TXA in the Trauma Bay

Written by: Jilan Shimberg, MD (NUEM ‘26) Edited by: Rafael Lima, MD (NUEM ‘23)
Expert Commentary by: Matthew R Levine, MD

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Expert Commentary

Unlike many of the treatments and interventions we use in the Emergency Department and the trauma bay, tranexamic acid (TXA) has rather robust studies to guide usage. Like many interventions, however, even when there are studies with large numbers of patients and positive results, there are still barriers towards implementation. TXA is no different.

Working at a Level 1 Trauma Center and frequently interacting closely with the trauma surgeons through the Trauma Quality Management Committee, I often follow their lead when it comes to promising trauma innovations through the years such as TXA, REBOA, permissive hypotension, and so on. What I have observed is that our trauma surgeons tend to believe that there is benefit to properly timed TXA in the right trauma patients and that we do not use it enough. Yet use of TXA in trauma at our hospital has not been protocoled.

Why not? Some possibilities:

1. Someone usually (but not always) thinks to give it to patients who would benefit despite there not being a protocol (thanks ED pharmacists!).

2. The patients who need it most also need something else even more – source control of hemorrhage. Anything that slows or distracts from that may be counterproductive. It may not seem like a simple TXA infusion would delay anything. But keep in mind the multiple lines sick trauma patients may need and the often already chaotic nature of “the bay” getting the sickest patients the tubes, meds, lines, products, studies, and, ultimately, proper disposition during their “golden hour”. The nurses have many tasks, to say the least. But maybe this is an argument for why use of TXA should just be protocolized.

I bounced this off of our trauma section head to make sure I was not misrepresenting their thoughts. As a result, we are looking into protocolling its use. Thanks NUEM Blog!

Matthew Levine, MD

Associate Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern Memorial Hospital

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Shimberg, J. Lima, R. (2024, Mar 11). TXA in the Trauma Bay. [NUEM Blog. Expert Commentary by Levine, M]. Retrieved from http://www.nuemblog.com/blog/txa-trauma

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Vasopressor Nonresponse

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

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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. 

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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

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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

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Physiologically Difficult Intubations

Written by: Samantha Stark, MD (NUEM ‘20) Edited by: Steve Chukwulebe, MD (NUEM ‘19) Expert Commentary by: Seth Trueger, MD, MPH

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It’s the first few minutes of your shift, and the paramedics roll by your workstation with your first patient, a young woman clutching an inhaler and breathing with every accessory muscle in her body. You direct them to your resuscitation room and they inform you that she has a history of asthma and is having an attack; she’s too exhausted from breathing to verify this, but it seems true. You quickly get her on BiPAP, which mildly improves her work of breathing, but as she becomes drowsy, you obtain a VBG showing a climbing CO2 of 45. You realize that it’s time to intubate this patient, and as you get set up, you collect your thoughts and quickly review everything you’ve heard about intubating asthmatics.

Obstructive Airway Disease

First, remember that asthma is an obstructive airway disease, meaning that there are two main processes to worry about during and after intubation:

• Auto PEEP

• Hypotension secondary to increased intrathoracic pressure from auto PEEP

*Note: auto PEEP is caused by breath stacking in a patient whose expiration is impaired (such as asthma or COPD) – the ventilator initiates a breath before there’s time for full exhalation, and this leads to progressively more volume retained in the lungs, increasing the risk of barotrauma. This can also lead to increased intrathoracic pressure, in turn decreasing preload to the heart and thus causing hypotension.

How to optimize the intubation:

• As you already have this patient on BiPAP, try to preoxygenate as much as possible with this mode of positive pressure

• Consider attempting delayed sequence intubation with ketamine

  • It will maintain the patient’s respiratory drive and may help with BiPAP synchrony and anxiolysis

  • It serves as a bronchodilator

• Use rocuronium for paralysis

  • It will last longer than succinylcholine, and initially help with vent synchrony

  • *Note: remember to fully sedate the patient after intubation, as they won’t tell us that they’re not sedated during their prolonged paralysis

• Decrease the dead space and resistance of your vent by using the largest endotracheal tube feasible

• Frequently reassess the ventilator to ensure that breath stacking is not occurring:

  • Low respiratory rate to allow for exhalation

  • Higher tidal volumes of 6-8 cc/kg IBW

  • Decreased I:E ratio (at least 1:3, may very well need to be longer)

You’ve successfully intubated this patient, and now the lab pages you to let you know that there is a patient in the waiting room with a bicarb of 9. When the patient is wheeled back, his marked tachypnea and work of breathing makes you think he may need to be intubated as well. But he’s so acidotic, and you’re sure you’ve hear something about intubating acidotic people…

Metabolic Acidosis

What you’ve heard is that if you intubate a severely acidotic patient, you’ve killed them. There are two reasons for this:

• It’s very difficult to keep up with their minute ventilation

• There is a transient increase in pCO2 with paralysis (this is normally inconsequential, but in the decompensating acidotic patient, can lead to cardiovascular collapse)

How to optimize the intubation:

• Optimize cardiovascular status as much as possible beforehand

• Bolus fluids

• Consider starting pressors pre-intubation, or having push-dose phenylephrine or epinephrine on hand during intubation

• Match the patient’s minute ventilation

• Ensure adequate pre-oxygenation, using NIPPV

• However, even if oxygenation is not an issue, BiPAP should be used to assess the minute ventilation the patient is maintaining on their own, to help determine what is needed post intubation

• Using delayed sequence technique with ketamine as the induction agent and a short acting paralytic like succinylcholine could theoretically help to avoid apnea as much as possible

• Once intubated, the patient’s pre-intubation minute ventilation (respiratory rate and tidal volume) MUST be matched on the ventilator

• Don’t be surprised to see higher tidal volumes of 8 cc/kg IBW

As you’re sitting down to catch up on notes, a nurse gets your attention to let you know that there is an altered, febrile, tachycardic patient with a pressure of 65/40 tucked away in a bed at the back of the ED that you should probably see right away. As it turns out, this patient needs to be intubated as well.

Shock

As mentioned above, increased intrathoracic pressure from PPV results in decreased venous return to the heart, leading to decreased preload. This obviously has the potential to be quite detrimental to a patient with shock.

How to optimize the intubation:

• Optimize cardiovascular status as much as possible beforehand

• Fluid resuscitation and vasopressors started prior to intubation

• Have push dose pressors available at the bedside should they be needed

• Induction agents:

  • Avoid propofol as it has a propensity to cause hypotension

  • Use etomidate or ketamine

  • Ketamine has been shown to be more hemodynamically stable than etomidate

  • Also, the body should prioritize cerebrovascular blood flow in shock, therefore if etomidate is used, consider decreasing the dose to minimize hemodynamic effects

At this point, you’re too tired to write any notes, so you decide to sit down and, given how your shift has been going so far, do some reading about patients that are dangerous to intubate or difficult to manage on the vent. The first topic you come across is pulmonary hypertension.

Pulmonary Hypertension

Mechanical ventilation is dangerous in these patients due to their inability to tolerate decreased preload, increased afterload, or really any alteration in their tenuous hemodynamics. Unfortunately, in patients with pulmonary hypertension but also systemic hypotension, IV fluids can over-distend the right ventricle and make things worse. There’s not a super reliable way to tell if these patients will be fluid responsive or not; most would suggest a small fluid bolus challenge to see how they respond. There may or may not be time for this prior to intubation, but if there is time, it’s probably worth a try.

How to optimize the intubation:

• Can consider pre-medication with fentanyl:

  • Thought to blunt the hypertensive response to laryngoscopy, similar to head-injured patients

  • In theory, this prevents increased afterload in the pulmonary vasculature

• Induction agent:

  • Consider etomidate

  • Theoretically should have less of an effect on preload than propofol

  • Additionally, less of an effect on afterload than ketamine

• Ventilator settings:

  • Closely monitor plateau pressures to keep them less than 30 cm H2O, to avoid drops in preload due to increased intrathoracic pressure

  • Consider placing an arterial line for frequent ABG checks

  • Both hypercapnia and hypoxia can cause vasoconstriction (increasing afterload in the pulmonary vasculature)

Two days later, while you’re following up on some of your prior patients, you note that the patient in septic shock that you intubated a couple of days ago now has ARDS, and it seems that the inpatient team is having some difficulty managing her on the vent.

ARDS

While this is an area of active research and there are different strategies and methods for helping to improve these patients’ oxygenation, the main thing to remember from the perspective of managing the ventilator is the lung protective strategy:

• Tidal volume 6 cc/kg IBW

• Plateau pressure less than 30 cm H2O

• Minimum PEEP of 5 cm H2O (and remember that these patients may often need significantly higher PEEP) 

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Expert Commentary

Thank you for this review of intubating sick patients - intubating complex physiology is arguably one of the most dangerous things we can do, but there are some straightforward, concrete steps we can take to do it as safely as possible.

For me, the first step is to consider every ED intubation potentially dangerous. Maximize resuscitation (IV fluids; pressors if needed, always ready) and optimize preoxygenation to provide the biggest possible safety net. It’s much more CBA than ABC.

Every patient we intubate in the ED has potential to crump: the sympatholysis from sedation will reduce endogenous catecholamines, and the switch to positive pressure ventilation impairs preload.

Every intubated patient needs post-intubation sedation. I generally default to a fentanyl drip and modify from there (eg add propofol if BP tolerates; add ketamine if not). Do not remove sedation for hypotension; do not use pain as a pressor. That is torture and it is bad. Sedate the patient adequately and if that means more resuscitation (fluid, blood, pressors, etc) then do that too. Do not torture patients to maintain BP.

The easiest tactic to ensure post-intubation sedation is to think of RSI as 3 medications: NMBA, induction agent, and post-intubation sedative. I should not be surprised that I will need post-intubation sedation shortly after intubation.

Perhaps the biggest lesson in ARDS management and prevention in recent years is that nearly everyone potentially benefits from lung protective ventilation, i.e. 6 ml/kg *ideal* body weight. I’ve changed my default tidal volume to 400-450ml (it was 550-600 when I was in med school). Otherwise, ventilation (minute ventilation, or CO2 management) is all about adjusting respiratory rate (my default is 16-18, not 12) as the patient’s height usually does not change in the ED.

Special situations: asthma patients don’t have a big enough tube to exhale properly. Pay special attention, make sure they have sufficient time to exhale (and they may the one group that may benefit from *not* being on 6 ml/kg IBW. Perhaps even more importantly, unlike many other situations, intubation does not fix asthma; it makes it even harder to manage, as even the largest ET tubes are, by definition, smaller than the patient’s natural airway. Maximize NIV and other management options (eg epinephrine) if at all possible.

Acidosis is tough and the key is maximizing ventilation before and after intubation. These patients may need absurd-seeming respiratory rates and regardless of how hypercarbic they are, acidosis does not make patients taller so there is no reason to adjust tidal volume.

Pulmonary hypertension is complex and scary. Prepare beforehand, and work with your intensivists and other relevant specialists.

The most important part of airway management is preparation – not just in the ED, but learning as much as I can beforehand.

Seth Trueger, MD, MPH

Assistant Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern University expert commentator

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Stark, S. Chukwulebe, S. (2020, Oct 5). Physiologically Difficult Intubations. [NUEM Blog. Expert Commentary by Trueger, S]. Retrieved from http://www.nuemblog.com/blog/physiologically-difficult-intubations

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