Case Review: 77 y.o. with acute respiratory failure previously discharged with PNA

[Catticus11]

I had a patient that I wasn't truly able to grasp. Below is my report, hopefully i'm including everything of note.

77 y.o. male was recently discharged 1/16 for PNA and new DVT, he was treated with IV Abx and discharged on Eliquis. He had an uncomplicated hospital stay. Then on 1/28, his wife called EMS because he was very dyspneic, per report his "O2 sat was in the 50s" and he was tachycardic. He was admitted to the ED where he was started on Hiflo which was unsuccessful, Bipap which was unsuccessful, and eventually intubated.

Past Med Hx: Paroxysmal afib, HTN, HLD, former smoker, pulmonary fibrosis, OSA, and DM II, diastolic heart failure, thrombocytopenia.

1/28

Patient arrived to unit, intubated. Patient was hypotensive, and started on Neo gtt.

Patient started on Levaquin, IV Solumedrol

Labwork:

WBC normal. Troponin elevated.

Tests/Procedures:

CXR showed atelectasis, bilateral airspace disease.

Vent settings: PRVC, TV 450, Rate 16, PEEP 5, FiO2 50%

1/29

BNP 1520, Patient started on IVP Bumex

Labwork:

Troponin peak at 17.10.

PSA is 12.5.

Tests Procedures:

Bronchoscopy and lavage performed, bronchial culture was negative, and pathology report showed benign cytology. Cell differential reports still pending.

Echo: EF 50-55%, mild-to-moderate AS

Chest CT: extensive bilateral ground glass opacities, worsening PNA, chronic interstitial changes.

1/30

Bumex discontinued.

IVF started at 50 mL/hr.

Started on IVP Lopressure 5mg q4hours. BP stabilized, and Neo gtt weaned off.

Patient started on Heparin gtt, and Eliquis was held for right heart cath.

Plan for weaning was held due to lack of improvement found on morning CXR (per report)

1/31

Right heart cath to rule out cardiogenic pulmonary edema.

Platelet count dropped from 104 to 73, but remained stable at 74 when rechecked.

Tests/Procedures

Right sided heart cardiac catherization -- CVP/RAP 1mmHg, PAOP 15mmHg

Patient experienced incident upon return from cath lab, where patient desatted to 80s, FiO2 increasd to 100, and PEEP was upped to 8. However, vent settings were adjusted back to original settings of 50% and 5 by the end of shift.

Repeat CXR showed worsening airspace disease.

Plan was for open lung biospy.

My assessment:

Patient was sedated for mechanical ventilation with Propofol and Fentanyl, with a RASS of -2. Breath sounds were rhonchorous in all lung fields, with scattered wheezes. Scant tan secretions with deep suctioning. Patient was SR on telemetry, no abnormal heart sounds noted. No edema noted, just bilateral venous stasis changes in legs. No bowel movement since PTA, foley in place draining dark urine at 30-125 mL/hr.

I'm not very good with acute respiratory failure, or understanding the etiology of this acute respiratory failure. I did walk away with several questions particularly:

1. Why an open lung biopsy?

2. There was a debate between the physicians whether this was ARDs, Cancer, interstitial lung disease. One doctor said it couldn't possibly be ARDS because he's tolerating the vent well, and vent settings didn't have to be adjusted much which I don't understand.

3. There was talk of interstitial lung disease, and his pulmonary fibrosis history. I don't understand ILD to be honest, but specifically how it relates to his pulmonary fibrosis.

4. What does "airspace disease" mean? What does "groundglass opacities" mean?

5. General vent question: With deep in-line suctioning, I always thought you always increase FiO2 temporarily to 100% and then you insert the tube until you hit gag, and intermittently suction while pulling out. However, my preceptor told me that this patient did not to be preoxygenated because he's tolerating the vent well and only on an FiO2 of 50%, which I didn't understand. And then my preceptor also told me when I begin to suction, to hold the suction catheter in place for a few seconds to "build pressure within the ET tube to create better suction" and then continuously hold suction as you pull out. I just want to verify.

[offlabel]

1. Why an open lung biopsy?

Because of all of the points you bring up in #2. Tissue bx will point to the actual problem.

2. There was a debate between the physicians whether this was ARDs, Cancer, interstitial lung disease. One doctor said it couldn't possibly be ARDS because he's tolerating the vent well, and vent settings didn't have to be adjusted much which I don't understand.

See #1

3. There was talk of interstitial lung disease, and his pulmonary fibrosis history. I don't understand ILD to be honest, but specifically how it relates to his pulmonary fibrosis.

ILD is broad category of lung disease with different causes. Pulmonary fibrosis is a type of an ILD.

4. What does "airspace disease" mean? What does "groundglass opacities" mean?

I've never heard anyone use "airspace disease" but it undoubtedly refers to disorders of the pulmonary interstitium, which is a fine layer of supportive tissue between alveoli and their airways. Ground glass is just a broad, non specific finding on CT that indicates interstitial thickening and partial alveolar filling. The interstitial tissue is this fine, lacy structure that shows up this way when it thickens.

5. Lots of ways to suction someone. If the patient doesn't desaturate, you're doing it right.

[ghillbert, MSN, NP]

Why biopsy? Because you ruled out cardiac causes of acute respiratory failure with an acceptable LVEF on echo and low filling pressures (CVP 1, WP 15). Mind you this was after aggressive diuresis with bumex, and BNP was elevated on admission so could have still account for some acute resp failure. Then you ruled out infective causes with bronch, BAL, antibiotics, steroids.

Ground glass opacities is a non specific way to describe what the lungs look like on CT scan. It can be from edema, pneumonia, fibrosis etc. Just a radiologists way of describing what they see. "Air space disease" is a nice way to say the lungs don't look right, without actually saying what you think the problem is. Like saying you see "bilateral pulmonary opacities" on a chest xray - so what does that mean? Is there edema, consolidation, atelectasis?

Now you need to figure out why the respiratory failure. So lung biopsy it is. Why open biopsy versus EBUS I don't know, but may be to do with the patient's specifics.

[offlabel]

Why open biopsy versus EBUS I don't know, but may be to do with the patient's specifics.

Isn't EBUS more for lymph node biopsy? Lung tissue biopsy usually a wedge of distal lung segment.

[ghillbert, MSN, NP]

Mostly but depends what they are looking for. They can evaluate intraparenchymal tissue and lesions also with transbronchial lung biopsy, especially if less invasive testing is preferred prior to surgical biopsy.