The U.S. is currently experiencing an epidemic of a severe lung disease termed Vaping-Associated Pulmonary Illness (VAPI), with over 500 cases and 7 deaths across 38 states and 1 U.S. territory since July 2019.

The clinical presentation of VAPI varies -- 

• Respiratory (SOB, cough, chest pain), constitutional (fever, tachycardia, headache, dizziness), and potentially GI symptoms (vomiting, diarrhea) after the use of vaping devices. GI symptoms may precede respiratory issues.
• Can take days or worsen over weeks and can present or end up with severe respiratory failure

Diagnostics --

• Labs nonspecific: Leukocytosis, elevated ESR, no specific infectious etiology
• Chest CT generally with bilateral infiltrates
• Bronchoscopy with BAL demonstrates PMNs and may have lipid-laden macrophages on Oil red O or Sudan staining

Treatment is supportive +/- steroids -- 

• Current recommendations to treat similarly to ARDS in intubated patients
• Potential benefit to steroids if not contraindicated

Bottom Line: Include vaping-associated pulmonary illness in your differential for patients presenting with acute lung disease.

• Ask patients about use of e-cigarette/vaping devices.
• Notify the CDC or your state health department of any suspected cases.
• Counsel your patients to avoid the use of these devices, at the very least until the specific causative agent is found.

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Managing the intubated patient with exacerbation of severe obstructive lung disease, especially asthma, can be very challenging as it carries higher risks of barotrauma due to higher pulmonary pressures and circulatory collapse due to auto-PEEP and decreased venous return. When measures such as medical therapy and noninvasive positive-pressure ventilation fail to prevent intubation, here are some tips to help:

1. Utilize a volume control ventilation mode to ensure a set tidal volume delivery / minute ventilation, as pressure-targeted modes will be more difficult due to the high pulmonary pressures in acute obstructive lung disease.

2. Set a low RR in order to allow for full exhalation, avoiding air-trapping / breath-stacking and circulatory collapse due to decreased venous return. This may require deep sedation and potentially paralysis.

• Permissive hypercapnea to >7.2 is generally well-tolerated except for pregnant patients, patients with high ICP, or patients with severe pulmonary hypertension

3. Increase your inspiratory flow by shortening your inspiratory time (thereby increasing your time for exhalation.

4. Monitor for auto-PEEP:

• Check your flow curve -- the waveform should return to zero before the start of the next inhalation, otherwise the next breath has been given before the patient has fully exhaled.
• Perform an expiratory hold at the end of exhalation. PEEP greater than set PEEP = auto-PEEP.

5. Peak inspiratory pressures will be high -- what is more important is the plateau pressure, measured by performing an inspiratory hold at the end of inspiration. Provided your plateau pressure remains <30, you don't need to worry as much about the peak pressure alarms.

6. If your patient acutely decompensates in terms of hemodynamics and oxygenation -- first attempt to decompress their likely auto-PEEPed lungs by popping them off the ventilator and manually press on their chest to assist with exhalation of stacked breaths allowing venous return to the heart.

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Background:  Previous systematic reviews^1,2,3 have indicated that the absence of cardiac activity on point-of-care ultrasound (POCUS) during cardiac arrest confers a low likelihood of return of spontaneous circulation (ROSC), but included heterogenous populations (both traumatic and atraumatic cardiac arrest, shockable and nonshockable rhythms).

The SHoC investigators⁴ are the first to publish their review of nontraumatic cardiac arrests with nonshockable rhythms, evaluating POCUS as predictor of ROSC, survival to admission (SHA), and survival to discharge (SHD) in cardiac arrests occurring out-of-hospital or in the ED.

• 10 studies, 1485 patients
• Compared to absence of cardiac activity, presence of cardiac activity = higher odds, increased incidence of ROSC, SHA, and SHD
• Pooled sensitivity for ROSC, SHA, SHD relatively low (60%, 75%, 69%, respectively)
  • On subgroup analysis, sensitivity higher in PEA group (77%) than asystole group (25%)

Bottom Line:  In nontraumatic cardiac arrest with non-shockable rhythms, the absence of cardiac activity on POCUS may not, on its own, be as strong an indicator of poor outcome as previously thought.

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When managing transplant patients it is important to keep in mind the anatomic and physiologic changes that occur with the complete extraction of one person's body part to replace another's. 

For cardiac transplant patients with symptomatic bradycardia:

• Remember that due to lack of autonomic/vagal innervation, resting HR should be around 90 bpm.
• HR will not respond to atropine. Use direct sympathomimetics like epinephrine instead.
• If medication is unsuccessful, proceed to transcutaneous or transvenous pacing.

For cardiac transplant patients with tachyarrythmias:

• They are particularly sensitive to adenosine; for SVT start with 1 to 3mg adenosine push (3mg is usually effective) to avoid sustained bradycardia or asystole.
• Digoxin is not effective as an antiarrhythmic.
• Diltiazem can decrease the metabolism of calcineurin inhibitor immunosuppressive agents (such as cyclosporine and tacrolimus), so while it can be used there may need to be dose adjustments to these medications. 

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The PROTRACH study recently compared preoxygenation with standard bag valve mask (BVM) at 15 lpm to preoxygenation + apneic oxygenation with high flow nasal cannula 60 lpm/100% FiO2 in patients undergoing rapid sequence intubation.

• There was no significant difference in the primary outcome of median lowest SpO2 during intubation. 
• There were more intubation complications in the BVM group compared to the HFNC group:
  • Severe complications: SpO2 <80%, severe hypotension (SBP < 80mmHg or vasopressor initiation/increase by 30%), and cardiac arrest (6% HFNC vs 16% BVM, RR 0.38, 95% CI 0.15-0.95, p=0.03). 
  • Moderate complications: aspiration, cardiac arrhythmia, agitation, and esophageal intubation (0% HFNC vs 7% BVM, p= 0.01). 
• There was no difference in ventilator days, ICU length of stay, or mortality.

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Despite ongoing research and efforts to improve our care of patients with ARDS, it remains an entity with high morbidity and mortality. Early recognition of the disease process and appropriate management by emergency physicians can have profound effects on the patient's course, especially in centers where ICU boarding continues to be an issue.

Recognition of ARDS (Berlin criteria)

• Acute in onset
• Bilateral infiltrates on chest imaging not due to cardiac failure/volume overload
• PaO2 : FiO2 < 300 despite PEEP of at least 5cmH2O 
• This is the standard ED patient who gets intubated with multifocal pneumonia and has continued hypoxemia

*An ABG should be obtained in the ED if physicians are unable to wean down FiO2 from high settings, if oxygenation by pulse ox is marginal, or if the patient is in a shock state.

Tenets of ARDS Management:

• Low tidal volume ventilation (6-8ml/kg ideal body weight*)
• Maintain plateau pressures (Pplat) < 30 cmH2O
• Driving pressure (Pplat – PEEP) < 15 cmH2O
• Goal PaO2 > 55-60 
• Permissive hypercapnia to pH >7.2

*IBW Males = 50 + 2.3 x [Height (in) - 60]   /  IBW Females = 45.5 + 2.3 x [Height (in) - 60]

Strategies for Refractory Hypoxemia in the ED:  You can't prone the patient, but what else can you do? 

1. Escalate PEEP in stepwise fashion

• ex: 2cmH20 every 10 minutes
• can use ARDSnet PEEP/FiO2 table as guide

2. Recruitment maneuvers

• "20 of PEEP for 20 seconds" or "30 for 30"
• if patient is "PEEP responsive," leave PEEP on a higher setting than when you started (ex: 10 instead of 5, 16 instead of 10)
• Risk of barotrauma with higher PEEPs and hypotension in underresuscitated or hemodynamically unstable patients due to decreased venous return

3. Appropriate sedation and neuromuscular blockade

• promotes patient synchrony with lung protective settings
• can result in improved oxygenation by itself

4. Inhaled pulmonary vasodilators (inhaled prostaglandins, nitric oxide) if known or suspected right heart failure or pulmonary hypertension

Bottom Line: Emergency physicians are the first line of defense against ARDS. Early recognition of the disease process and appropriate management is important to improve outcomes AND to help ICU physicians triage which patients need to be emergently proned or even who should potentially be referred for ECMO. 

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Neutropenic enterocolitis can occur in immunosuppressed patients, classically those being treated for malignancy (hematologic much more commonly than solid tumor). When involving the cecum specifically, it is known as "typhlitis."

It should be considered in any febrile neutropenic patients with abdominal pain or other symptoms of GI discomfort (diarrhea, vomiting, lower GI bleeding), and can be confirmed with CT imaging.

A recent study found that invasive fungal disease, most often candidemia, occurred in 20% of febrile neutropenic patients with CT-confirmed enteritis, a rate that increased to 30% if the patient was in septic shock.

Take Home: 

1. Have a lower threshold for abdominal CT imaging in your patients with febrile neutropenia and abdominal pain/GI symptoms, especially if they are critically ill.

2. Consider addition of IV antifungal therapy if they are hemodynamically unstable with enterocolitis on CT.

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Historically, there has been very limited data regarding the epidemiology of OHCA in pregnant females. Two recently-published studies tried to shed some light on the issue.

Both Maurin et al.¹ and Lipowicz et al.² looked at all-cause out-of-hospital maternal cardiac arrest (MCA) data in terms of numbers and management, in Paris and Toronto respectively, from 2009/2010 to 2014. Collectively, they found: 

• MCA was relatively rare: 0.8 MCA per 1000 OHCA (Maurin) and 1.71 MCA per 100,000 pregnant females (Lipowicz)
• Low incidence of bystander CPR in witnessed MCA (33% and 0%)
• Adherence to PMCS guidelines was poor 
• Maternal survival was lower than what has been previously quoted for in-hospital CA: 12.5 and 16.7% compared to 40-50%^3,4

A few reminders from the 2015 AHA guidelines for the management of cardiac arrest in pregnancy: 

• Hand location for chest compressions should be in the center of the chest as for nonpregnant patients (previous recommendations had been to shift upward to accommodate for the gravid uterus but there is no data to support this).

• Chest compressions should be performed with the patient supine, using manual lateral uterine displacement for aortocaval decompression. Left lateral tilt position is no longer recommended due to poorer quality of cardiac compressions, the lack of full aortocaval decompression, and further complication of other procedures such as airway management.

• IV or IO access should be obtained above the diaphragm, to ensure no interference to flow to the heart by the gravid uterus.

• Rate and depth of chest compressions, ACLS drugs and doses, and defibrillation all remain the same as in nonpregnant OHCA patients.
  • NB: As opposed to nonpregnant patients periarrest, oxygen saturation in the pregnant female should be maintained at 95% or greater, or PaO2 > 70mmHg, to ensure appropriate oxygen delivery to the fetus. The goal PCO2 is ~28-32 mmHg, to facilitate fetal CO2 removal.⁶  

• If advanced airway is pursued, the most experienced provider should perform intubation due to the higher intrinsic difficulties, more rapid decompensation, and propensity for airway trauma and bleeding in the pregnant female.

• Perimortem c-section should occur within the first 5 minutes of cardiac arrest / arrival to the ED in ongoing arrest. 

Bottom Line: Although maternal cardiac arrest is relatively rare, survival in OHCA is lower than perhaps previously thought. Areas to improve include public education on the importance of bystander CPR in pregnant females, and appropriate physician adherence to PMCS recommendations, with decreased on-scene time by EMS in order to decrease time to PMCS. 

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The European Society of Intensive Care Medicine (ESICM) recently released a review with recommendations from an expert panel for the use of IV fluids in the resuscitation of patients with acute circulatory dysfunction, especially in settings where invasive monitoring methods and ultrasound may not be available.

Points made by the panel include: 

• Circulatory dysfunction should be identified not only by HR and BP, but by other indicators of poor perfusion: altered mentation, decreased urine output, and skin abnormalities (poor skin turgor, mottling, delayed capillary refill)

• The absence of arterial hypotension does not preclude hypovolemia

• The lack of an increase in MAP (especially in patients with decreased vascular tone) does not exclude positive response to IVF

• The purpose of IVF administration is to improve tissue perfusion by increasing cardiac output

• Fluid "loading" as the rapid administration of large volumes of fluid to treat overt hypovolemia, while a fluid "challenge" is a test of fluid responsiveness

• In elderly patients or those with arteriosclerosis or chronic arterial hypertension, a low pulse pressure (e.g. less than 40 mmHg) indicates that stroke volume is low. PP = SBP - DBP

Recommendations from the panel include:

• The early measurement of lactate to incorporate in the assessment of perfusion

• The use of crystalloids as initial resuscitation fluid (unless blood products are indicated)

• When overt hypovolemia is unclear, the use of a fluid challenge of 150-350mL IVF within 15 minutes to help assess fluid responsiveness

• Avoidance of using jugular venous distension alone as a guide for resuscitation

• Avoidance of using acute urine output response alone as a guide for resuscitation, as renal response to fluids can be delayed

• A recommendation against using CVP as a target for resuscitation; if CVP is being measured, a rapid increase with IVF should suggest poor fluid tolerance

• Individualizing fluid resuscitation to the patient's current presentation, underlying comorbidities, and response to fluids

Bottom Line: Utilize all the information you have about your patient to determine whether or not they require IVF, and reevaluate their physical and biochemical (lactate) response to fluids to ensure appropriate IVF administration and avoid volume overload. 

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Hyperoxia has been repeatedly demonstrated to be detrimental in a variety of patients, including those with myocardial infarction, cardiac arrest, stroke, traumatic brain injury, and requiring mechanical ventilation,^1-4 and the data that hyperoxia is harmful continues to mount:

• Systematic review and meta-analysis of 16,000 patients admitted to hospital with sepsis, trauma, MI, stroke, emergency surgery, cardiac arrest: liberal oxygenation strategy (supplemental O2 for average SpO2 96%, range 94-100%) associated with increased in-hospital and 30-day mortality compared to conservative strategy.⁵

• ED patients requiring mechanical ventilation admitted to ICU: hyperoxia defined as PaO@ >120mmHg. Patients with hyperoxia in the ED had higher mortality than not only normoxic but hypoxic patients (30% v 19% v 13% respectively), and longer vent days and ICU/hospital LOS.⁶

• ICU patients, majority respiratory failure, 60% requiring mechanical ventilation; hyperoxia defined as PaO2 >100mmHg. Just ONE episode of hyperoxia an independent risk factor for ICU mortality (OR 3.80, 95% CI 1.08-16.01, p=0.047).⁷

Bottom Line: Avoid hyperoxia in your ED patients, both relatively stable and critically ill. Remove or turn down supplemental O2 added by well-meaning pre-hospital providers and nurses, and wean down ventilator settings (often FiO2). A target SpO2 of >92% (>88% in COPD patients) or PaO2 >55-60 is reasonable in the majority of patients.⁸

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A few (out of 10) tips for the care of sick patients with liver failure:

• Use of albumin is indicated to improve outcomes in spontaneous bacterial peritonitis (SBP), large-volume paracentesis, and hepatorenal syndrome (HRS).

• Norepinephrine remains the vasopressor of choice for nonhemorrhagic shock. Use vasopressin or terlipressin (outside the U.S.) in AKI due to HRS to maintain a target MAP and for splanchnic vasoconstriction.

• INR does not correctly reflect coagulation performance. Platelet count and fibrinogen are the best predictors of bleeding, and thromboelastography (via TEG/ROTEM) can reduce blood products administered for hemorrhage without affecting mortality.

• If a nasogastric tube is indicated (administration of lactulose, decompression of SBO, etcetera), presence of [non-recently banded] esophageal varices is not a contraindication.

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The most recent AHA guidelines for goal blood pressure after return of spontaneous circulation (ROSC) post-cardiac arrest recommend a definite mean arterial pressure (MAP) goal of > 65 mmHg.¹ There is no definitive data to recommend a higher specific goal, but there is some evidence to indicate that maintaining higher MAPs may be associated with better neurologic outcomes.²

A recently published prospective, observational, multicenter cohort study looked at neurologic outcomes corresponding to different MAPs maintained in the initial 6 hours post-cardiac arrest.³

Findings: 

1. Compared to lower blood pressures (MAPs 70-90 mmHg), the cohort with MAPs > 90 mmHg had:

• a higher rate of good neurologic function at hospital discharge (42 vs.15%, p < 0.001)
• a higher rate of survival to 72 hours (86 vs. 74%, p=0.01) and hospital discharge (57 vs 28%, p < 0.001)

2. The association between MAP > 90 mmHg and good neurologic outcome was stronger among patients with a previous diagnosis of hypertension, and persisted regardless of initial rhythm, use of vasopressors, or whether the cardiac arrest occured in or out of hospital.

3. There was a dose-response increase in probability of good neurologic outcome among all MAP ranges above 90 mmHg, with MAP >110 mmHg having the strongest association with good neurologic outcome at hospital discharge.

Note: The results of a separate trial, the Neuroprotect post-CA trial, comparing MAPs 85-100 mmHg to the currently recommended MAP goal of >65 mmHg, are pending.⁴

Bottom Line: As per current AHA guidelines, actively avoid hypotension, and consider use of vasopressor if needed to maintain MAPs > 90 mmHg in your comatose patients post-cardiac arrest, especially those with a preexisting diagnosis of hypertension.

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We know that high flow nasal cannula is an option in the management of acute hypoxic respiratory failure without hypercapnea. A newer iteration of high flow, "high velocity nasal insufflation" (HVNI), may be up-and-coming.

According to its makers (Vapotherm), it is reported to work mainly by using smaller bore nasal cannulae that deliver the same flows at higher velocities, thereby more rapidly and repeatedly clearing dead space, facilitating gas exchange and potentially offering ventilatory support. 

In an industry-sponsored non-inferiority study published earlier this year:

• 204 adult patients in 5 EDs
• Any acute respiratory failure deemed by the treating physician to require non-invasive positive pressure ventilation (NPPV)
• Patients randomized to either NPPV (bilevel positive airway pressure) or HVNI
• Rate of HVNI treatment failure (26%) and intubation @ 72 hours (7%) fell within predefined noninferiority margins
• Rates of PCO2 clearance were similar between HVNI and NPPV groups
• The study was not powered to detect differences between different etiologies for respiratory failure
• Authors concluded that HVNI is noninferior to NPPV for all-comer respiratory failure.

Bottom Line: 

The availability of a nasal cannula that helps with CO2 clearance would be great, and an option for patients who can't tolerate the face-mask of NPPV would be even better.

HVNI requires more investigation with better studies and external validation before it can really be considered noninferior to NPPV, but it certainly is interesting. 

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The recently published BICAR-ICU study looked at the use of bicarb in critically ill patients with severe metabolic acidemia...

• Multicenter, open-label, RCT, 26 French ICUs
• Adult patients with pH < 7.2 not secondary to hypercapnia, serum bicarb < 20 not due to bicarb wasting process 
• SOFA score > 4 or lactate > 2
• No bicarb versus 4.2% sodium bicarb infusion titrated to pH >7.3
• Primary outcome: Composite measure of 28-mortality and presence of any organ failure at 7 days post-randomization
• Secondary outcomes: Need for/length of life support measures (renal-replacement, vasopressors, mechanical ventilation), SOFA score after enrollment, electrolyte effects, occurrence of ICU-acquired infections, and ICU length of stay
• Major findings:
  • No difference in primary outcome overall
  • No difference in pressor-free days, days off RRT, dialysis dependence at ICU discharge, ICU LOS
  • Bicarb group had less need for RRT during ICU stay (35 vs 52%, p=0.0009)
  • In patients with AKI and AKIN score 2-3*, the bicarbonate group had a decrease in both 28-day mortality (46 vs 63%, p=0.0166) and presence of any organ failure at day 7 (66 vs 82%, p=0.0142)
• Limitations:
  • Unblinded
  • A quarter of the control group actually received bicarb
  • No data regarding vent settings, ABGs to r/o ventilation effects on pH
  • 4.2% is not a standard concentration of bicarb used in the U.S.

Bottom Line: 

Consider administration of sodium bicarbonate for your critically ill ED patients with severe metabolic acidosis and AKI, especially if acidosis &/or renal function is not improved with usual initial measures (such as IVF, etc).

*Acute Kidney Injury Network Staging Criteria

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The highly-awaited PARAMEDIC2 trial results are in:

• Multicenter, double-blinded, randomized controlled trial of prehospital OHCA care
• 1mg IV epinephrine vs saline placebo, every 3-5 minutes
• 8014 OHCA patients over the age of 16 (excluded pregnant patients, anaphylactic and asthmatic cardiac arrests)
• Primary outcome: 30 day survival
• Secondary outcomes: 
  • Survival to hospital admission
  • ICU and hospital LOS
  • Survival to hospital discharge and at 3 months
  • Neurologic outcomes at hospital discharge and at 3 months, "favorable" if mRS≤3
• Results: 
  • Higher 30 day survival in Epi group (3.2 vs 2.4%, unadj OR 1.39; 95% CI 1.06 to 1.82; P=0.02)
  • No difference in ICU or hospital LOS
  • No difference in favorable neurologic outcomes at discharge or 3 month
  • Worse neurologic outcomes in the epinephrine survivors (mRS 4 or 5 in 31% of epi group vs. 17.8% of placebo)

Interestingly, the authors also queried the public as to what mattered to them most: 

Bottom Line:

• As has been demonstrated in previous studies, use of bolus-dose epinephrine results in increased rates of ROSC. 
• This survival comes with the trade-off of worsened neurologic function, a condition not in a majority of patients' personal wishes.
• Epinephrine "1mg every 3-5 minutes'" should no longer be the dogma of OHCA resuscitation.

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When a do-not-intubate (DNI) hospice patient arrives in the ED with respiratory distress, consideration of non-invasive positive pressure ventilation (NIPPV) could invoke either a “What other option do I have?” or “Why torture the patient and prolong the dying process?” sentiment.

But what’s the data?

A recently-published meta-analysis¹ found that in DNI patients receiving NIPPV, there was a 56% survival rate to hospital discharge and 32% survival to 1-year.

• Higher survival was seen in patients with COPD and pulmonary edema as the cause of their respiratory failure, as opposed to pneumonia or malignancy.
• In surviving patients, there was no decrease in quality of life at 3 months; quality of life was not assessed in the time before death in nonsurvivors.
• In comfort-measures only (CMO) patients, patients receiving NIPPV had a mildly lower dyspnea score with less opiates required/administered.

Independent studies have demonstrated:

• Better survival with NIPPV for DNI COPD and CHF patients^2,3,4 who are awake and have a good cough.⁴
• No decrease in health-related quality of life or post-ICU psychological burden (symptoms of PTSD, anxiety, or depression) in DNI survivors receiving NIPPV.³
• 63% survival to hospital discharge & 49% survival to 90 days in DNI patients receiving NIVV, with no decrease in health-related quality of life in survivors. Survival was lower for CMO patients (14% and 0% at discharge and 90 days, respectively).⁵

Bottom Line:

1. NIPPV can benefit DNI patients -- most identifiably those with COPD or cardiogenic pulmonary edema as the etiology for their respiratory distress.
2. Mild benefits to dyspnea have been seen in CMO patients, without survival benefit. A trial of NIPPV therapy may be reasonable (especially in COPD or CHF) after frank discussion with the patient and his/her loved ones, with quick cessation if comfort is not achieved and/or more discomfort is caused.

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Although not specifically a part of current recommendations due to lack of data, the AHA has previously recommended shifting upward on the sternum during CPR in the pulseless pregnant patient in order to account for upward displacement of the heart by a gravid uterus. Should the same be done for our obese patients?

Lee et al. performed a retrospective study that reviewed chest CTs to determine the location on the sternum that corresponded to the optimal point of maximal left ventricular diameter (OPLV), in both obese and non-obese patients. 

They found that the OPLV was higher (more cranial) on the sternum for obese patients than for patients with normal weight, although 96% of obese patients' OPLV fell within 2cm of where the guidelines recommend standard hand placement should be, compared to a notable 52% in non-obese patients.

*as measured from the distal end of the sternum

Bottom Line: Radiographically, the location on the sternum that corresponds to optimal compression of the LV is more cranial in obese patients than in non-obese patients. It remains to be seen whether the recommendations for hand placement in CPR should be adjusted, but we may want to consider staying within 4cm of the bottom of the sternum in patients of normal weight. 

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• The Surviving Sepsis Campaign recently republished the 2018 update to their guidelines, namely, the recommendation that physicians initiate treatment measures using a "1-Hour Bundle" rather than the 3 and 6-hour bundles previously recommended:

• Also included was the level of evidence for each bundle component. There was no additional evidence provided to support the within-one-hour recommendation. 

• There has been no well-designed, randomized trial to demonstrate benefits to administration of the various bundle components at specific time points. There are observational studies that show benefits to early protocolized therapy, including a restrospective study by Seymour et al. that showed benefits to earlier administration of antibiotics (but notably, not IV fluid administration), primarily in patients with septic shock requiring pressors.²

• There have been a variety of studies demonstrating harm with unecessary IV fluid administration,^3-5 and inappropriate antibiotic use puts patients at risk for C.difficile colitis, drug reactions, and promotes drug-resistant organisms. Studies to date do not examine adverse events in patients initially treated for sepsis who do not end up being septic.

Take Home Points: 

1. Early recognition of sepsis is crucial to initiating necessary therapies and improving outcomes.
2. Patients with sepsis and septic shock benefit from early appropriate antibiotics, source control, and appropriate resuscitation.
3. Empiric treatment of all-comers with possible sepsis with broad spectrum antibiotics and 30ml/kg of IV fluids, in order to meet a 1-hour deadline, has definite potential for harm. 

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ED physicians frequently utilize modailities such as noninvasive positive pressure ventilation (NIV) and high flow nasal cannula (HFNC) to support and potentially avoid intubation in patients presenting with acute hypoxic respiratory failure. Unfortunately, failure of these measures, resulting in "delayed" intubation, has been associated with increased mortality.^1,2

A recent post-hoc analysis of data from a multicenter randomized controlled trial evaluated 310 patients with acute hypoxic respiratory failure managed with supplemental O2 by regular nasal cannula, HFNC, or NIV.³

The following factors were predictive of eventual intubation in the different groups: 

• For nasal cannula patients, RR > 30 at 1 hour
• For HFNC patients, tachycardia at 1 hour (No respiratory variables were found to predict intubation).
• For NIV patients, tidal volume > 9ml/kg predicted body weight or PaO2:FiO2 ratio < 200 at 1 hour

Of note, 45% of the 310 patients eventually required intubation, and these patients in general had a higher initial respiratory rate and lower PaO2 at presentation, and were more likely to have bilateral infiltrates on CXR. 

Bottom Line: Reevaluate your patients frequently. If RR remains high, P:F ratio remains low, or patient respiratory effort/work of breathing is not alleviated by noninvasive measures, consider pulling the trigger on intubation earlier.

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Background:

Animal studies in post-ROSC management after cardiac arrest have repeatedly demonstrated poorer neurological outcomes with higher amounts of oxygen administration.¹ Studies in humans have also demonstrated dose-dependent associations between hyperoxia and poorer neurologic outcomes, as well as in-hospital mortality.^2,3

Recent Data

A retrospective analysis of prospectively-collected data in 187 OHCA patients undergoing postarrest care with targeted temperature management found worse neurologic outcomes in patients experiencing hyperoxia in the first 6 hours following ROSC.⁴

This association was dose-dependent, with worsening outcomes as with higher PaO2 levels >200.

• Adjusted OR 1.659 [95% CI, 1.194–2.305] at 200 mmHg
• Adjusted OR 3.969 [95% CI, 1.450–10.862] for 300 mmHg
• Trend towards worsening at 150 mmHg that did not reach statistical significance

Bottom Line:

• Our initial management of these patients in the ED is crucial
• In post-cardiac arrest patients, titrate immediate FiO2 to SpO2 ≥ 94% and PaO2 75 to 150/200 mmHg to avoid hyperoxia and worsening neurologic and survival outcomes. 

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