Anatomic Alterations of the Lungs

The respiratory syncytial virus (RSV) moves down the respiratory tract by means of cell-to-cell transfer, causing bronchiolitis and, later, atelectasis and pneumonia in the child. The syncytium is defined as a “multinucleate mass of protoplasm produced by the merging of cells.” At the level of the bronchioles the virus causes neighboring cells to fuse to form a syncytium, hence the name respiratory syncytial virus. The lower airways may also become infected when secretions from RSV-infected upper airways are aspirated.

RSV infection causes peribronchiolar mononuclear infiltration and necrosis of the epithelium of the small airways. This condition leads to edema of the small airways and increased production of mucus. As the condition worsens, the epithelium of the small airways becomes necrotic and proliferates into the airway lumen. The combination of sloughing necrotic tissue, airway edema, and accumulation of mucus leads to (1) a decreased airway lumen, (2) a partially obstructed airway, or (3) a completely obstructed airway. Partial airway obstruction leads to alveolar hyperinflation as a result of a “ball-valve” mechanism (see Figure 36-1). Complete airway obstruction leads to alveolar collapse or atelectasis. Pneumonic consolidation is common. RSV is also referred to as bronchiolitis or pneumonitis.

The following major pathologic or structural changes are associated with RSV infection:

Etiology and Epidemiology

RSV is the most common viral respiratory pathogen seen in infancy and early childhood. Although RSV infection can occur at any age, it is most commonly seen in young children. Almost all children will be infected with RSV by their second birthday. At highest risk for severe respiratory distress syndrome (RDS) are premature infants, children less than 1 year of age, and children with weakened immune systems as a result of a medical condition or medical treatment. Adults with compromised immune systems and those 65 years of age and older are also at increased risk of severe RDS.

RSV is commonly transmitted by young children who are infected with RSV and demonstrate the signs and symptoms of a mild upper respiratory tract infection or a cold—for example, coughing, sneezing, runny nose, decreased appetite, irritability, decreased activity, and respiratory distress. RSV is easily transmitted when droplets containing the virus are coughed or sneezed into the air. Infection occurs when the particles touch the nose, mouth, or eyes of uninfected individuals in the immediate area. RSV can also spread from direct or indirect contact with nasal or oral secretions from an infected person. For example, RSV can be contracted by kissing the face or hands of a child infected with RSV who has a runny nose. Indirect contact may occur when touching the hard surface of a table, crib rail, or doorknob that has been touched by a person infected with RSV. RSV can survive several hours on a hard surface. Common areas of RSV transmission include elementary schools and day care centers. Frequent hand washing and wiping the hard surfaces with a disinfectant may help stop the spread of RSV.

Infants and children infected with RSV usually develop symptoms within 4 to 6 days of infection (range: 2 to 8 days). Most will recover in 1 to 2 weeks. Infected individuals are usually contagious for 3 to 8 days. However, even after recovery an infected person can spread the virus for 1 to 3 weeks. Some patients with a weakened immune system may be contagious for as long as 4 weeks.

Most otherwise healthy children with RSV do not require hospitalization. However, according to the Centers for Disease Control and Prevention, 75,000 to 125,000 children under the age of 1 year are hospitalized each year in the United States because of RSV infection. Of this group, most of the children hospitalized because of RSV are under 6 months old.

Although the outbreak of RSV cases varies by location each year, the number of RSV cases typically increases during the fall, winter, and early spring months. It is not fully known why RSV outbreaks occur in certain regions more than in others, but temperature, climate, and humidity appear to play a role. Figure 36-2 shows the typical RSV season in the United States by region and in Florida according to the Centers for Disease Control and Prevention.

Laboratory Testing for Respiratory Syncytial Virus

RSV infection should be suspected when the clinical manifestations correlate to the time of year, the presence of a local outbreak, the age of the patient, and the history of the illness. Through use of an oropharyngeal or nasopharyngeal secretion sample, RSV is most commonly diagnosed with commercially available antigen assay tests. RSV can also be confirmed with a nasopharyngeal culture. Both the antigen assay test and the nasopharyngeal culture are usually reliable in young children but are less sensitive in older children and adults. Highly sensitive reverse transcriptase–polymerase chain reaction (RT-PCR) assays are also available. The RT-PCR assay may be used to test adults.

 OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Respiratory Syncytial Virus Infection

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Alveolar Consolidation (see Figure 9-9), and Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with respiratory syncytial virus (RSV) infection (see Figure 36-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Normally a newborn’s respiratory rate is about 40 to 60 breaths/min. During the early stages of RSV infection the respiratory rate generally is well over 60 breaths/min. Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

• Stimulation of peripheral chemoreceptors (hypoxemia)

• Decreased lung compliance–increased ventilatory rate relationship

• Stimulation of central chemoreceptors

Increased Heart Rate (Pulse) and Blood Pressure

Apnea

Clinical Manifestations Associated with More Negative Intrapleural Pressures during Inspiration

• Intercostal retractions

• Substernal retraction and abdominal distention (seesaw movement or paradoxic chest motion)

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

• Flaring nostrils

Chest Assessment Findings

• Wheezes

• Rhonchi

• Crackles

Respiratory Secretions (Copious)

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 RESPIRATORY SYNCYTIAL VIRUS INFECTION

Acute Alveolar Hyperventilation with Hypoxemia (Acute Respiratory Alkalosis)

pH	Paco2		Pao2
↑	↓	↓ (slightly)	↓

SEVERE RESPIRATORY SYNCYTIAL VIRUS INFECTION

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	↑	↓

---

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

^†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.

RADIOLOGIC FINDINGS

Chest Radiograph

RSV infection appears as both bronchiolitis and bronchopneumonia in infants and young children. The chest radiograph commonly shows streaky peribronchial opacities associated with air trapping and hyperinflation. Lobar atelectasis frequently is seen, and alveolar and lobar pneumonic consolidation occasionally may be seen also (Figure 36-3).

Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in RSV most commonly is caused by the excessive airway fluid, atelectasis, and consolidation associated with the disorder. Hypoxemia caused by capillary shunting is often partially refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 9-1).

A premature baby boy was born in mid-November at 31 weeks’ gestation. He weighed 1300 g at birth and immediately demonstrated respiratory distress that rapidly progressed into respiratory distress syndrome (RDS; see Chapter 34). During the first hour after delivery, the baby was intubated, placed on a mechanical ventilator, and given a dose of pulmonary surfactant. An umbilical artery line was inserted, and antibiotics were given for several days. Over the next 10 days, the baby was slowly weaned off the ventilator and started on oral feedings. Both the umbilical artery and intravenous (IV) lines were discontinued. Over the next week, the baby gained weight and appeared to be doing well.

Two days later, however, the baby started to demonstrate more periods of apnea and signs of respiratory distress. His vital signs were as follows: heart rate 165 bpm, blood pressure 85/55, respiratory rate 65, and temperature 37° C. He demonstrated nasal flaring and intercostal retractions. Wheezing and rhonchi could be auscultated over both lung fields. His skin appeared cyanotic, and his oxygen saturation by pulse oximetry decreased from 90% to 83%. A chest x-ray examination revealed bilateral streaky infiltrates and scattered areas of atelectasis.

Because of the baby’s history, the time of year, and the increased number of colds and flu reported throughout the medical community, the neonatologist suspected RSV infection. The baby was placed in an oxygen hood at an Fio₂ of 0.50, and a nasopharyngeal swab was obtained and sent to the laboratory. The smear was positive for RSV. Because apnea is sometimes associated with RSV infection, the baby was reintubated and placed back on the ventilator for support. The ventilator settings were as follows: intermittent mandatory ventilation (IMV) mode 15, positive inspiratory pressure (PIP) +20 cm H₂O, positive end-expiratory pressure (PEEP) +4 cm H₂O, flow 6 L/min, and Fio₂ 0.4. His saturation increased to 88%. At this time, the respiratory therapist charted the following SOAP note.