Respiratory distress syndrome: Pathology review

Two people are admitted to the emergency department.

Mike, a 55-year-old man, presents with shortness of breath, high fever, and cough.

A chest x-ray was ordered and it showed a right lower lobe infiltrate, which is suggestive of pneumonia.

He was then started on IV antibiotics but the following day Mike became hypoxic and hypotensive.

Because his hypotension didn’t improve despite intubation, IV fluids, and vasopressors, he is diagnosed with septic shock.

Next, a repeat x-ray detected newly-developed bilateral alveolar opacities, heart echography ruled out heart failure, and arterial blood gas analysis revealed a PF ratio of 109 milligrams Mercury.

Then there was Dona, an infant delivered by cesarean section at 36 weeks’ gestational age, with an Apgar score of 9 at birth.

A few hours after delivery, she develops tachypnea, chest wall retractions with nasal flaring, and tachycardia.

Aside from increased work of breathing, her physical examination findings are normal.

A chest x-ray was ordered and it showed diffuse reticulogranular ground glass appearance with air bronchograms.

Now, both people are in respiratory distress.

But first, a bit of physiology.

Normally, when you breathe in, the air reaches the alveoli, which are made up of two types of pneumocytes.

First, type I pneumocytes are thin, and have a large surface area that that facilitate gas exchange.

More important for the exams are the type II pneumocytes, which are smaller, thicker and have the ability to proliferate in response to lung injury.

They are in charge of making a fluid called surfactant which contains various phospholipids.

This lets it act like droplets of oil that coats the inside of the alveoli, decreasing surface tension, so if it’s missing, the alveoli will collapse.