Anatomic Alterations of the Lungs

During normal intrauterine fetal development, the infant periodically demonstrates normal rapid, shallow respiratory chest movements. This normal action moves pulmonary fetal fluid into and out of the oropharynx while the glottis remains closed. During periods of fetal hypoxemia, however, the infant may demonstrate very deep, gasping inspiratory movements that may force the contents of the naso-oropharynx to pass through the glottis into the airways. The aspiration of minimal amounts of clear amniotic fluid usually is not associated with serious anatomic or functional problems of the lungs. During fetal hypoxemia, however, the aspirate may contain meconium and amniotic fluid—hence the phrase meconium aspiration syndrome (MAS).

MAS is a clinical entity seen primarily in full-term or postterm infants who have had some degree of hypoxemia either prenatally or during the birth process. When the fetus experiences in utero hypoxia, the intestinal response is vasoconstriction, increased gastrointestinal peristalsis, anal sphincter relaxation, and passage of meconium into the amniotic fluid. Meconium is the material that collects in the intestine of the fetus and forms the first stools of the newborn. Meconium is an odorless, thick, sticky, blackish green material. Meconium is a heterogeneous mixture of intestinal tract secretions, amniotic fluid, pulmonary fetal fluid, and intrauterine debris such as epithelial cells, mucus, lanugo, blood, and vernix. Aspiration of meconium leads to one or more of the following complications.

First, the physical presence of the meconium results in upper airway obstruction at birth because of the high viscosity of the meconium. Shortly after birth (within 1 hour), and especially if gasping inspirations are present, clumps of meconium rapidly migrate past the glottis and penetrate the smaller airways (see Figure 32-1). In cases of severe intrauterine hypoxemia, meconium may already be present in the distal airways at birth.

When thick particulate meconium is aspirated into the small airways, the meconium can partially or totally obstruct the airways. Airways that are partially obstructed are affected by a “ball-valve” effect, in which air can enter but cannot readily leave the distal airways and alveoli. This condition in turn leads to air trapping and alveolar hyperinflation. Excessive hyperinflation commonly leads to alveolar rupture and air leak syndromes (see Chapter 35) such as pneumomediastinum or pneumothorax. Totally obstructed airways lead to alveolar shrinkage and atelectasis. This combination of areas of overexpanded alveoli adjacent to areas of atelectasis creates both an increased functional residual capacity (FRC) and a decrease in air flow during exhalation.

The second chain of events that can develop from MAS is chemical pneumonitis, which is characterized by an acute inflammatory reaction and edema of the bronchial mucosa and alveolar epithelium. This reaction commonly leads to excessive bronchial secretions and alveolar consolidation. Meconium also promotes the growth of bacteria, which in turn augments the development of alveolar pneumonitis and consolidation. Meconium aspiration can also interfere with alveolar pulmonary surfactant production. When this occurs, respiratory distress syndrome (RDS) also may complicate MAS.

Third, as a consequence of the hypoxemia associated with MAS, infants with the condition often develop hypoxia-induced pulmonary arterial vasoconstriction and vasospasm, which cause a state of pulmonary hypertension. This results in blood shunting from right to left through the ductus arteriosus and the foramen ovale; intrapulmonary shunts occasionally are seen also. As a consequence, the blood flow is diverted away from the lungs (pulmonary hypoperfusion), which worsens the hypoxemia. Clinically, this condition is referred to as persistent pulmonary hypertension of the neonate (PPHN), previously called persistent fetal circulation (PFC).

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

Etiology and Epidemiology

About 10,000 to 15,000 infants are diagnosed with MAS annually. From this group, about 30% of the infants with MAS require mechanical ventilation, and 10% and 15% of the infants with MAS will develop a pneumothorax. The overall mortality rate is about 4%. As discussed earlier, the fetal passage of meconium is caused by fetal hypoxemia and stress. Fetal hypoxemia causes a vagal response that relaxes anal sphincter tone and allows meconium to move into the amniotic fluid.

MAS rarely is seen in infants younger than 36 weeks’ gestation because the release of meconium requires strong peristalsis and sphincter tone, which usually are not present among preterm infants. Thus, postterm infants (infants older than 42 weeks’ gestation) are especially at risk for MAS, because both strong peristalsis and sphincter tone are present in babies of this age. Other infants who are at high risk for MAS are those who are small for gestational age, those who are delivered in the breech position, and those whose mothers are toxemic, hypertensive, or obese.

 OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Meconium Aspiration Syndrome

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Alveolar Consolidation (see Figure 9-9), Excessive Bronchial Secretions (see Figure 9-12), and Airway Obstruction—the major anatomic alterations of the lungs associated with meconium aspiration syndrome (MAS) (see Figure 32-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Normally, a newborn infant’s respiratory rate is about 40 to 60 breaths per minute. In MAS the respiratory rate generally is well over 60 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

Apnea

Clinical Manifestations Associated with More Negative Intrapleural Pressure during Inspiration

• Intercostal retractions

• Substernal retraction and abdominal distention (seesaw movement)

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

• Flaring nostrils

Chest Assessment Findings

• Wheezes

• Rhonchi

• Crackles

Expiratory Grunting

Cyanosis

Common General Appearance Clinical Manifestations

• Meconium staining (brownish-yellow color) on:

• Skin

• Nails

• Umbilical cord

• Wrinkles and creases in the skin

• Barrel chest (when airways are partially obstructed)

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Extrapolated Data for Instructional Purposes) (Primarily 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 MECONIUM ASPIRATION SYNDROME

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓

SEVERE MECONIUM ASPIRATION SYNDROME

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.

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

When alveolar atelectasis and consolidation are present, the chest x-ray film shows irregular densities throughout the lungs. Although the chest x-ray picture clearly is different from that seen in respiratory distress syndrome, it is difficult to differentiate the x-ray appearance of MAS from that of pneumonia (Figure 32-2).

The chest x-ray film may show local or generalized problem areas. When significant partial airway obstruction, air trapping, and alveolar hyperinflation are present, the chest x-ray film appears hyperlucent and the diaphragms may be depressed. The practitioner should be alert for the sudden development of a pneumothorax or pneumomediastinum in infants with MAS (Figure 32-3).

General Management of Meconium Aspiration Syndrome

The respiratory care practitioner should be proactive whenever an infant is at risk for meconium aspiration. In other words, when the amniotic fluid is found to be stained with meconium—and when the infant is not actively breathing or crying immediately after delivery—the infant should be intubated and the upper airways should be suctioned until all the meconium has been cleared. This measure should be routine for all infants born through particulate meconium, even if meconium is not visualized in the oropharynx. Positive-pressure ventilation should not be administered until a thorough suctioning of the upper airways has been completed, because any particulate meconium remaining in the upper airways likely will be forced into the lower airways in response to positive-pressure ventilation.

After the infant is stabilized and has been transported to the neonatal intensive care unit, vigorous bronchial hygiene (e.g., postural drainage, percussion, suctioning) of the airways should be performed per protocol. Appropriate oxygen therapy should be administered per protocol; in severe cases, mechanical ventilation may be necessary. As already mentioned, however, mechanical ventilation should be avoided or applied cautiously to prevent the possibility of dislodging unseen particulate meconium and pushing it further down the infant’s airways. In addition, a high incidence of pneumothorax is associated with MAS. If some mechanical ventilation is necessary, an inspiration/expiration ratio that permits a long exhalation time (to allow expired gas enough time to flow past partially obstructed airways) should be used. Finally, the infant should be monitored closely for possible superimposed infection. Antibiotics may be indicated and steroids may be required to offset the inflammatory response in chemical pneumonitis. Because a decreased production of pulmonary surfactant is associated with MAS, exogenous pulmonary surfactant may be administered to infants with MAS.

A 38-week-gestation newborn male infant was delivered by emergency cesarean section because of sudden maternal vaginal hemorrhage. The mother was a primigravida Caucasian 19-year-old with a history of no prenatal care. She was a heavy smoker and had an uncertain history of recreational psychopharmaceutical drug use during pregnancy. Rupture of membranes was believed to have occurred about 18 hours before delivery.

At delivery, the infant’s umbilical cord was wrapped once around his neck. He was covered with meconium. He was limp and blue and did not show any spontaneous movement or respiratory effort when he was handed to the neonatologist, who was heading the resuscitation team of one registered nurse and a registered respiratory therapist. While receiving 100% free-flow oxygen to the oral and nasal area, the infant was dried and warmed. With the aid of a laryngoscope, several clumps of meconium were suctioned from the infant’s oral and pharyngeal areas. On two separate passes below the vocal cords, no meconium was visualized or suctioned.

In spite of these efforts, the infant demonstrated no spontaneous respirations, and his heart rate was less than 60 bpm. Because of this, manual ventilation could no longer be avoided. At this time, the respiratory therapist started to ventilate the infant with a bag-valve-mask resuscitation bag, at an Fio₂ of 1.0 and a respiratory rate of 30/min. The nurse started chest compressions at about 90 per minute, with a rhythm of three compressions to one breath. Bilateral crackles and rhonchi were auscultated.

At 1 minute, the Apgar score was 1 for the heart rate. By the third minute, the baby’s heart rate was 80/min. The infant was gasping occasionally and demonstrated some central pinkness. Although compressions were stopped, bagging continued at 40 breaths per minute. At the fifth minute, the Apgar score was 6 (heart rate 2, respirations 1, tone 1, reflex irritability 0, and color 2). The neonatologist decided at this time to intubate the baby with a 3.5-mm endotracheal tube. The respiratory therapist confirmed the correct position of the endotracheal tube by means of (1) careful auscultation, and (2) the appearance of a “yellow” color on the CO₂ detector (i.e., a yellow color confirms CO₂ and a purple color indicates no CO₂). The respiratory therapist then taped the tube at the 8.5-cm mark at the infant’s lips. The baby was transferred to the neonatal intensive care unit (NICU) and placed on a ventilator. Initial ventilator settings were respiratory rate (RR) 40, inspiratory time (Ti) 0.35 sec, Fio₂ 100%, positive inspiratory pressure (PIP) +25, positive end-expiratory pressure (PEEP) +5, and flow 8 L/min. A chest x-ray examination was ordered. At that time the respiratory therapist documented the following in the infant’s chart.