-85

Infection

The preterm infant is predisposed to infection as a result of decreased immune function and diminished concentration of immunologic factors.⁸⁶ The preterm infant, especially the VLBW baby is significantly hypogammaglobulinaemic as the level of immunoglobulin G (IgG) is proportional to gestational age.⁸⁶ The infant is at risk of

infections due to Eschericia coli and other enterobacteriaceae, as there is no transplacental transfer of immunoglobulin M (IgM).⁸⁶ The preterm infant also has a lower level of complement activity than the full baby resulting in a reduced complement derived chemotactic activity and their ability to opsonize certain organism in the absence of antibody.⁸⁶ The number of circulating neutrophils is elevated immediately after birth with a peak at 12 hours returning to normal by 22 hours, but their chemotaxis is diminished with a decreased adherence aggregation and deformability, all of which delay response to infection.⁸⁶ The number of circulating monocytes is normal but has impaired chemotaxis.⁸⁶ The function and mass of the macrophages is diminished.⁸⁶ Furthermore, these babies are likely to be on admission for a long period with indwelling catheters and multiple invasive procedures performed on them putting them at increased risk of nosocomial infection.

Many workers have reported prematurity to be risk factors for both neonatal sepsis and hospital acquired infections. Josh and colleagues⁸⁷ found prematurity and low birthweight to be the underlying condition in 60% of neonates with neonatal sepsis and formed the major contributing factor in total mortality. Kauffmann and Fairchaild⁸⁸ found that 20% of VLBW infants experienced serious systemic infection and, despite advances in neonatal intensive care and antimicrobial therapy, mortality is as much as threefold higher for these infants than in their counterparts without sepsis during their hospitalization.

Renal Problems

In utero, urine is produced by the fetus from about the twelfth gestational week through functioning developing but immature kidney.⁸⁹ Nephrogenesis is not

completed until 34 weeks gestation.⁸⁹ At term, the kidney is qualitatively able to perform its function compared to the older child and adult but quantitatively is limited in its ability to respond to abnormal stress. The degree of compromise is greater with increasing immaturity of the neonate.⁸⁹ As a result, the preterm baby has a decreased glomerular filtration rate and a reduced tubular function. The ability to handle sodium and water load is also reduced.⁸⁹ He is less able to concentrate urine to conserve water but can maintain normal acid base status.⁸⁹ He however has a reduced ability to excrete an acid load.⁸⁹ This immaturity also limits its ability to excrete drugs.⁸⁹ The more immature the baby, the more limited the excretory capacity for drugs.

The process of growth however, with its anabolic drive assists the kidney by reducing the excretory load of sodium, water, phosphorus, hydrogen and nitrogen.⁸⁹ This anabolic state will however be reversed promptly in period of acute stresses, thereby increasing the demand to excrete at a time when the kidney is possibly less able to respond quantitatively.⁸⁹ Following birth, a marked improvement in function occur within a few days followed by a slower progressive rise to essentially adult level by the end of the first year.⁸⁹ The pattern and rate of postnatal improvement is similar to those of a fetus of the same conceptual age.⁸⁹

Neurologic Problems

The preterm infant is at an increased risk of hyperbilirubinaemia because of a reduced activity of the glucoronyl transferase system in the liver leading to decreased bilirubin conjugation.⁸³ The less mature the infant, the greater the susceptibility to jaundice⁸³. They are more susceptible to developing bilirubin encephalopathy, at lower serum bilirubin levels than would be required in term infants.⁸³ This may be

related to their decreased albumin level and hence decreased albumin binding or to interference with bilirubin binding to albumin by a number of factors often present in the preterm infant like acidosis and increased free fatty acid level associated with hypothermia, hypoglycaemia and sepsis.⁸³ This risk is also increased by factors that increase permeability of the blood brain barrier which are often present in the preterm infant like hypoxia, hyperosmolality and meningitis.⁸³

Intra-cranial haemorrhage often involves the ventricles of preterm babies delivered spontaneously without apparent trauma.¹³ Intra-ventricular haemorrhage (IVH) occurs in 24 to 40% of all VLBW and ELBW babies.⁹⁰ Nzeh and Ajayi⁹¹ in Ilorin found an overall incidence of 24.5% among 110 preterm babies studied. The incidence was 28% among babies with birthweight less than 1500g and 11.8% among those with birthweight between 1500g and 2500g. These authors concluded that premature African children have a lower incidence of IVH compared to babies from temperate countries. IVH is associated with up to 65% of overall neonatal deaths and about 28% case fatality.⁹⁰ Survival is associated with a high risk of neurologic and developmental disability.⁹⁰ Predisposing factors include RDS, hypoxic ischaemic or hypotensive injury, pneumothorax, hypervolaemia and hypertension.⁹⁰ Various groups had Attempted to prevent IVH by antepartum administration of Vitamin K to the mother. Analyses of these attempts show inconclusive results. While Pomerance et al⁹² and Morales et al⁹³ found significantly reduced incidence and severity, Kazzi and colleagues⁹⁴ found no such effect. Some other researchers have demonstrated the efficacy of administration of phenobarbital to the mother before 32 gestational weeks in reducing the incidence of IVH.^{95- 97}

Peri-ventricular leukomalacia (PVL) is commonly associated with severe perinatal asphyxia (SPA) and intra-ventricular haemorrhage (IVH) and is characterized by necrosis of the white matter around the ventricle.^13,90 It is seen primarily in prematurely born infants and there is usually sparing of the cerebral cortex probably because of the presence of meningeal inter-arterial anastomosis which are present in the preterm infant but not in term infants.⁹⁰ Nzeh and Ajayi⁹¹ in Ilorin found an overall incidence of 26.4% among 110 preterm babies studied. The incidence was 23.7% among babies with birthweight less than 1500g and 41.2%

among those with birthweight between 1500g and 2500g. The incidence of PVL among premature African children was higher compared to babies from temperate countries. The high prevalence of PVL observed in this study is likely a consequence of SPA than IVH. Most common long term consequence of PVL secondary to IVH is spastic diplegia which is often associated with normal intellectual function in contrast to the cerebral palsy seen in term asphyxiated infants where the severity of the motor defect correlates directly with the severity of the intellectual deficit.⁹⁰

Apnoea is defined as cessation of breathing for greater than 15 seconds or cessation of breathing for less than 15 seconds associated with bradycardia, hypoxia and cyanosis.⁸³ About half of preterm infants have an apnoeic episode at some time during the first few weeks of life.⁸³ Among preterm babies, 55% of apnoea pauses are central, 12% are obstructive and 33% are mixed.⁹⁸ Apnoea of prematurity is a diagnosis of exclusion. It is thought to be a consequence of the immaturity of the respiratory centre and the relative insensitivity of this centre to acidosis and hypercapnoea.⁸³ Causes of symptomatic apnoea in preterm infants include IVH, PDA,

pneumonia, sepsis, seizures and metabolic abnormalities such as hypoglycaemia and hypocalcaemia.⁸³

Ophthalmological Problems

Retinopathy of Prematurity (ROP) is a retinal angiopathy that occurs primarily but not exclusively in preterm babies.⁸³ The acute proliferative changes are seen in as many as 75% of ELBW babies while about 25% develop the scarring cicatricial changes of chronic disease.⁹⁹ Only 0.5% of VLBW babies develop the chronic disease.⁹⁹ Retinal angiogenesis normally begin from 16 weeks of gestation proceeding from the optic disc to the outer rim of the retina nasally at 36 weeks and temporally at 40 weeks.¹⁰⁰ The factors that cause ROP and determine its outcome are not fully understood but prematurity, hyperoxia and degree of retinal immaturity at birth are major factors.¹⁰⁰ It is thought to occur when the immature retina suffers an ischaemic insult secondary to vasoconstriction of developing retinal arterioles most often because of oxygen radical induced vasoconstriction, but there have been numerous case reports of preterm infants who developed ROP with no increase in inspired oxygen at any time in their course.⁸³ The infant may present later with myopia, anisometropia, strabismus, amblyopia and nystagmus.⁸³

Haematologic Problems

Preterm babies, like term babies are predisposed to haemorrhagic disease of the newborn.¹³ This is a consequence of an accentuation and prolongation of the normally moderate decrease in the vitamin K dependent factors that occurs in all newborns by 48-72 hours to 7-10 days.¹³ They also suffer from anaemia of prematurity, an exacerbation of the normal physiologic anaemia of infancy.¹³ It is result of repeated

phlebotomies, shortened red blood cell life span, rapid growth with expanding intravascular volume, physiologic effect of transition from fetal life with relative hypoxia to extra uterine life and an attenuated erythropoietin response compared to the degree of anaemia.¹² Mokuolu et al¹⁰¹ found a slower rate of postnatal fall in packed cell volume among Nigerian preterms. The reason for this is not fully clear but may be due to the relative greater maturity of black babies compared to Caucasians at the same gestational age.

Metabolic Problems

Preterm babies are predisposed to metabolic problems like hypoglycaemia, hypocalcaemia, metabolic acidosis, hyperbilirubinaemia and rickets.¹² Hypoglycaemia is most likely to occur during the first 12 hours of life but may occur as late as 48 hours. It is a result of many factors including low and rapidly depleted glycogen stores and limited gluconeogenesis. Hypocalcaemia usually represents an exaggeration of the physiologic fall in calcium in the preterm infant. Reasons advanced for this exaggerated fall include interruption of calcium supply, failure of homeostatic control of the calcium partition between bone and serum, parathyroid hypofunction and calcitonin excess.¹⁰² Rickets of prematurity is usually seen in VLBW infants that have suffered significant problems like NEC, BPD, cholestasis and acidosis.¹³ Most of these babies have been on calciuric drugs like lasix on account of their problems and usually have diminished intake of calcium, phosphorus and vitamin D.¹³

Drugs

The preterm infant disposes off drugs less efficiently than the term infant.¹³ This is as a result of their large volume of distribution and the long half life of the drugs due to hepatic and renal immaturity.¹³