Diffuse alveolar damage
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Obesity, Sleep & Internal medicine
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| Diffuse alveolar damage | |
|---|---|
| Synonyms | DAD |
| Pronounce | N/A |
| Specialty | Pulmonology, Pathology |
| Symptoms | Acute respiratory distress syndrome, Hypoxemia, Dyspnea |
| Complications | Respiratory failure, Pulmonary fibrosis |
| Onset | Acute |
| Duration | Variable |
| Types | N/A |
| Causes | Sepsis, Trauma, Pneumonia, Aspiration, Inhalation injury |
| Risks | Mechanical ventilation, Severe infection, Shock (circulatory), Multiple organ dysfunction syndrome |
| Diagnosis | Chest X-ray, CT scan, Lung biopsy |
| Differential diagnosis | Pulmonary edema, Interstitial lung disease, Pneumonitis |
| Prevention | N/A |
| Treatment | Supportive care, Mechanical ventilation, Corticosteroids |
| Medication | N/A |
| Prognosis | Variable, often poor |
| Frequency | Common in intensive care unit settings |
| Deaths | N/A |
Diffuse Alveolar Damage (DAD) is a pathological condition characterized by damage to the alveoli, which are the small air sacs in the lungs where gas exchange occurs. It is a major histopathological pattern observed in Acute Respiratory Distress Syndrome (ARDS), a severe form of lung injury that can result from a variety of causes, including infection, trauma, pneumonia, and sepsis. DAD is considered the initial phase of ARDS and is critical in the progression of the disease.
Etiology
The causes of Diffuse Alveolar Damage are varied and often involve direct or indirect injury to the lung. Direct causes include inhalation of toxic substances, pneumonia, and aspiration of gastric contents. Indirect causes are systemic and include sepsis, severe trauma, and pancreatitis. The common pathway in DAD is an intense inflammatory response that leads to damage of the alveolar walls.
Pathophysiology
The pathophysiology of DAD involves three phases: the exudative phase, the proliferative phase, and the fibrotic phase.
- The exudative phase occurs within the first week and is characterized by the leakage of protein-rich fluid into the alveoli, leading to the formation of hyaline membranes. This phase is marked by significant inflammation and edema that disrupt gas exchange.
- The proliferative phase follows, characterized by the proliferation of type II pneumocytes and fibroblasts, which attempt to repair the alveolar epithelium. During this phase, the lung architecture begins to be restored, but the process can also lead to abnormal repair and fibrosis.
- The fibrotic phase is the final stage, where excessive fibrosis can lead to irreversible lung damage and decreased lung function.
Clinical Features
Patients with DAD typically present with rapid onset of respiratory failure. Symptoms include severe shortness of breath, hypoxemia (low blood oxygen levels), and cyanosis. The diagnosis is often made in the context of the underlying condition leading to ARDS and is supported by imaging studies, such as chest X-rays or CT scans, which show diffuse pulmonary infiltrates.
Diagnosis
Diagnosis of DAD is primarily based on clinical presentation and history of risk factors. Imaging studies are crucial for diagnosis, with chest X-rays and CT scans showing diffuse bilateral infiltrates. In some cases, a lung biopsy may be performed to confirm the diagnosis, revealing the characteristic histological features of DAD.
Treatment
Treatment of DAD focuses on addressing the underlying cause and supporting the patient with respiratory support. This may include mechanical ventilation with low tidal volumes and high positive end-expiratory pressure (PEEP) to improve oxygenation while minimizing further lung injury. Management of the underlying cause, whether it be infection, trauma, or another condition, is critical. Supportive care, including fluid management and nutritional support, is also important.
Prognosis
The prognosis of patients with DAD varies and depends on the severity of the initial injury, the underlying cause, and the presence of comorbidities. Despite advances in supportive care, the mortality rate remains high, particularly in severe cases.
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Contributors: Prab R. Tumpati, MD