Pulmonary Oedema: Causes, diagnostics, management

Introduction
Pulmonary edema refers to the abnormal accumulation of fluid in the lung parenchyma—specifically in the interstitial and/or alveolar spaces—resulting in impaired gas exchange and respiratory compromise. It is a frequent emergency in dogs and cats, commonly stemming from cardiac (cardiogenic) or non-cardiac (non-cardiogenic) causes. Prompt diagnosis and definitive management are essential to reverse hypoxia and stabilize these patients. This lesson explores the causes, diagnostic strategies, and therapeutic interventions for pulmonary edema, aligning with the high standards of care expected for Membership in the Australian and New Zealand College of Veterinary Scientists (MANZCVS) in Veterinary Emergency and Critical Care.

1. Pathophysiology of Pulmonary Edema

1.1. Basic Mechanisms

• Starling’s Forces

  • Hydrostatic pressure, oncotic pressure, and capillary permeability govern fluid movement across the pulmonary capillary membrane.

• Formation of Edema

  • Excess fluid accumulates when transvascular fluid filtration exceeds lymphatic drainage capacity.

1.2. Types of Pulmonary Edema

1. Cardiogenic (Hydrostatic) Pulmonary Edema

   • Increased pulmonary capillary hydrostatic pressure secondary to left-sided heart failure.

   • Commonly seen with degenerative mitral valve disease in dogs, hypertrophic cardiomyopathy in cats.

2. Non-Cardiogenic Pulmonary Edema

   • Increased Permeability (Acute Lung Injury or ALI/ARDS)

     • Inflammatory mediators disrupt alveolar-capillary barriers (e.g., sepsis, severe pneumonia, smoke inhalation).

   • Neurogenic Pulmonary Edema

     • Intense sympathetic discharge after CNS insult (seizures, head trauma) can trigger acute alveolar flooding.

   • Near-Drowning

     • Freshwater aspiration washing out surfactant, damaging alveoli.

2. Causes and Risk Factors

2.1. Cardiogenic Edema

• Left-Sided Congestive Heart Failure

  • Myxomatous mitral valve disease, dilated cardiomyopathy, arrhythmias resulting in reduced forward cardiac output, elevated left atrial pressure.

• Severe Volume Overload

  • Excessive IV fluid rates in a patient with marginal cardiac reserve.

2.2. Non-Cardiogenic Edema

• Vascular Permeability Increases

  • Sepsis, anaphylaxis, pancreatitis, disseminated intravascular coagulation (DIC).

• Electrocution

  • Damaged alveolar epithelium, leading to acute alveolar flooding.

• Severe Hypoalbuminemia

  • Rarely causes isolated pulmonary edema, but may exacerbate fluid shifts if alveolar-capillary membrane is compromised.

3. Clinical Presentation and Diagnosis

3.1. Clinical Signs

• Respiratory Distress

  • Tachypnea, increased inspiratory effort, orthopnea, open-mouth breathing in cats.

• Auscultation

  • Pulmonary crackles, especially in the perihilar or caudodorsal lung fields (cardiogenic).

  • Harsh lung sounds or diffuse crackles in non-cardiogenic edema.

• Cough

  • Often noted in dogs with cardiogenic edema; less consistent in cats.

3.2. Diagnostics

1. Thoracic Radiography

   • Cardiogenic: Perihilar or caudodorsal alveolar pattern in dogs; patchy interstitial-to-alveolar in cats.

   • Non-Cardiogenic: Often dorsocaudal alveolar infiltrates; look for normal cardiac silhouette.

2. Cardiac Evaluation

   • Auscultation for murmurs, gallop rhythms.

   • Echocardiography to confirm structural/functional heart disease.

3. Bloodwork

   • CBC, serum chemistry to identify underlying disease or triggers (e.g., renal failure, sepsis).

4. Pulse Oximetry or Arterial Blood Gas

   • Hypoxemia assessment, alveolar-arterial gradient calculations in severe cases.

3.3. Differentiating Cardiogenic from Non-Cardiogenic

• History: Heart disease signs vs. inciting event (electrocution, near-drowning, sepsis).

• Physical Exam: Cardiomegaly on auscultation or imaging suggests cardiogenic origin.

• Response to Furosemide: Marked improvement in alveolar infiltrates and clinical status strongly suggests cardiogenic fluid overload.

4. Management of Pulmonary Edema

4.1. Stabilization and Supportive Care

1. Oxygen Therapy

   • High-flow nasal cannula, oxygen cage, or mask to address hypoxemia.

2. Sedation

   • Mild sedation (butorphanol, low-dose acepromazine) to reduce anxiety and respiratory effort.

4.2. Cardiogenic Pulmonary Edema

1. Loop Diuretics (Furosemide)

   • IV or IM bolus (1–2 mg/kg), repeated as needed; CRI if severe edema.

   • Monitor renal function and electrolytes.

2. Vasodilators

   • Nitroglycerin ointment or sodium nitroprusside for afterload reduction (cautious use).

3. Positive Inotropes

   • Pimobendan or dobutamine in heart failure with systolic dysfunction.

4. Rate/Rhythm Control

   • Antiarrhythmics if arrhythmias complicate or precipitate edema (atrial fibrillation, VPCs).

4.3. Non-Cardiogenic Pulmonary Edema

1. Address Underlying Cause

   • Antibiotics if infection, anti-inflammatory management (e.g., ARDS).

   • Supportive care for CNS events (neurogenic edema) or near-drowning.

2. Careful Fluid Therapy

   • Aim to maintain perfusion; avoid excessive IV volumes that may exacerbate alveolar flooding.

3. Ventilatory Support

   • Mechanical ventilation if severe respiratory failure (PaO₂ <60 mmHg on supplemental oxygen).

4.4. Monitoring

• Respiratory Rate, Effort

  • Evaluate improvement in respiratory distress as therapy effect.

• Oxygenation

  • Pulse oximetry, arterial blood gases if available.

• Renal Values

  • Especially if repeated diuretics used.

• Thoracic Radiographs

  • Repeat imaging after stabilization to confirm resolution or improvement of edema.

5. Prognosis and Follow-Up

5.1. Prognostic Indicators

• Underlying Disease Severity

  • Reversible triggers (mild congestive episodes) have better outcomes than advanced heart failure or ARDS.

• Acute Response

  • Rapid resolution of edema and improved oxygenation favor a better prognosis.

5.2. Long-Term Management

• Cardiogenic

  • Chronic therapy (furosemide, ACE inhibitors, pimobendan).

  • Regular rechecks for heart disease progression.

• Non-Cardiogenic

  • Monitor for recurrent triggers (e.g., seizures leading to neurogenic edema).

  • Supportive lung protective strategies if chronic or recurrent.

Conclusion

Pulmonary edema is a serious emergency in dogs and cats, with cardiogenic or non-cardiogenic etiologies demanding distinct but overlapping management strategies. Accurate diagnosis hinges on clinical and radiographic findings, supplemented by echocardiography to confirm or exclude underlying heart disease. Immediate stabilization includes oxygen supplementation, sedation, and diuretics in cardiogenic edema, whereas non-cardiogenic edema often emphasizes cause-specific therapy, fluid management, and potential ventilatory support. By mastering these diagnostic and therapeutic principles, veterinarians uphold essential competencies for timely, life-saving intervention consistent with MANZCVS Veterinary Emergency and Critical Care standards.

Suggested References

1. Silverstein, D. C., & Hopper, K. (Eds.). (2014). Small Animal Critical Care Medicine (2nd ed.). Saunders.

2. Ettinger, S. J., Feldman, E. C., & Côté, E. (Eds.). (2017). Textbook of Veterinary Internal Medicine (8th ed.). Elsevier.

3. Fox, P. R., Oyama, M. A., & Macdonald, K. A. (2019). Canine and Feline Cardiology. Wiley-Blackwell.

4. King, L. G. (Ed.). (2013). Textbook of Respiratory Disease in Dogs and Cats. Saunders.

5. Proulx, J. (2017). Pulmonary edema in the critical care patient. Veterinary Clinics of North America: Small Animal Practice, 47(2), 349–366.