Notes by Harriet Wood. Preterm Infants

Transcription

1 Preterm Infants Prognosis Depends on gestational age at birth. Rate and severity of problems associated with prematurity decrease markedly with increasing gestation. Appearance of very preterm infants - Thin, dark red, transparent skin - No palpable breast tissue - Shapeless ears - Undecended testes/ Protruding labia minora - Lie with arms and legs extended - Poor muscle tone Medical Problems of a Preterm Infant - Need for resuscitation at birth - Necrotising enterocolitis - Temperature control - Nutrition - Respiratory o Respiratory distress - Fluid balance o Pneumothorax o Apnoea and bradycardia - Periventricular leukomalacia - Retinopathy of prematurity - Infection - Hypotension - Jaundice - Patent ductus arteriosus - Bronchopulmonary dysplasis (chronic lung disease of prematurity) - Metabolic o Hypoglycaemia - Intraventicular haemorrhage, o Hypocalcaemia parenchymal cerebral haemorrhage o Electrolyte imbalance o Osteopenia of prematurity - Anaemia of prematurity - Inguinal hernia - Iatrogenic 1

2 Birth Asphyxia (neonatal encephalopathy) oxygen delivery to the tissues hypoxic-ischaemic encephalopathy. Investigations: CTG Fetal blood sampling or cord blood analysis may identify metabolic acidosis APGAR scores Hypoxic-ischaemic encephalopathy: used to describe clinical manifestations of brain injury immediately or up to 48hrs after asphyxia It is graded: Stage 1 Mild Stage 2 Moderate Stage 3 - Severe Consciousness Hyperalert Lethargic Stuporose Seizure None Common Prolonged + often refractory to treatment Muscle Tone Normal Hypotonic Flaccid Duration <24hrs 2-14 days Hours-weeks Prognosis Good Variable Poor Other Irritable, staring of eyes, hyperventilation, impaired feeding Multi-organ failure Management: Effective resuscitation: respiratory support, circulatory, metabolic support. Fluid balance: avoid exacerbating cerebral oedema. Treat seizures: anticonvulsants e.g. phenobarbitone. Monitor other organs: kidneys, liver, gut. Withdrawal of care: consider if severe HIE asso. with poor prognosis. Neurological sequelae: motor problems, cognitive problems, school problems, epilepsy. 2

3 The Blue Baby Causes 1. Respiratory: - Transient tachypnoea of the newborn (esp. after C-section) - Surfactant deficiency (RDS) - Meconium aspiration - Pneumonia - Pneumothorax - Congenital anomalies: pulmonary hypoplasia, congenital diaphragmatic hernia, congenital cystic adenomatous malformation, chylothorax 2. CV: - Transposition of the great vessels - Pulmonary atresia - Critical pulmonary stenosis - Severe tetralogy of Fallot - Tricuspid atresia - Ebstein s anomaly - Total anomalous pulmonary venous drainage 3. Sepsis Respiratory Distress Syndrome (RDS) Also called Hyaline Membrane Disease Most infants born before 28 weeks have RDS. Pathophysiology - Deficiency of surfactant, which lowers surface tension. - This causes alveolar collapse and inadequate gas exchange. Prevention - Glucocorticoids (steroids) are given if preterm delivery is anticipated e.g. betamethasone or dexamethasone. o It stimulates surfactant production 3

4 S&S Onset of respiratory symptoms within 4hrs of birth: - Tachypnoea RR>60/min - Cyanosis - Subcostal / intercostal recession - Sternal recession - Expiratory grunting Radiological features: - Glass-ground appearance - Air bronchograms Treatment and Management - Avoid hypoxia, acidosis, hypothermia - Continuous positive airway pressure (CPAP) - Ventilate and give surfactant - Strict attention to fluid balance - Antibiotics Complications Short term: - Fluid overload, PDA, NEC, pneumothorax, PIE - Mortality Long term: - Morbidity - Chronic lung disease - risk of neurodevelopmental sequelae 4

5 Patent Ductus Arteriosus Shunting of blood across the ductus, from the left to the right side of the circulation is common in infants with RDS Signs and Symptoms - Apnoea - Bradycardia - Increased difficulty weaning the infant from artificial ventilation - Pulses are bounding - Signs of heart failure Investigations - Echocardiography Treatment - Fluid restriction and indomethacin - Surgical ligation Intracranial Lesions Occur in 25% of very low birth weight infants Major of haemorrhages are small and harmless Occurs in the germinal matrix region Retinopathy of prematurity (ROP) Pathophysiology - Affects developing blood vessels at the junction of the vascular and nonvascularised retina - There is vascular proliferation which may progress to retinal detachment, fibrosis and blindness 5

6 Necrotising Enterocolitis Cause - Ischaemia of the bowel wall and infection from organisms colonising the bowel. - May be accelerated by feeding with milk. Signs and Symptoms Xray - Infant stops tolerating feeds - Milk aspirated from the stomach - Vomiting (may be bile stained) - Distended abdomen - Stool may contain fresh blood - May be rapid shock - Distended loops of bowl - Thickening of bowel wall with intramural air - Air in the portal tract Disease may progress to bowel perforation Treatment - Stop oral feeding - Broad spectrum antibiotics - Parental nutrition - Artificial ventilation - Surgery (for bowel perforation) Long-term complications - Strictures - Malabsorption 6

7 Neonatal Intestinal Obstruction - Can be due to a variety of causes. - Clinical features often similar. - Bile-stain vomiting is never normal in a neonate and implies IO. - Failure to pass meconium is a feature. - The degree of abdo distension is variable. 1. Duodenal atresia - Occurs in 1/10000 live births. Pathology: - Site of obstruction commonly 2 nd part of duodenum. - Proximal duodenum becomes hypertrophied. Associations: - 50% asso. with polyhydramnios. - 60% of pregnancies are complicated or end prematurely. - 30% of babies also have Down s Syndrome. - Other asso. abnormalities inc. cardiac anomalies, malrotation, biliary atresia. S&S: - Postnatally presents with bilious or non-bile stained vomiting. Inv: - AXR: Double bubble and no gas within bowel distally. - Often diagnosed on antenatal USS. Management: - A nasogatric tube should be passed. - IV fluids. - Major cardiac and other defects should be excluded. - Duodenoduodenostomy should be performed when resuscitated. 2. Meconium Ileus - Commonest cause of neonatal intraluminal IO. - 80% cases are asso. with CF. Pathology: - Viscid pancreatic secretions cause autodigestion of pancreatic acinar cells meconium of abnormal + putty like consistency. - Meconium becomes inspissated in the lower ileum. - There is a micocolon. 7

8 S&S: - Presents with bilious vomiting and distension usually on 1 st day of life. - Passage of meconium is delayed. - Meconium filled loops of bowl may be palpable. Investigations: - X-ray: Ground-glass appearance, esp. in RUQ. Management: - Gastrogradin enemas (successful in 50% ptts). - Surgery. - Occasionally resection and stomas. 3. Malrotation Pathology: - Between 4-10wks of development intestines herniated into umbilical cord. - When they returned to abdo they rotate 270 anticlockwise. - As a result: o Duodenojejunal flexure lies to the left of the midline. o Caecum lies in the RIF. o Transverse colon lies anterior to the small bowel mesentery. - Partial failure of rotation results in malrotation. - Commonest abnormalities results in caecum lying close to DJ flexure. - Resulting midgut mesentery is abnormally narrow and liable to volvulus. Two principle clinical presentations: - Presents early with collapse and acidosis due to intestinal infarction. - Presents late with intermittent bile stained vomiting and distension. Radiological investigations often unhelpful. Management: - After resuscitation, early laparotomy may be required. - Any volvulus should be reduced. - Resection may be required if there has been small bowel infarction. - Any Ladd s bands should be divided. - The base of the mesentery should be elongated. - Colon should be placed on the left of the abdomen. - Inversion appendicectomy should be performed to prevent future diagnostic uncertainty. 8

9 Neonatal Jaundice (preterm and term) Over 50% of all newborn infants become visibly jaundiced. Commoner in prems. This is because: - Haemoglobin conc. rapidly in the first few days after birth from haemolysis. - The red cell life span of newborn infants is markedly shorter than that of adults. - Hepatic bilirubin metabolism is less efficient in the first few days of life. Causes of neonatal jaundice Starting <24h of age always pathological unconjugated: - Haemolysis - Haemolytic disorders e.g. Rhesus incompatibility, ABO incompatibility - Congenital infection 24h to 2 weeks of age unconjugated: - Physiological jaundice - Breast milk jaundice - Infection e.g. UTI - Haemolysis e.g. ABO incompatibility - Bruising >2 weeks of age: - should always be investigated. 1. Unconjugated: - Physiological or breast milk jaundice - Infection e.g. UTI - Hypothyrodism 2. Conjugated: - always pathological - Bile duct obstruction - Biliary atresia - Neonatal hepatitis Kernicterus: - a complication Caused by unconjugated neonatal jaundice. S&S: a type of brain damage asso. with cerebral palsy, hearing loss, problems with vision, yellow staining of teeth. Investigation Is it conjugated? Total conjugated bilirubin, LFTs If it haemolysis? FBC, Group + DAT Is it infection? Viral serology, blood cultures, urine cultures Is it metabolic? TFTs, a-1 antiutrypsin, cystic fibrosis IRT/DNA, plasma amino acids/ urinary organic acids. 9

10 Treatment - Treat underlying cause. - Phototherapy with/without exchange transfusion. Important Note These notes were written by Harriet Wood, as a medical student in They are presented in good faith and every effort has been taken to ensure their accuracy. Nevertheless, medical practice changes over time and it is always important to check the information with your clinical teachers and with other reliable sources. Disclaimer: no responsibility can be taken by either the author or publisher for any loss, damage or injury occasioned to any person acting or refraining from action as a result of this information. Please give feedback on this document and report any inaccuracies to: support@askdoctorclarke.com 10