DESCRIPTION

Pulmonary edema is the accumulation of fluid within the interstitial spaces and alveoli of the lung.

PATHOPHYSIOLOGY

• As fluid for pulmonary edema accumulates in the lung, the exchange of gas within the lung is impaired, resulting in hypoxia.
• The accumulation of fluid within the lung tissue also decreases lung elasticity and further impairs ventilatory function and gas exchange.

Pulmonary edema is classified as cardiogenic and noncardiogenic:

• Cardiogenic pulmonary edema results from left ventricular failure.
  • The fluid "backs up" into the pulmonary vasculature, resulting in increased pulmonary capillary pressure and transudation of fluid into the alveoli.
  • The increase in left atrial pressure is most commonly caused by poor systolic function of the left ventricle but also may result from valvular dysfunction, impaired relaxation of the left ventricle, or increased systemic resistance.
• Noncardiogenic pulmonary edema (adult respiratory distress syndrome) results from increased permeability of the capillaries within the pulmonary vasculature and can result from a direct toxic insult to the lungs (e.g., phosgene inhalation), from systemic drug toxicity (e.g., heroin), or from a systemic inflammatory response (e.g., sepsis).

EPIDEMIOLOGY

Elderly patients are more likely to have cardiac disease, which may increase their susceptibility to cardiogenic edema.

Section Outline:

• DESCRIPTION
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY

Diagnosis is based on symptoms of shortness of breath and clinical findings of rales, or wheezing, and tachypnea.

• Major symptoms include shortness of breath, chest pain, cough, dyspnea on exertion, production of frothy pink sputum, and air hunger.
• Other symptoms may be related to underlying causes (e.g., lethargy from narcotic overdose), and associated physical signs may help identify the poison involved.

DIFFERENTIAL DIAGNOSIS

Nearly all toxicologic etiologies produce noncardiogenic pulmonary edema. Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.

Common Toxicologic Causes

• Opioids are associated with pinpoint pupils and CNS and respiratory depression. Opioid-induced pulmonary edema responds to naloxone, although pulmonary edema also has occurred after naloxone treatment.
• Salicylate is associated with tachypnea, tinnitus, increased anion gap metabolic acidosis, and altered mental status.
• Cocaine or amphetamine use (both intravenous and inhalational) is associated commonly with tachycardia, agitation, and the possible development of hyperthermia, seizures, and dysrhythmia.
• Hydrocarbon aspiration is more common with low-viscosity agents. It is associated with initial persistent cough followed by fever and worsening pulmonary function over several hours.
• Inhalation injury from smoke, acrolein, ammonia, chlorine, chloramine, hydrochloric acid, isocyanates, nitrogen dioxide, ozone, or phosgene usually presents with symptoms of upper airway irritation; symptoms may be delayed with agents that have low water solubility.
• Metal fume or polymer fume fever is associated with fever, myalgia, malaise, and headache following inhalation exposure.
• Tricyclic antidepressants. Pulmonary edema may occur in up to 15% of admitted cases; tricyclic antidepressant toxicity is associated with altered mental status, seizures, widening of the QRS complex, dysrhythmia, and hypotension.
• Organophosphate or carbamate insecticides are associated with lacrimation, bradycardia, vomiting, and diarrhea.

Uncommon Toxicologic Causes

• Hydrochlorothiazide diuretic. Idiosyncratic cases of noncardiogenic pulmonary edema may occur after suicidal ingestion.
• beta-blockers or calcium channel blockers. Cardiac depression can result in cardiogenic pulmonary edema; bradycardia and widened QRS should be evident.
• Colchicine poisoning can result in myocardial depression, which can cause cardiogenic pulmonary edema, and is associated with nausea, vomiting, abdominal pain, and diarrhea.
• Nickel carbonyl, ethchlorvynol, or nitrogen dioxide and cadmium fume poisoning also can result in pulmonary edema.

Other Causes

• Cardiac disease. Myocardial depression from ischemic heart disease, cardiomyopathy, or myocarditis, among other diseases, may result in pulmonary edema.
• Systemic inflammatory syndromes are associated with sepsis, burns, or multisystem trauma, among other conditions.
• Aspiration of gastric contents may result in pulmonary edema.

SIGNS AND SYMPTOMS

• Pulmonary edema results in hypoxia, which is the main cause of signs and symptoms.
• Patients with cardiogenic edema may have findings of congestive heart failure such as a third heart sound, peripheral edema, jugular venous distention, or pulsus alternans.
• Patients with noncardiogenic pulmonary edema should have no evidence of cardiac dysfunction but may have signs caused by the precipitating poison.

Vital Signs

Tachycardia, tachypnea, and hypertension develop initially, followed by bradycardia and hypotension as hypoxia progresses.

HEENT

• Nasal flaring may occur.
• Jugular venous distention may develop in cardiogenic heart failure.

Dermatologic

• Diaphoresis is common.
• Cyanosis may occur as hypoxia worsens.
• Peripheral edema may develop with cardiogenic failure.

Cardiovascular

• Cardiogenic pulmonary edema
  • Patient may have signs of underlying heart disease: S3 and S4 signs of ventricular hypertrophy, pulsus alternans, ventricular lifts, or heart murmurs.
  • Pulmonary artery pressure will be elevated.
• Noncardiogenic pulmonary edema
  • Cardiac function and pulmonary artery pressure are generally normal.

Pulmonary

• Isolated tachypnea may be the first sign of pulmonary edema.
  • As fluid accumulates, rales and wheezing may develop.
  • Further accumulation may produce signs of consolidation such as bronchial breath sounds and egophony.
• Pleural effusions may develop, causing decreased breath sounds and dullness to percussion.
• Hypoxia and hypercarbia may develop as respiratory failure worsens.

Neurologic

Patients will initially be restless and agitated, with progression to CNS depression as hypoxia progresses.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• Arterial blood gases or pulse oximetry are used to assess oxygenation.
• Cardiac enzyme levels are used to assess contribution of myocardial ischemia, as is ECG, which may show evidence of acute or old myocardial infarction, nonspecific changes of myocarditis, or changes consistent with ventricular hypertrophy.
• Serum electrolytes, BUN, creatinine, and glucose detect presence of acidosis and other toxic effects.
• Chest radiographs
  • Cardiogenic edema. Radiographs classically show a butterfly distribution around the hilum, which is associated with Kerley B lines, increased heart size, and cephalization of pulmonary vessels.
  • Noncardiogenic edema. Radiograph may be normal initially, but as the toxicity progresses, septal lines develop, consolidation may occur, and pleural effusions may occur in the presence of normal heart silhouette.

Recommended Tests

• Serum levels of acetaminophen, aspirin, and ethanol are measured, and urine toxicology screen in overdose setting is used to detect occult ingestion.
• Urinalysis and serum creatine kinase are performed on comatose patients to evaluate for rhabdomyolysis.
• Head CT, lumbar puncture, cultures, and other tests are used as needed to assess CNS depression.
• Pulmonary artery catheterization is indicated if the etiology is uncertain and if the procedure may assist in patient management. Increased pulmonary wedge pressures typically indicate a cardiac etiology while normal wedge and pulmonary artery pressures indicate noncardiogenic causes.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
  • Common Toxicologic Causes
  • Uncommon Toxicologic Causes
  • Other Causes
• SIGNS AND SYMPTOMS
  • Vital Signs
  • HEENT
  • Dermatologic
  • Cardiovascular
  • Pulmonary
  • Neurologic
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Therapy should be focused on the rapid treatment of hypoxia and the underlying cause of pulmonary edema.
• Supportive care with appropriate airway management is vital, with specific treatment initiated while supportive care continues.
• Dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

The health-care provider should call the poison control center when:

• cause of pulmonary edema is unclear.
• coingestant, drug interaction, or underlying disease presents unusual problems.

Admission Considerations

All patients with pulmonary edema warrant inpatient treatment.

DECONTAMINATION

• Induced emesis is not recommended.
• Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult (tube size 36-42 French) patients for large ingestion presenting within 1 hour of ingestion or if serious effects are present.
• One dose of activated charcoal (1-2 g/kg) should be administered without cathartic if a substantial ingestion has occurred within the previous few hours.

ADJUNCTIVE TREATMENT

• If serious respiratory depression, difficulty in protecting the airway, or inadequate oxygenation on 100% oxygen develops, the patient should be intubated endotracheally.
• Intravenous access should be established and the patient should be placed on a cardiac monitor.
• Hypotension should be treated with a small isotonic fluid bolus.
  • Overly aggressive fluid administration should be avoided.
  • If the patient does not respond to fluid, vasopressors should be initiated early.
  • Early pulmonary artery catheterization should be considered to optimize therapy.
• Treatment of cardiogenic pulmonary edema includes morphine, furosemide, and nitrates.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

The patient's pulmonary and cardiovascular function should be monitored continuously.

EXPECTED COURSE AND PROGNOSIS

Most toxic causes of pulmonary edema respond well to therapy. Sequelae are determined by underlying cause, however, and permanent pulmonary dysfunction may occur.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS

Chest radiographs may be normal initially.

TREATMENT

Overadministration of fluid may worsen pulmonary edema.

ICD-9-CM 975

Poisoning by agents primarily acting on the smooth and skeletal muscles and respiratory system.

RECOMMENDED READING

Albertson TE, Walby WF, Derlet RW. Stimulant induced pulmonary toxicity. Chest 1995;108:1140-1149.

Reed CR, Glauser FL. Drug induced noncardiogenic pulmonary edema. Chest 1991;100:1120-1124.

Author: Kennon Heard

Reviewer: Luke Yip