CONSOLIDATION

Stuff INSIDE the lung


ATELECTASIS

Sleeping lung


Atelectasis refers to a benign temporary alveolar collapse in a portion of the lung. All of the air in the alveoli is ejected, leaving only compact lung tissue behind. The lung shrinks. You can imagine how that dense lung tissue would show up as a white patch on a chest x-ray. Atelectasis is frustrating because it mimics consolidation, but can also be caused by a consolidation! It’s common to see “possible atelectasis” on the radiologist’s read of a chest x-ray. Atelectasis can look mild, but it can also look quite terrifying! Here are the causes. 



Atelectasis is NOT the same thing as a pneumothorax, because the walls of the lung don’t rupture. It usually resolves after a few hours. It doesn’t usually require any treatment. It’s really common in real life, but I don’t think it’ll play a significant role in exams. 

Here is a rather dramatic example of atelectasis. The entire right lung is whited out. I want to draw your attention to the trachea. Notice how it’s not in the midline. Rather it seems to be deviated towards the opacified lung. This is a very important clue. It tells us that the opacity exerts a “pulling force'', rather than a “pushing force.” Atelectasis is the only opacity that pulls, whereas pneumonia, tumors and effusions will all push. 




RESPIRATORY DISTRESS SYNDROMES


Acute Respiratory Distress Syndrome (ARDS) is a common and catastrophic lung complication that can follow any severe illness (most often sepsis > pancreatitis > trauma). During a major illness or lung disease, the immune system normally floods the lung with WBCs and exudates. But if the immune response is disproportionately strong, then ARDS takes place. A few days after admission to the ICU, patients will suddenly develop dramatic dyspnea and hypoxia. Their CXR will show a diffuse bilateral “white out.” ARDS is high yield.


ARDS is caused by diffuse damage to pneumocytes by neutrophils. The damage creates holes allowing exudate spill into the alveoli. The fluid congeals along the wall of the alveoli, forming a hyaline membrane, which makes the alveolar wall really thick which obstructs gas exchange. The AA gradient is increased. Also these hyaline membranes are sticky and promote alveoli collapse with every exhalation. If the type 2 pneumocytes (stem cells) are killed, then the damage becomes permanent as the damaged alveoli are filled in with fibrosis. 

Neonatal Respiratory Distress Syndrome (NRDS) occurs when newborns don’t have enough SURFACTANT (made by type 2 pneumocytes). Surfactant is also called Lecithin or Dipalmitoylphosphotidylcholine. Surfactant production begins in utero during week 24 and reaches peak levels at week 34. The most common cause of NRDS is simple prematurity. But there are two other contributing factors to NRDS, and they each highlight the physiology of surfactant production. Cortisol increases surfactant production, while insulin decreases it. Therefore, NRDS is common in the absence of stress (a speedy c-section spares the fetus from hours of being squished) and with a surplus of insulin (maternal diabetes). 


If a premature newborn has trouble breathing immediately after birth (grunting, accessory muscles, hypoxia, cyanosis), then you should suspect low surfactant levels. You can order a screening test called the L:S ratio (Lecithin:Sphingomyelin). Lecithin is surfactant, while Sphingomyelin is another lipid that stays constant throughout fetal development. Therefore a low ratio suggests NRDS. A CXR will show diffuse granularity / haziness


You can prevent the worst of NRDS by giving mom Steroids before delivery. The steroids help to boost the baby’s surfactant production. Beware of giving too much supplemental O2. It increases free radical production, which can damage the fragile retina (blindness) and lung tissue (bronchopulmonary dysplasia). Bronchopulmonary Dysplasia is the lung injury that results from giving prolonged oxygen to premature kids with NRDS. The hyperoxidative environment results in reduced septation of the alveoli. Babies who spend more than a week or two on the vent are at risk. In the old days, this was a devastating illness. In the modern era, we have more supplemental treatments, so kids are able to come off of the vent much sooner, making this illness much less horrible.