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Acute respiratory distress syndrome (ARDS) 

acute inflammatory lung injury that causes non-cardiogenic pulmonary edema by increasing alveolar capillary permeability. 

The thickened diffusion barrier leads to hypoxemia via:

decreased lung compliance

inefficient gas exchange

Pulmonary hypertension

increased physiological dead space

Predisposing factors:

Direct lung injury: pneumonia, gastric aspiration, pulmonary contusion, near drowning, inhalation injury, transfusion-related acute lung injury

Indirect lung injury: sepsis, shock, acute pancreatitis, burns, crush injury, fat embolism, and massive transfusion

Diagnosis criteria for ARDS – Berlin definition (all 4 components must be present):

  1. Acute onset (1 week or less)

  2. Hypoxemia (PF ratio* < 200 mmHg with a minimum of 5 cmH2O PEEP (or CPAP))

  3. Pulmonary edema (bilateral opacities on CXR)

  4. Non-cardiogenic (not caused by cardiac failure)

*PF (PaO2/FiO2) ratio is the ratio of arterial oxygen partial pressure to fractional inspired oxygen. PaO2 value can be obtained from ABG, and FiO2 is 0.21 at sea level (room air) or depends on supplemental O2.


ARDS is a diagnosis of exclusion so consider first: 

Cardiogenic pulmonary edema, severe multilobar pneumonia, acute exacerbation of pulmonary fibrosis, diffuse alveolar hemorrhage, idiopathic acute eosinophilic pneumonia, dissemination of lymphoma/leukemia, and several others. 



Labs: CBC, BMP, LFTs, Coags, VBG followed by ABG, troponin, BNP, lipase, consider DD

Imaging: CXR, POCUS US ECHO and CHEST and consider CT



ED Management:

Supplemental O2

Treat the underlying condition (pneumonia, sepsis, etc.)

Tempered diuresis – non-cardiogenic pulmonary edema takes much longer to respond to treatment than cardiogenic CHF, so avoid being overly aggressive with diuresis, as this may worsen underlying shock and increase likelihood of multi-organ failure

Glucocorticoids — consider steroids when ARDS precipitated by a steroid-responsive process (eg, acute eosinophilic pneumonia)

Be cautious when using non-invasive positive pressure ventilation – the benefit of NIPPV in the initial management of ARDS remains controversial. 

Mostlikely patient will end up being intubated, for vent management suggested strategies are:

Use low tidal volume (6-8 mL/kg) to avoid barotrauma (ideal body weight should be calculated)

And careful FiO2:PEEP ratio titration:


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ARDS severity (mortality) predictor 

Mild ARDS – The PaO2/FiO2 is >200 mmHg, but ≤300 mmHg, on ventilator settings that include positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H2O


Moderate ARDS – The PaO2/FiO2 is >100 mmHg, but ≤200 mmHg, on ventilator settings that include PEEP ≥5 cm H2O

Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilator settings that include PEEP ≥5 cm H2O.

systematic approach to reading CXR and hidden pneumonias

For this pearl of the day we will talk about systematic approach to reading CXR and hidden pneumonias:

The key is to be very systematic when approaching CXRs and that is what radiologists do each time.

Here is the suggested approach by the Brown EM program (

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When ready to review the x-ray, consider the commonly used “A, B, C, D, E, F” system.

A - Airway- trachea, carina, right and left main bronchi

B - Bones and soft tissue- clavicles, ribs- posterior and anterior, vertebral bodies, and sternum on lateral films. Look for any fractures, dislocations, or lytic lesions.

C - Cardiac- cardiac silhouette and mediastinum. The cardiac silhouette should be less than half of the thoracic cavity. AP films exaggerate heart size, so this rule does not apply. Assess the borders of the heart and the hilar structures

D - Diaphragm- right should be higher than left and you should see a gastric air bubble on the left. Is there any free air under the diaphragm? Evaluate the costophrenic angle and pleura (normally invisible due to thinness).

E - Everything else (lines and tubes, pacemakers, artificial valves)

F - Fields- FINALLY, evaluate the lung fields. Lungs are the area of greatest interest, so it is helpful to keep this at the end to prevent distraction. Divide each lung into three “zones” when reading a chest x-ray. These do not correlate with the lobes. Remember, there are 2 lobes on the left (upper and lower) and 3 on the right (upper, middle and lower). 

Hidden pneumonias:

Go through your ABCDEFs and look at the signs of hidden pneumonias:

Silhouette sign

The loss of the normal silhouette of a structure is called the silhouette sign.  - It enables us to find subtle pathology and to locate it within the chest.

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R middle lobe pneumonia


LLL pneumonia

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LLL pneumonia

Hidden areas

There are some areas that need special attention, because pathology in these areas can easily be overlooked:

apical zones

hilar zones

retrocardial zone

zone below the dome of diaphragm

These areas are also known as the hidden areas.

But in doubt get another view or a chest CT.


POTD: Pulmonary Embolism Decision Rules - Beyond the Basics

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Special thanks to Dr. Errel Khordipour for giving this amazing review and Dr. Anna Bona for taking meticulous notes during this talk!


  • PE carries an 8% 30-day mortality after diagnosis (some studies higher)

  • CTA has a very high false positive rate

  • Step 1: based on the patient's history and presentation, do you think the patient has a PE? If yes, proceed. If no, STOP

    • Read more below for nuances re: features that makes a patient risky for PE

  • Step 2: Using your clinical decision rules (Well's, Geneva, or clinical gestalt), is the patient low, medium, or high risk?

    • Low risk: PERC

    • Medium: D-dimer --> then CTA if positive

      • Age adjust your d-dimer if possible

    • High Risk: CTA

  • Step 3: Treat! (or don't treat!)

    • Unstable --> tPA and MICU

    • Stable --> get labs, echo

      • Labs abnormal or echo w/ RV strain --> heparin +/- half-tPA

      • Labs/echo normal --> determine the pt's PESI score

        • High --> heparin

        • Low --> lovenox and discharge

  • Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome

    • May consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence

  • If the study is inadequate, refer to the d-dimer

    • If d-dimer positive, get bilateral lower extremity dopplers

      • Discharge if negative

      • If positive, consider anticoagulation based on risk factors and labs and f/u with PMD for repeat doppler in 3-7 days. 

Interested? Let's get more specific!

Let’s consider a patient that rolls into your emergency department. They’re complaining of chest pain and shortness of breath. You’re working with a medical student and they list pulmonary embolism as a differential diagnosis. How do we risk stratify our patients using our decision making tools.

First off, why do we care? First off, PE is a very much-feared missed diagnosis, which carries an 8% 30-day mortality** after diagnosis (this was much lower than I expected, to put this into context, hemorrhagic strokes carry a 25-40% mortality depending on your source and hip fractures carry a 4-10% mortality rate depending on your source).

**some studies show a 30% mortality, however those were autopsy studies, so it is unknown whether the patients died with a PE or as a result of a PE.

That being said, our testing methods are very much imperfect! The false positive rate on CTA for segmental PE is 25% and even scarier, the false positive rate for subsegmental PEs is 60%!! Not a great test! Plus, a CTA is not a benign test. Contrast can cause anaphylactoid reactions and lifetime risk of malignancy increases with each CT. Plus, once a patient is labeled as having a PE (even subsegmental), they’re much more likely to get scanned in the future.

So let’s talk about how we can determine who is high risk and who is low risk.

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Step 1: Consider the patient’s presentation and history

Vital signs:

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Risk Factors

Prior VTE (PE/DVT): Was the last PE/DVT unprovoked or provoked? More concerning if the last PE/DVT was unprovoked (e.g. the patient was not immobilized for a long period of time). This does not change if testing for hypercoagulability was negative. If provoked, this is less concerning.

Malignancy History: Higher risk with active cancer. This either means active treatment within the last 6 months or metastatic disease. Chemotherapy patients are also more at risk. Not all malignancies are created equal, though! Your risk is even higher with pancreatic cancer, multiple myeloma, colon cancer, glioblastoma, and melanoma.

Immobility: certain types of immobility are higher risk than others! Examples: patients in casts, hospitalized trauma patients (others not at higher risk). Surgical patients are higher risk if they were intubated, received general anesthesia, or received an epidural (e.g. knee surgery, abdominal surgery, neurological surgery). Being in a continuous seated position for > 6 hours might be a risk factor.

OCPs: estrogen of any form increases risk (e.g. OCPs, estrogen replacement, intra-vaginal estrogen). For transgendered patients, more study is needed to determine increased risk.

Pregnancy: Highest risk 2 weeks postpartum. If a patient is pregnant and symptomatic, they have a 70% risk of PE.

Increased risk at age 50: Risk of PE perpetually increases with age. 


Chest painpleuritic chest pain suggest peripheral PE (65%)

Hemoptysis: more indicative of pulmonary hemorrhage, not infarct

Exertional Dyspnea: concerning! You do not need to have chest pain to have a PE!! There is a syndrome that consists of subacute dyspnea that gets worse over days that is predictive of central PE.

Calf pain/Calf swelling: unilateral calf pain (the symptom) and calf swelling (the physical exam finding) are both concerning.

Syncope: corresponds to a large clot burden, but syncope  (likely does not confer an increased likelihood of PE)

Anticoagulation: if they are compliant with anticoagulation, they are less likely to have PE. While this is definitely true with NOACs, with Coumadin, it’s less certain because levels will vary regardless of compliance with medication. Symptoms that are not significant: orthopnea, palpitations, anxiety, dizziness 

Physical Exam Findings:

Abnormal pulmonary exam - decreases likelihood of PE

Clinical signs of DVT - such as calf swelling, redness, etc. increases likelihood 

STEP 1 (cont): Do you, based on the information above, feel that a PE is possible? Meaning, it is ABOVE the 2% threshold for PE. 

Professional recommendation: if the patient has risk factors in 2 or more of the above categories (e.g. vital sign and risk factors, or risk factors and exam findings), and there is no alternative explanation for the patient's presentation, you can say adequately that you have suspicion for PE. 

If you have less than a 2% clinical suspicion for PE, STOP. You do NOT think there is a PE and you do not evaluate further. I repeat - STOP! Evaluate for other suspected pathologies). ACEP Guidelines: 2% is an acceptable cutoff recognizing limitations of testing and risk of false positives (in latest NSTEMI guidelines) Now that you truly think your differential should include PE...  


It doesn't matter if you use Well's Score vs. Geneva vs. Gestalt; all have been shown to be equal. Keep in mind these decision tools SHOULD NOT used to rule out. They are only to RISK STRATIFY. Meaning that you clinically have a suspicion of said disease before you use them. This means you should NEVER document "Well's score low, not likely PE". 

 High risk: get a CTA! May consider empiric heparin before or after CTA.  

Moderate: D-dimer. 

  • In general, you should use age adjusted cutoffs for patients > 50. The conversion depends on which unit you use. 

    • FEU (fibrinogen unit, cutoff usually ~ 500): add the age x 10

    • DDU (d-dimer unit, cutoff usually ~ 250): add the age x 5


STEP 3: Further Management

Ever get a reading that said "evaluation for sub-segmental suboptimal due to motion artifact? What do you do? (Only if vital signs are stable)

  • Get a d-dimer (if not already obtained)

  • Positive --> LE dopplers

    • Yes DVT: anticoagulate!

    • No DVT: discharge with or without anticoagulation based on risk factors and lab values; follow-up with PMD for repeat surveillance ultrasound in 3-7 days. 

  • Negative -->  Discharge 

Now let's go over what you do if a PE is found...


Disposition: depends on if the patient is stable or unstable

Unstable: hypotensive, signs of shock, etc

  • Give tPa and admit to MICU

Stable: labs (BNP, troponin), echo

  • If the patient as abnormal labs or right heart strain, give heparin +/- half-dose tPA and admit to ICU/tele

  • If normal, determine the patient's PESI Score

    • High PESI score --> give heparin and admit to floor

    • Low PESI score --> give lovenox** and discharge

** There inadequate evidence and no FDA approval for NOACs at this time
  Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome, so you may consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence and have the patient f/u with PMD for surveillance of PE symptoms


POTD: TB in the ED

Approach to TB in the ED.

TB might be more common than you think: In NY alone, in 2016, 3.9 cases per 100,000 people, 761 cases in NY in 2016.

Reactivation TB is about 90% of active TB in the United States. 

Who is at high risk?

Those with no “usual source of care”

  • ethnic minorities

  • foreign born

  • HIV patient

  • drug users

  • nursing home patients

  • homeless patients

  • prisoners

Why is it often missed?

Non-specific presentation of TB

  • Cough present: 64%

  • Cough was chief complaint: 20%

  • Only 36% had respiratory complaint at triage

What to do if for high suspicion of TB:

  • Negative pressure isolation room

  • N95 fitted masks

  • CXR and rapid HIV

    • Why HIV test?

      • HIV increases risk of having reactivation TB

      • Immunosuppression will give you atypical cxr findings

  • Looking primarily for active tuberculosis 

Confirmatory testing:

  • PPD: Sensitivity 60-100%

  • QuantiFERON Gold: Sensitivity 81-96%

  • Sputum Looking for AFB on smear (Ziehl-Neelson stain)

    • Variable Sensitivity: 20-60%

    • High specificity: 90-100%

  • Culture

    • Slower results: 7days- 8 weeks

    • Gold standard: 99% sensitivity

  • Rapid TB testing/ Cepheid Xpert MTB/RIF PCR assay

    • Respiratory for assistance in collection

    • 5 ml specimen

    • Rifampin resistance detection

    • Supposed to be a 2 hr turnaround

    • 2 negative sputum specimens at least 8 hrs apart: can remove from isolation

    • Sensitivity about 75-93%

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*This is a sample rule out TB protocol that I adapted from Annals of Emergency Medicine October 2016 :

potd tb.png

Crashing Asthmatic POD

We treat asthma on a daily basis, especially in the peds ED. But what if duonebs x3, steroids, and mag isn’t doing the trick?


  • Nebulized epinephrine may help.

  • If no improvement, start dosing IM epi as if it were anaphylaxis: 0.5 mg (0.01 mg/kg) q 10 min, or start a drip at 5 mcg/min and titrate to effect.

  • Keep going with continuous albuterol nebs.

  • If pharmacy isn’t around to make an epi drip, consider a “dirty” epi drip: 1 mg epi (an entire vial of code cart epi) added to 1 L NS or LR, start at 2 drops per second and titrate up.

  • Alternatively, terbutaline IV can be started: 10 mcg/kg bolus over 10 min and then drip starting at 0.4 mcg/kg/min and titrate up. Terbutaline is a systemic beta agonist. Perhaps they’re so tight that the albuterol you’re nebulizing is not getting where it needs to go due to profound bronchoconstriction. The main adverse effect is here is vasodilation-related hypotension.

By this point, your intubation stuff should be ready and the patient should be in resus.

They also will be having insensible losses so should get as 20 cc/kg IVF bolus.

Still getting worse.

Now this gets interesting.

We are really trying to avoid intubating any asthmatic because of historically poor outcomes with intubation, but sometimes it is unavoidable.

Next step is to try BiPAP. BiPAP could also be started simultaneously with epi. If they can’t tolerate BiPAP, consider ketamine to help them tolerate BiPAP. Ketamine can be dosed numerous ways. If sub-dissociative dosing is pursued, you risk them freaking out. If dissociative dosing, there’s a higher risk of laryngospasm. But consider this, they’re on the brink of getting intubated anyway. If your last-ditch-effort-ketamine gives them laryngospasm, that might be your cue to push a paralytic.

Ketamine and BiPAP has failed.

Time to intubate. Preoxygenate as much as possible. Use the largest ETT possible. First pass success is key. Induce with ketamine 2 mg/kg if they’re not already in the K-Hole. Roc or Sux.

Now they’re intubated

  • They have OBSTRUCTIVE LUNG PHYSIOLOGY. It will take them way longer than usual to exhale. Thus:

  • Low respiratory rate! 8 breaths/min

  • Lung protective tidal volume: 7 cc/kg ideal body weight

  • Minimal PEEP: 0 (ZEEP) - 2 cc H2O

  • High inspiratory flow rate: 90 LPM or I:E 1:5

  • FiO2 100%

  • The ventilator will alarm due to high PEAK pressures. This is OK. Have the respiratory therapist fix it to raise the alarm threshold. The high peak pressures are a consequence of their tight bronchioles.

  • If running into issues with ventilator dyssynchrony, consider paralyzing with cisatracuium

  • Relative hypoxia (sat mid 80s, goal >90%) and hypercarbia (goal >7.15) is OK

  • Aggressive airway suctioning

  • If they begin crashing, disconnect from vent and push on chest to ensure breath stacking is not the issue; rule out pneumothorax; rule out displaced/clogged/kinked ETT

Still doing poorly

  • Call the ECMO team for VV ECMO

  • Anesthesia to set up inhaled anesthetics! e.g. desflurane, sevoflurane. Not tons of evidence, but in case series' and anecdotally, this works really well.

  • Fun fact, CO2 can be dialyzed out of someone rather than ventilated out of someone. However, you need to be in a center where ECMO is also done, because it’s basically putting a piece of the ECMO circuit into a CVVHD circuit. Yes. Blew my mind too.

See Reuben’s algorithm on this at


Hemoptysis Pearl

Let’s Talk Hemoptysis

So your patient thinks they’re coughing up blood...

Initial questions:

  • Are they actually coughing up blood?

  • Or are they having hematemesis?

  • Or epistaxis?

Seems like they actually are. So what could they have? What should you ask in your history?

  • Infectious/inflammatory causes are very common:

    • Acute bronchitis - if you cough enough, you will get some inflammation of your airways and BOOM, hemoptysis)

    • COPD can cause neoangiogenesis to enhance alveolar blood delivery, new fragile blood vessels can rupture

    • In immunosuppressed patients, consider aspergillus and of course TB causing necrotic badness, thus also ask travel history

    • Lung parasites! paragonimiasis, echinococcus, schistosomiasis - ask about travel

    • Neoplastic

      • Bronchogenic carcinoma, bronchial adenoma, squamous cell carcinoma — ask about weight loss and constitutional sx, but know that tumors can also cause massive hemoptysis

      • Structural

        • Aortobronchial fistula — good point, if their giant thoracic aortic aneurysm eroded into one of their bronchi, they would be in extremis to say the least and you wouldn’t be taking this detailed history…

        • Tracheo-innominate fistula — usually 3d-6w after tracheostomy placement, life-threatening and scary, we’ll save management of TIF for another POD

        • Other chronic lung diseases leading to bronchiectasis —> chronic inflammation —>destruction of cartellagenous support —> ruptured blood vessels

        • Vasculitides and collagen-vascular diseases

          • Goodpastures - remember this? Me neither. Autoimmune disease where antibodies attack the basement membrane of the kidneys and lungs — so if known renal failure or hematuria + hemoptysis, think about this

          • Granulomatosis with polyangiitis, SLE, and Behçet’s can all do similar things — h/o autoimmune disorders, family history…

          • Cardiovascular

            • PE can cause a pulmonary infarction —> ischemia/necrosis of lung tissue—> bleeding — ask about PE risk factors!

            • Pulmonary hypertension — ?CHF ?mitral stenosis

OK, enough of that. Let’s break down management.

Are they bleeding a lot? Coughing up large amounts of copious bright red frothy blood in front of you and in respiratory distress? 

Massive Hemoptysis

They need

airway management (often emergent intubation), STAT labs/portable CXR, bronchoscopy, CT surgery/IR/ICU consults, CT scan if stable enough

. Also,

position them on their side with the bleeding lung down

so that gravity doesn’t wash all the blood into their ventilated lung. I like this algorithm from Tinti’s below. The only confusing acronyms are MDCT (multidetector computed tomography) and BAE (bronchial artery embolization).

You may be able to intubate the healthy mainstream

as shown below in order to protect the side you’re able to ventilate. As another option pulmonology/IR may help with placement of a Fogarty catheter to tamponade the bleeding side.

Image not available.

If it’s

mild hemoptysis

, think about whether quarantine and TB workup is needed. If not, they most likely have bronchitis, and may only need a CXR, but refer to this simpler algorithm to tell you when you need a little more. It’s unlikely that they’ll have a diagnosis by the time they leave, but they will continue their workup with PCP or pulmonology for definitive diagnosis and management. 

Image not available.

Bipap Settings

BIPAP Principles:This one goes out to our rising Resus Residents: Bipap has settings that can ameliorate the two primary causes of respiratory failure: oxygenation (CHF, pneumonia) and ventilation (COPD, etc).

Improve hypoxemia two ways: 1. FiO2 2. PEEP (recruit more alveoli) Improve ventilation (hypercarbia) 1. Tidal Volume 2. Respiratory Rate

Settings on Bipap: IPAP – Inspiratory positive airway pressure (e.g. the high number) EPAP – Expiratory positive airway pressure (e.g. the low number) FiO2 – Fraction of inspired O2 (%) There are more, mentioned below, however lets touch on these first.

It is important to understand the cause of your respiratory failure to apply the proper settings. Physiology! Time to move on to practical application:

For HYPOXEMIA generally start with IPAP of 10cmH2O. EPAP can generally start at 5cmH2O


• CHF (hypoxemia): Start at IPAP of 10cmH2O with an EPAP of 5cmH20 (remember you want EPAP here to prevent atelectasis. o Pressure will improve oxygenation o May always increase FiO2 as well to improve oxygenation Conversely, for HYPERCARBIA (COPD) start with a similar IPAP of 5-10cmH20 however EPAP may not even be necessary. o Remember the difference in IPAP and EPAP is related to tidal volume, and this is one thing that effects hypercarbia!! Greater the difference = greater tidal volume. o You may also change the respiratory rate (described below)

Other settings/points: • Respiratory rate as well as I:E (inspiratory:expiratory) ratio can also be adjusted (however these settings may or may not be as helpful in a patient who is breathing on their own). I don’t want to get into this too much, but a couple points: • For HYPERCARBIA increased ventilation is desired with a HIGHER respiratory rate to blow off CO2. • For asthma keep EPAP lower (blow out more air in expiration) and setup a lower I:E ratio (e.g. 1:5) to prevent “breath stacking.” • Titrate by 2 – 3 cmH20 every 5 – 10 minutes. • Max IPAP is generally considered 20cmH2O (this is because lower esophageal sphincter tone is roughly 23 – 25cmH20, don’t over insufflate the stomach). • Remember to get a blood gas.

Sources: JB Life in the Fast Lane Rebel EM UpToDate


Pulmonary Contusion


  • Symptoms include SOB and chest pain.

    • Remember this may manifest as back pain depending on mechanism.

    • Look for in high impact injuries to chest (MVC, fall, pedestrian struck, trampled by livestock, etc)

    • MOA being compression-decompression.


  • Flail chest or crackles (however unlikely unable to auscultate in ED).

  • Observe for crepitus for possible pneumothorax.

  • Seatbelt sign.


  • CXR or CT chest

  • Extent of injury not apparent on CXR for 24-48 hours

  • Areas of lung opacification within 6 hours diagnostic of pulmonary contusion.

  • There are NEXUS chest guidelines (yes, chest!) for patients>14 to omit any imaging in chest trauma (see appendix below) - 98.8% sensitive.

  • Look for homogenous focal or diffuse opacity that may cross typical anatomical landmarks (i.e. lobes).



  • Primarily supportive. Watch for delayed presentation!

  • Consider Bipap; pain control with intercostal block or epidural inpatient. Avoid unnecessary fluids.

  • Up to 40-60% will require mechanical ventilation. Also may be necessary to sedate for pain control.

  • Place good lung in dependent position to improve V/Q mismatch 50% go on to develop ARDS (blood in alveoli activates inflammatory cascade).

  • If not improving - ECMO (V-V) is a possibility.

Bottom line:

  • Monitor patients suspicious for pulmonary contusion - if they have signs of CXR there is a good chance they may need more invasive support (e.g. intubation).

  • Have low suspicion for concurrent injuries including mediastinal and vascular injuries, diaphragmatic rupture, and cardiac contusion.

  • Be aware of patient fluid status and try not to overload patient.


Keywords:  Pulmonary Contusion NEXUS Chest Radiography Chest Trauma


Pearl of the Day: Empyema

Empyema Background - pleural space infection with pus, positive Gram stain/culture, or parapneumonic effusion - predisposing factors: aspiration pneumonia, respiratory disease impairing ciliary function, alcoholism, malignancy, immuncompromise

Causes and Common Organisms - pneumonia -> Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenza - lung abscess, esophageal rupture -> mixed oropharyngeal anaerobes - thoracotomy -> Gram-negative bacilli - immunocompromised pneumonia -> tuberculosis, fungal infections - chest trauma -> S. aureus, Gram-negative bacilli - contiguous abdominal infection -> Gram-negative bacilli, anaerobes

Signs/Symptoms - unresolving fever, cough, dyspnea, pleuritic chest pain, malaise - weight loss, night sweats, anemia - decreased tactile fremitus, friction rub, dullness to percussion

Diagnosis - diagnostic criteria: aspiration of grossly purulent material on thoracentesis and at least one of the following: thoracentesis fluid with positive Gram stain or culture, pleural fluid glucose < 40 mg/dL, pH < 7.1, or LDH > 1000 IU/L

Stages of Disease 1. Exudative: <48 hours, free-flowing pleural effusion amenable to chest tube drainage 2. Fibrinopurulent: fibrin strands form in pleural fluid -> loculations; chest tube drainage is unlikely 3. Organizational: several weeks later; extensive fibrosis with "pleural peel" that restricts lung expansion

Treatment - treat underlying cause - definitive treatment: drainage + antibiotics - respiratory or cardiac distress -> thoracentesis - recommended antibiotics: piperacillin/tazobactam 3.375 - 4.5 g IV q6h or imipenem 0.5 - 1 g IV q6h - may add vancomycin for increased risk of MRSA (e.g., patients recently hospitalized, invasive medical device, from long-term healthcare facility, in contact sports, live in unsanitary conditions) - exudative empyema -> chest tube thoracostomy with antibiotics +/- intrapleural fibrinolytic agents if in fibrinopurulent stage - loculated empyema -> video-assisted thoracoscopic surgery - organizational stage -> surgical removal of fibrous peel

Resources Tintinalli's Emergency Medicine, 8th Edition