Respiratory disorder Samah Suleiman 23/3/2006.

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Presentation transcript:

Respiratory disorder Samah Suleiman 23/3/2006

Introduction At birth major cardiopulmonary changes take place in order to prepare the baby for extra uterine existence The fluid in the fetal lung is rapidly replaced by air, associated with lung inflation and increased oxygenation there is a marked decrease in the pulmonary vascular resistance, with consequent increased pulmonary blood flow and closure of the ductus arteriosus, foramen ovale and ductus venosus

Respiratory distress Is a general term used to describe respiratory symptoms It is assessed clinically by the following signs:- Tachypnoea (R.R more than 60/ min) Expiratory grunt: the infant expires against a closed glottis, which maintains a higher residual lung volume, thus preventing alveoli from collapsing (preterm infant)

Chest retraction: this may be intercostal, lower costal, sternal or substernal Flaring of the ala nasae associated with infants used accessory respiratory muscles Cyanosis which is central (nitrogen wash out test to differentiate if the problem is cardiac or respiratory) Bilateral decrease air entry

diagnosis Full clinical history Physical examination Appropriate investigation Chest X-ray Perinatal history Vital signs

Investigations Bacteriological culture Viral culture Full blood count Lecithin/ sphingomyelin (L/S) ratio Chest transillumination with a cold light source if pneumothorax suspected Passage of NGT

Treatment Supportive care:- Vital signs Keep the baby warm I.V.F and nutrition (TPN) Keep monitoring Oxygen:- Is useful and life saving therapeutic agent but is potentially dangerous especially in preterm

Baby, may cause retinopathy and bronchopulmonary dysplasia Fluids:- Shouldn’t be breast or bottle fed With mild RDS gavage feeding may be adequate With sever RDS, IVF may be adequate

Acid-base studies:- If respiratory acidosis is sever (pH less than 7.2) assisted ventilation may be necessary For sever metabolic acidosis an infusion of sodium bicarbonate may be indicated

Mild respiratory distress Color presence of central cyanosis Chest retraction Grunt and flaring of the ala nasae Heart rate hourly recorded Respiratory hourly recorded Temperature q 4hrs B.P q 4hrs

Moderate to sever respiratory distress Heart rate monitoring with alarm system for bradycardia respiratory monitoring with alarm system for apnea Pulse oximetry Regular ABGs Hourly B.P 24hrs fluid balance chart

Umbilical artery catheterization For regular ABGs estimations Indication for insertion of an umbilical catheter:- Infant less than 1000 gm Infant require intensive care Infant with increasing RDS Infant with sever recurrent apnea

Transient tachypnea of the new born (TTN) It is RDS type 2 Occur in 1-2% of all newborn infants Is usually benign and self limiting

pathogenesis Most of the fetal lung fluid is squeezed out during descent through the birth canal or within the first few breaths after birth, but some is reabsorbed into the pulmonary capillaries and lymphatic In these cases retained fluid causes respiratory distress

Predisposing factors Prematurity Heavy maternal analgesia Birth asphyxia C\S Breach presentation Male sex Hypoproteinaemia and Polycythemia Excessive fluid administration to the mother in labor

treatment Doesn’t usually require respiratory support Extra inspired oxygen Regular blood gas measurement Usually improved within 48hrs Pulmonary hypertension or pneumothorax may have developed

RDS reliving factors Hydrocortisone (give 2 doses 4mg q 12hrs and before 4-8hrs of labor) Any stress IUGR Pre-eclampsia

Respiratory distress syndrome (hyaline membrane disease) Occurring in preterm infants due to a lack of surfactant in the alveoli Occur in 1% of all births Although there have been a number of recent advances in the management of premature delivery, including suppression of labor, estimation of L\S ratio and the use of steroids

Predisposing factors Prematurity Infant of a diabetic mothers Ante partum Hge Second twin Hypoxia, acidosis, shock Male sex C\S hypothermia

pathogenesis The lack of surfactant results in alveoli remaining unexpanded (atelectatic) and gas exchange is impaired Surfactant is a phospholipid secreted by the type 2 alveolar cells of the lung and is stored in lamellar bodies The major active component is lecithin, but other phospholipids and protein must be present for full activity

These surface-active agents are released into alveoli, reducing the surface tension and helping to keep the alveoli open Lung maturity is assessed by measuring the L\S ratio An L\S ratio less than 1.5 predict a high risk of RDS (70% incidence) An L\S ratio of 1.5-2 predicts a 40% risk of developing RDS

Mature ratio more than 2 indicates a very small risk unless the mother is diabetic Surfactant is secreted into the fetal lung at 3o-32 wks gestation

Clinical features The signs start immediately after birth or become obvious in the first 6hrs of life The infant lies in a frog-like position and may have difficulty with copious pharyngeal secretions Expiratory grunt may diminish and prolonged apnea may occur The infant is oliguric initially and has evidence of increasing peripheral edema

radiology Ground glass Air bronchograms Poorly inflated lung

Treatment Oxygen:- Maintain the pao2 within the normal range Increasing the inspired oxygen concentration In sever cases respiratory support may be necessary

Chest physiotherapy:- Regular position changes Air way suctioning to reduce the risk of mucus retention Active chest percussion and cupping Physiotherapy shouldn't be employed for at least 24hrs after surfactant instillation Antibiotics:- Broad-spectrum antibiotics

Surfactant replacement therapy:- Exogenous surfactant is administered via the endotracheal tube either to infants with established RDS or as a prophylaxis in high risk preterm infants It is general practice to give at least one dose of surfactant down the endotracheal tube as soon as RDS is diagnosed then put the baby on mechanical ventlation

Meconium aspiration syndrome Is a serious and potentially preventable cause of respiratory distress in the newborn Meconium staining of the amniotic fluid occurs almost always in full term or post term infants The passage of Meconium often indicates fetal distress

Clinical features Infant is born covered in Meconium stained liquor and has Meconium staining of the umbilical cord Hyper inflated chest Respiratory distress Cerebral irritability

pathogenesis Causes plugging of the airways with consequent atelectasis Meconium is irritating to the airways causing a chemical pneumonitis and secondary bacterial infection

Prophylactic management Once the head crowns, and before the shoulder are delivered, the oropharynx should be suctioned Transfer the baby to the resuscitation trolley In depressed infant intubeted is needed If the baby is healthy transfer to mother

Treatment Humidification of inspired oxygen Postural drainage positioning Suctioning of airways and chest percussion Antibiotic