Ideal Pathophysiology of Pulmonary Contusion

PRECIPITATING FACTOR:
 Motor Vehicle Crashes (trauma from steering
wheel, seat belt)
 Falls
 Bicycle crashes (trauma from handle bars)
 Explosion
 Assault with blunt object

Mechanism of Injury

Blunt Trauma

Rib Fracture Sternum Fracture Pulmonary Contusion Flail Chest

Leakage of serum protein & Injury of lung parenchyma &

Plasma capillary network

Abnormal accumulation of fluid

in the interstitial and intra- Fluid exerts osmotic pressure Enhance loss of fluid from
alveolar space capillaries

Enters the lung and

accumulate in bronchioles Cellular response to injury:
Interfere gas exchange Blood and cellular debris
and alveoli

Hypoxemia, CO2 retention,

Acute Respiratory Failure

Cardiac failure S/S:

 Breath sounds
Tachypnea
tachycardia
Impaired V/Q (Ventilation – Chest pain
Perfusion) Hypoxemia
Blood-tinged secretions &
Respiratory Acidosis
Large amount of mucus & constant
cough but cannot clear the
Acute Kidney Injury secretions
ARDS (Acure Respiratory Disease
Syndrome)

Hypovolemic shock

Death
NARRATIVE DISCUSSION FOR IDEAL PATHOPHYSIOLOGY

Pulmonary contusion is a common thoracic injury and is frequently associated with

flail chest. It is defined as damage to the lung tissues resulting in hemorrhage and localized
edema. It is associated with chest trauma when there is rapid compression and decompression to
the chest wall (i.e., blunt trauma). Pulmonary contusion represents a spectrum of lung injury
characterized by the development of infiltrates and various degrees of respiratory dysfunction
and sometimes respiratory failure. It is often cited as the most common potentially life-
threatening chest injury; however, mortality is often attributed to other associated injuries.
Pulmonary contusion may not be evident initially on examination but develops in the
posttraumatic period; it may involve a small portion of one lung, a massive section of a lung, one
entire lung, or both lungs. Depending on the extent of injury, this type of trauma may be
associated with a mortality rate greater than 50% (Mancini, 2018).

The primary pathologic defect is an abnormal accumulation of fluid in the interstitial and
intra-alveolar spaces. It is thought that injury to the lung parenchyma and its capillary network
results in a leakage of serum protein and plasma. The leaking serum protein exerts an osmotic
pressure that enhances loss of fluid from the capillaries. Blood, edema, and cellular debris (from
cellular response to injury) enter the lung and accumulate in the bronchioles and alveoli, where
they interfere with gas exchange. An increase in pulmonary vascular resistance and pulmonary
artery pressure occurs. The patient has hypoxemia and carbon dioxide retention (Brunner &
Suddarth’s Textbook of Medical-Surgical Nursing, 15th Edition, Vol.1, pag. 592-593).