Anatomic Alterations of the Lungs

Transient tachypnea of the newborn (TTN) (also called type II respiratory distress syndrome and “wet lung” syndrome) was first described in the literature in 1965. Within the first 4 to 6 hours after birth, TTN produces clinical signs very similar to those associated with the early stages of respiratory distress syndrome (see Chapter 34). However, the anatomic alterations of the lungs associated with TTN are much different from the pulmonary pathology seen in respiratory distress syndrome.

As shown in Figure 33-1, the infant with TTN has a delay in the pulmonary fluid absorption by the lymphatic system and pulmonary capillaries. It is thought that this condition results, in part, from the infant’s hypoxemia and inadequate inspiratory effort, producing a delay in clearance of pulmonary fluid. As this condition worsens, the infant develops pulmonary capillary congestion, interstitial edema, decreased lung compliance, decreased tidal volume, and increased dead space. Because the swallowing and cough efforts of infants with TTN are commonly depressed, the clearance of bronchial secretions is compromised. This condition often leads to air trapping and alveolar hyperinflation.

In severe cases, the excessive fluid accumulation throughout the alveolar-capillary interstitial tissue may also compress the bronchial airways. As a general rule, however, the abnormal anatomic alterations of the lungs associated with TTN usually begin to resolve about 48 to 72 hours after birth.

The major pathologic or structural changes associated with TTN are as follows:

Etiology and Epidemiology

TTN affects 1% to 2% of all newborns. Classically, TNN is most often seen in full-term infants. Risk factors include elective cesarean section, excessive administration of fluids to the mother during labor, male gender, and macrosomia (a newborn with excessive birth weight). The infant’s history often includes maternal analgesia or anesthesia during labor and delivery or episodes of intrauterine hypoxia. TTN is also commonly associated with maternal bleeding, maternal diabetes, and prolapsed cord. TTN is occasionally seen in very small infants.

Although the precise mechanism is not known, it is believed that TTN results from a delayed absorption of fetal lung fluid. The delayed absorption of lung fluid is thought to be caused by any condition that increases the central venous pressure, which in turn slows the clearance of lung fluid by the lymphatic system. Infants with TTN are often lethargic at birth, resulting in a depressed cough effort and accumulation of airway secretions and mucus. The typical baby with TTN usually has good Apgar scores at birth. During the next few hours, however, signs of respiratory distress develop. Early clinical manifestations include tachypnea, retractions nasal flaring, grunting, and cyanosis. It is common to see respiratory rates of 80 to 120 breaths/minute. In fact, the rapid and shallow breathing pattern often is considered a hallmark clinical manifestation of TTN. In addition, the infant may demonstrate a barrel chest and coarse breath sounds. Within 24 to 48 hours, the clinical manifestations of respiratory distress usually disappear.

 OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Transient Tachypnea of the Newborn

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), Excessive Bronchial Secretions (see Figure 9-12), and Airway Obstruction—the major anatomic alterations of the lungs associated with transient tachypnea of the newborn (TTN) (see Figure 33-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Infants with TTN frequently breathe rapidly and shallowly. In fact, this rapid and shallow breathing pattern often is considered a hallmark clinical manifestation of TTN. Normally, a newborn infant’s respiratory rate is about 40 to 60 breaths per minute. During the early stages of TTN, the respiratory rate is often 60 to 100 breaths per minute. Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

• Stimulation of the peripheral chemoreceptors (hypoxemia)

• Decreased lung compliance–increased ventilatory rate relationship

• Stimulation of the central chemoreceptors

Increased Heart Rate (Pulse) and Blood Pressure

Clinical Manifestations Associated with More Negative Intrapleural Pressure during Inspiration

Intercostal Retractions

• Substernal retraction and abdominal distention (seesaw movement)

• Cyanosis of the dependent portions of the thoracic and abdominal areas

• Flaring nostrils

Chest Assessment Findings

• Wheezes

• Rhonchi

• Crackles

Expiratory Grunting

Cyanosis

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Extrapolated Data for Instructional Purposes) (Restrictive Lung Pathophysiology)

FORCED EXPIRATORY FLOW RATE FINDINGS

FVC	FEVT	FEV1/FVC ratio	FEF25%-75%
↓	N or ↓	N or ↑	N or ↓
FEF50%	FEF200-1200	PEFR	MVV
N or ↓	N or ↓	N or ↓	N or ↓

LUNG VOLUME AND CAPACITY FINDINGS

VT	IRV	ERV	RV*
N or ↓	↓	↓	↓
VC	IC	FRC*	TLC*	RV/TLC ratio*
↓	↓	↓	↓	N

^*↑ When airways are partially obstructed.

Arterial Blood Gases

MILD TO MODERATE TRANSIENT TACHYPNEA OF THE NEWBORN

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓

SEVERE TRANSIENT TACHYPNEA OF THE NEWBORN*

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco2	†	Pao2
↓	↑	↑ (slightly)	↓

^†When tissue hypoxia is severe enough to produce lactic acid, the pH and values will be lower than expected for a particular Paco₂ level.

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^*The clinical manifestations of TTN usually disappear in the first 24 to 48 hours. Severe TTN is rare.

Oxygenation Indices*

	Do2†			O2ER
↑	↓	N	N	↑	↓

^†The Do₂ may be normal in patients who have compensated to the decreased oxygenation status with (1) an increased cardiac output, (2) an increased hemoglobin level, or (3) a combination of both. When the Do₂ is normal, the O₂ER is usually normal.

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^*, Arterial-venous oxygen difference; DO₂, total oxygen delivery; O₂ER, oxygen extraction ratio; , pulmonary shunt fraction; , mixed venous oxygen saturation; , oxygen consumption.

RADIOLOGIC FINDINGS

Chest Radiograph

Initially, the chest radiograph appears normal. Over the next 4 to 6 hours, however, signs of pulmonary vascular congestion develop. These are revealed on the chest radiograph as prominent perihilar streaking (commonly called starbursts or sunbursts), air bronchograms, and fluid in the interlobular fissures. Air trapping and hyperinflation may occur and are manifested by peripheral hyperlucency, flattened diaphragms, and bulging intercostal spaces. Patches of infiltrates may be seen in some infants. Mild cardiomegaly and pleural effusions also may be seen (Figure 33-2).

General Management of Transient Tachypnea of the Newborn

Because of the relatively short course of TTN, the treatment consists mostly of proper stabilization, close monitoring, and frequent and thorough evaluations to rule out other, more serious conditions that may develop. Oxygen therapy is provided to maintain adequate oxygenation, and bronchopulmonary hygiene therapy may be administered to keep the airways clear of bronchial secretions. Lung expansion therapy is often used as a preventative measure, but mechanical ventilation is usually not required. Fluid restriction is usually ordered until the signs associated with TTN resolve. Oral feedings are usually started as soon as the infant is able tolerate them. Diuretics do not affect the clinical course of the TTN. In cases in which pneumonia is suspected, the use of antibiotics is indicated.

A 27-year-old woman in the thirty-fifth week of her second pregnancy awakened at 2 am with sudden lower abdominal pain and some bleeding. She had no contractions at the time. She woke her husband, who in turn called the obstetrician. The doctor instructed him to bring his wife to the hospital. On arrival at the hospital, she was immediately taken to the labor and delivery room. The nurse on duty placed an oxygen mask on the patient’s face and started an intravenous (IV) line. The patient’s vital signs were monitored closely. An ultrasound Doppler belt also was placed around the mother’s lower abdominal area to monitor the baby’s heart rate. Over the next 20 minutes, the mother continued to bleed (saturating two pads with numerous blood clots), her blood pressure fell, and her heart rate increased. The baby’s heart rate had increased from 155/min to 170/min.

The obstetrician called the operating room and asked the staff to prepare for an emergency cesarean section. The doctor also called for the neonatal resuscitation team (which consisted of a neonatologist, nurse, and respiratory therapist) and asked that they be on standby. The cesarean section was uneventful. The baby was a 7-pound girl. The neonatologist assessed the baby and gave a 1-minute Apgar score of 8 (2 heart rate, 2 respiratory rate, 1 tone, 1 reflex irritability, and 2 skin color). The baby, however, was clearly having difficulty breathing. Auscultation revealed mild bilateral rhonchi and crackles. The baby was transferred to the neonatal intensive care unit (NICU).

In the NICU, the baby was placed in a warmed isolette, and an umbilical artery catheter was inserted. An IV line and nasogastric tube also were inserted. Warm, humidified oxygen was started via a high-flow nasal cannula (HFNC)* at 4 L/min and an Fio₂ of 0.5. Ten minutes later the infant’s vital signs were as follows: heart rate 155 bpm, blood pressure 75/40, and respiratory rate 75/min. The infant’s ventilatory pattern was described by the neonatologist as fast and shallow. In other words, even though the infant was breathing fast and not very deeply, she did not appear to be working hard to breathe. She had no intercostal retractions or nasal flaring at this time. Arterial blood gas values were as follows: pH 7.33, Paco₂ 31, 21, and Pao₂ 42. The baby’s Spo₂ was 75%.

About 2 hours later, however, the baby started to show signs of distress. Her vital signs were as follows: heart rate 170 bpm, blood pressure 75/45, and respiratory rate 110/min. She demonstrated abdominal movements and nasal flaring. Her skin appeared pale and blue. Auscultation revealed moderate to severe bilateral rhonchi and crackles. On the same HFNC settings (4 L/min and an Fio₂ of 0.5), her Spo₂ was 58%. Arterial blood gas values were as follows: pH 7.52, Paco₂ 28, 22, and Pao₂ 35.

A chest x-ray film showed areas of infiltrates and microatelectasis throughout both lung fields, as well as prominent white-lined lung fissures (indicating fluid in the fissures). A starburst pattern was seen at the hilum of the lungs (indicating increased lymphatic fluid). The chest x-ray film also showed air trapping and hyperinflation in the lower lobes (indicating fluid in the airways). The infant’s diaphragms were flattened. The neonatologist charted a diagnosis of TTN in the baby’s progress notes. The doctor also stated that he did not want to mechanically ventilate the baby at this time. The respiratory therapist entered the following assessment in the baby’s chart.

Respiratory Assessment and Treatment Plan

Over the next 48 hours, the baby’s condition progressively improved. She no longer required oxygen therapy, and her breath sounds were normal. Her last room air arterial blood gas values showed a pH of 7.38, Paco₂ 39, 24, Pao₂ 73, and Sao₂ 94%. Her chest x-ray film was normal. The baby was discharged the next day.

Discussion

This case reinforces the importance of observation and inspection in the assessment process. The respiratory care practitioner must continuously inspect and analyze infants with TTN. This baby, for example, born at 35 weeks, may have had respiratory distress syndrome (RDS; see Chapter 34), but the clinical symptoms ruled out the diagnosis. For example, babies with RDS have alveolar collapse and consolidation, whereas babies with TTN have airway trapping and alveolar hyperinflation. In addition, babies with RDS generally breathe hard, quickly, and deeply, whereas infants with TTN usually breathe rapidly and shallowly. In fact, this rapid and shallow breathing pattern often is considered a hallmark of TTN. Certainly, the rapid shallow breathing seen in this baby was caused, in part, by the Increased Alveolar-Capillary Membrane Thickness (Figure 9-10)—and decreased lung compliance—associated with TTN.

Although apnea may occur in these babies, it is not common. Therapeutically, most do quite well with just oxygen via an HFNC. Occasionally, nasal continuous positive airway pressure (CPAP) may be used. Caution, however, must be taken not to give the baby too much CPAP. The lungs of these babies are usually already hyperinflated. Too much CPAP expands the baby’s lungs even more and may cause a tension pneumothorax. CPAP at +3 to +4 cm H₂O is usually safe. Mechanical ventilation rarely is needed for babies with TTN.