Anatomic Alterations of the Lungs

Drowning is defined as suffocation and death as a result of submersion in liquid. Drowning may be classified further as near drowning, dry drowning, and wet drowning. Near drowning refers to the situation in which a victim survives a liquid submersion, at least temporarily. In dry drowning the glottis spasms and prevents water from passing into the lungs. The lungs of dry drowning victims are usually normal.

In wet drowning the glottis relaxes and allows water to flood the tracheobronchial tree and alveoli. When fluid initially is inhaled, the bronchi constrict in response to a parasympathetic-mediated reflex. As fluid enters the alveoli, the pathophysiologic processes responsible for noncardiogenic pulmonary edema begin—that is, fluid from the pulmonary capillaries moves into the perivascular spaces, peribronchial spaces, alveoli, bronchioles, and bronchi. As a consequence of this fluid movement, the alveolar walls and interstitial spaces swell, pulmonary surfactant concentration decreases, and the alveolar surface tension increases.

As this condition intensifies, the alveoli shrink and atelectasis develops. Excess fluid in the interstitial spaces causes the lymphatic vessels to dilate and the lymph flow to increase. In severe cases the fluid that accumulates in the tracheobronchial tree is churned into a frothy, white (sometimes blood-tinged) sputum as a result of air moving into and out of the lungs (generally by means of mechanical ventilation).

Finally, if the victim was submerged in unclean water (e.g., swamp, pond, sewage, or mud), a number of pathogens (e.g., Pseudomonas) and solid material may be aspirated. When this happens, pneumonia may occur, and in severe cases, acute respiratory distress syndrome (ARDS) may develop. Although the theory has been controversial in the past, it is now believed that the major pathologic changes of the lungs are essentially the same in fresh water and sea water wet drownings; both result in a reduction in pulmonary surfactant, alveolar injury, atelectasis, and pulmonary edema (see Figure 40-1).

The major pulmonary pathologic and structural changes associated with wet drowning are as follows:

Etiology and Epidemiology

Each year 6000 to 8000 people drown in the United States. Drowning is the third leading cause of accidental death in the United States. Drowning is the second leading cause of accidental death in people 5 to 44 years of age. About 15% of children experience near drowning by middle-school age. Drowning is most common in teenagers and in children younger than 4 years of age. More than 40% of drownings are in the under-4 age group. Swimming pools with poor adult supervision are the most common sites of drownings. Up to 33% of adults have experienced near drowning at some time. Alcohol use is present in about 50% of adult drownings. African-American children drown at a rate of 4.5 per 100,000 annually, usually in freshwater lakes and ponds. Caucasian children drown at a rate of 2.5 per 100,000 annually, usually in home pools.

Box 40-1 summarizes the general sequence of events that occurs in drowning or near drowning. Victims submerged in cold water generally demonstrate a much higher survival rate than victims submerged in warm water. Table 40-1 lists favorable prognostic factors in cold-water near drowning.

 OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Near Wet Drowning

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-8), Alveolar Consolidation (see Figure 9-9), Increased Alveolar-Capillary Membrane Thickness (see Figure 9-10), Bronchospasm (see Figure 9-11), and Excessive Bronchial Secretions (see Figure 9-12)—the major anatomic alterations of the lungs associated with near wet drowning (see Figure 40-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Apnea

Apnea is directly related to the length of time the victim is submerged. The longer the submersion, the more likely it is that the victim will not have spontaneous respiration. When spontaneous breathing is present, the respiratory rate is usually increased.

Vital Signs

Increased Respiratory Rate (Tachypnea)

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 J receptors

• Anxiety (conscious patient)

Increased Heart Rate (Pulse) and Blood Pressure

Cyanosis

Cough and Sputum Production (Frothy, White or Pink, Stable Bubbles)

Chest Assessment Findings

• Crackles and rhonchi

CLINICAL DATA OBTAINED FROM LABORATORY TESTS AND SPECIAL PROCEDURES

Pulmonary Function Test Findings (Extrapolated Data for Instructional Purposes) (Primary 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

DECREASED DIFFUSION CAPACITY (Dlco)

Arterial Blood Gases

EARLY AND ADVANCED STAGES OF NEAR DROWNING

Acute Ventilatory Failure with Hypoxemia (Acute Respiratory Acidosis)

pH*	Paco2	*	Pao2
↓	↑	↑ (slightly)	↓

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^*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	↑	↓

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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.

^†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

• Fluffy infiltrates

The initial appearance of the radiograph may vary from being completely normal to showing varying degrees of pulmonary edema and atelectasis (Figure 40-2). It should be emphasized, however, that an initially normal chest radiograph still may be associated with significant hypoxemia, hypercapnia, and acidosis. In any case, radiographic deterioration may occur in the first 48 to 72 hours.

For the first responder, the first objectives in treating a drowning victim are to remove the person from the water and, if the patient has no spontaneous ventilation and pulse, to call for help and immediately initiate cardiopulmonary resuscitation (CPR). When the patient has been submerged for less than 60 minutes in cold water, fixed and dilated pupils do not necessarily indicate a poor prognosis. Because water is an excellent conductor of body heat (cold water can cool the body 25 times faster than air at the same temperature) and because evaporation further reduces an individual’s body heat, the victim’s wet clothing should immediately be removed and replaced with warm, dry coverings.

A 12-year-old boy had a history of a seizure disorder but had not taken his medication for almost a year. On the morning of admission, he participated in a regular swimming class in the junior high school pool. According to the coach on duty, there had been a “pool check” 30 seconds before the patient’s partner reported that the patient seemed to stay under water “too long.”

When taken from the water, he was unconscious and “blue.” He was given mouth-to-mouth resuscitation, and by the time the emergency medical technician (EMT) squad arrived about 20 minutes later, he was breathing at a rate of 10 breaths/min, although his lips and fingers were still cyanotic. He remained comatose and was taken to the nearest hospital.

On admission the patient’s blood pressure was 100/60 and his pulse was 140 bpm. Auscultation of his chest revealed fine crackles bilaterally. Clear secretions were suctioned from his oral airway. An x-ray showed bilateral, diffuse increase in density, which suggested pulmonary edema or possible hemorrhage. His oxygen saturation on 5 L/min O₂ was 72%. Plans were made to transfer him to a nearby tertiary care medical center. The respiratory therapist in the emergency department entered the following assessment moments before the patient transfer.