RESPIRATORY DISTRESS IN NEWBORN

B. VISHNU BHAT Prof. of Pediatrics JIPMER Pondicherry 605 006.

Address for communication B. Vishnu Bhat,

Prof. of Pediatrics, JIPMER, Pondicherry - 605 006. Email: drvishnubhat@yahoo.com

RESPIRATORY DISTRESS IN NEWBORN

Respiratory distress in a newborn is diagnosed when any two of the following findings are present for more than 2 hours after birth:Respiratory rate more than 60/ minute. Grunting Apnea Central cyanosis Accessory muscles of respiration working. The time duration of 2 hours is set so that transient adaptation to extrauterine life is not included. The incidence of respiratory distress may vary from 7 8 % among live births. The incidence varies from 30% among preterms, 20% among post-terms to 4% in term babies. CAUSES: The cause of distress may be within the respiratory system or outside. Pulmonary causes account for 80 85% cases of respiratory distress in a newborn. Table 1: CAUSES OF RESPIRATORY DISTRESS PULMONARY Transient tachypnea of newborn Hyaline membrane disease Meconium aspiration syndrome Pneumonia Pneumothorax Congenital lung cysts Diaphragmatic hernia Choanal atresia Laryngeal web/ polyp EXTRA-PULMONARY Cardiac failure Anaemia, Polycythemia Septicemia Metabolic disorders Renal failure, renal tubular acidosis Meningitis/ intracranial bleed Ascites

In a newborn, upper airway obstruction like blocked nostril or choanal atresia can cause severe respiratory distress since they are primarily nose-breathers. Severity of respiratory distress can be assessed using Downes score as shown in Table 2. Table 2: DOWNES SCORE SCORE PARAMETER 0 1 2 Respiratory rate < 60/ min 60-80 > 80 Cyanosis Nil While in room air At 40% oxygen Grunting Nil Audible with stethoscope Audible to naked ear Retractions Nil Minimal Marked Air entry Normal Reduced Almost absent A normal baby has 0 score while score 10 indicate severe distress resulting in impending death.

TRANSIENT TACHYPNEA OF NEWBORN: It is also known as Type II Respiratory Distress Syndrome or Wet Lung. It is the commonest cause of respiratory distress accounting for 40 45 % of cases. It occurs mostly among term and near term babies. The cause is increased lung fluid in the lungs. Generally 40 % of lung fluids get squeezed out during passage through birth canal and the remainder gets absorbed into venous channels and lymphatics. This may result from rapid delivery (precipitate or caesarian section) or poor respiratory effort resulting from perinatal asphyxia, respiratory depression from drugs and prematurity. The diagnosis is usually done by exclusion of other causes. Chest radiography may reveal increased bronchovascular markings, sometimes interlobar or subpleural effision. The condition is usually self-limiting and lasts for 12 24 hours. The baby needs intravenous fluids and supplemental oxygen. They may rarely require ventilatory support suggesting myocardial failure. HYALINE MEMBRANE DISEASE (Type I Respiratory distress syndrome): It is usually seen among preterm babies and rarely after 36 weeks of gestation. It is caused by decreased surfactant level in the lung. Surfactant reduces the alveolar surface tension and prevents collapse of alveoli during expiration. Alveolar collapse leads to poor oxygenation, hypercapnea and acidosis. The incidence is increased with decreasing maturity. It may occur among 80% of babies less than 28 weeks of gestation and in less than 5% after 36 weeks. Asphyxia, hypothermia, blood loss, Diabetes in the mother, male sex, caesarian section and erythroblastosis fetalis increase the incidence while intrauterine growth retardation, premature rupture rupture of membrane, heroin addiction in the mother and antenatal steroids decrease the occurrence of hyaline membrane disease. Predicting the risk for HMD: 1. Lecithin/ Sphingomyelin ratio (L/S ratio): If this ratio is less than 2, then there is increased risk. But in cases of diabetic mothers and erythroblastosis, a ratio of more than 3 should be taken for adequate lung maturity. 2. Shake test: One should take 1 ml of amniotic fluid or gastric aspirate of the baby and 1 ml of absolute alcohol in a test tube. Then the test tube is shaken for 15 seconds and allowed to stand for 15 minutes. The amount of air bubbles at the meniscus is noted and graded as follows:+ -- 1/3 of meniscus has bubbles ++ -- 2/3 of meniscus +++ -- one row along the circumference of meniscus has bubbles ++++ -- more than one row of bubbles The risk of hyaline membrane disease is minimal if the test is more than ++. Clinical Features:

The baby develops grunting, tachypnea, accessory muscles of respiration working and cyanosis, soon after birth or within 6 hours. The distress gradually worsens during the first 72 hours and then improves.

Diagnosis: Respiratory distress in a preterm baby with L/S ratio < 2 or positive Shake test suggests Hyaline membrane disease. Chest radiography initially shows fine reticulogranular pattern with air bronchogram followed by opalescence and complete white out lung fields. Lung biopsy if done shows hyaline membrane, which is made up of eosinophilic material. Hyaline membrane will not be present if the baby dies too early in the disease. Treatment: The baby needs intravenous fluids because of respiratory distress. Temperature control in order to prevent hypothermia and maintenance of acid base balance are important. Supplemental oxygen through head box or nasopharyngeal catheter is effective in mild cases. The severe cases will require ventilatory support. Artificial surfactant can be given intratracheally both prophylactically as well as therapeutically. The cost is prohibitive. Since one cannot differentiate conclusively hyaline membrane disease from infective

bronchopneumonia, antibiotics are given if the child is sick after collecting samples for bacterial culture. The survival is directly proportional to the maturity of the baby. The survival may be 50% with supportive care alone and > 90% with surfactant therapy and ventilatory support. MECONIUM ASPIRATION SYNDROME (MAS): Meconium consists of bile, intestinal secretion, amniotic fluid and exfoliated epithelial cells. About 10 12 % of fetuses may pass meconium before delivery. Meconium aspiration syndrome develops in 1 2% of deliveries or 10% of thick meconium stained liquor cases. Only 25% of meconium aspiration will result in aspiration syndrome. If meconium is seen below the vocal cords, baby has barrel shaped chest and respiratory distress, meconium aspiration is present. Chest radiography shows coarse nodular opacities, hyperinflation, air leak and sometimes consolidation or collapse. The commonest cause for respiratory distress is blocking of the airways by the meconium particles and hence develops immediately after birth. Sometimes chemical pneumonitis, secondary infection or air leak may result in respiratory distress. When distress develops after 24 hours, it suggests infection or air leak.

Treatment: The babys nutrition, temperature and hydration should be maintained through intravenous fluids and warming devices. Correction of acidosis will result in improvement by increased pulmonary circulation. Acidosis results in pulmonary vasoconstriction and

increase in pulmonary pressure. Supplemental oxygen by head box or ventilatory support may be needed for maintaining oxygenation. Since there is air loculation and emphyseme in this condition, the baby should be maintained with low end expiratory pressure. Surfactant has been tried by some with improved survival. Antibiotics are initiated if there is evidence of infection like foul smelling liquor, prolonged rupture of membranes, positive septic screening tests. Persistent pulmonary hypertension is difficult to manage. Hyperventilation and alkali therapy will help in improving pulmonary ciruculation. If they do not work, then Tolazoline or Nitric oxide may be tried. If they also fail in improving oxygenation, then Extra corporeal membrane oxygenation (ECMO) is the treatment. Complications: Blocking of airways leading to apnea, collapse of lung, air leak, consolidation, hypoxic brain damage and Persistent pulmonary hypertension are the complications. Mortality may vary from 15 20%. APNEA OF PREMATURITY: It is the cessation of respiration for more than 15 seconds or less than that with cyanosis and / or bradycardia. It is classified as follows:1. Central or idiopathic 2. Peripheral or obstructive 3. Mixed (commonest type). It can also be classified as primary and secondary. Primary apnea is the idiopathic apnea of prematurity due to immaturity of the respiratory center. Primary apnea most often manifests on the second or third day. When a newborn develops apnea after 3 days one should always look for an underlying cause. Secondary apnea results from underlying cause like sepsis, intracranial bleed, temperature instability, metabolic abnormality, anaemia, convulsion etc. When apnea is a manifestation of convulsion, there is

tachycardia unlike other causes. Apnea when prolonged can result in hypoxia and brain damage. Hence it is essential to identify and treat apnea. Treatment: Idiopathic apnea of prematurity can be prevented by Aminophylline/ Theophylline in a dose of 5-6 mg/kg/day to maintain a blood level of 10 12 g/dl. Other drug that is effective is Caffeine citrate. Doxapram although effective is not used because of side effects. If

apnea is persisting and recurrent, then Continuous Positive Airway Pressure(CPAP) or Intermittent Positive Pressure Ventilation (IPPV) may be needed. In cases of secondary apnea, the primary cause should be identified and treated.

INFECTIVE BRONCHOPNEUMONIA: Pneumonia may be observed among 0.5% of live births and 10% of low birth weight and sick newborns. The infection may be acquired before, during or after delivery. Transplacental infections are usually caused by viruses like Cytomegalovirus and Rubella virus. It may also result from Listeria or Treponema pallidum. The baby may get infected from the maternal genital tract during delivery. Premature rupture of membranes, prematurity, birth asphyxia and invasive procedures increase the risk for infection. The organism responsible for intranatal infection may be Streptococcus, Escherichia coli, Klebsiella, Enterobacter, Chlamydia, Herpes and Varicella viruses. Postnatal infections are usually caused by bacteria like Klebsiella, Coagulase negative staphylococci, Pseudomonas, Acinetobacter. Sometimes Chlamydia and fungi may also cause infection. Clinical Features: The baby may have grunting, retractions, tachypnea or apnea. There could also be temperature instability, reduced activity and other features suggestive of systemic infection. Investigations:Laboratory tests can be done for diagnosing sepsis and pulmonary involvement. Blood cell count, Band cell count, micro-ESR, C-Reactive Protein and blood culture are helpful in diagnosing sepsis. Blood culture and lung aspirate culture may be helpful in identifying the etiological agent. When intrauterine infection is suspected, gastric aspirate and tracheal aspirate at birth are helpful. Chest radiography will reveal the extent of

pulmonary involvement. Blood gas analysis will indicate severity of pulmonary disease and the need for ventilatory support. Treatment: It includes general supportive care and specific against infection. The nutrition, hydration and temperature are to be maintained. Oxygenation is maintained by supplemental oxygen by hood or mechanical ventilation. Antibiotics are to be selected based on the type of organism prevalent in the neonatal unit and later modified based on sensitivity pattern of the bacteria identified. A combination of third generation cephalosporin with aminoglycoside may be the initial combination of choice. Other modes of therapy involve granulocyte transfusion, immunoglobulin therapy and administration of GM CSF (Colony stimulating factor).

Key messages 1. Respiratory distress is an important cause of neonatal morbidity and mortality. 2. Transient tachypnea of newborn (TTN) is the commonest cause but it should be diagnosed after excluding other causes. 3. More than 80-85% of the cases the etiology can be identified in the respiratory system. 4. Chest radiography and septic screen are must in all cases of persisting respiratory distress. 5. Ventilatory support and good nursing care can improve the outcome. Reference 1. Kumar A, Bhat BV. Respiratory distress in newborn. Ind J Mat&Chld Hlth 1996, 7:8-10. 2. Kumar A, Bhat BV. Epidemiology of respiratory distress in newborn. Ind J Pediatric 1996, 63:93-98 3. Shuba S, Bhat BV. Meconium aspiration - current concepts. Quality care in Pediatric 1997,2:10-17. 4. Field DJ, Milner AD, Hopkins IE, Madeley RJ. Changing pattern in neonatal respiratory distress. Pediatr pulmonol 1987, 3: 231-235. 5. Hjalmarson O. Epidemiology of neonatal disorders of respiration. Ind J Technol assess Hlth care. 1991, 7:9-15.