UMEM Educational Pearls

Summary:

The recent ARISS (Albumin Resuscitation in Septic Shock) trial showed no difference in 90-day mortality or other secondary outcomes, similar to other trials comparing albumin and crystalloid. Notably however, the trial did not meet its predetermined enrollment requirement of patients (in the setting of the COVID-19 pandemic) and had a large portion of its intervention group failing to meet goal serum albumin level. 

The Bottom Line:

There remains no evidence-based mortality benefit of albumin over crystalloid in patients with septic shock that do not have additional indications for albumin (such as hepatorenal syndrome). Crystalloid resuscitation remains a staple of appropriate and cost-effective care in septic shock. Albumin can be considered on a case-by-case basis after standard crystalloid resuscitation in this clinical setting.

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In a large, randomized trial conducted in 42 ICUs in France, high-flow oxygen did not reduce 28-day all-cause mortality in adult patients with acute hypoxemic respiratory failure when compared to standard oxygen support.

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The 2026 Acute Pulmonary Embolism Guidelines recommend a new approach to risk stratification of patients with acute PE, including measurement of at least one cardiac biomarker and serum lactate, evaluation of RV size and function with CTA or echo (preferred when feasible), and multidisciplinary PERT assessment for all patients with acute PE and elevated clinical severity scores to assist with further risk stratification.

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Bottom Line: Swimming-Induced Pulmonary Edema (SIPE) AKA Immersion Pulmonary Edema is a rare, though life-threatening pathology associated with water-based activities, especially among athletes or military personnel. Caused by physiologic effects of immersion, not from aspiration/ingestion. Consider in any patient with respiratory distress or chest discomfort onset during water activities such as swimming, diving, etc. Diagnose with physical exam and POCUS. Manage supportively, potentially including positive pressure ventilation. Screen for alternative diagnoses.

See the link for more thorough review of assessment diagnostics, pathophysiology, pharmacological options, risk factors, and long-term considerations.

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Click the link for below to read the bulleted, abridged version of the Executive Summary of the Updated SSC Guidelines for Adults with Sepsis and Septic Shock 2026…

• Strength of guidelines provided as conditional “suggestions” or strong “recommendations"
• Amount of certainty given existing evidence (very low [VL], low, moderate)
  • Note “very low” certainty may simply indicate there isn't a study or any reliable data
• Please refer to the article (linked in References) for given rationales from the SSC

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Beta-blocker is used for tachycardia among patients with sepsis. Landiolol, a new beta-blocker with highly selective B1-agonist (ratio of B1:B2 250:1) has recently been approved for use. In a network meta-analysis comparing landiolol with esmolol (B1:B2 ratio 30:1), landiolol was associated with increased 28-day mortality (relative risk [RR], 1.57; 95% CI, 1.08–2.30). This result carried low certainty as there were not as many studies using landiolol and there was no direct comparison between landiolol versus esmolol.

Similarly, landiolol  was associated with higher norepinephrine requirements (mean difference [MD], 0.17 ?g/kg/min; 95% CI, 0.02–0.32). Again, there was no direct head-to-head comparison between landiolol versus esmolol.

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It is a common scenario in the ICU, and occasionally in the ED, to be asked which pressor you would like to wean first, norepinephrine or vasopressin.  This is mostly an “art not science” question, but is there a right answer?  Does picking one vs the other to wean first lead to less hypotension?

Bottom Line: This meta-analysis doesn't suggest that either the norepi-first or vasopressin-first strategies for vasopressor wean are associated with an increased incidence of hypotension, although the literature is mixed.  Whatever your current practice is, it's probably reasonable to stick with that.  See the additional information for my personal approach.

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Bottom Line: Hypertonic sodium bicarbonate (8.4%) can be used judiciously as an alternative hyperosmolar therapy in the setting of increased intracranial pressure (ICP) or cerebral edema with impending herniation, particularly in setting of concomitant metabolic acidosis. Two 50 mL ampules of hypertonic sodium bicarbonate is the equivalent of approximately 200 mL of 3% sodium chloride (hypertonic saline).

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Diagnostic Errors in the Critically Ill

• Critical illness comprises numerous time-sensitive conditions in which diagnostic errors and delayed diagnoses markedly impact patient outcomes.
• Diagnostic errors in the critically ill can occur in up to 20% of patients and lead to overuse of resources, delayed recovery, and increased mortality.
• The most common cognitive biases leading to diagnostic errors in the critically ill include: 
  • Anchoring bias: over-reliance on your initial impressions
  • Availability bias: favoring diagnoses that easily come to mind
  • Premature closure: ending your diagnostic reasoning too early
  • Confirmation bias: seeking information that supports your diagnosis and discounting contradictory findings
• Recommended strategies to reduce diagnostic errors in the critically ill include implementation of checklists, standardized handoff protocols, multidisciplinary patient reviews, and explicitly discussing these cognitive biases.

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Etomidate is often a go-to agent for RSI because it is considered relatively hemodynamically neutral. However, lab studies have shown an association with transient adrenal suppression, and some observational studies and meta-analyses have suggested that patients intubated with etomidate face higher risk of cardiovascular collapse and in-hospital mortality than those intubated with ketamine.

The RSI trial was a pragmatic open-label multi-center randomized control trial conducted in 6 EDs and 8 ICUs across the US and compared induction with ketamine 1-2mg/kg versus etomidate 0.2-0.3mg/kg for RSI of critically ill adults (excluding trauma patients). They found no significant difference in overall 28 day hospital mortality across the cohort. They found an increased risk of cardiovascular collapse during intubation in the ketamine group. This increased risk was more pronounced in patients with sepsis or septic shock and patients with APACHE II ?20.

Some details:

• Cardiovascular collapse during intubation was defined as systolic BP <65mmHg, new or increased vasopressors, or cardiac arrest within 2 minutes of induction
• The prevalence of 28 day hospital mortality was 28.1% in the ketamine group vs 29.1% in the etomidate group, with an absolute difference -0.8%, 95% CI ?4.5% to 2.9%; P=0.65
• The prevalence of peri-intubation cardiovascular collapse was 22.1% in the ketamine group vs 17.0% in the etomidate group, absolute risk difference 5.1%; 95% CI, 1.9% to 8.3%. 
  • Among patients with sepsis or septic shock, 30.6% vs 20.9%, absolute risk difference 9.7%; 95% CI, 4.6% to 14.9%. 
  • Among patients with APACHE II ?20, 31.4% vs 20.7%, absolute risk difference 10.7%, 95% CI 5.5% to 16.0%.
• Both ketamine and etomidate were dosed using actual body weight, whereas data is more supportive of using ideal body weight for ketamine. The dose used for ketamine was also on the higher end of that recommended for critically ill patients. There was no investigation of how the impact of the dose of either drug on the outcomes assessed.

Overall - this was a well conducted randomized control trial that  - at the very least - suggests that etomidate is likely as safe (if not safer) than ketamine with respect to 28d mortality and peri-intubation cardiovascular collapse, even among patients with critical illness or septic shock.

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A crucial part of cardiac arrest management is identification of the underlying rhythm, with key aspects of management diverging depending whether shockable (pulseless ventricular tachycardia/pVT or ventricular fibrillation/VF) or unshockable (pulseless electrical activity/PEA or asystole). 

A recent study prospectively evaluated adult atraumatic out-of-hospital-cardiac-arrests (OHCAs) presenting to the ED, to determine what percentage of cases had “Occult VF” –  VF found point-of-care echocardiogram but not by ECG. The researchers only included cases with simultaneous ECG and echo assessments for the initial 3 pulse checks. Echo and ECG determinations for the study were adjudicated by research team members.

They found that:

• 5.3% of patients had occult VF (43/811), with ECG reading PEA in 81.4%  (35/43) and asystole in 18.6% (8/43)
• Of the 202/811 patients with VF on ECG, only 23.3% had echo VF
• Interestingly, patients with ECG VF but no VF on echo had a lower rate of ROSC and successful defibrillation than those with Occult VF
• There was no statistically significant difference in survival to hospital discharge between the two
• A higher percentage of patients evaluated by TEE compared to TTE were found to have occult VF (12.5% vs 4.9%)

Major limitations: 

• Only have the cases with simultaneous ECG + echo for the first 3 pauses
• Only have the recorded echo clips, which are not the same as in-the-moment viewing during the arrests
• No comparison to how research team interpreted ECGs to how the treating team managed

Bottom Line: Point-of-care echocardiogram continues to have value in the management of cardiac arrest, potentially changing management and affecting post-ROSC decisions. Ensuring high-quality CPR, with appropriate defibrillation and anti-arrhythmic strategies, remains paramount in management of shockable OHCA.

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Settings: Secondary analysis of the Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) trial.

Participants:

1368 patients who survived on day 28 after enrollment, and were retrospectively assigned different subtypes:

1. Low risk, barriers to care. Younger patients with few comorbidities, less severe disease, 

2. Unhealthy baseline with severe illness: Previously healthy with severe illness and complex needs after discharge, barriers to care.

3. Multimorbidity. Older patients with more comorbidities and are frequently readmitted. 

4. Low functional status: Poor functional status. Older patients with high prevalence of frailty at discharge and high functional needs who are  often discharged to a facility.

5. Unhealthy baseline with severe illness: Existing poor health with severe illness and complex needs  after discharge. Older patients with severe comorbidities,  more severe illness, high functional needs, prolonged hospital stay, 

Outcome measurement: 

A) 90-day mortality, 

B) 6-month and 12-month EuroQol 5D five level score

Study Results:

A) 90-day mortality:

Unhealthy baseline  with severe illness (37.6%) >  low functional status (45.5%) > multimorbidity (17.4%) >  unhealthy baseline, severe illness (13.2%) > Low risk (5.1%).

B) 6-month EuroQol 5D-Five Level: lower score, lower functional outcomes)

Unhealthy baseline  with severe illness (0.53) >  unhealthy baseline, severe illness (0.68) > low functional status (0.69) > multimorbidity (0.78) >  Low risk (0.80).

Discussion:

a) The framework, readily available to clinicians provides good prognostic tools for mortality.

b) Although there was prediction of poor functional outcomes at 6-month and 12-month, the differences between subtypes in their EuroQoL 5D-5L did not seem to correspond to 90-day mortality. Low functional status group had 2nd-highest rate of mortality, but only 3rd in their EuroQoL 5D-3L score. Thus, there needs to be more studies in these nuances.

Conclusion: 

Sepsis survivor subtypes—assigned using only three routinely available discharge variables—are strongly associated with 3-month mortality and long-term disability and HRQOL up to 12 months

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Attachments

• 2026 Flick Figure 3-696f822c68572.jpg (137 Kb)

Recall that MAP = (cardiac output) x (systemic vascular resistance)

Consequently, a patient can be normotensive due to increased SVR despite a very low cardiac output and shock. In fact, normotensive shock may have worse outcomes compared to patients with isolated hypotension. 

Take home points: 

• Shock does not equal hypotension
• In critically ill patients with reduced cardiac output, additionally use other markers for end-organ perfusion (mental status, renal function/urine output, LFTs, cap refill, lactate etc.) to assess for possible shock

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Yet another study (this time ED focused) has shown benefits to patients and hospital systems when implementing a Phenobarbital-based treatment algorithm. Shorter ED LOS, fewer admissions, and treatment with phenobarbital alone was independently associated with discharge when compared to mixed treatment regimens. Higher age and heart rate, as well as treatment with benzodiazepines alone were independently associated with hospitalization.

Cautions/contraindications include: pregnancy, cirrhosis with history of hepatic encephalopathy (consider dose reduction in hepatic dysfunction), acute intermittent porphyria, and prior chronic phenobarbital use.

Phenobarbital has a long half life (one of its benefits in AWS) and works synergistically with benzodiazepines, so should be used preferentially as monotherapy in patients where the diagnosis is relatively certain and who have not received high doses of benzos. Once the diagnosis is made, go with phenobarbital and stick with it. 

PulmCrit has an excellent in-depth article on this and also see Dr. Flint's pearl describing another centers experience in a hospital-wide rollout (links below).

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Perintubation hypotension is a major problem, and can precipitate hemodynamic collapse and cardiac arrest for a multitude of reasons.  To prevent this, many different strategies have been explored (some of which work and some of which don't), including empiric IV fluid boluses, additional resuscitation before intubation, switching or dose-reducing induction agents and much more.  But we know pressors  like norepinephrine raise blood pressure effectively, so should we just put everybody on a norepinephrine drip before we intubate them?

Probably not.  The EPITUBE trial included 210 patients at a single-institution undergoing cardiac surgery, and randomized them to empirically starting a norepinephrine infusion before induction vs just rescue ephedrine when needed (fairly standard anesthesia practice).  For the empiric norepinephrine group, they started at 0.06 ug/kg/min, and once the drip was up and running, they titrated for a MAP of 65-80 (which could include stopping the norepi if that the patient remained above 80 despite downtitration)

The incidence of severe hypotension (MAP < 55) did not differ between the groups, although fewer empiric norepinephrine patients had a MAP < 65 at any point (which was a secondary outcome).  Naturally, the differences between this practice setting (the cardiac surgery OR) and the emergency department should be noted and are not addressed by this study.

Bottom line: There isn't good evidence to support empirically starting all patients on a norepinephrine infusion prior to intubation as a method to prevent perintubation hypotension.  You should always have rapid access to vasopressors when intubating, and should continue to tailor your therapy to the individual patient, but probably don't start just putting everyone on norepinephrine before you intubate them.

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The emergency department serves many critically ill patients that require airway management and mechanical ventilation. Most of these patients go on to require ICU care. However, some patients require only brief intubation and should be appropriate candidates considered for emergency physician-driven extubation. Early extubation can minimize the risks associated with mechanical ventilation for patients such as ventilator associated pneumonia (VAP), ventilator induced lung injury (VILI), and others. Additionally, in setting of high levels of ED boarding and limited ICU resources, extubating appropriate candidates in the ED can reduce boarding times and improve patient flow.

Who?

1. Patients with temporary neurologic dysfunction (alcohol/drug intoxication)
2. Need for brief procedural sedation that cannot be accomplished without a definitive airway (endoscopy)
3. Patients transitioning to a palliative, comfort-focused approach to treatment

Screening Checklist

• Returned to baseline mental status, able to follow commands
• Appropriate vital signs on minimal ventilator support
• Breathing spontaneously with RR <30, FiO2 of 30-40%, PEEP 5-8 cmH2O, achieving TV > 6-8 cc/kg
• May be on low-dose vasopressor to manage sedation-related hypotension
• No history of difficulty intubation (in case emergent reintubation is required)

Testing

• Perform spontaneous breathing trial (SBT):
  • IPAP 10 cmH2O over EPAP of 5 cmH2O, also described as pressure support of 5 cmH2O over PEEP of 5 cmH2O
  • 30 minutes
  • Assess the RSBI (Rapid Shallow Breathing Index — available on MDCalc)
• Patient fails for EP-driven extubation if one or more of the following is present:
  • respiratory distress
  • severe anxiety
  • hypoxemia (SaO2 < 90%)
  • tachypnea (usually RR > 30)
  • somnolence
  • RSBI > 105 breaths/min/L

Prepare - depending on institution, may require consultation with the hospital intensivist

• Notify the respiratory therapist (extubation ideally performed by the RT, if available)
• Have standard AND difficult airway equipment at bedside
• These specifically selected patients can usually be extubated to temporary standard nasal cannula
  • Optimal respiratory support post-extubation for palliative patients depends on patient-specific care plan
• For patients with respiratory distress with plan for compassionate extubation, we advise palliative opiate and anxiolytic administration closely titrated to patient comfort, adjusted as ventilator support is weaned down to a pressure support of 0 over PEEP of 0-5. This ensures the patient remains comfortable with minimal distress and air hunger when ventilator support is removed. Other palliative patients with no tachypnea or distress do not necessarily require this measure.
• Some of these patients may be anxious when transitioning off mechanical ventilation; consider use of dexmedetomidine in the peri-extubation period to facilitate patient comfort while maintaining respiratory drive

Perform - see this video courtesy of Respiratory Skills - LSC on performing extubation

• Make sure to monitor for post-extubation hypoxemia and post-extubation stridor
• Always be prepared for the potential need for re-intubation

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Pitfalls in Lactate Interpretation

• Lactate is one of the most common biomarkers used in critical care.
• While an elevated lactate level is often attributed to impaired tissue oxygenation, an important pitfall in lactate interpretation in the critically ill is the failure to consider non-hypoxic causes of increased levels.  These include:
  • Enhanced glycolysis (B2-agonist administration, increased metabolic activity)
  • Reduced clearance (hepatic failure, renal dysfunction, muscular dysfunction)
  • Impaired tissue metabolism (mitochondrial dysfunction due to drug intoxication)
• Additional pitfalls in lactate use in the critically ill include:
  • Use of an isolated value rather than assessing longitudinal trends
  • Failure to correlate elevated lactate levels with other markers of perfusion (i.e., capillary refill time)
  • Use of rigid normalization targets rather than targeting therapeutic interventions to the full clinical picture

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Last month, Mark Sutherland posted an overview of a new article investigating the use of personalized MAP targets in resuscitation for septic shock (1). Now, the authors of ANDROMEDA-SHOCK-2 (2) suggest a new multimodal approach to personalize resuscitation in septic shock that largely operates outside of the traditional focus on MAP and lactate.

In 2019, the ANDROMEDA-SHOCK Trial (3) suggested that capillary refill time (CRT) may be a better resuscitation in septic shock than lactate. Now, the same group is suggesting that a stepwise algorithm to guide resuscitation may provide more optimal and “personalized” results when compared to usual care for patients with abnormal CRT:

Tier 1: If CRT is abnormal, assess pulse pressure (PP) and DBP: 

• PP (<40mmHg) OR DBP (>50mmHg)?  Assess for fluid responsiveness and challenge with up to 1L IVF if fluid responsive.
• PP (>40mmHg) AND DBP (<50mmHg)? Increase norepinephrine (NE) for DBP >50mmHg, followed by assessment for fluid responsiveness and possible fluid challenge if CRT remains abnormal.

Tier 2: If CRT remains abnormal despite the above, use POCUS to assess for cardiac dysfunction.

• LV dysfunction? Trial dobutamine @ 5-75 mcg/kg/min (stop for HR > 120 or tachyarrhythmia, or if it doesnt help CRT)
• RV dysfunction? The authors recommend avoiding fluids, increasing pressors if needed, as well as decreasing PEEP, limiting plateau pressures, and/or proning the patient if they have ARDS
• If there is no cardiac dysfunction, assess for fluid responsiveness and fluid challenge if fluid responsive. Continue this cycle until CRT normalizes or there is evidence of harm (evidence of pulmonary edema, worsening oxygenation/ventilation, or high central venous pressure).
  • If the patient is not fluid responsive, investigate for a history of HTN
    • If they have a history of HTN, push MAP to 80-85 for 1h and see if it improves CRT (if not, revert back)
    • If they do not, trial dobutamine @ 5 for 1h and see if it improves CRT (if not, DC dobutamine)
• If CRT remains abnormal after all of this, move on to “rescue therapies” (high dose steroids, hemofiltration, ECMO).

The authors found that at 6 hours, following the protocol resulted in increased use of dobutamine, lower fluid balance, and similar CVP and MAP with lower lactate levels and CRT. They reported an improvement in their composite hierarchical outcome at 28 days, primarily driven by a shorter duration of organ support (vasoactives, mechanical ventilation, renal replacement therapy) and among sicker patients. No difference in mortality was observed between groups.

Food for Thought:

• CRT is a subjective assessment, and all participating clinicians in this study underwent mandatory training. Other, more objective measures that can be used to assess organ perfusion (lactate clearance, urine output, MAP) were excluded from this protocol.
• Fluid responsiveness was assessed using the “preferred technique by each center.” Suggested techniques included pulse pressure/stroke volume variation, change in VTI with passive leg raise, IVC variability, or change in CO with end expiratory pause.
• There was no standardization regarding the integration of vasopressin, and steroids were reserved as “rescue therapies” and considered at the same point as mechanical hemodynamic support. 
• The effect of other inotropic agents (like low dose epinephrine) was not discussed.

Study Details:

• Setting: multicenter randomized control trial conducted in 86 ICUs across 19 countries
• Patients:
  • >1450 adults from the ED, ICU, OR, or floor with septic shock based on Sepsis-3 criteria - suspected/confirmed infection + lactate >2 + pressor requirement to maintain MAP> 65 despite 1L+ IVF bolus.
  • Patients with Child B or C cirrhosis, acute hematologic malignancy, severe ARDS, or anticipated surgery or HD within 8h of being diagnosed with septic shock, or who could not be enrolled within 4h of diagnosis were excluded. Pregnant patients were also excluded.
  • Almost half had an abdominal source of infection, followed by respiratory and urinary.
  • The median time to enrollment was 2h from meeting sepsis criteria
• Outcome: a hierarchical composite outcome using all-cause mortality, duration of vital support (vasoactives, invasive mechanical ventilation, or renal replacement therapy), and hospital LOS at 28d.
  • The primary outcome was assessed in a hierarchical fashion using “wins” and “losses.” The intervention group “won” in 48.9% of cases, while the usual care group “won” in 42.1%, for a Stratified Win Ration of 1.16 (95% CI 1.02-1.33).

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We have all been there – an ED patient with circulatory shock requiring vasoactive medications and, therefore, an arterial line for accurate and close monitoring of the MAP and appropriate titration of the infusions. But does it save lives?

The recently published NEJM article by Muller et al. takes a look at noninvasive BP monitoring (NIBP) by cuff versus early arterial catheterization in patients with hypotension and evidence of tissue hypoperfusion: 

• Open-label, pragmatic, parallel-group, noninferiority, multicenter RCT across 9 ICUs in France
• Adult patients enrolled within 24h of ICU admission, randomized to NIBP (n=506) or arterial line placement within 4h of enrollment (n=504)
  • 15% of NIBP group received art line during study period as deemed necessary by predefined safety criteria (unable to get NIBP or SpO2, for ex)
  • 50% septic shock, >90% medical patients, 90% on pressors at randomization
• Notable exclusions: BMI >40, high-dose vasopressors (total norepi tartrate* + epi infusion rate >2.5 mcg/kg/min) 
• Findings: 
  • No difference in primary outcome of 28-day mortality (34.3% NIBP vs. 36.9% art line)
  • No difference in 90 day mortality, 28-day ventilator, vasopressor, or RRT-free days
  • More arterial puncture attempts in the NIBP group (742 vs. 269 per 1000 ICU days)
  • No increase in arterial line-associated infections or ischemia
  • More (8 vs 1%) hematoma or hemorrhage at art line site in arterial line group
  • More patients in NIBP group reported serious pain/discomfort related to device (13 vs 9%)

Bottom Line: This trial indicates that in appropriately-selected patients with shock, such as those not on high doses of vasopressors, with BMI < 40 and an ability to consistently obtain NIBP measurements, early arterial line placement in the ED for vasopressor titration is unlikely to improve outcomes. It is important to note other potential indications for arterial line placement (severe hypoxia, inability to obtain reliable SpO2 with need for ABG monitoring, cardiac arrest, pain related to NIBP cuff monitoring, intracranial hemorrhage, etcetera) may still make arterial line placement in the ED prudent and better for overall patient care.

*France refers to norepi by the tartrate formulation dose, US refers to the base norepi dose (ratio is 2:1 tartrate: base).

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Settings: this is a meta-analysis of 17 observational studies about boarding of critically ill patients in US Emergency Departments. All studies were from urban, academic centers.

Participants:

• There was a total of 407,178 patients, 194,814 (485) were boarding vs. 212,364 (52%) non-boarding patients.
• 355,86 (87%) patients were at centers with the presence of a resuscitation service.
• Ther was a mixture of critical illnesses: trauma (29.4 %), medical conditions (29.4 %) and mixed critical illness (41.2 %).

Outcome measurement: all cause mortality, as reported by the authors of the original studies.

Study Results:

• Overall, boarding patients were not associated with higher mortality, than non-boarding patients (Odd ratios 1.06, 95 % CI 0.94–1.19 p=0.383).
• Boarding patients were not associated with longer hospital length of stay (mean difference 0.38 days, 95%CI 0.94-1.50, P=0.51).
• However, among subgroup analyses, boarding patient population with mixed critical illnesses was associated with higher odds for mortality (OR 1.2, CI 1.04–1.4, p = 0.02 ) and longer HLOS (difference = 1.9, 95 % CI 0.81–3.1, I2 = 0 %, p = 0.001).

Discussion:

• All studies were observational so there was risk of bias and there was a presence of a small publication bias. This means that there were a few unpublished studies out there that showed that Boarding patients might have better outcomes.
• The findings that patient population with mixed illnesses were associated with higher odds for mortality, compared with Trauma-only or medical-only patients, might suggest that ED are not well equipped to take care of a wide spectrum of disease states. We seem to do better with populations with protocols such as sepsis, stroke, trauma.
• There was no clear consensus about how researchers approach this topic. A few studies did not even report their patient populations’ age (I cannot understand how these got published). Researchers used different thresholds for boarding, likely reflecting their institutional variabilities. There was quite a significant heterogeneity about patients’ acuity: some studies used SOFA, others used mSOFA.
• All of the studies were from urban academic centers so their results may not be applicable to non-academic centers which may not have many boarding issues

Conclusion: 

Critically ill patients boarding in the U.S. Emergency Departments were associated with a non-statistically signi?cant increase in odds of mortality and hospital length of stay compared to non-boarded patients

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