Traumatic Arthrotomy

**Written by:** Parisa Kermani, MD (NUEM ‘23) **Edited by:** Alex Herndon, MD (NUEM ‘21)
**Expert Commentary by**: Matt Levine, MD

Case: A 25-year-old male comes into the ER after a saw accident at work. The patient was using a circular saw to cut wood when it slipped and the saw touched up against his knee. The patient has a 10cm linear vertical laceration over the anterior surface of his left knee (Figure 1). Bleeding is controlled. Patient ambulatory. Reporting 10/10 pain over the laceration.

What are the next best steps for evaluation and treatment of his injury?

Background

Traumatic arthrotomy is defined as a soft tissue injury over a joint that penetrates the joint space. Violation of the joint capsule exposes the sterile intra-articular space to the environment which can result in a deep infection and sepsis. The morbidity associated with septic arthritis is high, so it is important that providers have a high index of suspicion when evaluating wounds over joint surfaces.

The knee joint is the most common joint to be affected, followed by the ankle. Penetrating injuries have a higher rate of capsule violation so a history of knives or bullets should raise suspicion, though MVCs, falls, motorcycle accidents can also result in a deep injury. The capsule has little protection lateral to the patella (Figure 2 & 3), so even if the laceration does not appear deep there is potential that it penetrates the joint space.

Evaluation

Exploration: The first step of evaluation is local wound exploration. It is useful to anesthetize the wound at this point, as this will make the patient more comfortable and allow for a better exam. Irrigate the wound with sterile saline. It is extremely important to visualize the base of the wound. Using a hemostat or q-tip to probe the tissue at the base can be helpful as to not miss any tunneling segments. Keep a close eye out for bubbles, synovial fluid (appears straw colored and oily) or visible bone/tendon as all of these indicate joint involvement. It is important to note that the absence of these findings does not rule out a traumatic arthrotomy.

X-ray: Many times, next step will be to get an X-ray to look for associated fractures. Though this is not the most sensitive test for evaluating for joint space violation, if you see intra-articular air, this signifies joint involvement and no further imaging is required before calling the orthopedic surgeons. Many times, the X-ray will be normal and further testing will need to be completed. Of note, an x-ray is not required if there is no concern about injury to the bone as it is unlikely going to give a definitive answer on traumatic arthrotomy in less obvious cases.
CT Scan: As far as imaging goes, CT scan is the imaging modality of choice for traumatic arthrotomy. Though not currently the gold standard for ruling out joint violation, CT scan has become more accepted as an alternative to saline load testing the joint. Although limited, a 2013 study by Konda et al, where direct arthroscopic visualization or septic arthritis at follow-up were used as the gold standard for diagnosis, found imaging by CT scan to be 100% sensitive and specific for diagnosing traumatic knee arthrotomy. When viewing a CT scan to evaluate for traumatic arthrotomy, the presence of gas in the joint, known as pneumarthrosis, indicates intra-articular extension (Figure 4).

Figure 4: Traumatic arthrotomy on CT scan
Source: Konda et al, 2013

Saline Load Test (SLT): Though not strongly backed by the literature, SLT is a standard tool used to assess for traumatic arthrotomy. SLT is done by performing an arthrocentesis of the affected joint away from laceration, once confirmed in the correct space, sterile saline is injected into the joint and the laceration site is observed for extravasation. The provider should also passively range the joint while injecting to ensure greater sensitivity. Table 1 below summarizes how much sterile saline should be injected to obtain 95% sensitivity for traumatic arthrotomy. Adding methylene blue to the saline has not been proven to increase sensitivity and generally no longer recommended. The sensitivity will be highly variable based on provider experience with the procedure and patient tolerance. It is important to remember that this procedure can be exquisitely painful and special attention should be paid towards the patient’s comfort.

Table 1: Amount of saline for 95% sensitivity SLT

Because strong, conclusive literature is lacking, the choice between CT versus SLT to rule out traumatic arthrotomy will depend on many different factors including provider procedural comfort, local practice patterns, available resources and patient input.

Treatment

Once a diagnosis of traumatic arthrotomy is confirmed through an above modality, orthopedics should be emergently consulted. Tetanus prophylaxis should be updated and the patient should be started on an IV antibiotic that covers both strep and staph. A 1st generation cephalosporin is usually sufficient. Other antibiotics should be considered if injury is from a human/animal bite, happened underwater, or if there is concern for fecal/other contamination. Definitive treatment is joint wash out in the Operating Room.

If the above modalities do not show evidence of arthrotomy the patient’s laceration may be repaired in usual fashion. The patient should be given strict return precautions and have close follow-up for wound/joint reevaluation and suture removal.

Sources

Browning BB, Ventimiglia AV, Dixit A, Illical E, Urban WP, Jauregui JJ. Does the saline load test still have a role in the orthopaedic world? a systematic review of the literature. Acta orthopaedica et traumatologica turcica. 2016;50(6):597-600. doi:10.1016/j.aott.2016.01.004

Gittings D, Dattilo J, Fryhofer G, Martin A, Hast M, Mehta S. The saline load test is effective at diagnosing traumatic arthrotomies of the shoulder. Journal of surgical orthopaedic advances. 2019;28(4):268-271.

Gittings DJ, Fryhofer GW, Hast MW, Steinberg DR, Levin LS, Gray BL. The saline load test is effective at diagnosing traumatic arthrotomies of the wrist. Techniques in hand & upper extremity surgery. 2019;23(2):59-61. doi:10.1097

Jonathan Michael Strong. Saline Load or CT: What’s the Best Test for Traumatic Arthrotomy. Acepnow magazine. 2020; https://www.acepnow.com/article/saline-load-or-ct-whats-the-best-test-for-traumatic-arthrotomy

Konda SR, Howard D, Davidovitch RI, Egol KA. The saline load test of the knee redefined: a test to detect traumatic arthrotomies and rule out periarticular wounds not requiring surgical intervention. Journal of orthopaedic trauma. 2013;27(9):491-497. doi:10.1097/BOT.0b013e31828211f3

Konda SR, Davidovitch RI, Egol KA. Computed tomography scan to detect traumatic arthrotomies and identify periarticular wounds not requiring surgical intervention: an improvement over the saline load test. Journal of orthopaedic trauma. 2013;27(9):498-504. doi:10.1097/BOT.0b013e31828219bc

Metzger P, Carney J, Kuhn K, Booher K, Mazurek M. Sensitivity of the saline load test with and without methylene blue dye in the diagnosis of artificial traumatic knee arthrotomies. Journal of orthopaedic trauma. 2012;26(6):347-349. doi:10.1097/BOT.0b013e3182255167

Nord RM, Quach T, Walsh M, Pereira D, Tejwani NC. Detection of traumatic arthrotomy of the knee using the saline solution load test. The journal of bone and joint surgery american volume. 2009;91(1):66-70. doi:10.2106/JBJS.G.01682

Timothy D. Roberts. Traumatic arthrotomy with pneumarthrosis on plain radiograph of the knee. Western journal of emergency medicine. 2016;17(2):184-185. doi:10.5811/westjem.2015.12.29317

Expert Commentary

What a great review of traumatic arthrotomy! You now have a concise reference that teaches you everything you would probably ever need to know about this tricky diagnosis! These injuries are so uncommon that the first hurdle to overcome is actually considering the diagnosis. If you don’t consider it, then you hopefully just get lucky by a diagnostic x-ray that was ordered for other reasons!

Physical exam and exploration is indeed important but has limitations and does not rule out the diagnosis if the suspicion is high enough. The tract may be small, jagged, or there may be soft tissue destruction that limits your visualization. Be sure to inspect the wound while passively ranging the joint in question since it is often unclear the precise position of the joint (fully flexed, fully extended, or somewhere in between) when the wound occurred. This may bring the wound tract into your field of view. Ideally your exploration should be in a bloodless, painless field and documented as such.

While x-rays lack sensitivity, they are a worthwhile starting point since they are less expensive, noninvasive, readily available, and you can stop if they are positive. X-rays may also better define the extent and trajectory of the wound tract which my either heighten your suspicion or provide reassurance that the trajectory was away from the joint.

If the diagnosis is still in question, I prefer CT in most scenarios. It provides additional information about any associated fractures. CT is painless. Intra-articular air is very easy to see on CT. The downside is increased cost. Saline load testing seems to have more room for error. The joint must be properly entered. Enough fluid must be injected to fill the joint enough to cause visible extravasation. And the diagnosis can still be missed if it is forgotten to range the joint during the SLT. It is also quite painful. Consider all the patients you see who present with a painful joint effusion that has gradually accumulated. In the SLT you are giving the patient a sudden acute joint effusion. Ouch! So just be thoughtful about the route you choose to go.

Matthew Levine, MD

Associate Professor

Department of Emergency Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Kermani, P. Herndon, A. (2022, Apr 25). Traumatic Arthrotomy. [NUEM Blog. Expert Commentary by Levine, M]. Retrieved from http://www.nuemblog.com/blog/traumatic-arthrotomy

Toxic Alcohols

**Written by:** Rafael Lima, MD (NUEM ‘23) **Edited by:** Laurie Aluce, MD (NUEM ‘21)
**Expert Commentary by**: Zachary Schmitz (NUEM ‘21)

Methanol Toxicity

Methanol itself is not toxic to the body. Methanol’s metabolite, formic acid, causes toxicity at serum levels greater than 20mg/dl [1].

Clinical Findings of Methanol Poisoning

CNS sedation
Seizures
Rapid, Deep Breathing
Hypotension
Ocular findings:
- Blindness
- Afferent pupillary defect
- Optic disk hyperemia
- Mydriasis

Ethylene Glycol Toxicity

Similarly, the toxic metabolites of ethylene glycol cause end-organ damage at levels greater than 20mg/dl. The most notable toxic metabolites are glycolic acid and oxalic acid.” [1] .

Clinical Findings of Ethylene Glycol Poisoning

CNS sedation
Seizures
Cranial nerve palsies
Rapid, deep breathing
Hypotension
Hypocalcemia (can result in tetany)
Renal findings:
- Oliguria
- Acute renal failure
- Flank pain
- Hematuria
- Oxalate crystals in the urine under fluorescence

Isopropyl Alcohol Toxicity

Found in hand sanitizers and disinfectants, isopropyl alcohol is a less common source of alcohol poisoning. The parent molecule does exhibit toxic effects here, unlike methanol and ethylene glycol. If untreated, the lethal dose is between 4-8 g/kg [2].

Alcohol dehydrogenase metabolizes isopropyl alcohol into acetone. Because acetone is a ketone, and ketones are not oxidized into carboxylic acids, isopropyl alcohol poisoning does not result in anion gap metabolic acidosis.

Clinical Findings of Isopropyl Alcohol Poisoning

CNS sedation
Disconjugate gaze
Fruity breath odor
Hypotension
Hematemesis
Pulmonary edema

Plasma Osmolal Gap

One of the most reliable laboratory markers of toxic alcohol poisoning is a large osmolal gap. The osmolal gap is defined as the difference between the measured serum osmolality and the calculated, or expected, plasma osmalality:

OSMOLAR GAP = Measured plasma osmolality – calculated/expected plasma osmolality

The common equation for calculating the expected plasma osmolality is listed below [3]. Of note, there are other formulas with slight variations. Using an online calculator can be helpful.

Expected Serum Osmolality=2[Na]+BUN/2.8+Glucose/18

A gap < 10 is considered normal. Any elevation above 10 should raise the clinician’s suspicion of toxic alcohol ingestion.

Note: this tool is not helpful in late presentations as the metabolized forms of the different alcohols do not contribute to the osmolal gap. The calculated gap will be falsely low in late-stage poisoning.

Treatment of Toxic Alcohol Ingestions

Consult your medical toxicologist or poison control center if toxic alcohol ingestion is suspected.

The national poison control center hotline telephone number is 1(800)-222-1222.

Fomepizole

Fomepizole should be used only for methanol and ethylene glycol ingestions. It is not indicated for isopropyl alcohol intoxications [4]. It is an inhibitor of alcohol dehydrogenase (ADH). Evidence shows that it is a superior antidote to ethanol [5].

Loading dose 15 mg/kg IV
Then 10 mg/kg every 12 hours

Continue until blood pH is normal and serum alcohol concentration is less than 20 mg/dL in the presence of retinal or renal injury.

Ethanol

Ethanol works as a competitive inhibitor of ADH, having a higher affinity for the enzyme compared to the other alcohols. Ethanol was used historically before the effects of fomepizole were studied. Fomepizole is now the preferred treatment because the administration of ethanol is more difficult, ethanol causes sedation, and titration of the therapy is challenging in co-ingestions [6]. If ethanol must be used, the preferred route is IV and the studied therapeutic target level is 100 mg/dL [7].

Supplemental Therapy

Methanol poisoning patients should also receive folic acid (50mg IV every 6 hours) [7].

Ethylene glycol poisoning patients should also receive thiamine (100mg IV) and pyridoxine (50mg IV) [8].

Hemodialysis

Consult your nephrologist early if you are considering hemodialysis. Renal replacement therapy should be considered in the following situations [9]:

Anion gap metabolic acidosis with known toxic alcohol ingestion
End-organ damage
- Renal failure
- Vision changes
Unexplained anion gap metabolic acidosis with elevated osmolal gap in suspected toxic alcohol ingestion

References

1. Liesivuori, J. and H. Savolainen, Methanol and formic acid toxicity: biochemical mechanisms. Pharmacol Toxicol, 1991. 69(3): p. 157-63.

2. Slaughter, R.J., et al., Isopropanol poisoning. Clin Toxicol (Phila), 2014. 52(5): p. 470-8.

3. Bhagat, C.I., et al., Calculated vs measured plasma osmolalities revisited. Clin Chem, 1984. 30(10): p. 1703-5.

4. Su, M., R.S. Hoffman, and L.S. Nelson, Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med, 2002. 9(2): p. 175.

5. McMartin, K., D. Jacobsen, and K.E. Hovda, Antidotes for poisoning by alcohols that form toxic metabolites. Br J Clin Pharmacol, 2016. 81(3): p. 505-15.

6. Zakharov, S., et al., Fomepizole versus ethanol in the treatment of acute methanol poisoning: Comparison of clinical effectiveness in a mass poisoning outbreak. Clin Toxicol (Phila), 2015. 53(8): p. 797-806.

7. Barceloux, D.G., et al., American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol, 2002. 40(4): p. 415-46.

8. Ghosh, A. and R. Boyd, Leucovorin (calcium folinate) in "antifreeze" poisoning. Emerg Med J, 2003. 20(5): p. 466.

9. Moreau, C.L., et al., Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. META Study Group. J Toxicol Clin Toxicol, 1998. 36(7): p. 659-66.

Expert Commentary

Thank you for this great review of a difficult subject! The combination of a lack of quick, confirmatory testing with delayed onset of symptoms makes toxic alcohol poisoning an incredibly difficult diagnosis to make. Additionally, even small ingestion can lead to major complications. For example, if a typical four-year-old (19kg) child drank windshield washer fluid that contained 50% methanol (a fairly standard formulation), it would take only 5.7 mL to potentially produce a methanol serum concentration of 25 mg/dL. Given the average 4-year-old’s mouthful is 8.9 mL, you can run into trouble quickly.[1]

We frequently see misuse or misunderstanding of osmol and anion gaps in diagnosing toxic alcohol ingestion when history is unclear. First, although a normal osmol gap is generally less than 10, baseline osmol gaps range from -10 to +14.[2] Therefore, a gap of 16 may represent a true gap of +2 in one person and +26 in another. Second, ethanol must be included in the osmol gap equation. An ethanol concentration of 200 mg/dL would increase your osmol gap by 43.5. Third, given metabolism over time, all values included in an anion gap calculation need to be drawn off of the same blood sample.

These considerations make finding the diagnosis even more complicated, but there are a few things that can help you out. First, an osmol gap > 50 is highly concerning for toxic alcohol. Second, an ethanol concentration > 100 mg/dL is sufficient to block ADH, meaning that few toxic metabolites from methanol or ethylene glycol could be made.[3] This means that an anion gap present with an ethanol > 100 mg/dL is not from toxic alcohol (unless the patient drank the ethanol after the toxic alcohol, which is very rare). Third, sequential values over time can be helpful. Metabolism of toxic alcohols should lead to a decreased osmol gap and increased anion gap over time. Proper use of the osmol and anion gap can help identify patients at high risk for morbidity and mortality while decreasing unnecessary administration of fomepizole, which typically costs thousands of dollars.

References

Ratnapalan S, Potylitsina Y, Tan LH, Roifman M, Koren G. Measuring a toddler's mouthful: toxicologic considerations. Journal of Pediatrics. 2003 Jun;142(6):729-30. doi: 10.1067/mpd.2003.216
Hoffman RS, Smilkstein MJ, Howland MA, Goldfrank LR. Osmol gaps revisited: normal values and limitations. J Toxicol Clin Toxicol. 1993;31(1):81-93. doi: 10.3109/15563659309000375.
Jacobsen D, McMartin KE. Methanol and ethylene glycol poisonings: mechanism of toxicity, clinical course, diagnosis and treatment. Med Toxicol. 1986;1:309-334.

Zachary Schmitz, MD

Toxicology Fellow

Ronald O. Perelman Department of Emergency Medicine

NYU Langone Health

How To Cite This Post:

[Peer-Reviewed, Web Publication] Lima, R. Aluce, L. (2022, Jan 24). Toxic Alcohols. [NUEM Blog. Expert Commentary by Schmitz, Z]. Retrieved from http://www.nuemblog.com/blog/toxic-alcohols

Marine Envenomations

Expert Commentary

An excellent post by Drs. Tandlich and Renshaw. Marine envenomations are common problems around the world. Like with land-based envenomations, the venomous organisms of note vary with geography; jellyfish encountered in Australia are different from those encountered in Florida, for example. As a result, we will focus on major envenomations in the United States.

The invertebrates account for a large but ultimately unknown number of envenomations. Cnidaria includes jellyfish, hydrozoa, anemones, and fire coral. A majority of stings from this group result in painful dermatitis; tentacles create a “whip-like” pattern on the skin, whereas fire coral creates localized skin wheals. The sea nettle and Portuguese man-of-war are of greatest interest, given their potential to cause severe systemic symptoms. Box jellyfish are rare in US coastal waters but produce a life-threatening toxicity.

Initial treatment is somewhat controversial. Many resources advocate for the use of seawater for the initial decontamination, given concern for vinegar triggering nematocyst release in some species common to US waters. However, further research is needed to determine which is best. At this time, seawater is recommended for empiric decontamination in the US unless a box jellyfish is strongly suspected, in which case vinegar is appropriate (a very rare circumstance). Systemically ill box jellyfish envenomations should be treated with pain and blood pressure control. The antivenom is not readily available in the US and is unlikely to be beneficial in the time course it would take to obtain it.

Echinodermata, which includes sea urchins, have mild venom on their spines that can cause local tissue irritation and pain. There are reports of severe envenomations with systemic symptoms, but this is ultimately quite rare. These injuries respond well to hot water immersion. Imaging and local wound exploration for retained spines are recommended. Soaking the wound in vinegar may help dissolve superficial spines.

Of the vertebrates, stingrays and spiny fish are of primary concern.

Stingrays stings are common and can cause serious penetrating trauma but envenomation mainly produces localized pain and swelling. The venom is heat-labile, so significant pain relief can be achieved with hot water immersion. Stingrays stings have the potential for both retained stinger and wound infections; evaluation for retained stinger with radiographs and local wound exploration is recommended along with prophylactic antibiotics.

Spinyfish, in particular stonefish, lionfish, and scorpionfish, have venom located in their spines. Stonefish have the most potent venom of any known fish. Lionfish are not native to the US but have become an invasive species. Human contact with these fish occurs both in the wild and in aquariums. These fish also have heat-labile venom susceptible to hot water immersion. However, systemically ill stonefish envenomations should receive the antivenom as this envenomation can be life-threatening; the antivenom will likely work against other spiny fish too, however, these other envenomations are usually much less severe and rarely require more than hot water immersion and supportive care.

So key learning points:

Most marine envenomations involve heat-labile venom. Hot water immersion is likely to help reduce local symptoms.
Systemic illness is rare but some marine envenomations can produce life-threatening toxicity. Be very wary of a systemically ill envenomation and try to figure out the source due to the limited availability of antivenoms.
Prophylactic antibiotics are recommended for stingray stings as they tend to get infected but otherwise are generally not necessary in most populations. Good wound care, evaluation for retained foreign bodies, and tetanus prophylaxis are the mainstays.
For further information, see this review article

Justin Seltzer, MD

UCSD Health Toxicology Fellow

Emergency Physician, UCSD Health

How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Renshaw, C. (2022, Mar 7). Marine Envenomations. [NUEM Blog. Expert Commentary by Seltzer, J]. Retrieved from http://www.nuemblog.com/blog/marine-envenomations

Crashing Patient on a Ventilator

Expert Commentary

Thank you for this succinct summary of an incredibly important topic. We as emergency physicians spend a lot of time thinking about peri-intubation physiology but the challenges do not end once the plastic is through the cords. The frequency with which our ventilated patients stay with us in the ED has been increasing for years and will likely continue to do so1. This means that managing both acute decompensation and refractory hypoxemia needs to be in our wheelhouse.

The crashing patient on the ventilator can be truly frightening and your post effectively outlines a classic cognitive forcing strategy for managing these emergencies. A truism in resuscitation is to always rule out the easily correctable causes immediately. In this case, it means removing the complexity of the ventilator and making things as idiot-proof as possible. Once you’ve ruled out the life threats like pneumothorax, tube displacement, and vent malfunction, you can try to bring their sats up by bagging. Just make sure that you have an appropriately adjusted PEEP valve attached to your BVM for your ARDS patients; the patient who was just requiring a PEEP of 15 isn’t going to improve with you bagging away with a PEEP of 5.

Once you’ve gotten the sats up and the patient back on the vent, your ventilator display can provide you with further data as to why your patient decompensated. Does the flow waveform fail to reach zero suggesting breath stacking and a need for a prolonged expiratory time? Is the measured respiratory rate much higher than your set rate with multiple breaths in a row indicating double-triggering? The measured tidal volume might fall short of your set tidal volume. This points towards a circuit leak, cuff leak, or broncho-pleural fistula. Maybe you’re seeing the pressure wave dip below zero mid-inspiration and the patient is telling you that they are in need of faster flow, a bigger breath, or deeper sedation. In these situations, your respiratory therapist is going to be your best friend in managing this patient-ventilator interactions2.

As your post alludes to, sometimes patients remain hypoxemic despite our usual efforts and refractory hypoxemia can be an intimidating beast when you’ve got a busy ED burning down around you. If your cursory efforts to maintain vent synchrony by playing with the ventilator dials have failed, there’s no shame in deepening sedation which will work to decrease oxygen consumption and prevent derecruitment. Once sedated, work with your RT to find appropriate PEEP and tidal volumes to meet your goals.

Most patients can be managed with usual lung-protective ventilation but some patients will require more support and you’ve correctly identified several salvage therapies. My general approach is to pursue prone positioning in any patient with a P:F ratio approaching 150 despite optimal vent settings as it has the only strong mortality benefit of the therapies outlined above. Proning in the ED is resource intensive and is probably better pursued as a department-wide protocol rather than you and your charge nurse trying to figure it out in the middle of the night3.

As you’ve pointed out, the neuromuscular blockade has more limited evidence and is not required for prone ventilation. Upstairs, we accomplish this with continuous infusions but in the ED you may be more comfortable using intermittent boluses of intubation dose rocuronium. Just make sure your patient is unarousable. I reach for this if I’m unable to achieve ventilator synchrony with sedation alone as it allows for very low tidal volumes and inverse ratio ventilation. I see inhaled pulmonary vasodilators in a similar light: there’s no data on patient-oriented outcomes but they can make your numbers look prettier while you wait for more definitive interventions such as transfer.

This finally brings me to VV ECMO for refractory hypoxemia. It’s worth considering that while there is some evidence for a mortality benefit for ECMO in ARDS, the evidence base is mixed. The CESAR trial did show a mortality benefit in patients transferred to an ECMO center but only 76% of patients actually received ECMO upon transfer4. The larger and more recent EOLIA trial failed to demonstrate this improvement in mortality5. The conclusion I take from this is that treatment at a high volume center matters and that a boarding patient with refractory hypoxemia warrants an early consideration for transfer to a tertiary center if high-quality ARDS care can’t be accomplished upstairs at your shop.

References

Mohr NM, Wessman BT, Bassin B, et al. Boarding of Critically Ill Patients in the Emergency Department. Crit Care Med. 2020;48(8):1180-1187. doi:10.1097/CCM.0000000000004385
Sottile PD, Albers D, Smith BJ, Moss MM. Ventilator dyssynchrony – Detection, pathophysiology, and clinical relevance: A Narrative review. Ann Thorac Med. 2020;15(4):190. doi:10.4103/atm.ATM_63_20
McGurk K, Riveros T, Johnson N, Dyer S. A primer on proning in the emergency department. J Am Coll Emerg Physicians Open. 2020;1(6):1703-1708. doi:10.1002/emp2.12175
Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet Lond Engl. 2009;374(9698):1351-1363. doi:10.1016/S0140-6736(09)61069-2
Combes A, Hajage D, Capellier G, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. Published online May 23, 2018. doi:10.1056/NEJMoa1800385

Matt McCauley, MD

How To Cite This Post:

[Peer-Reviewed, Web Publication] King, P. Akehtuamhen, A. (2022, Feb 28). Crashing Ventilator Patient. [NUEM Blog. Expert Commentary by McCauley, M]. Retrieved from http://www.nuemblog.com/blog/crashing -vent-patient.

End of Life Care in the ED

**Written by:** Savannah Vogel, MD (NUEM ‘24) **Edited by:** Logan Wedel, MD (NUEM ‘22)
**Expert Commentary by**: Matt Pirotte, MD

References

“Discussing Goals of Care.” UpToDate, www.uptodate.com/contents/discussing-goals-of-care

Ganta, Niharika, et al. “SUPER: A New Framework for Goals of Care Conversation.” SGIM Forum, vol. 40, no. 3, 2017.

“Transitions/Goals of Care.” VitalTalk, 9 May 2019, www.vitaltalk.org/guides/transitionsgoals-of-care

Expert Commentary

This is a nice review of the steps of what can be a very difficult conversation from Drs. Vogel and Wedel; I encourage emergency providers (especially residents) to run towards these situations aggressively and not expect other doctors to begin these challenging discussions.

While their piece is chock full of great tips, let me throw out a few of my own that might help you on your next shift.

“I am worried” is a great phrase to open the conversation. These are confusing topics for families and loved ones, our medical jargon is usually not fully suppressed and generally makes things even worse. While a family member can misunderstand a diagnosis or a prognosis, no one can misunderstand another person’s worry. “I am worried that your husband might not survive this illness” is very clear.
Be the first step. Remember that you might be the first step in what might be a series of conversations. When you are admitted to a patient who you think is in big trouble, have a frank honest conversation with the family but do not force them to make decisions. Then your conversation becomes part of your handoff to the inpatient team. The care of the patient will benefit from open communication upfront that minimizes false hope. Emergency doctors know intuitively what trajectory patients are on, a chronically ill elderly patient presenting with shock requiring pressors have an extremely high mortality risk and we should be clear with families about that.
Reassure and validate at every opportunity. Jim Adams gave me a great pearl when I was training at Northwestern which was that when you see worried first-time parents at 3am in the ED with a benign newborn issue you compliment, reassure, and validate. “This kid looks great, you guys are doing a great job.” Same thing with families. Simple statements like “it’s obvious that you care about them” and “I know you are trying to make the right decision and you’re asking great questions” will go a long way towards helping families process this information.
Humanize the body filled with tubes and lines. A few minutes to ask about the patient at the beginning of a tough conversation go a long way. What did they do for a living? What were their hobbies? Families usually end up smiling a little bit here, reminiscing, and telling you some really cool stuff. Sometimes you find yourself laughing with a family that came in the door sobbing. I find these few minutes spent getting to know your patient also helps to steer discussions towards what the patient would have wanted.
Anticipatory guidance is not just for well-child checks! After tough goals of care conversations especially those that end in decisions to move towards palliative care goals I always do 2 things. First I tell the decision-maker that they are making a good and loving decision, that it is the decision I would make for a member of my family, and to not let anyone tell them otherwise. Second, I insist that the family especially the decision-maker drink a bottle of water and eat a sandwich. We’ve all seen an end-of-life situation generate a second patient with dehydration mediated syncopal episode at the bedside, let’s try to prevent that.

I am forever grateful to my PD at NUEM Mike Gisondi for sparking my interest in this topic, it has been an unbelievable gift to me in my clinical practice. As I frequently say in the ED, you cannot avoid difficult goals of care conversations and then complain about the lack of beds in the hospital.

Matt Pirotte, MD

Program Director & Associate Professor of Emergency Medicine

Vanderbilt University Medical Center

How To Cite This Post:

[Peer-Reviewed, Web Publication] Vogel, S. Wedel, L. (2022, Feb 21). End of Life Care in the ED. [NUEM Blog. Expert Commentary by Pirotte, M]. Retrieved from http://www.nuemblog.com/blog/end-of-life-care

Review of the ATHOS 3 trial

**Written by:** Saabir Kaskar, MD (NUEM ‘23) **Edited by:** Amanda Randolph, MD (NUEM ‘20)
**Expert Commentary by**: Matt McCauley, MD (NUEM’ 21)

Review of the ATHOS 3 Trial: Angiotensin II for the Treatment of Vasodilatory Shock

Angiotensin, first isolated in the late 1930s, in recent years has become the new innovative vasopressor used in intensive care units, a change driven largely by the results of the ATHOS-3 trial. The ATHOS-3 trial in 2017 explored the efficacy of angiotensin II as a vasopressor for severe vasodilatory shock. Severe shock is defined as persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65mmHg and serum lactate <2 despite adequate volume resuscitation. Two classes of vasopressors have been used in the past for hypotension. They are catecholamines and vasopressin-like peptides. The human body, however, employs a third class which is angiotensin. Angiotensin II is an octapeptide hormone and a potent vasopressor that is an integral component of the renin-angiotensin-aldosterone system. It works by activating the ANGII type 1 receptor which subsequently activates a G coupled protein pathway and phospholipase C, thereby inducing vasoconstriction.

The ATHOS-3 trial compared the efficacy and safety of angiotensin II versus placebo in catecholamine-resistant hypotension, which is defined as an inadequate response to standard doses of vasopressors. The study was designed as a phase III multicenter randomized placebo control trial taking place across 75 intensive care units in the United States from 2015 to 2017. The three main inclusion criteria were catecholamine-resistant hypotension (defined as >0.2ug/kg/min of norepinephrine or equivalent for 6-48 hours to maintain a MAP 55-70 mmHg), adequate volume resuscitation (25mL/kg of crystalloid), and features of vasodilatory shock (mixed venous O2 >70% and CVP >8mmHg or cardiac index >2.3 L/min/m2).

Patients in vasodilatory shock that met the criteria of catecholamine-resistant hypotension were randomized to treatment with angiotensin II or placebo. Angiotensin II was initiated at an infusion rate of 20ng/kg/min and adjusted during the first three hours to increase MAP to at least 75mmHg. The primary outcome of the study was the response in MAP three hours after the start of angiotensin II infusion. A response was deemed as a MAP increase of 10mmHg from baseline or a MAP over 75mmHg without an increase in baseline vasopressor infusions. During the first three hours, the angiotensin II group had a significantly greater increase in MAP than placebo (12.5mmHg vs 2.9 mmHg). Angiotensin II also allowed for rapid increases in MAP which permitted decreases in doses of baseline catecholamine vasopressor. Additionally, improvement in the cardiovascular SOFA score was significantly greater in the angiotensin II group than in the placebo group. However, the overall SOFA score did not differ between groups. Rates of adverse events such as tachyarrhythmias, distal ischemia, ventricular tachycardia, and atrial fibrillation were similar in the angiotensin II and placebo groups. Overall serious adverse events that included infectious, cardiac, respiratory, gastrointestinal, or neurologic events were reported in 60.7% of patients who received angiotensin II and 67.1% of patients who received placebo.

The strengths and limitations of the ATHOS 3 trial are critical to how its author’s conclusions should be interpreted. The strengths of the study include that it was a randomized double-blind control trial examining a new class of vasopressor for refractory vasodilatory shock. Refractory shock is a common condition with high mortality, and so the investigation of an additional treatment modality can be of great clinical impact. However, one limitation of the study was that it was underpowered to demonstrate a mortality difference. It showed improvement in blood pressure which is a clinically important parameter but not a patient-oriented outcome. Interestingly, when vasopressin was studied in 2008, it similarly did not show a mortality benefit when added to norepinephrine infusion in septic shock2. It did, however, show a decrease in norepinephrine dosing which parallels the findings of the ATHOS 3 trial.

An additional point of contention with the ATHOS 3 trial is that the manuscript does not report an increase in thrombotic risk. It has been shown that angiotensin II increases thrombin formation and impairs thrombolysis3. The FDA even reports angiotensin II has a risk for thrombosis as there was a higher incidence (13% vs 5%) of arterial and venous thrombotic events in the angiotensin II vs placebo group in the ATHOS 3 trial itself. For this reason, the FDA recommends concurrent VTE prophylaxis with the use of angiotensin II. Further data regarding the thrombotic risk of angiotensin II would be helpful to determine which patient populations the vasopressor should be avoided in.

Overall, the author’s conclusion in the ATHOS 3 trial is that angiotensin II increased blood pressure in patients with a vasodilatory shock that did not respond to high doses of conventional vasopressors. It has been shown to raise mean arterial pressure over 75 mm Hg or by an increase of 10 mm Hg within three hours. The ATHOS 3 trial, however, did not demonstrate a mortality benefit when using angiotensin II. Further studies are needed to elucidate whether Angiotensin II truly improves patient outcomes in vasodilatory shock.

Expert Commentary

Thank you for this great summary of the ATHOS 3 trial. While this trial paved the way for the clinical use of angiotensin II as a vasopressor, you’ve raised some salient points as to why we should approach this emerging intervention with skepticism. The biggest shortcoming in my mind is the primary outcome of the study; it’s not particularly impressive that a vasopressor resulted in higher blood pressures compared to a placebo. Mortality benefit is an extremely elusive goal in critical care research1 but that doesn’t discount the fact that ATHOS 3 wasn’t designed to demonstrate an improvement in any patient-oriented outcome. ICU length of stay, hospital length of stay, ventilator-dependent days, or rate of renal replacement therapy: these are all things that matter to our patients and to our health systems and they are more fruitful targets when we investigate interventions.

There’s been some study of angiotensin II in the years since it has landed in our hospital formularies and there has not been robust data supporting its use. Some of the most recent data come from a multi-center retrospective study that includes patients from Northwestern. This review of 270 patients receiving angiotensin II demonstrated that 67% of patients were able to maintain a MAP of 65 with stable or reduced vasopressor doses. Univariate analysis showed that these patients that responded did have a statistically significant mortality benefit over the patients deemed nonresponders (41% vs 25%)2. If we are going to find a benefit of this drug, further study predicting which patients will be responders is necessary but this study did note that patients already receiving vasopressin and those with lower lactates (6.5 vs 9.5) were more likely to respond. Outside of septic shock, there is interest in the use of angiotensin II in refractory vasoplegia associated with post-cardiac surgery3 and anti-hypertensive overdose4. These are, of course, only hypothesis-generating.

But what does that mean to us clinically in the ED and ICU? This data shows us that angiotensin II can make the blood pressure better but I would never let it distract you from the things we know matter in sepsis resuscitation. Source control timely antibiotics, rational fluid resuscitation, and ruling out other causes of vasopressor refractory shock to include anaphylaxis, hemorrhage, adrenal insufficiency, LVOT obstruction, and any other cause of cardiogenic shock need to be ruled out and addressed. In my personal practice, I make sure to optimize these and start vasopressin shortly after the initiation of norepinephrine. In a patient already on vaso that has stopped responding to escalating doses of norepinephrine, I reach for my ultrasound probe and reassure myself that there isn’t significant sepsis-related myocardial dysfunction because those patients may benefit from a trial of an inotrope like epinephrine. In those with a good cardiac squeeze, I think it’s appropriate to discuss with your intensivist and clinical pharmacist the utility of adding angiotensin II as part of a kitchen-sink approach. Until we have more data about the benefits of this extremely expensive intervention, I wouldn’t lose sleep if you’re unable to secure it for your patient.

References

Chawla LS et al. Intravenous Angiotensin II for the Treatment of High-Output Shock (ATHOS Trial): A Pilot Study. Crit Care 2014; 18(5): 534. PMID: 25286986
Russell JA et al. Vasopressin Versus Norepinephrine Infusion in Patients with Septic Shock. NEJM 2008; 358(9): 877 – 87. PMID: 18305265
Celi A et al. Angiotensin II, Tissue Factor and the Thrombotic Paradox of Hypertension. Expert Review of Cardiovascular Therapy 2010; 8(12): 1723-9 PMID: 21108554
Santacruz CA, Pereira AJ, Celis E, Vincent JL. Which Multicenter Randomized Controlled Trials in Critical Care Medicine Have Shown Reduced Mortality? A Systematic Review. Crit Care Med. 2019;47(12):1680-1691. doi:10.1097/CCM.0000000000004000
Wieruszewski PM, Wittwer ED, Kashani KB, et al. Angiotensin II Infusion for Shock: A Multicenter Study of Postmarketing Use. Chest. 2021;159(2):596-605. doi:10.1016/j.chest.2020.08.2074
Papazisi O, Palmen M, Danser AHJ. The Use of Angiotensin II for the Treatment of Post-cardiopulmonary Bypass Vasoplegia. Cardiovasc Drugs Ther. Published online October 21, 2020. doi:10.1007/s10557-020-07098-3
Carpenter JE, Murray BP, Saghafi R, et al. Successful Treatment of Antihypertensive Overdose Using Intravenous Angiotensin II. J Emerg Med. 2019;57(3):339-344. doi:10.1016/j.jemermed.2019.05.027

Matt McCauley, MD

How To Cite This Post:

[Peer-Reviewed, Web Publication] Kaskar, S. Randolph, A. (2022, Feb 14). Review of ATHOS 3 trial. [NUEM Blog. Expert Commentary by McCauley, M]. Retrieved from http://www.nuemblog.com/blog/review-athos3-trial.

Nursemaid's Elbow

Expert Commentary

This is an excellent summary of the diagnosis and management of radial head subluxation (nursemaid’s elbow) in children. Clinically, as pointed out, these patients are usually toddlers and will come in after an injury to the arm. Usually, the clinical history will involve the child’s arm having been pulled on while the elbow was extended leading to sudden onset of pain and reduced mobility of the arm. The patient will most often be holding the elbow in flexion and be resistant to having it manipulated. In general, I have a low threshold to obtain radiographs on these patients. If the story and exam is classic for a radial head subluxation, imaging is technically not indicated, and reduction can be attempted. However, more often than not, the history can be vague, and the mechanism of injury may be unclear. In this situation, it is better to rule out a fracture first than to attempt a reduction without imaging. Attempted reduction could worsen or lead to displacement of a supracondylar humerus fracture if that is present. Keep in mind that it is not uncommon for the subluxation to reduce spontaneously during the process of obtaining x-rays.

There are two preferred techniques for reduction of a radial head subluxation. The method I start with is to support the patient's elbow and forearm and gently supinate the forearm while flexing the elbow and applying gentle pressure over the radial head. A “pop” sensation will often be felt as the radial head reduces. The other technique that can be used is to hyper-pronate the forearm while maintaining the elbow in a flexed position. Both of these techniques have a high success rate. Typically, the child will start using the arm again, but it may not be immediate. I will typically reassess the patient about 10-15 minutes post-reduction to ensure they are using their arm normally again. If the child is using their arm and able to extend and flex at the elbow without pain, they can be discharged, and no splinting is necessary. If no radiographs were obtained prior to reduction and the patient is not back to baseline post-reduction, x-rays should be obtained to rule out a fracture. Keep a broad differential, especially if the patient is not responding as you would expect or has other vital sign or exam abnormalities.

Jacob Stelter, MD, CAQ-SM

Division of Emergency Medicine | NorthShore University HealthSystem

NorthShore Orthopaedic Institute | Primary Care Sports Medicine

Clinical Assistant Professor | University of Chicago Pritzker School of Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Castillo, R. Luo, F. (2022, Feb 7). Nursemaid’s Elbow. [NUEM Blog. Expert Commentary by Stelter, J]. Retrieved from http://www.nuemblog.com/blog/nursemaids-elbow.

Vasopressor Nonresponse

**Written by:** Elizabeth Stulpin, MD (NUEM ‘23) **Edited by:** Aaron Wibberly, MD (NUEM ‘22)
**Expert Commentary by**: Joshua Zimmerman, MD (NUEM ‘17)

Non-Response to Vasopressors

Shock is defined as a state of cellular and tissue hypoxia resulting in end organ dysfunction. This state may arise due to impaired oxygen delivery to tissues, impaired oxygen utilization by the tissues themselves, increased oxygen consumption, or a combination of these mechanisms. Due to its extremely high morbidity and mortality as well as high healthcare costs, the prompt recognition, diagnosis and resuscitation of shock is key. And for most forms, EM physicians are not typically shocked by shock. They have a toolbox of strategies, mainly fluids and vasopressors, to stabilize these critically ill patients.

However, what happens when the trusted treatment paradigm fails? There is a subset of patients who, despite aggressive conventional resuscitation, have an inadequate hemodynamic response and develop refractory shock. This is seen in approximately 7 percent of patients, with short-term mortality ranging from 50 to 80 percent. Due to this significantly lower incidence and increased mortality, alternate causes for refractory shock must be considered when vasopressors do not have the desired effect.

Acidosis

Acidosis in shock states can present from multiple different sources, including sepsis, hypoxemia, ingestions, hyperlactatemia from hypoperfusion, amongst others. With increasing acidosis, calcium influx is reduced, contractility is inhibited and the binding affinity of pressors is reduced, all of which lead to excess vasodilation and refractory hypotension. While bicarbonate is sometimes given in an effort to increase cellular pH, it is controversial for any pH >7.0. At those levels, bicarbonate administration has not been shown to improve cardiac output, MAP or pressor response. While a bicarbonate drip and hyperventilation can temporize an acidosis, emergent HD or CRRT is a definitive treatment if the cause cannot be quickly reversed.

Adrenal Insufficiency

Cortisol has a myriad of functions in the body, not limited to its synergistic effects with catecholamines to help cause vasoconstriction. Thus, when the adrenal glands are chronically suppressed and then experience an acute stressor, hypotension can ensue. The most common cause of chronic suppression is long-term steroid use, and a stressor can include surgery, infection, hypovolemia, pregnancy, medications, or reduced steroid use. Clues that suggest adrenal insufficiency include nausea/vomiting, cutaneous hyperpigmentation, and multiple electrolyte abnormalities (hyponatremia, hyperkalemia, hypoglycemia). Previously healthy individuals, in the setting of critical illness, can also infrequently decompensate into a state of relative adrenal insufficiency. To reverse these effects as well as refractory hypotension, hydrocortisone is the preferred agent due to both its glucocorticoid and mineralocorticoid properties. A loading dose of 100mg IV should be given, followed by 50mg every 6 hours thereafter.

Alternate Shock

Not all shock is declared equal. For example, a patient in cardiogenic shock will likely worsen with the administration of fluids and the wrong vasopressors. Similarly, obstructive shock as seen in massive PEs, tension pneumothoraces or cardiac tamponade will not improve without addressing the cause.

Anaphylaxis

Anaphylaxis may present as hypotension alone. Thus, it may easily be confused with a different form of shock and treated with vasopressors such as norepinephrine and vasopressin, which are not first line for anaphylaxis. Along with using epinephrine as the pressor of choice and other conventional therapies for anaphylaxis, there are alternate medications available for persistent refractory hypotension. One of these is methylene blue. While typically reserved for treatment of methemoglobinemia, the cellular mechanism of methylene blue can decrease vasodilation. Data suggest that this effect can be seen with a one-time dose of 1-2mg/kg.

Hemorrhage

Often a common cause of refractory shock in the post op setting, bleeding can be obscure in its early stages before a hemoglobin drop is appreciated or before the patient develops abdominal distension and flank dullness (retroperitoneal bleed). If concerned, empiric uncrossed unmatched blood can be transfused.

Hypocalcemia

Calcium homeostasis is necessary for the proper maintenance of myocardial contractility and vascular tone. Hypocalcemia can be hinted at through history or by hints such as a prolonged QTc on an ECG. Those at higher risk of hypocalcemia (vitamin D deficiency, ESRD, hyperparathyroidism, burns, multiple blood transfusions, etc.) may have greater severity of shock with increased mortality. In repleting calcium, co-administration of phosphorous and magnesium may allow for reversal of the patient’s shock state.

Hypothyroidism

Decompensated hypothyroidism can have profound effects, including bradycardia, impaired myocardial contractility, and decreased peripheral vasoconstriction. However, even subclinical hypothyroidism with an elevated TSH but normal T4 increases risk of poor outcomes due to effects on cardiac function. While the diagnosis of hypothyroidism can be delayed by lab results, clues to the diagnosis include thyroidectomy scar, non-pitting edema of the extremities, macroglossia, altered mental status, hypoglycemia and hypothermia. Initial hypotension may not respond to vasopressors, but shock should improve once thyroid hormone is given. Stress dose steroids (hydrocortisone 100mg IV) should also be given due to the association between adrenal insufficiency and hypothyroidism, and giving thyroid hormone without steroids can precipitate adrenal crisis.

Ingestions

When in doubt, look at the medication list! Both beta blocker and calcium channel blocker toxicity can cause profound myocardial depression, bradycardia and hypotension due to their inhibition of calcium signaling. Refractory hypotension can be overcome with the use of direct cardiac pacing, calcium, glucagon, or high dose insulin. And if all else fails, ECMO can overcome medication toxicity until it can be fully metabolized or cleared.

When conventional resuscitation for shock with fluids, vasopressors and/or inotropes fails, it is time for a cognitive pause. By running through this list of alternate causes of refractory shock, other methods of resuscitation can be added to improve patient outcomes and stabilize the patient.

Sources:

1) Amrein K, Martucci G, and Hahner S. Understanding adrenal crisis. Intensive Care Medicine. 2018; 44(5): 652-655.

2) Boyd J, Walley K. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Curr Opin Crit Care. 2008;14:379-83.

3) Farkas J. Decompensated Hypothyroidism. The Internet Book of Critical Care. 2016. Accessed https://emcrit.org/ibcc/myxedema/

4) Ho H, Chapital A, and Yu M. Hypothyroidism and Adrenal Insufficiency in Sepsis and Hemorrhagic Shock. Arch Surgery. 2004; 139(11):1199-1203.

5) Kerns W. Management of B-Adrenergic Blocker and Calcium Channel Antagonist Toxicity. Emergency Medicine Clinics of North America. 2007; 25: 309-331.

6) Levy B, Collin S, Sennoun N, et. al. Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside. Intensive Care Medicine. 2010; 36: 2019-2029.

7) Manji F, Wierstra B, and Posadas J. Severe Undifferentiated Vasoplegic Shock Refractory to Vasoactive Agents Treated with Methylene Blue. Case Reports in Critical Care. 2017.

8) Minisola, S et al. Serum Calcium Values and Refractory Vasodilatory Shock. Chest. 2019; 155(1): 242.

9) Nandhabalan P, Ioannou N, Meadows C and Wyncoll D. Refractory septic shock: our pragmatic approach. Critical Care. 2018; 22(1):215.

10) Smith L, and Branson B. Refractory Hypotension – Diagnosis and Management in Surgical Patients. California Medicine. 1961; 95(3): 150-155

11) Velissaris D, Karamouzos V, Ktemopoulos N, Pierrakos C, and Karanikolas M. The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate. Critical Care Research and Practice. 2015.

12) Wang H, Jones A, and Donnelly J. Revised National Estimates of Emergency Department Visits for Sepsis in the United States. Critical Care Medicine. 2017; 45(9): 1443-1449.

Expert Commentary

Dr. Stulpin's review of a very critical topic is well articulated and concise. I would like to particularly emphasize her final points before delving into the details. As she pointed out, patients failing to respond to typical resuscitative efforts represent quite a quagmire to the ED physician. It is easy to arrive at premature closure and presume all shock to be sepsis simply needing more fluids or vasopressors. However, there is significant risk in this practice, and I would thus advocate very strongly for a “pause” and thorough reassessment of the patient’s presentation and condition. Much akin to a pre-procedural time out, this should be deliberate and uninterrupted to prevent diagnostic momentum from building and arriving at a premature closure on the etiology of the patient’s condition.

This review covers much of the differential and pathophysiology that is germane to a discussion of refractory shock. Rather than review this in detail, I would like to discuss a practical approach to application of this knowledge at the bedside. So, as we approach the patient who is refractory to standard resuscitation, one’s first task is to confirm the patient is receiving the desire therapy and that this is truly shock refractory to intervention. Check all access points for infiltration –the single most reversible cause for refractory hypotension is that the patient is not receiving fluids/vasopressors, etc. due to inadequate access. Check dosing and confirm with nursing that infusions have been running appropriately. If access is the issue, I would advocate placing a more reliable form such as central access or, in the very unstable, IO access early in the reassessment. While I am an advocate for US guided access in stable patients and feel that this is often a great tool, this is a scenario I would advocate against US guided peripheral access. This form of access is often time consuming, and more importantly, signs of infiltration are less evident in deeper IV sites which is a serious concern if you are running peripheral vasopressors.

Presuming your access is adequate, the next task is to reassess perfusion in its entirety. While not mandatory, this is a point where I would consider placing an arterial line for optimally reliable BP monitoring. One must perform a complete re-examination as well. If not already completed, a rectal exam for the occult GI bleeding. One should additionally particular attention on reassessment to skin and perfusion. Check capillary refill, skin temperature and coloration as a matter of habit for cases of refractory shock. Cool extremities are not typically associated with distributive shock and should make you consider shock states with high SVR such as cardiogenic or acute blood loss. In addition, a repeat skin exam may reveal new rashes – I look specifically for the presence of petechiae, purpura or urticaria. Urticaria should prompt consideration of anaphylaxis. If the patient has received any antibiotics yet this is an important consideration given antibiotics are one of the most common medication precipitants of anaphylaxis and this may be the source of their worsening shock state.

After completing your thorough exam, I strongly advocate for a sonographic assessment as well. This is where the RUSH exam, or at least a modified version, fits well into patient assessment and can offer a great deal of information. I pay particularly close attention to the cardiac and abdominal windows. This can aid in the rapid diagnosis of an obstructive shock state such as cardiac tamponade, or acute RV failure in the setting of massive PE. Free intra-abdominal fluid should be considered hemorrhage until proven otherwise in the shock patient. One reminder is that when assessing for occult bleeding, the FAST exam views are an excellent tool but not sufficiently sensitive for definitive rule out. In particular, the FAST exam lacks sensitivity for retroperitoneal bleeding and therefore if there remains high clinical concern, CT imaging should also be considered.

Once a thorough re-examination is completed, reconsider the patient’s medications as another source. Patients are on a myriad of antihypertensives and other agents that can lower blood pressure. Many of the pathways that metabolize or eliminate these drugs are compromised in a state of hypoperfusion and can lead to a synergistic worsening of hypotension. One example of this is the case of BRASH Syndrome. In addition to antihypertensives, a review of the patient’s medication list should include a particular search for steroids or other adrenal replacements such as fludrocortisone. An extremely important cause of refractory hypotension to consider is that of adrenal insufficiency. As Dr. Stulpin reviewed in her discussion above, this can come in both primary and secondary forms. The latter is far more common and induced by exogenous steroid use. A wise ICU attending once taught that no patient should die without stress dose steroids. While perhaps a bit morbid, the take home point here was that adrenal insufficiency can present in any patient, not just those with underlying disorders of glucocorticoid production. Pay particular attention to patients with autoimmune disorders or others on chronic steroid therapy as these are the populations that are particularly at risk. Patients presenting with unexplained hypoglycemia in the setting of sepsis or shock of any kind should also be strongly considered to receive stress dose steroids. Do not wait for a cortisol level to treat this condition. Consider, as well, checking TSH and free T3/T4 as patients with adrenal insufficiency can simultaneously harbor other endocrinopathies.

To summarize, refractory hypotension or failure to respond to traditional interventions is relatively uncommon but critical to identify in shock patients. Often these patients have a primary diagnosis of septic shock but can suffer from concurrent shock related to one or more of the differential considerations we have reviewed above. A thoughtful reassessment, both of the patient’s physical exam findings, US and other diagnostics, medication list and history of present illness will offer clues that may uncover an additional etiology critical to treat and to ensure the best outcome possible.

Joshua D. Zimmerman, MD

Health System Clinician

Feinberg School of Medicine

Northwestern Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Stulpin, E. Wibberly, A. (2022, Jan 24). Vasopressor Nonresponse. [NUEM Blog. Expert Commentary by Zimmerman, J]. Retrieved from http://www.nuemblog.com/blog/vasopressor-nonresponse

Hyponatremia

Expert Commentary

Thanks for a great review on hyponatremia by Drs. O’Brien & Kaltman. I’ve recruited the expert insight from one of my favorite colleagues and fellow Northwestern University Feinberg School of Medicine graduate Joshua Waitzman, MD PhD, Instructor of Nephrology at Beth Israel Deaconess Medical Center in Boston, MA.

I’ll highlight a few points from an emergency medicine point of view with Dr. Waitzman’s additional commentary from the nephrology perspective.

I’d argue the primary question you need to answer in the ED for hyponatremia patients is whether or not hypertonic saline is indicated. For those well-appearing neurologically intact hyponatremia patients w/ sodium levels > 120, further work-up & analysis of the underlying etiology can be deferred to the inpatient side. It’s always appreciated to send the hyponatremia labs (eg urine lytes, osms, TSH, etc) for the admitting team, however differentiating SIADH from cerebral salt-wasting should not be at the top of your priority list. Especially as the etiology of hyponatremia is commonly multifold.
- Dr. Waitzman: additionally, a key reminder is to STOP AND THINK before giving isotonic fluids (0.9% NS, LR, bicarb gtt, etc). For most patients with moderate-to-severe hyponatremia, giving a liter of normal saline is normally the wrong answer.
  - If your patient has SIADH, heart failure, or cirrhosis (common causes of hyponatremia), additional IV fluids will end up worsening the hyponatremia.
  - If your patient is volume depleted, isotonic fluids will fix the volume problem and shut off ADH, leading to rapid increases in urine output and rises in sodium. The worst thing we can do to patients with bad hyponatremia is overcorrect them too quickly.
If you are considering hypertonic saline, make sure to get your nephrologist on board early. Nephrology is the primary team that will be following your patient from arrival in the ED through discharge so if you’re debating whether the patient requires 3% NaCl, please consult your nephrology team ASAP. Though w/ that said, if your patient is seizing due to hyponatremia, push the hypertonic then get nephrology on board afterwards.
- Dr. Waitzman: 100%. If you’re debating on hypertonic saline, call nephrology at any time. However, for the sake of your friendly overworked nephrology fellow, please wait until the AM before calling about patients who appear well and have sodium > 125. When consulting nephrology for hyponatremia, please have a urine sodium, potassium, and creatinine at the ready.
Hypertonic saline is not only indicated for seizures, coma, suspected cerebral herniation or focal neurological deficits as noted above. Keep in mind the indication for 3% also extends to altered mental status and can present w/ simple confusion or even “just acting off” from baseline. Do keep in mind the acuteness of the neurologic status is also imperative to determining the need of hypertonic. More acute symptoms = higher likelihood of needing 3%. It’s essential to get background information from family/friends if the patient is unable to provide any additional history regarding their own baseline level of functioning.
- Dr. Waitzman: In my mind, using hypertonic saline should be based on three things.
  - First, how bad is the sodium level? It’s normally not worth it for most patients above 120.
  - Second, how acute is the hyponatremia? Hypertonic can be risky for those with chronic hyponatremia but curative for those with hyperacute hyponatremia like marathon runners.
  - Third, how severe are the symptoms? Seizures attributed to hyponatremia need treatment ASAP.
- Because I’m a nephrologist, I approach the use of hypertonic saline like an equation, combining the acuteness of the hyponatremia with the severity of symptoms. For example, the more recent the sodium drop w/ more severe symptoms = more comfortable w/ hypertonic. The more chronic the hyponatremia and the less severe symptoms = hypertonic may have more risk than benefit.
Of note, you do NOT need a central line for hypertonic saline administration. Though this is dictated by your own hospital protocols, hypertonic saline has been shown to be safe when pushed in small doses through a large-bore peripheral (proximally placed) IV [1,2]. Though if your administration says differently, do not waste time putting in a triple lumen catheter if hypertonic is truly indicated in your hyponatremia patient. Drill an IO and push the 100-150cc 3% NaCl as soon as possible.
- Dr. Waitzman: PREACH.
Do remember that pseudo-hyponatremia is a thing. Most commonly seen in our ED patients w/ hyperglycemia, other solutes which can lead to pseudo-hyponatremia are mannitol, glycol, or maltose (all three most commonly encountered on the inpatient side or post-outpatient urologic procedures). If you appreciate an elevated glucose on your chemistry panel, you can use the following equation

Corrected Na = Measured Na + [(1.6 * (glucose-100)/100)] [3]

or this helpful link via MDCalc (https://www.mdcalc.com/sodium-correction-hyperglycemia) to determine the appropriate corrected sodium.

Dr. Waitzman: If you hate math, consider a blood gas sodium. There is no pseudohyponatremia on a blood gas sodium and it results faster than your normal chemistry panel sodium level.

MDMA/ecstasy use is an uncommon cause of hyponatremia that should not be forgotten [4]. Keep that in mind in your presumed “intoxicated” young party-goers, especially those where these drugs are prevalent (eg raves, music-festivals, etc). MDMA leads to hyponatremia by activation of arginine vasopressin which increases kidney free water absorption [5].
Vaptans have not been established as standard of care for hyponatremia in emergency medicine. If these are to be utilized in an ED patient, it is essential that there is a nephrologist on board who is actively involved in the patient’s management.
- Dr. Waitzman: wholeheartedly agree. Vaptans don’t have a place in the acute settings (like the ED) and have a huge risk of over-correcting the sodium. If you need to acutely correct hyponatremia, hypertonic is the answer, not vaptans.
With boarding being a nation-wide issue, one final piece of commentary from both the emergency medicine & nephrology perspective: if you’re sending your patient to the ICU for hyponatremia, it’s because they require q2hr sodium levels. Please continue those q2hr sodium levels while they remain under your care in the ED while waiting for an ICU bed. Blood gas sodiums are a great way to trend sodium levels as they’re accurate & result quickly (and avoid the potential for pseudohyponatremia as described above).

I’d like to extend an incredibly huge thank you & sincere gratitude to Dr. Waitzman for his assistance & expertise on this expert commentary. We’re all exceptionally lucky to work with such fantastic nephrology colleagues and are eternally appreciative for all their help, insight, and expertise.

References:

Alenazi AO, Alhalimi ZM, Almatar MH, Alhajji TA. Safety of Peripheral Administration of 3% Hypertonic Saline in Critically Ill Patients: A Literature Review. Crit Care Nurse. 2021 Feb 1;41(1):25-30. doi: 10.4037/ccn2021400. PMID: 33560431.
Mesghali E, Fitter S, Bahjri K, Moussavi K. Safety of Peripheral Line Administration of 3% Hypertonic Saline and Mannitol in the Emergency Department. J Emerg Med. 2019 Apr;56(4):431-436. doi: 10.1016/j.jemermed.2018.12.046. Epub 2019 Feb 8. PMID: 30745195.
Katz MA. Hyperglycemia-induced hyponatremia--calculation of expected serum sodium depression. N Engl J Med. 1973 Oct 18;289(16):843-4. doi: 10.1056/NEJM197310182891607. PMID: 4763428.
Petrino R, Marino R. Fluids and Electrolytes. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; Accessed July 21, 2021.
Campbell GA, Rosner MH. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clin J Am Soc Nephrol. 2008 Nov;3(6):1852-60. doi: 10.2215/CJN.02080508. Epub 2008 Aug 6. PMID: 18684895.

Sarah Dhake, MD

Division of Emergency Medicine, NorthShore University HealthSystem

Clinical Assistant Professor, University of Chicago - Pritzker School of Medicine

Twitter: @ssandersEM

sdhake@northshore.org

Joshua Waitzman, MD PhD

Instructor in Medicine, Harvard Medical School
Division of Nephrology, Department of Medicine
Beth Israel Deaconess Medical Center

Twitter: @Jwaitz
jswaitzm@bidmc.harvard.edu

How To Cite This Post:

[Peer-Reviewed, Web Publication] O’Brien, J. Kaltman, D. (2022, Jan 10). Hyponatremia. [NUEM Blog. Expert Commentary by Dhake, S and Waitzman, J]. Retrieved from http://www.nuemblog.com/blog/hyponatremia

References

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Posted on January 10, 2022 by NUEM Blog and filed under Endocrine and tagged hyponatremia endocrine hypertonic Marathon mdma.

Running Injuries

Written by: Eric Power, MD (NUEM ‘24) Edited by: Justin Seltzer, MD (NUEM '21) Expert review by: Terese Whipple, MD (NUEM '20)

With over 40 million runners in the United States alone and an ever-increasing interest in fitness among the general population, the frequency of running injuries presented to urgent care and emergency departments will only grow with time. This is especially true due to the high rate of injury among runners, with a published annual incidence rate ranging from 19% to 79%; with even conservative estimates, that is nearly 8 million running injuries annually.

There are several risk factors for running injuries with which the emergency physician should be familiar. Running injuries are generally the sequela of repetitive stress. Acute injuries represent a small minority of cases and are usually not serious. The strongest risk factors include older age, high mileage running, beginners or suddenly restarting running, those making a rapid increase in speed and/or distance, low bone density, and those with a history of previous injuries.

This article will focus primarily on several “low acuity” running injuries along with their initial evaluation and management. A vast majority of running injuries are not serious, however, the evaluation of the injured runner still demands detailed musculoskeletal examination and thoughtful consideration of more dangerous potential causes of the symptoms. Proper clinical diagnosis and recommendations can certainly speed recovery and return to activity.

Iliotibial (IT) band syndrome

Major population: Young, active with a recent change in running mileage and/or runs on hilly terrain

Presentation: Lateral knee pain, especially with activity, with or without lateral thigh and hip pain

Diagnosis: Tenderness along lateral thigh extending into the lateral knee, swelling at the distal aspect may be present, Ober’s test for IT band tightness (not diagnostic)

EM differential: meniscus injury, stress fracture, lateral ligamentous injury

Initial treatment: No running until pain resolves then gradual return at painless speeds, distances, home exercise program to stretch IT band

Follow-up: Routine primary care, consider PT referral

Patellofemoral pain syndrome

Major population: Young, usually female, participating in sports with high volume running and/or jumping

Presentation: Anterior, aching knee pain worse with knee flexion (e.g. climbing stairs)

Diagnosis: Anterior patella tenderness; pain with patellar grind test, deep knee flexion

EM differential: meniscus injury, stress fracture, ligamentous injury

Initial treatment: home exercise program or formal physical therapy to strengthen quadriceps, core, and hip abductors. consider a patella stabilizing knee brace

Follow-up: Routine primary care, consider PT referral

Medial Tibial Stress Syndrome (“Shin Splints”)

Major population: Any patient with a recently initiated intense exercise regimen

Presentation: Anteromedial tibial pain provoked by activity and improved with rest

Diagnosis: Reproduction of pain with palpation of a diffuse area of the posteromedial border of the tibia

EM differential: stress fracture, DVT, exertional compartment syndrome

Initial treatment: Rest, icing (~20 minutes per hour) until the pain has resolved, then a gradual return to activity at painless speeds, distances

Follow-up: Routine primary care, consider PT, sports medicine referral due to high failure rate of conservative management

Achilles Tendinopathy

Major population: Usually middle-aged with recently initiated exercise or increased intensity/frequency

Presentation: Chronic, gradually worsening posterior heel and foot pain, often worst in the morning, with an impaired plantarflexion and explosive movements of the ankle

Diagnosis: Tendon palpation reproduces the pain, diminished range of motion and strength, calf muscle atrophy (late finding)

EM differential: calcaneal stress fracture, DVT, Achilles tendon rupture

Initial treatment: Reduce the intensity of activity to walking only until pain resolves, home exercise program to stretch and eccentrically load the Achilles tendon

Follow-up: Sports medicine and PT referrals due to benefit of rehabilitation and availability of multiple specialized therapies; some cases are treated surgically

Plantar Fasciitis

Major population: High volume or newly initiated/increased running or sports, slightly more common in women

Presentation: Classically plantar midfoot to heel pain worse with the “first step” in the morning

Diagnosis: Pain reproduced with palpation of the medial tubercle of the calcaneus and proximal plantar fascia, positive windlass test

EM differential: Foot stress fracture

Initial treatment: Avoid triggering activities, home exercise program to stretch and deeply massage the plantar fascia

Follow-up: Referral to PT and a foot and ankle specialist (orthopedic surgeon or podiatrist) as chronic symptoms are common

Key points

A majority of running injuries are not serious or acute but can be function limiting if not properly diagnosed and managed
It is important to rule out major relevant differential diagnoses such as stress fractures, DVT, and ligament/tendon injuries prior to discharge
Universal management is with rest, as needed NSAIDs, a gradual return to activity when the pain has resolved, and routine primary care follow up; primary care sports medicine or orthopedic surgery should be reserved for severe symptoms or failure of conservative management
Alongside home exercises and stretches, consider PT referral routinely

References

Li HY, Hua YH. Achilles Tendinopathy: Current Concepts about the Basic Science and Clinical Treatments. Biomed Res Int. 2016;2016:6492597.
McClure CJ, Oh R. Medial Tibial Stress Syndrome. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538479/
Petersen W, Ellermann A, Gösele-Koppenburg A, et al. Patellofemoral pain syndrome. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2264-2274.
Petraglia F, Ramazzina I, Costantino C. Plantar fasciitis in athletes: diagnostic and treatment strategies. A systematic review. Muscles Ligaments Tendons J. 2017;7(1):107-118. Published 2017 May 10.
Strauss EJ, Kim S, Calce JG, Park D. Iliotibial Band Syndrome: Evaluation and Management. American Academy of Orthopaedic Surgeon. 2011;19(12):728-736.
van der Worp MP, ten Haaf DS, van Cingel R, de Wijer A, Nijhuis-van der Sanden MW, Staal JB. Injuries in runners; a systematic review on risk factors and sex differences. PLoS One. 2015;10(2):e0114937. Published 2015 Feb 23.

Expert Commentary

Thank you to Drs. Power and Seltzer for their concise and relevant review of common overuse injuries seen in runners. Although most of these injuries would not be considered emergent, correct diagnosis and referral of these patients is important to keep them active and decrease their likelihood of suffering the heart attacks, strokes, and chronic pain we see daily. This post did an excellent job of walking through several common injuries however, there is one more that I would like Emergency Physicians to consider in their differential for runners with extremity pain: Stress Fracture.

A stress fracture is break down in bone that occurs when abnormal stress is applied to healthy bone or normal stress is applied to unhealthy bone (osteopenia/porosis)
Female athletes are at particular risk if they are not fueling well enough, sometimes manifesting in menstrual dysfunction and decreased bone density
Commonly occurs in healthy runners when an athlete is increasing their training volume or intensity, or other new stress is applied such as a new running surface
Complain of insidious onset pain that worsens with running and other pounding activity. Pain is often better with rest early on.
If the bone is palpable from the surface, it will have point tenderness over the area. Pain will be reproduced with the hop test and the fulcrum test.
X-rays may be normal early on, later in the course, they may show periosteal reaction or fracture line. MRI can be obtained on an outpatient basis if needed.
Most stress injuries can be managed by decreased weight bearing through alterations in training, however, sometimes offloading with a walking boot or crutches may be necessary depending on severity and location.
High-risk stress injuries that warrant prompt sports medicine or orthopedics referral: femoral neck (superior aspect), patella, anterior tibia, medial malleolus, talus, tarsal navicular, the proximal fifth metatarsal, tarsal sesamoids.
- If strong suspicion of a high-risk stress injury or diagnosis is confirmed in the ED, these patients should be given crutches and made non-weight bearing until follow-up.

Hopefully, this post will help you build a differential for overuse injuries you may encounter in the ED, and provide proper follow-up in order to keep our patients healthy, active, and engaged in the activities they enjoy.

Terese Whipple, MD

Assistant Professor

Department of Emergency Medicine

University of Iowa Hospitals and Clinics

How To Cite This Post:

[Peer-Reviewed, Web Publication] Power, E. Seltzer, J. (2022, Jan 3). Running Injuries. [NUEM Blog. Expert Commentary by Whipple, T]. Retrieved from http://www.nuemblog.com/blog/runninginjuries

Top Blogs of 2021

Congratulations to all of the authors with the most popular posts of 2021!

1. Pill in the Pocket (23,646 views)

The runaway favorite of this year was Dr. David Feiger’s (NUEM ’22) and Dr. Jon Andereck’s (NUEM ’19) post reviewed by Dr. Kaustubha Patel of Northwestern's Bluhm Cardiovascular Institute about the “pill-in-the-pocket” approach to treating atrial fibrillation.

Take-Home Point: In select patients, the “pill-in-the-pocket” approach is a safe and effective way to treat infrequent but symptomatic paroxysmal atrial fibrillation that reduces ED visits and improves patients’ quality of life.

2. Peripheral Vasopressors: Do I need that central line? (8,683 views)

In the second most popular blog of the year, Dr. Saabir Kaskar (NUEM '23) and Dr. Abiye Ibiebele (NUEM '21), with commentary by Northwestern pulmonologist/intensivist, Dr. Marc Sala, summarize the current literature on the peripheral infusion of vasopressors, which is becoming more and more commonplace as the evidence evolves to support earlier initiation of pressors and more judicious use of crystalloid for many forms of shock.

Take-Home Point: While the evidence at this time is limited, clinicians should feel comfortable administering peripheral vasopressors as a bridge to central infusion for a limited time. Peripheral vasopressors have a lower risk of complications than previously thought and allow clinicians to minimize delays in administering vasoactive medications that may have a mortality benefit.

3. Pericardiocentesis (2,553 views)

Rounding out the top three is Dr. David Feiger's (NUEM '22) and Dr. Abiye Ibiebele's (NUEM '21) post on emergent pericardiocentesis, a potentially life-saving procedure in a patient with hemodynamically significant cardiac tamponade, with expert commentary by Northwestern interventional cardiologist, Dr. Dan Schimmel.

Take-Home Point: Bedside pericardiocentesis is a rare but important procedure that can be performed emergently using ultrasound or landmark guidance. While a subxiphoid approach is commonly performed, an apical or parasternal approach may be considered to minimize potential complications. Consider exchanging the needle for a drain once the pericardium is accessed to bridge to definitive therapy.

4. Hanging Injury (959 views)

Dr. Vytas Karalius (NUEM '22), Dr. Nery Porras (NUEM '21), and expert commentator Dr. Kevin Emmerich describe the mechanisms of injury and management of patients presenting with hanging injuries, an unfortunate but all-too-common method of self-harm worldwide.

Take-Home Point: Hanging injuries can have wide-ranging immediate and delayed complications on multiple organ systems and clinicians should evaluate for cervical spine and cerebrovascular injury and anticipate a difficult airway due to evolving airway edema. Clinicians should have a high index of suspicion for polytrauma or toxic ingestion. Even with an initial negative workup, all patients should be admitted for observation (with a low threshold to transfer to a trauma center) and ultimately a psychiatry consult.

5. Paronychia (623 views)

In one of two procedural infographics to make the top ten this year, Dr. Richmond Castillo (NUEM '23), Dr. Andra Farcas (NUEM '21), and Dr. Matthew Kippenhan provide a visual guide to diagnosing and treating a common "fast-track" complaint.

Take-Home Point: Paronychia is a common infection of the nail fold that often requires an incision and drainage procedure if a purulent fluid collection is present. Be wary of several other "can't miss" visual diagnoses on the differential, such as herpetic whitlow, felon, and proximal onychomycosis.

6. Antiemetics/Gastroparesis (572 views)

With expert commentary by NUEM faculty Dr. Howard Kim, Dr. Nery Porras (NUEM '21) and Dr. Terese Whipple (NUEM '20) provide an overview of the role of antipsychotics in the treatment of gastroparesis and other cyclic vomiting syndromes. These conditions can be difficult to treat, frustrating for both patients and providers, and refractory to traditional antiemetic therapies.

Take-Home Point: Antipsychotic medications such as haloperidol and droperidol are effective therapies for nausea, vomiting, and abdominal pain associated with gastroparesis. Despite previous black box warnings on droperidol causing it to fall out of favor, it is safe and well-tolerated at the doses typically used in an emergency department setting.

7. Basic Capnography Interpretation (560 views)

Dr. Shawn Luo (NUEM '22) and Dr. Matthew McCauley (NUEM '21) review the basics of interpreting continuous waveform capnography, a versatile tool with multiple uses in both the emergency department and critical care settings. Dr. Seth Trueger, NUEM faculty, provides expert commentary.

Take-Home Point: Continuous waveform capnography (otherwise known as end-tidal CO2) is a valuable tool that can inform real-time management decisions in both intubated and non-intubated patients. Recognizing several common patterns can guide providers during several use-cases such as confirming endotracheal tube placement, cardiac arrest, and procedural sedation.

8. Knee Dislocation (436 views)

Knee dislocations are a rare but highly morbid condition for which Dr. Andrew Rogers (NUEM '22) and Dr. Amanda Randolph (NUEM '21) provide a streamlined approach to diagnosing and treating. NUEM's own emergency orthopedic guru, Dr. Matthew Levine, provides expert commentary.

Take-Home Point: Knee dislocations are time-sensitive injuries that require rapid diagnosis and treatment because of the high rate of vascular complications. Emergent closed reduction is key, with a thorough neurovascular exam before and after. All patients require ABIs (with CT angiography if the ABI is abnormal) and admission for neurovascular checks. Speak with your consultants early.

9. TPA in Frostbite (422 views)

For those who practice in colder climates, Dr. Patrick King's (NUEM '23) and Dr. Nery Porras's (NUEM '21) review of the current literature on the role of tPA in frostbite is timely as we enter into the winter season. Expert commentary is provided by Dr. Anne Lambert Wagner, medical director of the Burn and Frostbite Center at the University of Colorado Health.

Take-Home Points: While literature continues to evolve, current evidence supports the use of tPA in select patients with severe frostbite injuries in multiple digits, multiple limbs, or proximal limb segments presenting within 24 hours of injury. Combined with active rewarming strategies, tPA use results in significantly improved outcomes.

10. Felon (381 views)

Rounding out the top 10 for 2021 is the second procedural infographic, which is closely related to our Paronychia post. The expert review of Dr. Matthew Levine, Dr. Daniel Levine (NUEM '23), and Dr. Will LaPlant (NUEM '20) illustrate the diagnosis and management of felons in the emergency department.
Take-Home Point: Understanding finger anatomy is key to understanding felons, which present as tense, throbbing, purulent infections of the distal finger pad. Incision and drainage is the mainstay of therapy for felons, with a course of oral antibiotics and mandatory hand surgery follow-up to avoid complications such as flexor tenosynovitis or osteomyelitis of the distal phalanx.

Posted on December 27, 2021 by NUEM Blog and filed under top 10 2021 and tagged Top 10.

Hip Pain in Pediatrics

Written by: Tommy Ng, MD (NUEM ‘24) Edited by: Patricia Bigach, MD (NUEM ‘22) Expert review by: Terese Whipple, MD '20

So your kid won’t walk

One of the most common complaints in a pediatric Emergency Department is a child refusing or inability to ambulate. For normal development, a child is typically able to stand at 9 months, walk at 12 months, and run at 18 months. There is a certain degree of variability for these age constraints however any acute decrease in mobility should prompt an evaluation. A limp is defined as any abnormality in gait caused by pain, weakness, or deformity [1]. There are a plethora of conditions that can manifest with an antalgic gait or refusal to bear weight and it may be difficult to distinguish between etiologies given a child’s age.

History and physical

Age is an important factor as certain conditions are more likely depending on the patient’s age

Acuity should be determined as the chronicity of limp as certain etiologies are more acute while others are indolent. Additionally, certain infectious etiologies are more likely to present acutely or chronically.

Fever may suggest an infectious or rheumatologic cause

Trauma can help distinguish soft tissue vs orthopedic injuries

Past medical history is important to be focused on recent illnesses, antibiotic use, history of sickle cell disease, or hormonal diseases.

Physical examination should always include an attempt to ambulate the child unless there is an obvious contraindication noted immediately (eg open fracture). If the child refuses to bear weight, the child should be made non-weight bearing until serious pathology which can be worsened by walking is ruled out. Strength and range of motion of both lower extremities should also be examined [2].

Differential: the bad, the worse, and the ugly

Infectious

Transient Synovitis - Relatively common with a lifetime risk of 3%. Affects ages 3-8, males to females 2:1 [3]. Typically well appearing with normal labs, however, this is a diagnosis of exclusion and a septic joint should be ruled out. Management includes NSAID use and return to activity as tolerated [4].
Septic Arthritis - A “do not miss” diagnosis, commonly ages 3-6 with a slight male predominance [5]. Typically presenting with fevers and abnormal labs. The Kocher Criteria (originally developed in 1999 and validated in 2004) can be helpful in determining the likelihood of septic arthritis [6]. Management includes imaging studies, typical ultrasound to assess for a joint effusion, then a diagnostic arthrocentesis & antibiotics. The antibiotic regimen should be tailored to the child’s age and other predisposing factors to certain pathogens.

Osteomyelitis - Occurs in 1:5000-7700 kids in increased prevalence with MRSA communities; 2:1 male to female predominance with half of all cases occurring in ages less than 5 [7]. Commonly hematogenous spread from bacteremia; clinical suspicion should prompt radiologic evaluation. X-rays may be likely to be normal/inconclusive early in the disease course and MRI may be often indicated. Labs can be helpful but are not specific; a systematic review of >12,000 patients showed that elevated WBC was only present in 36% of patients [7]. ESR and CRP are non-specific but have a sensitivity of 95% [7]. Antibiotic therapy guidelines are similar to the management of septic arthritis. Surgical intervention may be indicated if there is a lack of improvement after 48-72 hours [8].

Osteomyelitis of the distal tibia (orthobullets.com)

Orthopedic

Legg-Calve-Perthes / Avascular Necrosis of the Hip - Age range 3-12 with a peak at 5-7, male to female ratio 3:1, can be bilateral in 10-20% of patients [9]. Radiographs should be obtained with high clinical suspicion but are often normal early in the course. An MRI would show fragmentation of the femoral head. The patient should be made non-weight bearing and be referred to a specialist. Children under 8 typically have a better prognosis however long-term management is poorly defined as there has been no long-term study [10].

Avascular necrosis of bilateral hip (orthobullets.com)

Slipped Capital Femoral Epiphysis - Typically obese child, median age 12, bilateral in 20-40% of cases [11]. Presentation is classically chronic hip pain with antalgic gait however may present with knee pain. Physical exam classically shows external rotation and abduction of the hip during hip flexion. Management is orthopedic consultation for operative stabilization [12].

References

Smith E, Anderson M, Foster H. The child with a limp: a symptom and not a diagnosis. Archives of disease in childhood - Education & practice edition. 2012;97(5):185-193. doi:10.1136/archdischild-2011-301245.
Naranje S, Kelly DM, Sawyer JR. A Systematic Approach to the Evaluation of a Limping Child. Am Fam Physician. 2015 Nov 15;92(10):908-16. PMID: 26554284.
Landin LA, Danielsson LG, Wattsgård C. Transient synovitis of the hip. Its incidence, epidemiology and relation to Perthes' disease. J Bone Joint Surg Br. 1987;69(2):238-242.
Kermond S, Fink M, Graham K, Carlin JB, Barnett P. A randomized clinical trial: should the child with transient synovitis of the hip be treated with nonsteroidal anti-inflammatory drugs?. Ann Emerg Med. 2002;40(3):294-299. doi:10.1067/mem.2002.126171
Bennett OM, Namnyak SS. Acute septic arthritis of the hip joint in infancy and childhood. Clin Orthop Relat Res. 1992;(281):123-132.
Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-1670. doi:10.2106/00004623-199912000-00002
Dartnell J, Ramachandran M, Katchburian M. Haematogenous acute and subacute paediatric osteomyelitis: a systematic review of the literature. J Bone Joint Surg Br. 2012;94(5):584-595. doi:10.1302/0301-620X.94B5.28523
Kaplan SL. Osteomyelitis in children. Infect Dis Clin North Am. 2005;19(4):787-vii. doi:10.1016/j.idc.2005.07.006
Johansson T, Lindblad M, Bladh M, Josefsson A, Sydsjö G. Incidence of Perthes' disease in children born between 1973 and 1993. Acta Orthop. 2017;88(1):96-100. doi:10.1080/17453674.2016.1227055
Canavese F, Dimeglio A. Perthes' disease: prognosis in children under six years of age. J Bone Joint Surg Br. 2008 Jul;90(7):940-5. doi: 10.1302/0301-620X.90B7.20691. PMID: 18591607.
Herngren B, Stenmarker M, Vavruch L, Hagglund G. Slipped capital femoral epiphysis: a population-based study. BMC Musculoskelet Disord. 2017;18(1):304. Published 2017 Jul 18. doi:10.1186/s12891-017-1665-3
Reynolds RA. Diagnosis and treatment of slipped capital femoral epiphysis. Curr Opin Pediatr. 1999;11(1):80-83. doi:10.1097/00008480-199902000-00016

Expert Commentary

Thank you to Drs. Ng and Bigach for compiling a concise approach to a common chief complaint encountered by Emergency Physicians across the county: a child with a new limp or the refusal to bear weight.

The first step to this often-challenging problem is to try to localize the pain, and in non-verbal kiddos, this can be the most difficult task. As highlighted above, if the child is able, observe their ambulation and establish laterality of the limp and when it occurs during the gait cycle. Most of the disease processes we as Emergency Physicians are concerned about will cause an antalgic gait or a shortened stance phase. Shortening the stance phase decreases the amount of time that the child is bearing weight on the painful limb in an effort to decrease their pain. Sometimes this is so effective that their parents will observe a limp, but the child will not complain of any pain. A thorough exam of the back and lower extremities including inspection, palpation, and range of motion of all joints is also imperative for trying to localize the cause of their symptoms.

Let your exam and history guide lab evaluation and imaging, however, a good place to start is usually basic labs and inflammatory markers and a plain film of the affected joint. In some cases, you won’t be able to localize pain or exam findings at all, and a broad workup including plain film imaging of the entire extremity may be necessary.

A few additional pearls:

Always consider non-accidental trauma in children with new limp or refusal to bear weight.
Systemic symptoms such as fever should raise your suspicion for infectious etiology such as osteomyelitis or septic arthritis.
Classically children with transient synovitis will have had a recent viral illness, but this is not always the case.
Always examine the hips and consider hip plain films in children complaining of knee or thigh pain, but with a benign knee exam. They could be hiding an SCFE or Leg-Calve-Perthes disease.
Don’t forget to examine the SI joint, as it too can become infected or inflamed.
History of night pain should raise your antenna for malignancy like osteosarcoma, Ewing’s sarcoma, or leukemia.
Consider Lyme arthritis in your differential for joint pain and swelling in endemic areas.
Ultrasound can be useful when evaluating for septic arthritis and transient synovitis and can be performed at the bedside. However, both septic arthritis and transient synovitis can cause effusion, and therefore it is not useful in differentiating between the two. (That’s where the Kocher Criteria should be used to risk-stratify and determine if joint aspiration and fluid analysis are warranted)

Ultrasound evaluation of a pediatric hip joint demonstrating effusion courtesy of Dr. Maulik S Patel (https://radiopaedia.org)

Finally, make sure that the parents understand the diagnosis, expected course, and follow-up plan. If the child continues to refuse to bear weight, their symptoms worsen or do not improve, or they develop new concerning symptoms such as new fever or new urinary retention, they should return to the Emergency Department or their pediatrician for re-evaluation. More than once I’ve had patients who seemed for all the world to have transient synovitis eventually be diagnosed with spinal cord tumor, chronic recurrent multifocal osteomyelitis, etc.

Terese Whipple, MD

Assistant Professor

Department of Emergency Medicine

University of Iowa Hospitals and Clinics

How To Cite This Post:

[Peer-Reviewed, Web Publication] Ng, T. Bigach, P. (2021, Dec 20). Hip Pain in Pediatrics. [NUEM Blog. Expert Commentary by Whipple, T]. Retrieved from http://www.nuemblog.com/blog/hippainpediatrics

Resuscitative Hysterotomy

**Written by:** Aldo Gonzalez, MD (NUEM ‘23) **Edited by:** Justine Ko, MD (NUEM ‘21)
**Expert Commentary by**: Paul Trinquero, MD (NUEM '19) & Pietro Bortoletto, MD

Introduction

Resuscitative hysterotomy (RH) is the new term for what was previously called perimortem cesarean delivery (PMCD). The new nomenclature is being adopted to highlight the importance of the procedure to a successful resuscitation during maternal cardiopulmonary arrest (MCPA). It is defined as the procedure of delivering a fetus from a gravid mother through an incision in the abdomen during or after MCPA. The goal of the procedure is to improve the survival of the mother and the neonate.

Physiology

There are physiologic changes that occur during pregnancy which reduce the probability of return of spontaneous circulation (ROSC) during cardiac arrest. Physiologic anemia of pregnancy reduces the oxygen carrying capacity of blood and results in decreased delivery of oxygen during resuscitation. The large gravid uterus elevates the diaphragm and reduces the lung’s functional reserve capacity (FRC), which when combined with increased oxygen demand from the fetus results in decreased oxygen reserves and resultant risk for rapid oxygen desaturations. The size of a gravid uterus at 20 weeks results in aortocaval compression which reduces the amount of venous return from the inferior vena cava and reduces cardiac output during resuscitation. The theory behind resuscitative hysterotomy is to increase the probability of ROSC by reducing the impact of aortocaval compression.

Supporting Evidence

A 2012 systematic review primarily investigated the neonatal and maternal survival rates after perimortem cesarean delivery and secondarily attempted to evaluate maternal and fetal neurological outcome and the ability to perform the procedure within the recommended time frame.

Inclusion Criteria

original articles, case series, case reports and letters to the editor, and reports from databases
had minimum of least five clinical details of the case (e.g. patient age, gravidity, parity, obstetric history, medical history, presenting rhythm, or location of arrest)
AND
the care administered (chest compression, ventilation, monitoring, drug administration)
AND
maternal return of spontaneous circulation or survival to hospital discharge or fetal neonatal outcome

Exclusion Criteria

Post-delivery arrests
Studies without enough data to understand the details of the arrests
Studies with unclear maternal and fetal outcomes

Population

Pregnant woman that
- (1) had a cardiac arrest or a non-perfusing rhythm
- (2) received chest compression and/or advanced life support medications and/or defibrillation
Average maternal age: 30.5±6.5 years (median 32, range 17–44, IQR, 26.5–35.5, n = 80)
Gravidity: 2.5±1.5 (median 2, range 1–7, IQR 1–4, n = 59)
Parity: 1.1±1.3 (median 1, range 0–6, IQR 0–2, n = 57)
Singleton Pregnancies: 90.4% (n = 85)
Average gestational age at arrest: 33±7 weeks (median 35, range 10–42, IQR 31–39, n = 85)

Results

for cases undergoing PMCD, earlier time from arrest to delivery was associated with increased survival (p < 0.001, 95%CI 6.9–18.2)
- surviving mothers: 27/57; 10.0±7.2 min (median 9, range 1–37)
- non-surviving mother: 30/57; 22.6±13.3 min (median 20, range 4–60)]
for neonates delivered by PMCD/RH earlier time from arrest to delivery was associated with increased survival (p = 0.016)
- surviving neonates: 14±11 min (median = 10, range = 1–47)
- non-survivor neonates: 22±13 min (median = 20, range = 4–60)
Only 4 cases met the timeframe of less than minutes

Take-Aways: Performing a PMCD/RH in the 4-5 minutes time frame is difficult. However, PMCD/RH beyond the proposed time is still beneficial and earlier time to delivery from arrest is associated with better outcomes

Guideline Recommendations

Perform basic life support (BLS) in the same way as non-pregnant patients

Place patient in supine position
- Left lateral decubitus (left lateral tilt) positioning is no longer recommended during compressions because of reduced efficacy of chest compressions
No modification of Chest compressions
- Rate: 100-120 per minute
- Depth: at least 2 inches (5 cm)
- Allow for full chest recoil between compressions
- Avoid interruptions as much as possible
No modification of Ventilation
- Use bag-ventilation
- Compression to breath ratio: 30:2 before advanced airway

Perform advanced cardiac life support (ACLS) as in non-pregnant women

No modification of Ventilation
- Once breath every 6 seconds (10 BPM) with advanced airway
No modification of medications
- Use 1 mg Epinephrine of epinephrine every 3-5 minutes
No modification to defibrillation
- Use adhesive pads on patient
- Place in anterolateral position
  - Lateral pad should be placed under breast tissue
- Defibrillate for Ventricular fibrillation or Ventricular tachycardia
- Use usual Voltages
  - Biphasic: 120-200 Joules
- Resume compressions after shock is delivered

Special considerations during resuscitation

Obtain access above the diaphragm to minimize the effect of aortocaval compression on the administration of drugs
Perform left uterine deviation during resuscitation to reduce aortocaval compression
If a gravid patient suffers a cardiac arrest mobilize resources to prepare for the need for resuscitative hysterotomy and the resuscitation of the fetus early

Palpate the size of the gravid uterus
- If above the height of the umbilicus then patient is most likely greater than 20 weeks gravid and a candidate for RH
Strongly consider performing RH (PMCD) if the patient does not achieve ROSC by the 4-minute mark and qualified staff to perform the procedure are present
Aim to have the procedure done by the 5-minute mark
Consider performing RH (PMCD) sooner if maternal prognosis is poor or prolonged period of pulselessness
RH should be performed at the site of the resuscitation
Do not delay procedure to prepare abdomen
- May pour iodine solution over abdomen prior to incision
Do not delay procedure for surgical equipment if scalpel is available
Continue performing LUD while performing RH

Figure 1: One-handed left uterine deviation technique

Figure 2: Two-handed left uterine deviation technique

Steps for Resuscitative Hysterectomy

Pre-procedure

Gather supplies to perform RH
- Personal Protective Equipment
  - Gloves
  - Face mask
  - Apron/gown
- Resuscitative Hysterotomy Equipment
  - Scalpel(the minimum equipment to perform procedure)
  - Blunted Scissors
  - Clamps/Hemostats
  - Gauze
  - Suction
  - Large absorbable sutures
  - Needle Holder
  - Antiseptic Solution
- Neonatal resuscitation equipment
  - Dry Linens
  - Neonatal Bag Valve Mask
  - Neonatal Airway supplies
  - Suction
  - Umbilical venous access equipment
  - Neonatal resuscitation drugs
  - Baby Warmer
  - Plastic Bag
Form teams to perform Resuscitative Hysterotomy
- Resuscitative Team
- Resuscitative Hysterotomy Team
- Neonatal Resuscitation Team

Procedure

Maintain patient in supine position and continue compressions
Continue Left Uterine Deviation until the start of incision
Quickly prepare the skin with antiseptic solution (do not delay for skin prep)
Perform midline vertical Incision with scalpel on the abdomen from pubic symphysis to umbilicus and cut through skin and subcutaneous tissue until fascia is reached
Use fingers to bluntly dissect the rectus muscle fascia access the peritoneum (can use scalpel or blunt scissors)
Locate the uterus and differentiate it from the bladder (bladder yellow and enveloped in fatty tissue)
Make a vertical incision from the lower uterus to the fundus with scalpel (can use blunt scissors)
If the placenta is encountered while entering the uterus, cut through it
Use a cupped hand to locate the fetal part closest to pelvis
Elevate the located fetal part and pass through uterine incision while applying transabdominal pressure with other hand
Use traction and transabdominal pressure to deliver the rest of the baby
Clamp the cord at two spots and cut in between both clamps
Hand the baby to the neonatal team
Deliver placenta with gentle traction

Post-procedure

Continue performing compressions
Consider stopping if ROSC not achieved after several rounds and depending on the cause of PMCA
Give medications to promote uterine contraction
Analgesia and sedation may be required if patient achieves ROSC
Bleeding will be worse if ROSC achieved and may require pharmacologic and nonpharmacologic interventions
Closure will depend on whether the patient achieves ROSC and may necessitate careful closure to prevent further bleeding. Best performed by an obstetrician. If an obstetrician is unavailable, pack the uterus with gauze and clamps actively bleeding vessels to reduce bleeding.
Administer prophylactic antibiotics

References

Einav, S., et al. (2012). "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?" Resuscitation 83(10): 1191-1200.
Jeejeebhoy, F. M., et al. (2015). "Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association." Circulation 132(18): 1747-1773.
Kikuchi, J. and S. Deering (2018). "Cardiac arrest in pregnancy." Semin Perinatol 42(1): 33-38.
Parry, R., et al. (2016). "Perimortem caesarean section." Emerg Med J 33(3): 224-229.
Rose, C. H., et al. (2015). "Challenging the 4- to 5-minute rule: from perimortem cesarean to resuscitative hysterotomy." Am J Obstet Gynecol 213(5): 653-656, 653 e651.
Soskin, P. N. and J. Yu (2019). "Resuscitation of the Pregnant Patient." Emerg Med Clin North Am 37(2): 351-363.
Walls, R. M., et al. (2018). Rosen's emergency medicine: concepts and clinical practice. Philadelphia, PA, Elsevier.

Expert Commentary

This is an excellent review of an extremely rare, but potentially life-saving procedure. It may seem daunting to perform (and it should), but the evidence would say that a resuscitative hysterotomy (RH), especially if performed promptly, drastically improves survival during the catastrophic scenario of maternal cardiac arrest. This is even more important because these patients are young (and often relatively healthy) and could potentially have decades of meaningful quality of life if they can survive the arrest. That being said, this procedure is so rare that most of us not only have never performed it, but often have never even seen it. Not only that, but unlike other rare lifesaving procedures (such as cricothyroidotomy or resuscitative thoracotomy), RH is extremely difficult to practice in cadaver labs due to the unavailability of pregnant cadavers. So, we are left with the next best thing: familiarizing ourselves with the anatomy, physiology, and simplified technique of the procedure and mentally rehearsing it so that when the time comes, we can be ready.

For these rare procedures, in addition to the excellent and thorough review above, it is also helpful to simplify and rehearse the fundamental steps. I’m not an obstetrician and certainly not an expert on this procedure, but I’ve mentally prepared myself for what I would do in the event that I am faced with this grave situation and categorized it into the following simplified five step plan. Also, prior to writing this commentary I got a curbside consult from a friend from med school and actual obstetrician and gynecologic surgeon, Dr. Pietro Bortoletto.

First off, the indications-- basically, a pregnant woman estimated to be >20 weeks EGA who has suffered a cardiac arrest. Don’t worry about the 4 minutes, make the decision to perform a RH right away and start prepping. Delegate someone to call the appropriate resuscitation teams if available. Then start the procedure.

Step 1: Setup. You probably don’t have a c section kit in your trauma bay, so instead open the thoracotomy tray and you’ll have most of what you need. Go ahead and set aside the finochietto rib spreaders so that you don’t have a panic attack trying to remember how to put those together with other people watching. But everything else you’ll need will be in that tray (basically a scalpel, blunt scissors, and hemostats).

Step 2: Cut into the Abdomen. Splash prep the abdomen with betadine. Then make your long vertical incision from the uterine fundus to the pubic symphysis. Cut through the skin and subcutaneous tissue then bluntly separate the rectus and enter the peritoneum with scalpel or blunt scissors. Extend the peritoneal incision with blunt scissors.

Step 3: (carefully) Cut into the Uterus. First, locate the uterus. Then, take a deep breath and remember that there is a fetus inside the uterus. With that terrifying thought in mind, cut vertically into the uterus, insert your fingers, and extend the incision upwards with blunt scissors and a steady hand. If you encounter an anterior placenta, cut right through it.

Step 4: Delivery. Deliver the fetus either by cupping the head and elevating it through the incision or by grabbing a leg, wiggling out the shoulders, and then flexing the head. Hand over the neonate to whoever is taking the lead on the neonatal resuscitation (will need to be warmed, stimulated, and potentially aggressively resuscitated). Clamp and cut the cord, leaving a long enough umbilical stump for an easy umbilical line if needed. Then using gentle traction, attempt delivery of the placenta. If it isn’t coming easily, leave it alone so as not to stir up more bleeding.

Step 5: Extra credit. If you’ve made it this far as an emergency physician and there is still no obstetrician in sight, you can continue resuscitation, focusing on stopping the uterine bleeding. While you don’t need to close the fascia or skin, it can be helpful to close the uterine incision to prevent additional blood loss. You can do this with a whip stitch using 0-0 vicryl (or if that seems like showing off, you can just pack it with sterile gauze. If you’ve got it handy, give 10 IU oxytocin to stimulate uterine contraction and further slow bleeding. Feel free to order some antibiotics as well. Otherwise, continue maternal resuscitation following typical ACLS.

The big picture here is that this is a heroic, potentially life-saving procedure that most of us will never do. But we can all take a few minutes to read an excellent review like the blog post above, watch a video, and mentally walk ourselves through the simplified steps. That preparation will afford us some much-needed confidence if we are ever faced with this terrifying scenario.

Paul Trinquero, MD

Medical Director

Department of Emergency Medicine

US Air Force Hospital - Langley

Pietro Bortoletto, MD

Clinical Fellow

Reproductive Endocrinology & Infertility

Weill Cornell Medical College

How To Cite This Post:

[Peer-Reviewed, Web Publication] Gonzalez, A. Ko, J. (2021, Dec 13). Resuscitative Hysterotomy. [NUEM Blog. Expert Commentary by Trinquero, P and Bortoletto, P]. Retrieved from http://www.nuemblog.com/blog/resuscitative-hysterotomy.

Nail Trauma

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Written by: Jon Andereck, MD, MBA (NUEM PGY-3) Edited by: Rachel Haney, MD, (NUEM Graduate 2017, US Fellow MGH) Expert review by: Danielle McCarthy, MD

Why Nails are Important

Nail injuries may have significant associated functional and cosmetic morbidity
Nail bed provides adherence and support for the nail

Nail Anatomy

Nail bed overlies the cortex of the distal phalanx and lies directly beneath the nail plate
Eponychium is the skin that covers the proximal end
Hyponychium is the skin edge at the distal nail margin

Cuticle is an outgrowth of the eponychium that provides a seal between the proximal nail fold and nail plate
Germinal matrix is the proximal portion of the nail bed responsible for nail formation and begins 7 to 8 mm under the eponychium; the distal end of the germinal matrix is the lunula

Subungual Hematoma

A simple subungual hematoma is not an indication to remove the nail; trephination is not indicated if the hematoma encompasses only 25%, there is no significant pain, or if injury was over 24 hours ago as the blood likely clotted and will not flow out.
Blood under the cuticle proximal to the nail is a clue that there is a deeper injury and usually the nail should be removed if there is significant pain.
There is controversy regarding treatment of subungual hematomas and whether simple trephination is enough or whether inspection of the nail bed for injury is required.
- It was suggested that for subungual hematomas involving more than 50% of the nail bed, the nail should be removed given the risk of nail bed laceration. This was based on an initial study in 1987 that found that 16/27 patients with hematomas >50% had associated nail bed lacerations that required repair This study did not follow up with patients and did not have a control group so long term outcomes are unknown.
- However, subsequent studies have shown that if there is no other significant finger tip injury, treatment by trephinating alone provides a similar good cosmetic and functional result.
If you don’t have a trephinator, what else can you use?
- Heated paper clip
- 23-gauge 1-inch needle. Hold the needle over the hematoma, avoiding the lunula, twist and rotate the needle back and forth like a drill; no pressure needed.
- Number 11 scalpel (slower, more painful, larger hole but better drainage)
- Insulin syringe needle (29-gauge) can be used on toenails.
What if there is a fracture underneath?
- Though there is a risk of turning the fracture into an open fracture, consider still performing the procedure if the injury is painful.
Can consider antibiotics if trephination is pursued, though there is no data.
It is always important to obtain an x-ray with any traumatic injury.

Nail Bed Repair

Suture the nail bed if a large subungual hematoma is associated with an unstable or avulsed nail
Good outcome depends on maintaining the space under the cuticle where the new nail will grow out from (the germinal matrix). If this area scars down, a new nail will not grow
If the nail is only partially avulsed or loose, especially at the base, lift the nail slightly to assess the nail bed.
If the nail is completely transected, it is best to remove the entire nail to suture the nail bed; in this case, suture the proximal and lateral nail folds first for better approximation prior to repairing the actual nail bed.
A sturdy needle (3-0 or 4-0) is needed to suture the nail back in place. Before replacing the nail and suturing it back in place, you can poke a hole through so the needle and suture can pass more easily.
A study in 2008 used dermabond for nail bed laceration repair showed similar follow up cosmetic and functional outcomes; using dermabond took about 1/3 of the time. It was a small study with only 40 patients and repair was done by orthopedic residents, but definitely a consideration
Some physicians will use dermabond to secure the nail in place as well
Key to success is achieving hemostasis and making sure you have a dry field before dermabond application

Another method to secure the nail in place is the figure 8 stitch proposed by hand surgeons
Protecting the exposed nail bed is essential, which can be done with the nail itself (wash well beforehand with normal saline), with the sterile aluminum foil from the suture pack, or with a piece of vaseline gauze. The nail should be reinserted under the eponychium to protect the open space for nail growth.
Consider a hand surgeon consult if the nail bed is extensively lacerated or if part of the nail bed is lost, as the patient my need a matrix graft.
Tell the patient to return for a wound check 3-5 days post repair. Replace any non-adherent material that was inserted into the proximal nail fold. Afterwards, the patient should perform dressing changes every 3-5 days.
Sutures that were used to reattach the nail should be removed in 2 weeks.
Nails grow at a rate of 0.1 mm/day and it takes approximately 6 months for a new nail to grow.
Instruct the patient to avoid any trauma or chemical irritants to the healing nail.

Tips:

Always use absorbable suture to repair the nail bed

Use a large suture and sturdy needle when suture the nail back in place; consider dermabond as an option
Use a finger tourniquet to maintain a bloodless field
Clean the nail bed prior to repair; clean the nail very well before replacement
Digital blocks are key
Repair the proximal and lateral nail folds first
If possible use the avulsed nail to protect the exposed nail bed and maintain the space for a new nail to grow

Batrick N. Treatment of uncomplicated subungual hematoma. Emerg Med J 2003;20:65.

Bowen WT, Slaven EM. Evidence-based management of acute hand injuries in the emergency department. Emergency Medicine Practice EB Medicine. 2014;16(12):1-28. http://www.ebmedicine.net/media_library/files/1214%20Hand%20Injuries

Guthrie, Kane. “Minor Injuries 001.” Life in the Fastlane. <http://lifeinthefastlane.com/minor-injuries-001/>.

Last, First M. “Article Title.”Website Title. Website Publisher, Date Month Year Published. Web. Date Month Year Accessed.

Hedges, Jerris, James Robers. “Methods of Wound Closure.” Clinical Procedures in Emergency Medicine, 6th ed. Philadelphia: Elsevier/Saunders, 2014.

Roser SE, Gellman H. Comparison of nail bed repair versus nail trephination for subungual hematomas in children. J Hand Surg [Am]1999;24:1166–70.

Strauss E, Weil W, Jordan C, Paksima N. A prospective, randomized, controlled trial of 2-octylcyanoacrylate versus suture repair for nail bed injuries. J Hand Surg Am. 2008;33(2):250-253.

Posted on December 9, 2021 by NUEM Blog.

Bicarb in Cardiac Arrest

**Written by:** Kishan Ughreja, MD (NUEM ‘23) **Edited by:** Sean Watts, MD (NUEM ‘22)
**Expert Commentary by**: Dana Loke, MD (NUEM ‘21)

Utility of Sodium Bicarbonate in Cardiac Arrest

Use of sodium bicarbonate as empiric therapy in cardiac arrest has been an area of controversy. During cardiac arrest hypoxia and hypoperfusion results in severe metabolic acidosis and subsequent impaired myocardial contractility, decreased efficacy of vasopressors, and increased risk of dysrhythmias. Previous ACLS guidelines recommended use of sodium bicarbonate to mitigate these effects; however, harms are also associated with its routine use including compensatory respiratory acidosis, hyperosmolarity, increased vascular resistance, and reduction in ionized calcium. 1 Current guidelines no longer recommend routine use of sodium bicarbonate, except in cases of arrest secondary to hyperkalemia, TCA overdose or preexisting metabolic acidosis.2 Regardless of these recommendations, sodium bicarbonate continues to be utilized during routine management of cardiac arrest, and studies are limited in investigating its appropriate use.

The study below investigates the effect of sodium bicarbonate in patients suffering out-of-hospital cardiac arrest with severe metabolic acidosis during prolonged CPR.

Article

Clinical Question

In patients with prolonged, atraumatic out-of-hospital cardiac arrest (OHCA) and severe metabolic acidosis, does sodium bicarbonate (SB) administration with transient hyperventilation improve acidosis without increased CO2 burden, enhance rates of return of spontaneous circulation (ROSC), survival to admission, and favorable neurologic outcomes?

Study Design

Double-blind, prospective, randomized, placebo-controlled, single-center pilot clinical trial

Population

Inclusion criteria: Atraumatic arrest in patients ≥18yo without ROSC after 10 minutes of CPR in ED and with pH <7.1 or bicarbonate <10 mEq/L on ABG

Exclusion criteria: DNR, ECPR, ROSC w/i 10 minutes of ACLS, absence of severe metabolic acidosis on ABG after 10 minutes of CPR

Data collection over 1 year at Asan Medical Center, a tertiary referral center in Seoul, Korea

Intervention

Sodium bicarbonate administration of 50 mEq/L over 2 minutes with concurrent increase in ventilation rate from 10 to 20 breaths per minute for 2 minutes

Control

Normal saline administration of 50 mL over 2 minutes (with same transient hyperventilation)

Outcomes

Primary

Change in acidosis (per methods section)

Secondary

Sustained ROSC — defined as restoration of a palpable pulse ≥20 min (per methods section, but listed as primary outcome in abstract)
Survival to hospital admission
Good neurological survival at 1 and 6 months (defined as cerebral performance category 1 or 2)

Results

157 patients presented with cardiac arrest, 50 enrolled per inclusion criteria
No significant differences between study and control groups regarding demographics, PMH, witnessed arrest, bystander CPR, pre-hospital and initial cardiac rhythm
10% (n=5) of enrolled patients with sustained ROSC and admitted
No patients survived at 6 months follow up

Pre-Intervention

ABG results at 10 minutes were not significantly different between groups

Post-intervention

ABG results at 20 minutes demonstrate that pH and HCO3- were higher in the study group than in the control group
- pH 6.99 vs 6.90, p=0.038
- HCO3- 21.0 vs 8.00, p=0.007
Within the study group, the increase in pH was not statistically significant after sodium bicarbonate administration; the increase in HCO3- was statistically significant (using Wilcoxon signed rank test)
No statistically significant findings in the control group after normal saline administration
No significant differences in any secondary outcomes (sustained ROSC, survival to admission, good neurologic outcome)

Strengths

Randomized, double-blinded, placebo-controlled study design
This study adds additional information to a clinical question that has limited previous research
This study added a practical clinical intervention (hyperventilation) to counteract excessive CO2 accumulation secondary to sodium bicarbonate administration, a known deleterious effect of this compound.
Strong control over sodium bicarbonate administration (no pre-hospital administration allowed in South Korea), so authors could control when it was given and analyze ABG results at desired intervals)

Weaknesses

Small, single-center study with only 50 enrolled patients
Primary endpoint unclear from abstract vs methods, whether it was change acidosis or sustained ROSC; however, neither is truly patient-centered clinical outcome (good neurological outcome would be the ideal primary outcome)
Dosing was universal — 50 mEq/L instead of weight based (1-2 mEq/L/kg), which could result in improper dosing
Hyperventilation strategy may have benefited sodium bicarbonate administration group by countering respiratory alkalosis, however, it could have harmed the placebo group
Possible venous sampling rather than arterial for blood gas analysis at 10-minute point, though this would be a concern in any arrest setting if an arterial line could not be established in this time frame

Author’s Conclusion

“The use of sodium bicarbonate during CPR with transient hyperventilation improves acid-base status without CO2 elevation which is one of the most concerned adverse effects of sodium bicarbonate administration, but it had no effect on the improvement of the rate of ROSC and good neurologic survival. At this point, we could not advise for or against its administration, our pilot data could be used to help design a larger trial to verify the efficacy of sodium bicarbonate.”

Bottom Line

Based on this study, the use of sodium bicarbonate does not appear to improve clinically significant outcomes, though it improved acid-base status. Sodium bicarbonate should not be indiscriminately used in all cardiac arrests, and larger trials should be performed to further evaluate its impact on patient-centered outcomes.

Citation

Ahn, S., Kim, Y. J., Sohn, C. H., Seo, D. W., Lim, K. S., Donnino, M. W., & Kim, W. Y. (2018). Sodium bicarbonate on severe metabolic acidosis during prolonged cardiopulmonary resuscitation: a double-blind, randomized, placebo-controlled pilot study. Journal of thoracic disease, 10(4), 2295.

References

White, S. J., Himes, D., Rouhani, M., & Slovis, C. M. (2001). Selected controversies in cardiopulmonary resuscitation. Seminars in respiratory and critical care medicine, 22(1), 35–50. https://doi.org/10.1055/s-2001-13839
Merchant, R. M., Topjian, A. A., Panchal, A. R., Cheng, A., Aziz, K., Berg, K. M., Lavonas, E. J., Magid, D. J., & Adult Basic and Advanced Life Support, Pediatric Basic and Advanced Life Support, Neonatal Life Support, Resuscitation Education Science, and Systems of Care Writing Groups (2020). Part 1: Executive Summary: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 142(16_suppl_2), S337–S357. https://doi.org/10.1161/CIR.0000000000000918

Expert Commentary

Thank you Dr. Ughreja and Dr. Watts for this excellent blog post on an important topic. In medicine, we often ask “what else can we do?” but less often do we ask “is what we’re already doing effective?” This is especially important for resuscitation and cardiac arrest. Not everything that is standard-of-care is ultimately effective care, and overtreating patients can lead to other untoward effects.

In addition to the points made in the above blog, I would add a few important notes into the equation. First, the study excluded in-hospital cardiac arrest and therefore should not be considered in those patients. Second, the study also excluded those patients with early ROSC and absence of severe metabolic acidosis, effectively biasing towards inclusion of sicker patients. It is unclear how administration of sodium bicarbonate may have influenced those patients. Third, the study population was quite small and a striking majority of that population were found to have an initial rhythm of asystole. Fourth, ventilation rates were purposefully increased during bicarb administration. Though this may be practical and can potentially counteract excessive CO2 accumulation secondary to sodium bicarbonate administration, this is not common practice which leads to questions of this study’s external validity at other institutions.

So, despite this study, at this point in time we still must grapple with the “should-we-or-should-we-not” of sodium bicarbonate administration in prolonged cardiac arrest. Some scenarios certainly do require sodium bicarbonate, most notably TCA overdose and hyperkalemia. In these cases, it’s obvious what to do. But so often what we do in emergency medicine is riddled with uncertainty. An unclear cause of cardiac arrest is certainly one of those situations. Perhaps instead of mindlessly giving sodium bicarbonate to cardiac arrest patients, we should give it once or twice and look for evidence that it has had an effect. Is the rhythm narrowing? Did you obtain ROSC shortly after administration? If not, giving dose after dose of sodium bicarbonate in hopes of meaningful recovery may not be the best path forward.

Dana Loke, MD

Department of Emergency Medicine

Northwestern University Feinberg School of Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Ughreja, K. Watts, S. (2021, Dec 6). Bicarb in Cardiac Arrest. [NUEM Blog. Expert Commentary by Loke, D]. Retrieved from http://www.nuemblog.com/blog/bicarb-arrest

Hand Nerve Blocks

**Written by:** Aldo Gonzalez, MD (NUEM ‘23) **Edited by:** Jason Chodakowski, MD (NUEM '20)
**Expert Commentary by**: Mike Macias, MD

Hand Nerve Blocks

Nerve blocks are the use of anesthetics to anesthetize an area by injecting directly around the nerve that innervates a certain area. It is useful when there is a large area to provide anesthesia, the area might get distorted by local infiltration and make it difficult to close the tissue, or the distribution of the area to be anesthetized is well-suited to a nerve block.

Indications

Nerve blocks of the median, ulnar, radial, and digital nerves are useful for injuries of the hand including fractures, lacerations, and burns.

Contraindication

Overlying infection
Previous allergic reaction to anesthetic

Anesthetics

Landmark versus Ultrasound guidance

Ultrasound guidance is preferred given the ability to visualize the desired nerve and proper instillation of the anesthetic around the nerve. On ultrasound nerves are circular or triangular hyperechoic structures with hypoechoic structures within. Often described as having a “honeycomb” appearance as seen in the image of the median nerve below.

Materials

Ultrasound with Linear Transducer
Probe Cover
Sterile Ultrasound Gel
Anesthetic
10 cc syringe
18 gauge needle (to draw medication)
25-27 gauge needle at least 1.5 in in length
Antiseptic Solution (ex. Chlorhexidine)
Towel

Positioning

The patient can be either supine or seated with their arm slightly abducted and rested on a flat surface. Their elbow can be flexed with the wrist supinated and in slight extension. A rolled towel can be used for patient comfort and help in maintaining slight extension.

Figure 1: Nerves, arteries, and muscles of the human forearm

Radial Nerve Block

The superficial radial nerve travels between the flexor carpi radialis and the radial artery on anterior (volar) and lateral (radial) aspect of the forearm. Near the wrist the radial nerve splits into the medial and lateral branch of the superficial radial nerve. The block of this nerve should be performed at the mid-forearm to distal third of the forearm before the nerve splits. The nerve may be difficult to see at the distal forearm so instead it can be found proximally and followed distally. A lateral (radial) approach of the forearm provides the most direct route to the nerve.

Ulnar Nerve Block

At the distal forearm the ulnar nerve runs on the medial (ulnar) and anterior (volar) aspect of the forearm between the flexor carpi ulnaris tendon and the ulnar artery. The ulnar nerve lies in very close proximity to the ulnar artery in the distal forearm and increases the risk of accidental intravascular injection. It is safer to identify the ulnar nerve distally and the follow the artery and nerve proximally. Around the proximal third of the forearm the ulnar artery dives deeper and separates from the ulnar nerve. This provides a safer target. A medial (ulnar) approach of the forearm provides the most direct route to the nerve.

Median Nerve Block

At the mid to distal forearm the median nerve runs in the middle of the anterior (volar) aspect of the forearm between the flexor digitorum superficialis and flexor digitorum profundus muscles/tendons. Near the wrist the nerve can be difficult to appreciate due to all the tendons of the anterior compartment of the arm. The nerve can be best appreciated at the mid-forearm. A lateral (radial) or medial (ulnar) approach can be used for in-plane technique or a mid-line approach using out-of-plane technique. Be mindful to avoid accidentally puncturing the radial or ulnar artery If using an in-plane technique with a lateral or medial approach.

Figure 5: Demonstration of a median nerve block using a median (ulnar) approach with in-plane ultrasound technique on a patient’s right hand. Median nerve (yellow line) and ultrasound probe location (blue line).

Figure 6: Demonstration of a median nerve block using a lateral (radial) approach with in-plane ultrasound technique on a patient’s right hand. Median nerve (yellow line) and ultrasound probe location (blue line).

Steps for Ultrasound-Guided Nerve Block

Document a neurological exam prior starting the procedure
Select the nerve or nerves best suited to achieve best anesthesia for the injury
Use the linear transducer to visualize the nerve prior beginning the procedure
Plan an approach and select the best site
Draw up anesthetic in the 10 cc syringe with an 18 G needle
Replace 18 G needle with 25-27 G needle
Use antiseptic solution to prepare the skin
Dawn sterile gloves
Cover transducer in sterile cover
Use ultrasound to visualize the nerve and confirm approach
Insert the needle into the skin
Advance the needle using in-plane or out-of-plane technique
Come close to the nerve but do not puncture the nerve
Draw back to confirm not with-in a vessel
Deliver 5mL of anesthetic
The nerve will become enveloped in hypoechoic anesthetic and peel away from the fascia of nearby muscles
Withdraw the needle.
Wait 3-5 minutes until patient is fully anesthetized

References

Drake, R., Vogl, A. W., & Mitchell, A. W. (2015). Gray's Anatomy for Students (3rd ed.): Elsevier.
Farag, E., Mounir-Soliman, L., & Brown, D. L. (2017). Brown’s Atlas of Regional Anesthesia (5th ed.): Elsevier.
Gray, H. (2000). Gray's Anatomy of the Human Body. 20th edition. Retrieved from https://www.bartleby.com/107/
Harmon, D., Barrett, J., Loughnane, F., Finucane, B. T., & Shorten, G. (2010). Peripheral Nerve Blocks and Peri-Operative Pain Relief (2nd ed.): Elsevier.
Pester, J. M., & Varacallo, M. (2019). Ulnar Nerve Block Techniques. In StatPearls [Internet]: StatPearls Publishing.
Roberts, J. R., Custalow, C. B., & Thomsen, T. W. (2019). Roberts and Hedges' clinical procedures in emergency medicine and acute care (7th ed.): Elsevier.
Waldman, S. D. (2016). Atlas of Pain Management Injection Techniques E-Book (4th ed.): Elsevier.
Waldman, S. D. (2021). Atlas of Interventional Pain Management E-Book (5th ed.): Elsevier.

Expert Commentary

Thank you Drs. Gonzalez and Chodakowski for the excellent post on forearm nerve blocks! This is an important skill that definitely improves the care of our patients, especially since hand injuries are such a common emergency department presentation. This is especially true for injuries that are difficult to anesthetize using traditional local injection such as dog bites, burns, abscesses, large lacerations, and fractures of the hand. I’d like to dive a little deeper into a few aspects of forearm nerve blocks:

Ultrasound guidance

I think that the days of a landmark based approach to the majority of nerve blocks are gone with the widespread availability of ultrasound and its superiority with respect to block success and reduced complications. So if you have it, use it!

Which nerve to block?

Once you have made the commitment to block one forearm nerve, it doesn’t require much additional time or effort to block a second or even a third! Often, hand injuries will span several nerve distributions so make sure you are providing adequate anesthesia. Here is a quick way to think of it:

Major hand injury (ie burn, multiple hand fractures): Triple block
Injury to radial aspect of hand or digits 1-4: Radial + median nerve block
Injury to ulnar aspect of hand or 5th digit (ie Boxer’s fracture): Ulnar nerve block

It is important to remember that forearm nerve blocks do not provide anesthesia to the volar forearm or wrist and therefore will not be adequate for distal radius fracture reduction. In this case, an above the elbow Radial nerve block should be performed.

Which local anesthetic should I use?

It’s always important to consider what the goals of your local anesthetic are when determining which one to use. If you are performing a quick procedure, the shorter the better such as lidocaine. If you are providing prolonged pain management such as with a burn, bupivicaine is a better choice. I tend to prefer lidocaine + epinephrine (duration of acton 2-2.5 hours) for most of my hand injuries. Why? In a busy emergency department managing many patients at a time, the initial block and the procedure you plan on performing (ie lac repair, fracture reduction, etc) do not always happen simultaneously (ie patient may still need x-ray, irrigation, ring removal, etc). Using lidocaine + epinephrine will allow you to provide immediate pain relief for your patient but give you time to do other tasks before the patient is ready for the procedure

Positioning

As with any procedure, the set up is extremely important. You nicely described positioning earlier but I just want to highlight a couple additional points. Make sure your patient is comfortable and your ultrasound screen is in-line with your procedure. You don’t want to be turning your head away from your block to look at the screen. For the median and radial nerve block, the patient’s arm should be supinated and resting on a hard flat surface. Both nerves can then be approached using an in-plane technique from the radial aspect of the arm. The ulnar nerve can be cumbersome to get to with this same patient positioning so I recommend abducting the shoulder to about 90 degrees and placing the arm on a Mayo stand next to the patient. This will allow an in-plane approach from the ulnar aspect of the arm. I have also found this positioning technique helpful for the ulnar nerve block.

Procedural Tips

I wanted to end with a couple of important procedural pearls I have learned during my experience with performing these blocks:

Perform a pre-block exam! Always make sure to perform and document a full neurological exam of the hand before you block any nerve. This is important because you want to make sure you know if any sensory or motor changes are present before your perform the block otherwise if a neurological deficit is noted after, it makes it difficult to tell if the block caused the new symptom (you can always wait until the anesthetic wears off but it may be awhile if you used bupivicaine).

Follow the arteries! Sometimes it can be tricky to find the ulnar and radial nerves. The easiest method is to always start distally at the wrist. Both the radial and ulnar nerves run with their paired artery so if you start here and slide proximally, you should see the nerve split away from the artery around the mid forearm. Block them here!
Target the fascial plane! The key to an effective forearm nerve block is “bathing” the nerve in anesthetic. You will want to see spread of the anesthetic around the nerve in a crescent shape, full circumferential spread is not needed. Since these nerves run in the fascial plane the goal is to get your needle tip into this plane to deposit anesthetic. There is never a need to actually touch the nerve so avoid this by aiming for the fascia and not the nerve.
Protect the hand! After you perform a forearm nerve block be sure to communicate with nursing, consultants, and the patient regarding what block was performed and how long the effects will last. If a long acting agent was used such as bupivicaine, the hand should be splinted or arm placed in a sling and instructions provided to patient regarding care at home if they are being discharged.

Thank you again for providing this excellent piece on forearm nerve blocks. I cannot stress enough how essential I think these blocks are to the toolkit of the modern emergency physician. I promise you once you add these to your practice your patient’s will thank you!

Michael Macias, MD

Global Ultrasound Director, Emergent Medical Associates

Clinical Ultrasound Director, SoCal MEC Residency Programs

How To Cite This Post:

[Peer-Reviewed, Web Publication] Gonzalez, A. Chodakowski, J. (2021, Nov 29). Hand Nerve Blocks. [NUEM Blog. Expert Commentary by Macias, M]. Retrieved from http://www.nuemblog.com/blog/hand-nerve-blocks

Sono Pro Tips and Tricks for Acute Appendicitis

**Written by:** Morgan McCarthy, MD (NUEM ‘24) **Edited by:** David Feiger, MD (NUEM ‘22)
**Expert Commentary by**: Shawn Luo, MD & John Bailitz, MD

Welcome to the NUEM SonoPro Tips and Tricks Series where Local and National Sono Experts team up to take you scanning from good to great for a particular diagnosis or procedure.

For those new to the probe, we recommend first reviewing the basics in the incredible FOAMed Introduction to Bedside Ultrasound Book, 5 Minute Sono, and POCUS Atlas. Once you’ve got the basics beat, then read on to learn how to start scanning like a Pro!

Did you know, appendicitis is one of the most common surgical emergencies. Despite this, some data suggests that appendicitis is missed in 3.8% to 15% of children and 5.9% to 23.5% of adults in ED visits. Appendicitis is difficult to diagnose due to the early nonspecific generalized symptoms (anorexia, generalized pain, nausea, diarrhea or constipation). We can use point of care ultrasound (POCUS) to help evaluate your differential diagnosis. One study showed that after only a 20-minute training ED physicians at various levels of experience were able to scan for appendicitis with a specificity of 97.9% and a sensitivity to 42.8%.

Beyond the classic pediatric patient, who else does the SonoPro scan?

Pocus use for appendicitis is one of the leading diagnostic tools in pediatrics for acute appendicitis. In the pediatric population limiting radiation is generally thought to be of utmost importance. The lack of exposure to radiation and small habitus makes ultrasound a great alternative in the pediatric patient. These tips and tricks can be useful in other high risk adult patients, like pregnant women. It is well known that in adults there is often a higher chance of pathology and surgeons are managing the ultimate say on whether more imaging is necessary. However, the use of ultrasound for acute appendicitis may save time, expedite care, lead to quicker consultation, and potentially augment patient satisfaction and improve outcomes.

How to scan like a Pro:

There are a few ways to scan for the appendix. To start, we recommend simply asking for the patient to point to where the pain is worst and place the probe directly over that spot.
A simple trick is to have the patient cross their right leg over their left leg; this brings the appendix closer to the abdominal wall.
If neither of these work, start to look for visual landmarks to orient yourself: iliac artery and vein, and the psoas muscle. The psoas muscle will be posterior, the iliac artery will be medial and the iliac crest lateral. Many times the appendix may be on top of the iliac artery. ‘Lawn mowing’ the probe up and down in this area may help it come into view.

What to Look For:

Try to look for a blind ending tubular structure that is not undergoing peristalsis. When you locate this, turn your probe to view the appendix in short axis and measure the anterior to posterior diameter. In a normal appendix this may be shorter than the lateral measurements as a normal appendix is compressible!
There are two main criteria for diagnosing appendicitis on ultrasound:

> 6mm*
non-compressible

*Note: Make sure to consider your patient’s age; the criteria may not apply to young children as their appendix may be naturally smaller. Appendix growth typically occurs at 3 to 6 years, therefore in this population you may depend more on secondary findings.

There are many secondary findings that many experts believe may be more useful than the measurements of the appendix itself as this can be very difficult to accurately measure:

What to do next:

Ultrasound for appendicitis is very specific, however not very sensitive. If you see a dilated non-compressible blind ending loop of bowel without peristalsis, you may have identified an appendicitis - call your surgeon, follow recommendations and start antibiotics! If you are uncertain, look for secondary signs of appendicitis as above; if they are found you can increase your suspicion of appendicitis. If these findings are not present, more advanced diagnostic imaging may be required with respect to your clinical suspicion. Consider an MRI in a young patient or CT scan with contrast in an adult for further evaluation.

Where to Learn More (References)

Mahajan P, Basu T, Pai C, et al. Factors Associated With Potentially Missed Diagnosis of Appendicitis in the Emergency Department. JAMA Network Open. 2020;3(3):e200612. doi:10.1001/jamanetworkopen.2020.0612.
Y Ravichandran, P Harrison, E Garrow, and JH Chao. Size Matters: Point of care Ultrasound in Pediatric Appendicitis. Pediatric Emergency Care. 2016; 32: 815-816.
Ma, John, et al. Ma and Mateer's Emergency Ultrasound. McGraw-Hill Education, 2020.
Macias, Micheal. TPA, The Pocus Atlas.
Availa, Jacob. 5 minute Sono.
US G.E.L. Podcast
Nelson, Chiricolo, Raio, Theodoro, Patel, Johnson. Can Emergency Physicians Positively Predict Acute Appendicitis on Focused Right Lower Quadrant Ultrasound?. Annals of Emergency Medicine, 2005; 46: 27-28

Expert Commentary

Excellent job by Morgan and David on this engaging and informative post summarizing the latest and greatest pro-tips and tricks for POCUS for Appendicitis. POCUS again has been demonstrated to be a helpful adjunct to improve time to diagnosis and treatment when utilized by trained clinicians for appropriate patients. On your next pediatric, pregnant, or otherwise thin “Rule out Appy”, begin the exam by asking the patient to cross their leg to flex the psoas muscle to bring the appendix closer to probe. Have the patient point to the pain to identify where to start. If the appendix is not visualized, then go to McBurney’s point in the axial plane, visualizing the iliac artery & vein to find the nearby appendix. Next, start “lawn mowing” by compressing slowly but with adequate depth to displace bowel gas. Once you see what appears to be an inflamed appendix, trace the structure to verify the blind-ending and hold your probe for a few seconds to confirm the lack of peristalsis. Measure the diameter, then turn on color flow and look for other secondary signs of inflammation. Since the specificity is high, when appendicitis is visualized, call your surgeon, and consider skipping the CT. But remember, since the appendix often “hides” within the bowel the sensitivity is low, so other comprehensive imaging will be needed to reach the correct diagnosis.

John Bailitz, MD

Vice Chair for Academics, Department of Emergency Medicine

Professor of Emergency Medicine, Feinberg School of Medicine

Northwestern Memorial Hospital

Shawn Luo, MD

PGY4 Resident Physician

Northwestern University Emergency Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] McCarthy, M. Feiger, D. (2021, Nov 22). Sono Pro Tips and Tricks for Acute Appendicitis. [NUEM Blog. Expert Commentary by Luo, S and Bailitz, J]. Retrieved from http://www.nuemblog.com/blog/sonopro-tips-and-tricks-for-acute-appendicitis

Stingray Stings

**Written by:** Mike Tandlich, MD (NUEM ‘24) **Edited by:** Peter Serina, MD, MPH (NUEM ‘22)
**Expert Commentary by**: Mike Macias, MD (NUEM ‘17)

Expert Commentary

Thank you Drs. Tandlich and Serina for this excellent infographic summarizing stingray envenomation! The good news is that the majority of stingray injuries are nonfatal and will heal without any complications! You hit all of the key points however I just wanted to highlight a few management tips below:

Treat as a Trauma!

While majority of the pain from stingray envenomation occurs as a result of its venom, it is important to remember that this is also a traumatic injury. Treat the injury just like you would any other penetrating trauma. Consider the location as well as surrounding structures and make sure to properly examine for tendon, nerve, and vascular injury. Injuries to the chest or abdominal regions should prompt advanced imaging and trauma consultation.

Hot Water is Key!

Stingray envenomation is noted to cause severe pain that is often out of proportion to your examination findings. While the exact mechanism is not clear, the venom can lead to not only pain but also local tissue necrosis. The good news is the venom is heat labile! The faster you can get the injured area into hot water the better. You want the water to be as hot as tolerable without causing a thermal burn. A good rule of thumb is to have the patient place their unaffected limb in the water first to see if it is tolerable. As this often occurs at a beach, lifeguards are often your best resource to get hot water fast! Oral analgesics can be administered if needed however often they are unnecessary as soon as the injured area is submerged in hot water.

Retained Barb?

While uncommon, a retained barb from the envenomation can occur so be sure to consider this and evaluate appropriately. Traditionally, x-ray imaging of the affected area is performed to evaluate for a radio-opaque barb however some evidence suggests this to be a relatively low yield practice [1]. Ultrasound can also be considered if there is suspicion for retained barb or other material. In general ultrasound has been shown to be highly sensitive for identification of foreign body [2]. Not only can it be used to identify the barb but it can be used to facilitate removal [3].

Give Prophylactic Antibiotics

Prophylactic antibiotics are recommended for stingray envenomation given that the limited data suggest a higher rate of wound infection in patients who were not initially treated with antibiotics [1]. Given these injuries often occur in the ocean make sure to cover for salt water species such as Vibro. Levofloxacin is my go to option.

Teach The Stingray Shuffle!

Keeping these key management points in mind, the good news is that the majority of stingray injuries are nonfatal and will heal without any complications! Before your patient is discharged don’t forget to remind them that the next time they are going out for a surf to do the stingray shuffle!

References

Clark RF, Girard RH, Rao D, Ly BT, Davis DP. Stingray envenomation: a retrospective review of clinical presentation and treatment in 119 cases. J Emerg Med. 2007 Jul;33(1):33-7
Aras MH, Miloglu O, Barutcugil C, Kantarci M, Ozcan E, Harorli A. Comparison of the sensitivity for detecting foreign bodies among conventional plain radiography, computed tomography and ultrasonography. Dentomaxillofac Radiol. 2010;39(2):72-78. doi:10.1259/dmfr/68589458
Nwawka OK, Kabutey NK, Locke CM, Castro-Aragon I, Kim D. Ultrasound-guided needle localization to aid foreign body removal in pediatric patients. J Foot Ankle Surg. 2014;53(1):67-70. doi:10.1053/j.jfas.2013.09.006

Michael Macias, MD

Systems Clinical Ultrasound Director,
Emergent Medical Associates

Ultrasound Director,
UHS SoCal MEC Residency Programs

How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Serina, P. (2021, Nov 15). Stingray Stings. [NUEM Blog. Expert Commentary by Macias, M]. Retrieved from http://www.nuemblog.com/blog/stingray-stings

Ankle Injuries

**Written by:** Eric Power, MD (NUEM ‘24) **Edited by:** Brett Cohen, MD (NUEM ‘21)
**Expert Commentary by**: Jake Stelter, MD (NUEM ‘19)

Stepwise Approach to Management of Ankle Injuries in the Emergency Department

Introduction

Ankle injuries are a common presentation to the emergency department. This group of injuries varies in severity with different treatments, discharge instructions, and follow up plans based on the injury classification.. Ankle fractures also have a large degree of variability in severity and require different initial management. In this post, we will focus on the most common types of ankle injuries and discuss the most important steps for initial assessment, management, and discharge instructions ED clinicians should be giving to their patients.

Ankle Sprains

A very common presentation of ankle injuries, especially for young athletes, is a patient coming in saying they “rolled” their ankle. This most often infers a mechanism of an inversion injury to the ankle, often after making a cut or sudden change in direction in a sporting event or landing on another competitor’s foot. In fact, it is estimated that 25% of all musculoskeletal injuries are inversion ankle injuries, and that half of all these injuries occur during sporting events. Sudden, forced inversion of the ankle, often while in slight plantar flexion, may result in injury to one or more ligaments of the lateral ankle ligament complex. The anatomy of this complex, from anterior to posterior, consists of the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL) [1].

Isolated damage to the ATFL is by far the most frequent injury after “rolling an ankle”, making up two-thirds of all cases. With increased amounts of inversion force there is injury to the CFL followed by the PTFL, which are involved in about 20% of cases [2]. However, as with almost all complaints that come into the ED, a focused history and physical exam is the most important initial step to assess and correctly diagnose an ankle injury. The exam should start with assessments of neurovascular status with pulses, sensation, and capillary refill. The ankle should also be examined for gross deformity, tenderness, swelling, range of motion (ROM), strength, and associated injuries of the foot or knee.

Assessing for other Injuries

It is also important to recognize that ligamentous injuries often do not happen in isolation. Studies have found the prevalence of concurrent bony injuries in patients with ankle sprains to be 15-21%, with an anterior talofibular avulsion injury being the most common type [3,4]. When trying to decide whether to image these patients with ankle pain and likely sprains to assess for bony injury, many EM physicians may be familiar with the Ottawa rules. The rules and several interactive clinical decision-making tools are available online. For review, if the patient meets any of the following criteria, they require imaging of the ankle to assess for bony injuries.

Tenderness at the distal 6cm of the posterior edge of the fibula or tibia
Tenderness at the tip of either malleolus
Tenderness at the base of the fifth metatarsal or navicular
Inability to take four steps immediately after injury and on initial evaluation in the Emergency Department

A recently conducted review by Beckenkamp et al. revealed these rules to be highly sensitive (99.4%), but poorly specific (35.3%) to rule out visible fractures on plain films [6].

If x-rays are negative for fracture, the patient still may require orthopedic follow-up, surgery, and have a longer recovery if there is concern for a syndesmotic injury, or “high-ankle sprain”. This is the result of an injury to the tibiofibular ligament and is further discussed in a post by Ford et al [7]. Important considerations when there is clinical concern for this injury include looking for bony overlap on the malleolar films and performing specific exam maneuvers such as a “squeeze test”.

Symptom Management

When deciding what analgesic to use, providers should use clinical gestalt. In order to limit the use of opioid pain medications to prevent dependence and other associated side effects, we recommend they are only used in severe injuries where the patient is in obvious, uncontrolled pain or after a trial of non-opioid pain medications has failed. It is also our recommendation that physicians should not hesitate to use NSAIDs for pain management in fractures without other contraindications, as overall there is limited evidence to suggest it impairs bone healing [8,9]. These medications also provide the benefit of reducing inflammation in patients with swelling and/or joint effusion.

Generally accepted principles to promote healing, decrease swelling, and reduce pain are frequently referred to as the acronym “RICE” or “PRICE”. PRICE is now preferred because it includes protection of the affected structures, along with the other classic teachings. The remainder of the useful acronym includes rest of the injured joint, using ice for 20 minutes on, followed by at least one hour off while there is still pain and effusion, wearing a compression sock or stocking to decrease swelling, and elevating the affected joint above the level of the heart when possible [10]. These strategies should be used in conjunction with anti-inflammatory medications as previously mentioned to provide symptomatic relief while the injury is healing, followed by a focused home exercise program or physical therapy, often after an evaluation and referral from their primary care physician.

For a mild ankle sprain, PRICE with encouragement of early weight bearing is the ideal management. Semi-rigid braces such as an ankle stirrup brace may be superior to an ace wrap [11]. For moderate ankle sprains, give the patient crutches and have them avoid weight bearing for 2-3 days after injury, with encouragement to begin crutch walking when they are able to tolerate it [12]. A common error in treatment of mild and moderate sprains is prolonged immobilization which may delay recovery, these patients should be encouraged to perform range of motion exercises at home. For severe ankle sprains, immobilize the patient in a splint and refer them to follow-up closely with Orthopedic surgery [13].

Summary and Recommendation of Steps in Evaluation of Ankle Injuries for the ED Physician:

Expose the joint
Focused history: mechanism, ability to ambulate immediately after injury, co-injuries
Physical examination of the ankle: with a focus on neurovascular status, gross deformity, swelling, point tenderness, ability to ambulate or bear weight, strength, and ROM of the joint
Physical examination of the rest of the extremity: Evaluate the foot, knee and tibia/fibula for associated injuries.
Analgesia: NSAIDs and acetaminophen, adjuncts if needed based on severity of injury and initial pain control
Imaging, if appropriate: recommendation to use tools such as the Ottawa Ankle Rule and Ottawa Foot Rule
Protection: ace wrap, air cast, walking boot up to splint and crutches, if needed
Discharge instructions for acute recovery (“PRICE”) from injury and follow-up appointment

References:

van den Bekerom MP, Kerkhoffs GM, McCollum GA, Calder JD, van Dijk CN. Management of acute lateral ankle ligament injury in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013 Jun;21(6):1390-5. doi: 10.1007/s00167-012-2252-7. Epub 2012 Oct 30. PMID: 23108678.
Brostrom L (1966) Sprained ankles. V. Treatment and prognosis in recent ligament ruptures. Acta Chir Scand 132:537–550
Debieux P, Wajnsztejn A, Mansur NSB. Epidemiology of injuries due to ankle sprain diagnosed in an orthopedic emergency room. Einstein (Sao Paulo). 2019 Sep 23;18:eAO4739. doi: 10.31744/einstein_journal/2020AO4739. PMID: 31553355; PMCID: PMC6905160.
Bachmann LM, Kolb E, Koller MT, Steurer J, Ter Riet G (2003) Accuracy of Ottawa ankle rules to exclude fractures of the ankle and mid-foot: systematic review. BMJ 326:417–423
Stiell IG, McKnight RD, Greenberg GH, McDowell I, Nair RC, Wells GA, et al. Implementation of the Ottawa ankle rules. JAMA. 1994;271(11):827-32.
Beckenkamp PR, Lin CC, Macaskill P, Michaleff ZA, Maher CG, Moseley AM. Diagnostic accuracy of the Ottawa Ankle and Midfoot Rules: a systematic review with meta-analysis. Br J Sports Med. 2017;51(6):504-10. Review.
[Peer-Reviewed, Web Publication] Ford W, Li-Sauerwine S. (2019, May 27). Not All Ankle Sprains are Created Equal. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from http://www.nuemblog.com/blog/high-ankle-sprain.
1. Adolphson, P., Abbaszadegan, H., Jonsson, U., Dalen, N., Sjoberg, H.E., Kalen, S. No effects of piroxicam on osteopenia and recovery after Colles’ fracture: A randomized, double-blind, placebo-controlled prospective trial. Archives of Orthopaedic and Trauma Surgery, 1993; 112: 127-130.
[Peer-Reviewed, Web Publication] Farcas A, Bode, J. (2020, April 6). Clinical Question: are we impeding our patients’ fracture healing by giving them NSAIDs? [NUEM Blog. Expert Commentary by Levine, M]. Retrieved from http://www.nuemblog.com/blog/fx-nsaids
Ivins D. Acute ankle sprain: an update. Am Fam Physician. 2006 Nov 15;74(10):1714-20. PMID: 17137000.
Lardenoye S, Theunissen E, Cleffken B, Brink PR, de Bie RA, Poeze M. The effect of taping versus semi-rigid bracing on patient outcome and satisfaction in ankle sprains: a prospective, randomized controlled trial. BMC Musculoskelet Disord. 2012;13:81.
Birrer RB, Fani-Salek MH, Totten VY, Herman LM, Polit V. Managing ankle injuries in the emergency department. J Emerg Med. 1999;17(4):651-660.

Expert Commentary

This is a great review of ankle sprain injuries. Ankle sprains are one of the most common musculoskeletal injuries to present to the Emergency Department. From an emergency perspective, these injuries do not often require extensive intervention and are usually treated as discussed above with PRICE therapy. However, there are some important pitfalls to mention in regard to more serious injuries that can often be missed. The ankle joint is complex. It has multiple directions of motion and receives and distributes a lot of force and weight. It is the connection point between the lower leg and the foot, with multiple muscles and tendons originating in the lower leg, passing through the ankle and attaching to insertions on the foot. As a result of this anatomy, it is essential to not only evaluate the ankle, but to also pay attention to the foot and lower leg when evaluating an ankle sprain.

As pointed out, the most important first step in evaluating an ankle injury is to assess for neurovascular compromise and deformity. Dislocations or fractures causing neurovascular compromise require immediate reduction. Next, identifying the amount of swelling and ecchymosis is important. The more swollen and ecchymotic the ankle is, the more likely there is to be a severe injury. Palpation of the ankle is essential to guide further workup. Examining and palpating the base of the 5th metatarsal is important to evaluate for potential fractures to that bone. In addition, palpation of the entire fibula is important as well. External rotation injuries of the ankle can lead to syndesmotic sprains and a fracture of the proximal fibula called a Maisonneuve fracture. This will not be readily apparent on isolated ankle radiographs. In addition, I have a low threshold to image ankle injuries. Often when patients are in acute pain, it can be difficult to narrow down areas of tenderness. In addition, these patients will get x-rays if they follow up in an orthopedic clinic regardless.

My treatment of ankle sprains involves protecting the ankle, usually with an ace wrap and a stirrup ankle brace. I will provide crutches for non-weight bearing for the first 24 hours, after which I encourage patients to weight bear as tolerated. I also give instructions on ankle exercises to be done at home to prevent stiffness. For severe swelling or for high ankle sprains (discussed in a separate blog post), I will place the patient in a high rise controlled ankle movement (CAM) walking boot. Intermittent ice application for the first forty-eight hours definitely helps with swelling and pain, as does elevating the ankle when sitting. Compression stockings can be used, but are often painful. Hence, I prefer using an ace wrap for localized compression. Avoiding activities more intense than walking can worsen the injury and delay healing, so I typically tell patients to avoid running and returning to sports for a week or until reassessed, depending on the extent of injury. Reevaluation after a week with a sports medicine or orthopedic provider is beneficial to assess for healing, determine if further imaging, such as an MRI, is required, and begin rehab therapy.

Jacob Stelter, MD CAQ-SM

Division of Emergency Medicine

NorthShore Orthopaedic Institute

NorthShore University HealthSystem

How To Cite This Post:

[Peer-Reviewed, Web Publication] Power, E. Cohen, B. (2021, Nov 8). Ankle Injuries. [NUEM Blog. Expert Commentary by Stelter, J]. Retrieved from http://www.nuemblog.com/blog/ankle-injuries.

Mechanical Ventilation Oversimplified

**Written by:** Shawn Luo, MD (NUEM ‘22) **Edited by:** Sam Stark, MD, MA (NUEM ‘20)
**Expert Commentary by**: Ruben Mylvaganam, MD

The ventilator: we’ve all learned about it - the lectures, the bed-side demonstrations on those mind-numbingly long ICU rounds. But we were also told, repeatedly, “Don’t touch it!” Unless you are an attending, fellow, or respiratory therapist (RT) of course. So for a lot of us, the ventilator is a black box, mythical and intimidating.

In this blog, I hope to demystify ventilators a little so when duty calls, you can set initial settings and make some basic adjustments.

Physiology

1. How Mechanical Ventilation affects Oxygenation: PEEP & FiO2

You can reference this nice ARDSnet table for FiO2/PEEP combinations.

FiO2 – its effect is immediate

PEEP – takes up to an hour to show full effect

Therefore, when weaning, wean FiO2 before weaning PEEP so that if the patient desaturates, you have room to go up on FiO2.

2. How Mechanical Ventilation affects Ventilation: Tidal Volume, Respiratory Rate, Inspiratory Pressure or Inspiratory Time

This should be titrated in response to the patient's CO2 levels. Patients in respiratory failure from profound metabolic acidosis will need you to set higher minute ventilation to attempt respiratory compensation.

3. Peak Pressure and Plateau Pressure

Peak pressure is the summation of both airway resistance (dynamic compliance) and plateau pressure (static compliance). Most modern ventilators will automatically report peak pressures without any special maneuvers required. When thinking about airway resistance, think of when you blow air through a straw – the narrower the tubing the higher the resistance and thus a lot of pressure is needed to generate that flow. To measure airway resistance, have the RT set the flow rate to 60 LPM, adjust the flow pattern to a square wave form, and ask them to perform an inspiratory hold.

Plateau pressure is related to lung compliance (higher plateau pressure = less compliant lung). It is the pressure “felt” by the alveoli, and keeping it less than 30 cm H2O helps to prevent barotrauma. It’s only measured after the air stops moving (via an inspiratory hold maneuver – ask RT how to do this on your ventilator) so that dynamic airway resistance is not a factor.

4. Breath-stacking / Auto-PEEP

This occurs when the patient does not have enough time to finish exhalation before the next breath is delivered. This results in progressive hyperinflation of the lung, high peak pressures, and eventually hemodynamic collapse if not identified and intervened upon. It is most common in obstructive airway diseases such as asthma and COPD. Be vigilant for the flow diagram below on the ventilator to detect it early.

Modes

Volume vs Pressure – WHAT TYPE of breath is targeted

Volume mode means the vent will deliver a set tidal volume of air and results in whatever pressure (i.e. stiffer lungs result in higher pressure)
Pressure mode in turn means the vent will deliver at a set inspiratory pressure, and results in whatever volume (i.e. stiffer lungs result in lower volume)

A/C (Assist/Control) vs Support – WHEN the breath is delivered

In A/C mode, the machine delivers breath at a pre-set frequency (control), but the patient can also trigger additional breaths (assist) to faster than the set frequency. A quick and dirty trick is that any mode that contains the word “Control” means there will be a minimal respiratory rate set by the clinician.
Support (or Spontaneous) mode, in turn, will only deliver a breath when the patient initiates it. It senses the negative pressure generated by the patient and delivers a breath. If the patient does not breathe, it will not deliver. Usually safety back-up is in place to prevent prolonged apnea.

Volume Control

Delivers set tidal volume at or above a set rate
You set: tidal volume (6-8mL/kg ideal body weight), respiratory rate (16-22 breaths per minute), flow rate (60-80 LPM), and PEEP & FiO2 as needed
Check: Plateau pressure <30 (inspiratory hold maneuver)
This is a good initial setting for most of the patients you just intubated

Pressure Control

Delivers set pressure at or above set rate
You set: inspiratory pressure (5-15 cm H2O), inspiratory time (“I-time”; 0.6-0.8), respiratory rate (16-22), PEEP & FiO2 as needed
Check: to make sure the patient is getting tidal volumes of 6-8 mL/kg
This can be a helpful setting in some patients that do not tolerate volume control. Adjust pressure support to achieve tidal volume of 6-8 mL/kg while ensuring total pressure is less than 30-35 cm H20.

Pressure Support

Delivers set pressure when the patient initiates a breath to help the patient move the air
You set: Pressure support (5-15 cm H2O), PEEP & FiO2 as needed
Check: to make sure the patient is getting tidal volumes of 6-8 mL/kg
Usually a weaning mode to check if the patient is likely to tolerate extubation

*The bottom line is, by adjusting the parameters, you can achieve the same result with different ventilation modes.

My step-wise approach to initiate mechanical ventilation on most patients:

Build initial settings around Volume Control (tidal volume 6-8mL/kg ideal body weight, respiratory rate 16-22, PEEP 5, FiO2 100%)
Tweak according to patient’s clinical scenario – e.g. higher respiratory rate for acidotic patients, higher initial PEEP for hypoxemic respiratory failure, longer expiratory time for asthmatics/COPD patients with auto-PEEP
Start mechanical ventilation, quickly wean FiO2 for a goal SpO2 of 94-98%
Adjust settings further based on clinical response and ABGs
When in doubt, disconnect and bag the patient.

References:

The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308.

Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Annals of Emergency Medicine, Volume 68, Issue 5, November 2016, Pg 614-617

Hyzy, R. Modes of Mechanical Ventilation. In: UpToDate, Parsons P. Finlay G (Ed), UpToDate, Waltham, MA. (Accessed on May 5, 2020.)

Expert Commentary

Thank you for the opportunity to review this very helpful and concise review on the basics of invasive mechanical ventilation. I hope to make this commentary brief, a contrast to our notoriously long ICU rounding habits. I would recommend any reader to view this editorial for a more in depth and nuanced understanding of mechanical ventilation. (1)

As you have described above, one way in which to think about mechanical ventilation is in the context of the most common scenarios in which we implement it, ie: hypoxemia and hypercapnia. Understanding that for hypoxemic patients, our tools to improve physiology are by manipulating the set FiO2 and PEEP to achieve specified targets for oxyhemoglobin saturation or P/F ratios (with regard to ARDS management). It is important to note that a few studies have demonstrated that an FiO2 greater than 50-60% can be toxic and may result in an increase in reactive oxygen species, increased airway damage (tracheobronchitis), and secondary infection from impaired bactericidal action of immune cells. (2,3) For our hypercapnic patients, knowing their prior baseline PCO2 is helpful in determining how to adjust the respiratory rate and tidal volume to appropriately improve their respiratory acidosis.

An important common 3 part methodology to better appreciate modes of mechanical ventilation is understanding the “trigger”, “target”, and “cycle” of each ventilator mode. In the simplest of terms, the “trigger” is what prompts the ventilator to deliver the breath (ie: an assisted breath when the ventilator senses a patient generated decrease in flow/pressure or a control breath when enough time has elapsed as mandated by the set respiratory rate). The “target” is what the ventilator aims to achieve with each breath (in the mode of AC-VC: a targeted flow rate [often ~60 L/min] or in the mode of AC-PC: a targeted inspiratory pressure [often ~15 cwp]). Finally, the “cycle” is a term that describes how the ventilator recognizes when it is time to terminate the breath that is delivered (in the mode of AC-VC: cycling off after the goal TV is reached [~600cc] or in the mode of AC-PC: cycling off after the set inspiratory time has occurred [~ 0.7 seconds]). See table below for a quick summary.

Finally, the best practical way to simplify mechanical ventilation is to request the changes by the respiratory therapist and see the effects. I encourage you to interpret all VBGs and ABGs, approach your respiratory therapist, pulmonary/CCM fellow, and suggest everything from initial ventilator settings, changes to both modes and individual parameter settings, and see the reflection of this work in your subsequent blood gases.

References

1. Walter JM, Corbridge TC, Singer BD. Invasive Mechanical Ventilation. South Med J. 2018 Dec;111(12):746-753. doi: 10.14423/SMJ.0000000000000905. PMID: 30512128; PMCID: PMC6284234.

2. Suttorp N, Simon LM. Decreased bactericidal function and impaired respiratory burst in lung macrophages after sustained in vitro hyperoxia. Am Rev Respir Dis. 1983 Sep;128(3):486-90. doi: 10.1164/arrd.1983.128.3.486. PMID: 6311064.

3. Griffith DE, Garcia JG, James HL, Callahan KS, Iriana S, Holiday D. Hyperoxic exposure in humans. Effects of 50 percent oxygen on alveolar macrophage leukotriene B4 synthesis. Chest. 1992 Feb;101(2):392-7. doi: 10.1378/chest.101.2.392. PMID: 1310457.

Ruben Mylvaganam, MD

Instructor of Medicine

Department of Pulmonology & Critical Care Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Luo, S. Stark, S. (2021, Nov 1). Mechanical Ventilation Oversimplified. [NUEM Blog. Expert Commentary by Mylvaganam, R]. Retrieved from http://www.nuemblog.com/blog/mechanical-ventilation-tips

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