Pulmonary Medicine Shock Lung                                      ISSN 1930-6741



 

 

SHOCK LUNG

                                                  

 

                            

 

 

 

Author: Professor. Anil Aggrawal, MD

                                    Shock lung

 Shock lung is known by several names - adult Respiratory Distress Syndrome "ARDS" , adult respiratory failure, diffuse alveolar damage, acute alveolar injury, and traumatic wet lungs

  It is seen in a number of conditions most commonly with mechanical injuries including head injury and infections (table 1). Trauma and infection cause mediators such as cytokines, oxygen radicals, complement, and eicosanoids to be released, which damage the endothelium of the lung capillaries, allowing fluid and proteins to leak across them. This gives rise to intra-alveolar edema and formation of hyaline membranes. These are somewhat waxy in appearance.

It must be noted that it is an exudate which is released in trauma and infection in contrast to simple transudate which is seen in conditions like left-sided congestive heart failure, where simple hemodynamic mechanisms such as increased hydrostatic pressure play a part.

It must be noted that it is an exudate which is released in trauma and infection in contrast to simple transudate which is seen in conditions like left-sided congestive heart failure, where simple hemodynamic mechanisms such as increased hydrostatic pressure play a part.

Interestingly hyaline membrane is also seen in the respiratory distress syndrome of premature newborns, but the pathogenetic mechanism is completely different. In the respiratory distress syndrome of premature newborns deficiency in pulmonary surfactant is seen. At birth, the first breath of life requires high inspiratory pressures to expand the lungs. With normal levels of surfactant, the lungs retain up to 40% of the residual air volume after the first breath; thus, subsequent breaths require far lower inspiratory pressures. With a deficiency of surfactant, the lungs collapse with each successive breath, and so infants must work as hard with each successive breath as they did with the first.

This reduced lung compliance leads to a train of events, resulting in a protein-rich, fibrin-rich exudation into the alveolar spaces with the formation of hyaline membranes. The mechanism can shortly be described as below:

 

hypoventilation -> hypoxemia + CO2 retention -> acidosis -> pulmonary vasoconstriction -> pulmonary hypo-perfusion -> epithelial and endothelial damage -> plasma leak into alveoli -> fibrin + necrotic cells (hyaline membrane)

Pathology

Shock lungs are heavy, firm, red, boggy and almost liver like. They exhibit congestion, interstitial and intra-alveolar edema, and inflammation. The following table gives a complete list of conditions associated with shock lungs.

 

Table1: Conditions Associated With Development Of Shock lungs (Adult Respiratory Distress Syndrome)

1. Infection

    Sepsis*

    Diffuse pulmonary infections*

         Viral, Mycoplasma, and Pneumocystis pneumonia; miliary tuberculosis

    Gastric aspiration*

 

2. Physical trauma/Injury

    Burns   

    Fractures with fat embolism   

    Ionizing radiation

    Mechanical trauma, including head injuries*

    Pulmonary contusions

    Near-drowning

   

3. Inhaled Irritants

    Irritant gases and chemicals

    Oxygen toxicity

    Smoke

   

4. Poisons

    Acetylsalicylic acid

    Barbiturate overdose

    Heroin or methadone overdose

    Paraquat

 

5. Hematological Conditions

    Disseminated intravascular coagulation

    Multiple transfusions

   

6. Other conditions

    Cardiopulmonary Bypass   

    Pancreatitis

    Uremia

   

 

* More than 50% of cases of Shock lungs are associated with these four conditions. ( Sepsis, Infection, Aspiration & Trauma)

 

 

 

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