ARDS

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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. 

 

Workup:

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

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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.





When your Nose Knows Best

A new sick patient rolls into the busy Emergency Department, satting in the low 80s. As you prepare for a likely intubation, you appropriately assess your patient and see

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PLUS THIS:

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Hopes at bagging this patient's O2 sat up for pre-oxygenation start to dwindle as quickly as your fit summer body over the holiday winter season.

If only there was another way... but wait! Rudolph isn't the only nose that can be useful this holiday season!

Nasal trumpet for ambu bagging:

1. Collect Supplies: nasal trumpet, 6.0 ETT, ambu bag and access to oxygen. 

2. Separate ETT connector from ETT.

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3. Connect ETT Connector to Nasal Trumpet

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4. Connect joined ETT Connector-Nasal Trumpet to your ambu bag attached to the high flow oxygen (>>15 L/min, crank it all the way on)

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 5. Place into patient's nasopharynx, seal patient's mouth, and bag!

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Thanks to Anya for her photography skills!
As always, comments, feedback and input appreciated!

Happy airways and holidays to all! 



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References:

Dr. David Saloum's clinical teaching (even though he was not aware that this would be become today's pearl - thanks anyway!)

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Fancier double trumpet anesthesia option article: http://anesthesiology.pubs.asahq.org/article.aspx?articleid=2492128


POTD: Dexmedetomidine

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Dexmedetomidine

A polysyllabic exercise in typographic errors, dexmedetomidine is a drug more commonly known by its trade name “Precedex.” It was FDA approved in 1999 and has obtained an expanded role in emergency rooms as a generic version has tilted costs downward over the past few years. A 4 mcg/mL manually mixed generic concoction costs about $23 with the trademarked version costing $50. You can have the pre-mixed version for about $50 as well (which appears to be under patent past 2030).

FDA approved indications include sedation for ICU patients that are intubated for less than 24 hours and as a premedication for sedation though the non-FDA uses vary immensely.

It works as an alpha-2 agonist that sedates while providing analgesia through both spinal cord and peripheral antinociception. It works at the locus ceruleus in the medulla to halt transmission of noradrenergic output. This differs from GABA based medications which do not halt sympathetic transmission. Side effects include bradycardia and hypotension. Rapid administration activates alpha 2b receptors and causes vasoconstriction with resultant hypertension/reflex bradycardia. It is metabolized by the liver.

Our case today involves the following head CT of a patient brought to the emergency room unresponsive. They would no longer protect their airway and were subsequently intubated.

Sedating with propofol may be a good idea but what about dexmedetomidine?

 

Dexmedetomidine is a useful tool in managing patients with increased intracerebral pressure with whom you would like to maintain a salvageable neurologic exam. When sympathetic overdrive is a concern, it provides lysis to that environment creating a more stable environment. It creates a mild decrease in ICP and decreases CNS glutamate/catecholamines. If light levels of sedation are used with precedex, patients will rouse easily and then return to sedation when left alone. They simply aren’t as confused because GABA receptors are not the pharmacologic target.

 

To use dexmedetomidine you start with a 0.2-0.7 mcg/kg/hr infusion. The bolus should probably be avoided to avoid hemodynamic surprises.

 

Do you have success employing dexmedetomidine in your ER workflow?

 

 

https://www.ncbi.nlm.nih.gov/books/NBK268691/

Goldfrank, L. R., & Flomenbaum, N. (2006). Goldfrank's toxicologic emergencies. New York: McGraw-Hill.

Lee, K. (2018). The neuroICU book. Ch 20

http://www.micromedexsolution.com/

https://lifeinthefastlane.com/ccc/dexmedetomidine/