Respiratory Disorders of the Newborn

Published on 01/06/2015 by admin

Filed under Pulmolory and Respiratory

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 4 (1 votes)

This article have been viewed 3584 times

Respiratory Disorders of the Newborn

Persistent Pulmonary Hypertension in the Newborn (PPHN)

Etiology

Pathophysiology (Figure 27-1)

Clinical presentation

Diagnostic tests for PPHN

1. Contrast or “bubble” echocardiography

2. Hyperoxia test

3. Comparison of preductal and postductal arterial Pao2

4. Hypoxemia-hyperventilation test

Management of PPHN

1. Management goals:

2. Minimize handling and stimulation of the infant to avoid transient hypoxemia.

3. Inhaled nitric oxide (iNO)

4. Mechanical ventilation and oxygen

a. Conventional mechanical ventilation (CMV) and high frequency oscillatory ventilation (HFOV) have been used with success.

b. Hyperventilation and induced alkalosis have been widely used but are controversial.

c. A widely practiced approach is to set the ventilator to produce mild hypocapnia and respiratory alkalosis.

d. Success has been reported using lung protective ventilator strategies without inducing alkalinization.

e. Muscle relaxants and sedatives to prevent patient-ventilator dysynchrony and resulting fluctuations of Pao2.

5. Administer surfactant if the infant has respiratory distress syndrome (RDS).

6. Pharmacologic treatments

7. Extracorporeal membrane oxygenation (ECMO) is used for severe cases.

II Respiratory Distress Syndrome

Etiology

Factors that increase the risk of developing RDS

Pathophysiology (Figure 27-2)

Clinical presentation

Radiographic findings (Figure 27-3)

Management

1. Monitoring of vital signs and arterial blood gases.

2. Manage hypoxemia; maintain Pao2 of 60 to 80 mm Hg.

3. Continuous positive airway pressure (CPAP) may be used initially.

4. Mechanical ventilation is usually required to manage severe acidemia, hypercapnia, and hypoxemia.

5. High respiratory rate, FIO2, and airway pressures are often required.

6. HFOV may be used either initially or in cases in which CMV is unsuccessful.

7. Surfactant replacement therapy

a. Synthetic and animal-derived products are available (Table 27-1).

TABLE 27-1

Surfactant Replacement Therapy

Generic Name Brand Name Source Characteristics Route Dosage
Colfosceril Exosurf Synthetic surfactant No surfactant associated proteins Side port on endotracheal tube adaptor Initial: Two 2.5-ml/kg half-doses; avoid endotracheal suctioning for 2 hr after treatment
Beractant Survanta Exogenous surfactant from bovine lung extract Contains surfactant associated proteins Intratracheal Initial: 4 ml/kg; if needed, 4 doses in the first 48 hr of life; ≥ 6 hr between each dose
Poractant alfa Curosurf Derived from minced porcine lung extract Contains surfactant associated proteins Intratracheal Initial: 2.5-ml/kg dose divided in 2 aliquots; up to 2 more doses of 1.25 ml/kg, 12 hr apart, if needed
Calfactant Infasurf Derived from lavage of calf lungs Contains surfactant associated proteins Intratracheal Initial: 3-ml/kg dose divided into 2 aliquots; 3 doses of 3 ml/kg, 12 hr apart, if needed

image

b. Method of administration depends on the drug used.

c. Results in rapid and dramatic improvement in lung compliance and gas exchange.

d. High levels of ventilatory support usually can be significantly reduced.

e. Widespread use of surfactant has markedly decreased mortality from RDS.

f. To avoid potential pneumothorax, it is important to decrease airway pressures and tidal volumes promptly when compliance improves during or immediately after surfactant administration.

g. The most common adverse effects are transient oxygen desaturation and bradycardia.

8. iNO

9. Maintain normal body temperature, and minimize stimulation of infant.

10. Provide appropriate fluid, electrolytes, glucose, and calories.

11. Maintain blood pressure and hematocrit.

12. Use secretion clearance techniques if necessary.

13. ECMO is used in severe cases.

Prognosis

Prevention of RDS

III Meconium Aspiration Syndrome (MAS)

Description

Etiology

Pathophysiology

1. The effects of meconium aspiration on the lower airways:

2. During the first few hours after aspiration, hypercapnia, hypoxemia, and metabolic acidosis develop.

3. As pulmonary vascular resistance increases, the infant often develops PPHN.

4. If mechanical ventilation is required, recovery may be complicated by barotrauma and pneumothorax.

Radiographic findings

Clinical presentation

Management

1. If meconium-stained amniotic fluid is present, the mouth, nose, nasopharynx, and oropharynx are always suctioned when the newborn’s head presents during birth, before the first breath is taken.

2. If meconium is present in the oropharynx, the vocal cords are viewed under direct vision, and the airway is suctioned above the cords.

3. If meconium is suctioned above the vocal cords, the trachea is intubated with a meconium aspirator, and the airway below the cords is suctioned.

4. The airway must be cleared of meconium by suction before any positive pressure breaths are given.

5. Supplemental blow-by oxygen is usually necessary.

6. CPAP is often used to improve oxygenation.

7. Mechanical ventilation is initiated if the infant fails to respond to oxygen with CPAP and develops worsening hypoxemia, hypercapnia, and acidemia.

8. HFOV may be used as primary therapy or when ventilation with CMV is unsuccessful.

9. Term infants often require sedation and sometimes muscle relaxers to maintain synchrony with the ventilator.

10. Inhaled nitric oxide can be used if PPHN is present.

11. Secretion clearance techniques, such as frequent endotracheal suctioning and chest physical therapy, are often useful.

12. ECMO may be required to manage severe MAS (Table 27-2).

TABLE 27-2

ECMO/ECLS Use and Survival for Neonates

Diagnosis Number of Cases* Percentage Survival
MAS 6263 94
CDH 4101 53
Sepsis 2307 75
PPHN 2649 79
RDS 1357 84
Others 1411 65

image

MAS, Meconium aspiration syndrome; CDH, congenital diaphragmatic hernia; PPHN, persistent pulmonary hypertension in the newborn; RDS, respiratory distress syndrome.

*Includes all cases reported to the registry.

From ELSO registry data. January 2003.

Prognosis

IV Pneumothorax

Etiology

Pathophysiology

Clinical presentation

Diagnosis (Figure 27-4)

Management

Pneumonia

Incidence of pneumonia during birth or after delivery

Etiology

Pathophysiology

1. The neonate can acquire infection via three routes.

2. Rupture of placental membranes ≥12 hours before birth increases the chance that infectious agents will spread to the amniotic fluid and the fetus.

3. Bacterial pneumonia causes inflamed, fluid-filled alveoli more often than viral pneumonia, and in severe cases necrosis of lung tissue develops.

4. Sepsis can rapidly develop from gram-negative pulmonary infections.

5. Bacterial pneumonia acquired in utero leads to stillbirth and premature delivery in many cases.

6. Pneumonia caused by viruses and mycoplasmae involve the bronchi and interstitium, resulting in loss of ciliary function and mucus stasis.

7. Fungal infections can produce a layer of hyphae that line the upper and lower respiratory tract, eventually leading to ulcerations in the airway.

Clinical presentation

Laboratory findings

1. Chest radiographs have various patterns of infiltrates that are often characteristic of a specific causative organism (Table 27-3).

TABLE 27-3

Chest X-ray Findings in Neonatal Pneumonia

Causative Agent Appearance of Chest Radiograph
Group B β -hemolytic Streptococcus (GBS) Diffuse opacities (“white out”), patchy infiltrates, pleural effusions
Streptococcus pneumoniae Patchy lobar infiltrates, pleural effusion
Klebsiella Bilateral consolidation, lung abscess, pneumatocele
Pseudomonas and Serratia Parenchymal consolidation (patchy or basilar), pneumatocele
Respiratory syncytial virus Hyperexpansion, patchy consolidation
Candida albicans Diffuse granularity, coarse infiltrates, opacification

From Merenstein GB, Gardner SL: Handbook of Neonatal Intensive Care, ed 5, St. Louis, Mosby, 2002.

2. Tracheal aspirates and blood cultures help identify causative organisms and diagnose sepsis.

3. Complete blood count (i.e., neutrophil count, platelet count) may be useful to diagnose sepsis and other infections, but results from these tests are not specific enough to differentiate between causative factors.

Management

Prognosis

VI Transient Tachypnea in the Newborn (TTN)

Etiology

Pathophysiology

1. The fetal lung is normally filled to the functional residual capacity level with fluid that is produced in the lungs (not amniotic fluid).

2. As the neonate passes through the birth canal during a normal delivery, “thoracic squeeze” removes one third of the fluid present in the lungs at birth.

3. The remaining fluid is removed slowly by the neonate’s lymphatic system.

4. The excessive fluid in the lungs and interstitium interferes with the ability to hold bronchioles and alveoli open.

5. Air trapping and small airway collapse result, causing changes in pulmonary mechanics and breathing pattern of the infant.

6. TTN is usually a benign and self-limiting condition.

7. However, TTN may be complicated by PPHN or evolve into RDS.

Clinical presentation

Radiographic findings

Management

VII Apnea in the Neonate

Apnea of prematurity or primary apnea

1. The younger the gestational age, the greater the incidence of apnea.

2. Not caused by a specific disease entity.

3. There are several factors that have been associated with primary apnea.

a. Response to hypoxemia and hypercapnia

b. Immaturity of the neurons that control respiratory rate and rhythm may contribute to primary apnea. Premature infants have fewer dendrites and synaptic connections, and this may alter transmission of impulses involved in control of breathing.

c. Apnea in infants occurs more often during sleep, especially rapid eye movement (REM) sleep. The known neurologic effects during REM sleep include inhibition of spinal motor neurons, increased movement of the eyes, muscle twitching, and increased cerebral blood flow. There may be other effects that directly or indirectly influence drive to breathe.

d. Respiratory muscle fatigue: The premature infant has an increased workload from the combination of a compliant chest wall and less compliant lungs.

Secondary apnea is caused by specific disorders that directly or indirectly lead to hypoxemia and depression of the drive to breathe.

Iatrogenic causes of apnea

Management

1. Spo2 and heart rate should be monitored, and alarm systems should remain active.

2. Reduce environmental stress

3. During apneic spells use the least invasive intervention that stimulates the infant to breathe.

4. Manage disorders that cause secondary apnea.

5. Methylxanthines are sometimes used to manage apnea of prematurity.

VIII Chronic Disorders Associated with Prematurity

Bronchopulmonary dysplasia (BPD)/chronic lung disease (CLD)

1. BPD is a chronic disorder in premature infants characterized by

2. Originally BPD described a classic progression of radiographic and functional changes in the lungs of survivors of RDS.

3. The BPD seen today is not as severe; with current treatment premature infants do not necessarily progress through all of the classic stages.

4. CLD is a term used to describe premature infants who require supplemental oxygen at 28 to 30 days of life or at 36 weeks’ postmenstrual age.

5. Etiology: The causes of BPD/CLD are iatrogenic.

6. Predisposing factors

7. Pathophysiology

8. The classic stages of BPD

a. Stage I

b. Stage II

c. Stage III

d. Stage IV

9. Clinical presentation

Management

1. Maintain adequate oxygenation and ventilation

2. Weaning from mechanical ventilation

3. Provide adequate nutrition to facilitate healing of damaged lung tissue.

4. Drug therapy is used to improve lung mechanics.

a. Aerosolized medications

b. Effectiveness of aerosolized medications

c. Methylxanthines are used to promote weaning from low-level ventilatory support.

d. Diuretics can improve lung mechanics and facilitate weaning.

e. Antenatal and postnatal steroids are widely used and have been linked to decreased mortality and faster weaning.

f. Studies comparing the efficacy of inhaled versus systemic steroids have yielded conflicting results.

5. Unfortunately very small premature infants almost always have complications from BPD as children (Box 27-1).

IX Retinopathy of Prematurity (ROP)

ROP is a common complication of prematurity.

Etiology

Pathophysiology

1. Most blood vessels supplying the retina are developed by 32 weeks’ gestation, but those in the peripheral regions may not develop until 40 weeks.

2. Retinal vessels constrict in response to hyperoxia.

3. Some vessels dilate and revascularize their surrounding areas.

4. Other vessels constrict permanently and become necrotic in a process called vasoobliteration.

5. The remaining blood vessels begin to proliferate as they attempt to provide blood flow to the obliterated areas of the retina.

6. If the vessels continue to proliferate, the damage can progress from hemorrhage to retinal scarring, retinal detachment, and blindness.

7. Early changes are often seen in the temporal periphery of the retina, the region where vascularization develops in the last few weeks of gestation.

8. ROP can no longer occur when the vascular development of the retina is complete.

Classification of the severity of ROP (Figure 27-5)

Management and prevention

Congenital Heart Disease (Box 27-2)

Approximately 1% of newborns are born with a heart defect.

Etiology

Newborns with severe cardiac defects generally have one or more of the following signs and symptoms.

CHF is a syndrome characterized by decreased cardiac output and decreased tissue perfusion.

1. Results from the inability of the myocardium to fulfill the body’s metabolic needs.

2. Causes of CHF

3. Signs and symptoms of CHF

4. Management of CHF

PDA (Figure 27-6)

Atrial septal defect (ASD) (Figure 27-7)

Ventricular septal defect (VSD) (Figure 27-8)

1. Cyanosis is rarely present because the shunt is from left to right.

2. Defects vary considerably in size and may occur in conjunction with other cardiac defects.

3. VSD (either alone or associated with other anomalies) account for 50% of congenital heart defects.

4. Two factors influence the effect of the VSD on circulation.

5. Management

Aortic stenosis (Figure 27-9)

image
FIG. 27-9 Aortic stenosis.

Pulmonary stenosis (Figure 27-10)

image
FIG. 27-10 Pulmonary stenosis.

Coarctation of the aorta (Figure 27-11)

Tetralogy of Fallot (Figure 27-12)

Truncus arteriosus (Figure 27-13)

image
FIG. 27-13 Truncus arteriosus.

1. Cyanosis is present because of right-to-left shunt.

2. Characterized by a common artery (truncus) originating from both ventricles and overriding a VSD.

3. The truncus carries a mixture of oxygenated and unoxygenated blood and is the origin for the aorta, coronary arteries, and both branches of the pulmonary arteries.

4. Pulmonary blood flow varies, depending on the location of the branching of the pulmonary arteries off the truncus and the degree of pulmonary hypertension.

5. Pulmonary blood pressure is usually equal to systemic blood pressure.

6. Right and left ventricular hypertrophy and CHF commonly occur.

7. Surgical correction involves

Complete transposition of the great vessels (Figure 27-14)

1. Cyanosis is present because of right-to-left shunting.

2. Characterized by reversed position of aorta and pulmonary arteries.

3. Venous and arterial blood may mix through an ASD, VSD, or PDA (Table 27-4).

TABLE 27-4

Congenital Heart Diseases

Cardiac Defect Anatomic Characteristics Direction of Shunt Presence of CHF Presence of Cyanosis Treatment
Patent ductus arteriosus (PDA) Failure of ductus arteriosus to close at birth Left-to-right Present Acyanotic Medical: Indomethacin
          Surgical: Ligation of PDA
Atrial septal defect (ASD) Failure of foramen ovale to close or malformation in atrial septal wall Left-to-right Present Acyanotic Surgical closure
Ventricular septal defect (VSD) Malformation in ventricular septal wall Left-to-right Present, if large VSD Acyanotic Large VSD requires surgical closure
Aortic stenosis Most common type an aortic valve with fused leaflets No shunt, if isolated lesion Present Acyanotic Surgical correction is aortic valvulotomy
Pulmonary stenosis Most common type is defect in the pulmonary valve with fused leaflets No shunt, if isolated lesion Present Acyanotic Pulmonary valvulotomy
Coarctation of the aorta Constriction in lumen of aorta near ductus arteriosus No shunt Sometimes Acyanotic Surgical resection of the stricture
Tetralogy of Fallot VSD with overriding aorta, outflow obstruction of RV, RV hypertrophy Right-to-left Rare Cyanotic Surgery to create shunt from aorta to PA, VSD closure, correction of outflow obstruction
Truncus arteriosus Common artery (truncus) overriding a VSD Right-to-left Present Cyanotic VSD closure, separation of pulmonary arteries from truncus, reattachment to RV
Complete transposition of the great vessels Aorta originates from RV; PA originates from LV, with ASD, VSD, and/or PDA Right-to-left Not present Cyanotic Most common surgical correction is arterial switch procedure
Total anomalous pulmonary venous return (TAPVR) Pulmonary veins return oxygenated blood to the RA, ASD Right-to-left Not present Cyanotic Surgical connection of pulmonary veins to LA, ASD closure
Tricuspid atresia Agenesis of tricuspid valve, small RV, large LV Right-to-left Sometimes Cyanotic Surgical connection of PA to RA, ASD and VSD closure

image

CHF, Congestive heart failure; RA, right atrium; RV, right ventricle; LV, left ventricle; PA, pulmonary artery.

4. Profound cyanosis may occur if the ventricular septum is intact or the ductus arteriosus begins to close.

5. In this situation oxygen therapy has a limited benefit because the only oxygenated blood reaching systemic circulation is that which is shunted through the VSD, ASD, or PDA.

6. This amount is determined by the size, position, and number of communications where shunting can occur.

7. The most common surgical repair is the arterial switch procedure.

Total anomalous pulmonary venous return (TAPVR) (Figure 27-15)

1. Cyanosis and right-to-left shunting are present.

2. Characterized by all pulmonary veins returning oxygenated blood to the right atrium.

3. Several types of TAPVR are classified according to route of pulmonary venous return to the right atrium.

4. To sustain life, there must be a passage between the right and left atria (ASD) so that right-to-left shunting can occur.

5. Surgical management consists of reimplantation of anomalous pulmonary veins from the right atrium to the left atrium and closure of the ASD.

Tricuspid atresia (Figure 27-16)

image
FIG. 27-16 Tricuspid atresia.

XI Other Congenital Anomalies with Effects on the Respiratory System

Choanal atresia

1. Characterized by blockage, to varying degrees, of the posterior opening into the nasopharynx by a membranous tissue, usually with bony implants.

2. Occurs in approximately 1 in 7000 live births.

3. Can be an isolated anomaly or part of a syndrome with multiple anomalies.

4. Clinical presentation

5. Computerized tomography scan usually confirms diagnosis of choanal atresia.

6. Management

Esophageal atresia (EA) (Figure 27-17)

1. Characterized by an esophagus that ends in a blind pouch before joining the stomach and usually occurs in conjunction with a tracheoesophageal fistula (TEF).

2. There are several types; the most common involves atresia of the upper esophagus with the lower esophagus connected to the trachea or mainstem bronchi.

3. Clinical presentation

4. Management

Congenital diaphragmatic hernia (CDH) (Figure 27-18)

1. Characterized by incomplete development of diaphragm, the presence of abdominal organs in the thoracic cavity, and small, underdeveloped lung(s).

2. CDH occurs in 1 of every 4000 live births.

3. At least 90% of occurrences of CDH involve the left side, allowing the intestines to migrate into the chest.

4. The primary factors that influence outcome are

5. Antenatal diagnosis is confirmed by ultrasound.

6. Early diagnosis allows the mother to plan for delivery at a high-risk perinatal center.

7. Management

8. Prognosis

XII Nonrespiratory Disorders of Preterm Neonates

Intraventricular hemorrhage (IVH)

1. Significant cause of brain injury in premature infants, particularly those weighing <1500 g or born at <32 weeks’ gestation.

2. Incidence of IVH

3. Etiology is multifactorial, but all risk factors relate in some way to an alteration in the infant’s cerebral blood flow.

4. Pathophysiology

5. Clinical presentation of IVH varies from subtle to catastrophic.

6. Management involves supportive care to prevent extension of the IVH.

7. Prognosis

Necrotizing enterocolitis (NEC) is an inflammatory bowel process resulting in injury to the intestinal mucosa.

1. Etiology

2. Pathophysiology

3. Clinical presentation

4. Management of NEC

5. Prognosis