Emergency physicians are familiar with posterior reversible [leuko]encephalopathy syndrome as an entity associated with untreated hypertension. It also happens to be a well-documented entity amongst solid organ transplant patients.  

While the exact pathophysiology remains unclear, PRES is characterized by posterior subcortical vasogenic edema due to blood-brain barrier disruption, usually in the setting of elevated blood pressure with loss of cerebral autoregulation and/or endothelial dysfunction.

The immunosuppressants used in this population, namely calcineurin inhibitors (CNI) such as tacrolimus and cyclosporine, are thought to contribute most to this endothelial dysfunction and development of PRES in transplant patients, although high-dose corticosteroids, ischemia-reperfusion injury during surgery, and antibiotics have also been implicated. 

Presentation of PRES post-transplant:

Clinical symptoms:

• Seizures (75-85%)
• AMS - confusion/somnolence (30-40%)
• Headache (25-50%)
• Vision disturbance (20-40%)

Time course:

• Within weeks to a year posttransplant, rarely after a year
• Rapid onset once it starts, can develop over hours to days

Diagnostics:

• Labs nonspecific, although supratherapeutic CNI levels are often associated with:
  • Acute renal injury
  • Hyperchloremic metabolic acidosis
  • Hyperkalemia
  • Hypomagnesemia
  • Hypercalciuria
• Thoughts on checking FK506 (tacrolimus) levels
  • For transplant patients, usually advise only checking troughs (~12 hrs after last dose)
  • A low random level may rule out CNI toxicity but not PRES
  • A high random level isn't really helpful
• MRI is diagnostic modality of choice >> subcortical edema, usually bilateral, symmetric, in parieto-occipital regions

Management:

1. Stabilization via supportive care – seizure, cerebral edema, BP management as applicable, etc.
2. Withdrawal/holding of offending agent – will require consultation with transplant physician and pharmacist usually by inpatient team
   • Mixed data re: use of CYP-inducers to lower CNI levels in CNI toxicity

Bottom Line: 

Patients with a history of solid organ transplant are at risk for PRES. While ED stabilization of these patients remains the same, recognition of PRES as a potential etiology for a transplant patient's presentation is crucial to proceed with important testing and necessary changes to their immunosuppressive regimen. 

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Deep sedation in the ED has previously been associated with longer duration of mechanical ventilation, longer lengths of stay, and higher mortality.¹ Current guidelines recommend light sedation, consistent with a goal RASS of -2 to 0, for most critically-ill patients in the ICU.²

The ED-SED³ multicenter, pragmatic, before-and-after feasibility study implemented an educational initiative (inservices, regular reminders, laminated sedation charts) to help target lighter sedation depths in newly-intubated adult patients without acute neurologic injury or need for prolonged neuromuscular blockade.

• 415 patients (196 pre-, 219 post-intervention), majority white (50%) and black (40%)
• Main reasons for intubation: sepsis, trauma, airway protection
• Majority of patients on fentanyl (85%) and propofol (76%), midazolam (20%)

After educational intervention:

• 21% fewer patients with deep sedation & 20% more patients achieving light sedation
  • 10% decrease in comatose levels of sedation (RASS -4 to -5)
• Lower hospital mortality (20.4 vs 10%, p < 0.01)
• Similar rates of self-extubation and paralysis awareness
• More patients extubated in the ED, downgraded from ICU admission, and discharged from the ED

Even with the caveats of the confounding and bias that can exist in before-and-after studies, these results are consistent with prior sedation-related studies and offer more evidence to support for avoiding deep sedation in our ED patients. The study also demonstrates the importance of nurse-driven sedation in achieving sedation goals.

Bottom Line: Our initial care in the ED matters beyond initial stabilization and compliance with measures and bundles. Avoid oversedating intubated ED patients, aiming for a goal RASS of -2 to 0. 

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Background: It is classically taught that the tenets of DKA management are IV fluids, electrolyte repletion, and an insulin infusion that is titrated until approximately 2 hours after anion gap closure, when long-acting subcutaneous insulin is administered if the patient is tolerating oral intake. It has been previously found that earlier administration of subcutaneous long-acting insulin can shorten the time to anion gap closure, while other small studies have noted similar efficacy in subcutaneous insulin compared to IV in mild/moderate DKA. 

A recent JAMA article presents a retrospective evaluation of a prospectively-implemented DKA protocol (see "Full In-Depth" section) utilizing weight-based subcutaneous glargine and lispro, rather than IV regular insulin, as part of initial and ongoing floor-level inpatient treatment.

When compared to the period before the DKA protocol: 

• ICU admissions decreased (27.9% from 67.8%, p<0.001)
• There was no difference in overall amount of insulin and time to anion gap closure
• There was no difference in 30-day mortality
• There was no difference in incidence of hypoglycemc events.

The only exclusion criteria were age <18 years, pregnancy, and presence of other condition that required ICU admission. 

Bottom Line: Not all DKA requires IV insulin infusion.

At the very least, we should probably be utilizing early appropriate-dose subcutaneous long-acting insulin. With ongoing ICU bed shortages and the importance of decreasing unnecessary resource use and hospital costs, perhaps we should also be incorporating subcutaneous insulin protocols in our hospitals as well.

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Based on prior studies¹ indicating possibly improved outcomes with vasopressin and steroids in IHCA (Vasopressin, Steroids, and Epi, Oh my! A new cocktail for cardiac arrest?), the VAM-IHCA trial² compared the addition of both methylprednisolone and vasopressin to normal saline placebo, given with standard epinephrine resuscitation during in hospital cardiac arrest (IHCA).

The use of methylprednisolone plus vasopressin was associated with increased likelihood of ROSC: 42% intervention vs. 33% placebo, RR 1.3 (95% CI 1.03-1.63), risk difference 9.6% (95% CI 1.1-18.0%); p=0.03.

BUT there was no increased likelihood of favorable neurologic outcome (7.6% in both groups).

Recent publication on evaluation of long-term outcomes of the VAM-ICHA trial³ showed that, at 6-month and 1-year follow-up, there was no difference between groups in:

• Survival
• Favorable neurologic outcome (CPC 1 or 2; mRS 0-3)
• Health-related quality of life (per EQ-5D5L survey)

Bottom Line: Existing evidence does not currently support the use of methylprednisolone and vasopressin as routine code drugs for IHCA resuscitation. 

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Background: Conventional medical wisdom long held that patients with pneumothorax (PTX) who require positive pressure ventilation (PPV) should undergo tube thoracostomy to prevent enlarging or tension pneumothorax, even if otherwise they would be managed expectantly.¹

• Small retrospective and observational studies have demonstrated safety to an observational approach for both occult (only detectable on CT) and larger PTXs even in patients requiring noninvasive or invasive mechanical ventilation, whether traumatic/iatrogenic or spontaneous.^2-6
• The Western Trauma Association recently released a guideline for the management of traumatic PTX, which includes observation with 6-hour follow up CXR for patients with small (<20% aka <2cm from chest wall on CXR or <35 mm on CT scan) hemodynamically stable pneumothoraces, even if mechanical ventilation is required.⁷
  • They note a 10% subsequent failure rate (i.e. chest tube requirement) with no difference between patients who do or do not undergo PPV. 
• The OPTICC trial, found however, that while the rate of respiratory distress development was not different between those randomized to observation vs initial chest tube management, there was an increase from a 25% chest tube requirement in the obs group to a 40% failure rate in patients requiring >4 days of mechanical ventilation.⁸ 

Bottom Line: The cardiopulmonar-ily stable patient with small PTX doesn’t need empiric tube thoracostomy simply because they’re receiving positive pressure ventilation. If you are unlucky enough to still have them in your ED at day 5 in these COVID times, provide closer monitoring as the observation failure rate may increase dramatically around this time.

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Fever has long been understood to be associated with worse outcomes in patients post-cardiac arrest. Whether ascribing to the goal of 33-34°C, 36°C, or simply <38°C, close monitoring and management of core temperatures are a tenet of post-cardiac arrest care.

A recently published study compared the effectiveness of several methods in maintaining temperatures <38°C…

• Both ICHA and OHCA, shockable and unshockable, nontraumatic arrests
• Single center retrospective cohort study looking at 1/2012 – 9/2015
• Treatment and temperatures over first 48 hours

Results:

Maintenance of temp <38°C:

• Antipyretics only group: 57.7% 
• Invasive cooling by intravascular catheter +/- antipyretics:  82.1%

Mean change in temp from baseline:

• Antipyretics only: +1.1°C
• Intravascular alone: -3.4°C
• Antipyretics + Intravascular cooling: -5.2°C

Limitations:

• Varied range of antipyretic dosing per body weight
• No mention of noninvasive cooling methods (cooling pads, ice packs, etc.)
• Patients w/ intravascular cooling likely getting more aggressive care in general
• Not powered for clinical outcomes assessment

Bottom Line:

• Antipyretics alone greatly ineffective at preventing fever 
• Even with invasive cooling -- not meeting goal 18% of the time
• With longer ED boarding times nationwide, we must pay active attention to body temperature management and not assume that that we can set it and forget it, even with techniques as invasive as intravascular cooling.

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Background:

There are also no clear guidelines regarding how fast fluid boluses should be administered, and there has been debate about whether different infusion rates could lead to different outcomes in patients receiving intravenous fluid (IVF) boluses (i.e. fast infusions may cause more third spacing due to the rapidity of the expansion of the intravascular space compared to fluid administered more slowly). A recent study compared IVF infusion rates in ICU patients.

-- Unblinded, randomized

-- 10,520 patients clinically requiring a fluid challenge, from 75 ICUs in Brazil

-- Infusion rate 333 mL/hr vs 999 mL/hr

   * (Trial also compared plasmalyte vs 0.9% saline, analyzed in separate study)

-- Some notable exclusion criteria: severe hypo/hypernatremia, AKI or expected to need RRT 6 hrs after admission

--Other caveats:

   * Faster infusion rates allowed at physician discretion in patients with active bleeding or severe      hypotension (SBP < 80 or MAP < 50 mmHg); patient was returned to assigned rate after condition resolved

   * Almost 1/2 the patients received at least 1L of IVF in 24 hours prior to enrollment

-- Results: No sig difference in 90-day survival, use of RRT, AKI, mechanical ventilator free days, ICU/hospital mortality/LOS 

Bottom Line: There is not yet compelling evidence that there are differences in patient outcomes in patients receiving fluid boluses given at 333 cc/hr vs. 999 cc/hr.

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Approximately 15,000 children experience an in hospital cardiac arrest (IHCA) with little improvement in outcomes over the last two decades. During that time, epinephrine has been the constant basis for resuscitation of these patients. Current recommendations by the AHA recommend bolus dosing of epinephrine every 3-5 minutes in a pediatric cardiac arrest. Animal studies suggest that more frequent dosing of epinephrine may be beneficial. 

This was a retrospective study of 125 pediatric IHCAs with 33 receiving “frequent epinephrine” interval (≤2 minutes). Pediatric CPC score 1-2 or no change from baseline was used as primary outcome to reflect favorable neurologic outcome, with frequent dosing associated with better outcome (aOR 2.56, 95%CI 1.07 to 6.14). Change in diastolic blood pressure was greater after the second dose of epinephrine among patients who received frequent epinephrine (median [IQR] 6.3 [4.1, 16.9] vs. 0.13 [-2.3, 1.9] mmHg, p=0.034). 

This study is subject to all sorts of confounding and should be studied more rigorously, but suggests that more frequent dosing for pediatric IHCA may be of benefit.

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Despite the knowledge that minimizing interruptions in chest compressions during CPR is key to maintaing coronary perfusion pressure and chance of ROSC,^1-4 difficulties in limiting hands-off time remain. 

Dewolf et al.⁵ recently performed a prospective observational study using body cameras to find that 33% (623/1867) of their CPR interruptions were longer than the recommended 10 seconds:

• 51.6% Rhythm/pulse checks
• 11.1% Installation/use mechanical CPR device
•   6.7% Manual CPR provider switch
•   6.2% ETT placement

Previous studies have shown an increase in hands-off time associated with the use of cardiac POCUS during rhythm checks as well.^6,7

Bottom Line:

• Physicians must be mindful of hands-off time to improve their chance of obtaining ROSC, minimizing each CPR interruption to <10 seconds, and maintaining a hands-on time (also known as chest compression fraction) of >80%. 
• Change your pulse check to a rhythm check utilizing arterial line placement, end-tidal monitoring, or US/doppler at the femoral artery in order to minimize the search for a pulse as a reason for prolonged CPR interruption.
• Consider having someone on the team count the seconds out loud during pauses so the entire team is aware of the interruption time and will recognize when CPR needs to be resumed.

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A recent prospective observational study examined the diagnostic usefulness of head-to-pelvis sudden death computed tomography (SDCT) in 104 patients with ROSC and unclear OHCA etiology.

• Obtained within 6 hours of hospital arrival
• Noncontrast head CT + ECG-gated chest CTA with abbreviated coronary imaging + contrasted CT of the abdomen to just below the pelvis. 

Diagnostic performance: 

• Detected 95% of OHCA etiologies diagnosable by CT
• Detected 98% of time-critical diagnoses requiring emergent intervention (including complications of resuscitation)
• The sole reason for diagnosis of OHCA etiology in 13%

Safety:

• 28% of patients with elevated creatinine at 48h (down from 55% at presentation; study excluded GFR < 30ml/min unless treating provider felt the data was needed for care)
• 1% (1 patient) required RRT 
• No false positives noted, no allergic contrast reactions, 1 contrast IV extravasation

Bottom Line: For OHCA without clear etiology, SDCT explicitly including a thoracic CTA may have diagnostic benefit over standard care alone with the added benefit of identification of resuscitation complications. 

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Supplemental oxygen therapy is frequently required for patients presenting with acute respiratory distress and COPD exacerbation. Over-oxygenation can derail compensatory physiologic responses to hypoxia,¹ resulting in worsening VQ mismatch and, to a lesser degree, decreases in minute ventilation, that cause worsened respiratory failure.

The 2012 DECAF (Dyspnea, Eosinopenia, Consolidation, Acidaemia, and Atrial Fibrillation) score was found to predict risk of in-hospital mortality in patients admitted with acute COPD exacerbation.^2,3 Data from the DECAF study’s derivation and external validation cohorts were examined specifically to look at outcome associated with varying levels of oxygen saturation.

• 1027 patients from 6 UK hospitals receiving supplemental oxygen at admission

• Lowest in-hospital mortality seen in the 88-92% cohort 

• Adj OR for in-hospital mortality in ≥97% vs 88-92% group: 2.97 (95% CI 1.58-5.58, p=0.001)

• Adj OR for in-hospital mortality in 93-96% vs 88-92% group: 1.98 (95% CI 1.09-3.60, p=0.025)

• Surprisingly, mortality risk seen more in normocapnic than hypercapnic patients

• Association between admission SpO2 and mortality persisted after adjusting for baseline risk and disease severity using the DECAF and NEWS 2 score

Bottom Line

In patients presenting to the ED with acute COPD exacerbation requiring oxygen supplementation, a target oxygen saturation of 88-92% is associated with the lowest in-hospital mortality, and higher oxygen saturations should be avoided independent of patients' PCO2 levels.

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Background: In respiratory failure due to COPD and cardiogenic pulmonary edema, noninvasive positive pressure ventilation decreases need for intubation and improves mortality,¹ while its utility in other scenarios such as ARDS and pneumonia has yet to be proven.^1,2 We know that patients on NIV with delays to needed intubation have a higher mortality,^1,3 but intubation and mechanical ventilation come with risks that it is preferable to avoid if possible.

So how and when can we determine that NIV is not working?

The HACOR (Heart rate, Acidosis, Consciousness, Oxygenation, Respiratory rate) score at 1 hour after NIV initiation has been demonstrated to be highly predictive of NIV failure requiring intubation.^4,5 

Bottom Line:

• Patients on NIV require close reassessment to prevent worsened survival due to intubation delay should invasive mechanical ventilation be indicated.

• A HACOR score >8 after 1 hour of NIV should prompt intubation in most instances, with strong consideration given to a score >5.

*Note: ABGs were obtained for PaO2 assessment in the above studies -- the use of SpO2 was not evaluated -- but we are often not obtaining ABGs in our ED patients with acute respiratory failure. The following chart provides an estimated SpO2 to PaO2 conversion.

WHO 2001

Caveats: 

1. Pulse oximetry may be inaccurate in darker skin tones (overestimated by ~2%)⁶ and in certain disease processes (e.g. CO poisoning, profound shock states, etc.)
2. The oxyhemoglobin dissociation curve shifts right with increasing pCO2/decreasing pH (lower saturation for a given PaO2).

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As the number of COVID-19 cases rises worldwide, prehospital and emergency department healthcare workers remain at high risk of exposure and infection during CPR for patients with cardiac arrest and potential SARS-CoV-2. 

Existing evidence supports similar cardiac arrest outcomes in airways managed with a supraglottic airway (SGA) compared to endotracheal intubation (ETT).¹  It is generally accepted that the best airway seal is provided with endotracheal intubation + viral filter, but how well do SGAs prevent spread of aerosols? 

In CPR simulation studies:

• Cuffed endotracheal tube + viral filter provides effective seal to prevent aerosolization during CPR.²
• SGA + viral filter decreases AP spread compared to facemask and compared to bag-valve mask ventilation during CPR.³
• Notable aerosolization is seen with SGAs, with no difference between AuraGain, I-gel, LMA Proseal, LMA Supreme, Combitube, or LTS-D.²

• Ventilating through an SGA + viral filter is likely better to limit spread of aerosolized particles than bag-valve mask ventilation.
• SGAs allow egress of aerosolized particles, although the amount and area of distribution in clinical practice is unclear, and endotracheal intubation with a cuffed endotracheal tube remains the best way to avoid ongoing aerosolized particle spread with chest compressions. 
• Appropriate PPE remains crucial to limiting healthcare workers' risk of infection and must be prioritized, even/especially in the management of patients in cardiac arrest. 

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While the invasive monitoring of central venous pressure (CVP) in the critically ill septic patient has gone the way of also transfusing them to a hemoglobin of 10 mg/dL, it remains that an elevated CVP is associated with higher mortality^1,2 and renal failure.^2,3

Extrapolating from existing data looking at hepatic vein, portal vein, and renal vein pulsatility as measures of systemic venous hypertension and congestion,^4,5,6 Beaubien-Souligny et al. developed the venous excess ultrasound (VExUS) grading system incorporating assessment of all 3, plus the IVC, using US to stage severity of venous congestion in post-cardiac surgery patients.⁷ They evaluated several variations, determining that the VExUS-C grading system was most predictive of subsequent renal dysfunction.

(Image from www.pocus101.com)
 

High Points

       VExUS Grade 3 (severe) venous congestion:

• Correlated with higher CVP & NTproBNP levels, as well as overall fluid balance
• Had a 96% specificity for development of subsequent AKI

Caveats

• Evaluating all parameters yields the most benefit to avoid false positives
• Can be difficult to obtain all views (>25% of subjects excluded due to poor US image quality)
• Studied in a limited population, notably not primarily RV failure patients

Clinical Uses

• To limit harmful fluid administration in shock
• To help answer the prerenal vs cardiorenal AKI question in CHF
• To indicate when volume removal (diuresis) should be the strategy, even in patients with vasopressor-dependent shock

A great how-to can be found here:

https://www.pocus101.com/vexus-ultrasound-score-fluid-overload-and-venous-congestion-assessment/

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The RECOVERY (Randomized Evaluation of COVid-19 thERapY) investigators recently published a non-peer reviewed article on their findings utilizing dexamethasone to treat patients with COVID-19. 

Rx: Dexamethasone 6mg daily* x 10 days (PO or IV) *or steroid equivalent

• 2104 in the dexamethasone group vs 4321 in the “usual care” group
• Did not exclude children or pregnant/breastfeeding mothers
• Follow-up at 28 days, hospital discharge, or death

Primary outcome:         All-cause mortality at 28-days

Secondary outcomes: 

• Major arrhythmia
• Time to discharge from hospital
• Duration of mechanical ventilation
• Need for renal replacement therapy
• In patients not ventilated at enrollment, need for intubation/ECMO & death

Results:

• Decrease in overall mortality at 28-days with 3% absolute risk reduction.
  • NNT of 25 in patients requiring O2, HFNC, or NIV
  • NNT of 8 in patients requiring invasive mechanical ventilation
• More mortality benefit seen the higher the respiratory support required, with no benefit and apparent trend towards increased mortality in the group not requiring any respiratory support at all. 
• When stratified by symptoms < or > 7 days, mortality benefit only seen in the >7 days group (which was more of the ventilated patients).
• Less progression to intubation, shorter hospital duration, greater likelihood of hospital discharge.

Limitations:

• Not yet peer-reviewed, haven't seen all the data, additional analyses could be helpful in determining if treatment effect is real
• Unblinded study
• 7% of control group received dexamethasone

Bottom Line: Strongly consider admininstering dexamethasone to your patients with known COVID-19 who require respiratory support, and look for the peer-reviewed publication from the RECOVERY Trial investigators.

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Background:

· Empiric broad spectrum antibiotic therapy is a mainstay of the management of critically ill patients with septic shock.

· Vancomycin is widely used for the coverage of potential MRSA infection

• PROS: cheap, widely available, relatively widespread tissue penetration when given IV, and is generally well-tolerated

• CONS: has a complicated dosing regimen requiring specifically-timed serum concentration sampling and subsequent dose changes, frequently subtherapeutic, carries a risk of AKI especially when used concomitantly with piperacillin/tazobactam,¹ as it commonly is during empiric therapy for septic shock.         

· Continuous infusion of vancomycin has been repeatedly demonstrated to reach target serum concentrations faster, maintain consistent serum vancomycin levels better, with fewer serum concentration sampling required, and less overall vancomycin required to do so, in both adult and pediatric populations.^2-5

Current Article: 

Flannery AH, Bissell BD, Bastin MT, et al. Continuous Versus Intermittent Infusion of Vancomycin and the Risk of Acute Kidney Injury in Critically Ill Adults: a Systematic Review and Meta-Analysis. Crit Care Med. 2020;48(6):912-8.

· Systematic review and meta-analysis of 11 studies for a total of 2123 patients

· Comparing continuous versus intermittent vancomycin infusion.

· Primary outcome of AKI, secondary outcome of mortality

· Found a reduction in the incidence of AKI in the continuous infusion cohort:

• OR 0.47 (95% CI 0.34-0.65) even when taking into account trough levels /area under the curve concentrations and the severity of AKI examined by the individual studies.

· No association between infusion strategy and mortality

Considerations:

· Initial loading dose used in most of the studies (15 mk/kg) probably underdosed, current recommendation for 25mg/kg initial loading dose⁷ (which is not even always effective by itself)⁸ (Reardon)

· Continuous infusion may be difficult with limited IV access

· AKI associated with increased hospital stay, costs, mortality (although didn’t pan out in study) – worth preventing if possible.

Take Home:

· Give a 25-30mk/kg loading dose of vancomycin in critically ill patients with suspicion of MRSA to achieve target serum concentrations sooner.

· Continuous vancomycin is a viable option and could be considered in ED boarders, especially if there is concern for impending renal injury.

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There is currently a high, and appropriate, concern regarding the aerosolization of viral particles during various methods of respiratory support. While studies are limited, here is some of the currently available data (mostly-simulated) on the approximate maximum distances of particle spread:

Nasal Cannula 5LPM:¹ 1 ft 4.5 in

Non-Rebreather Mask, 6-12LPM: 4 in, minimal change with increasing flows¹

High Flow Nasal Cannula

• Simulation:² 30 LPM = 5.6 in / 60 LPM = 8.1 in
• Actual volunteers:³
  • Use of HFNC decreased aerosol dispersion during “violent exhalation” through nares
  • No difference in aerosol dispersion w/normal breathing using HFNC until 60lpm
  • Max spread = 14.4 ft without HFNC (violent exhalation) and 6.2 ft with HFNC (violent exhalation); aerosols airborne for max of 43 seconds

CPAP (20 cmH2O) provided by oronasal mask with good fit (leak from exhaust port):² 11.5 in

Bilevel positive airway pressure w/ oronasal mask (IPAP 10-18/EPAP 4): max dispersal:⁴ 1 ft 7.7 in

Bilevel positive airway pressure with full facemask⁵ (IPAP 18 / EPAP 5): 2 ft 8 in

Bilevel positive airway pressure with helmet:⁴

• IPAP 20 / EPAP 10 = 9 in
• Using helmet w/ air cushion = negligible dispersal

Utility of Surgical Mask:⁶

• No therapy:                 31% of exhaled particles travel, some >3.3 ft
• No therapy + mask:    5% of exhaled particles leak, some >3.3 ft
• 6LPM O2 + mask:       6.9% of exhaled particles leak, some >3.3 ft
• High Velocity Nasal Insufflation (40LPM) + mask: 15.9% of exhaled particles leak, some >3.3 ft

Bottom Line: 

In vivo data from actual patients is lacking, however there is potentially lower risk of aerosol spread with HFNC than regular nasal cannula, perhaps due to higher likelihood of a tighter nare/nasal cannula interface. Nonrebreather mask performs well indirectly with the shortest dispersal distance. Noninvasive positive pressure ventilation with an oronasal mask and good seal has a relatively short dispersal distance, and a surgical mask over respiratory support interventions actively decreases amount, if not distance, of particle spread. Use of appropriate PPE and negative pressure rooms, if available, remains key.

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With ED-boarding of critically-ill patients becoming more common, it is likely that ED physicians may find themselves caring for a patient who develops ACS – that is, abdominal compartment syndrome. While intraabdominal hypertension (IAH) is common and is defined as intraabdominal pressure > 12 mmHg, ACS is defined as a sustained intraabdominal pressure > 20mmHg with associated organ injury.

WHY you need to know it:

ACS → Increased mortality & recognition is key to appropriate management

WHO is at risk:

• Decreased abdominal wall compliance (obese, post-surgical)
• Increased intrabadominal contents (hemoperitoneum, ascites, tumor)
• Increased intraluminal contents (gastroparesis, ileus)
• Capillary leak / aggressive fluid resuscitation (sepsis, burns)

HOW it kills:

• Decreased blood flow to organs due to extraluminal pressure (mesenteric, renal, hepatic ischemia)
• Decreased diaphragmatic mobility, hypoventilation/oxygenation
• Decreased venous return, decreased cardiac output

→ Lactic acidosis, respiratory acidosis, multisystem organ failure, cardiovascular collapse & death

WHEN to consider it:

• Most patients who develop ACS are already intubated or altered – but consider in responsive patients c/o severe abdominal pain, marked distension, and SOB with tachypnea
• Intubated patients – recurrent, ongoing high pressure alarms with relatively low lung volumes, tachypnea
• Abdomen distended and minimally ballotable
• New / worsening oliguria / anuria
• Labs demonstrate increased creatinine, LFTs, lactate elevated “out of proportion” to patient presentation prior to decompensation 
• Imaging may reveal underlying etiology or sequelae of ACS but cannot rule it out

WHAT to do:

1. Confirm diagnosis with bladder pressure (via urinary catheter) *see cited paper for how-to in the ED*
2. Emergent surgical consultation (emergent laparotomy → improved hemodynamics, organ function, & survival. 
3. Optimize abdominal perfusion pressure (MAP - intraabdominal pressure; recommended > 60mmHg) as much as possible:

• Adequate analgeisia and sedation, if needed, to avoid agitation
• Avoid intubation if able, to avoid the positive pressure. In intubated patients, aim for low PEEPs and plateau pressures and consider short-term paralytic
• Lower the head of bed (supine to 30mmHg) to minimize abdominal "crunch"
• Aim for intravascular euvolemia. If volume overload is a contributing factor then IVF for hypotension will worsen the ACS -- start vasopressor instaed
• Evacuate intraluminal contents if able (NGT/rectal tube for decompression, consider erythromycin/reglan, or neostigmine for colonic pseudoobstruction)
• Evacuate intraabdominal extraluminal contents if able (therapeutic paracentesis for ascites(
• Burn patients with restrictive abdominal eschar should get escharotomy

Bottom Line: Abdominal compartment syndrome is an affliction of the critically ill, is assosciated with worsened mortality, and requires aggressive measures to lower the intraabdominal pressure while obtaining emergent surgical consultation for potential emergent laparotomy. 

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The arrival of a critically ill pregnant patient to the ED can be anxiety-provoking for emergency physicians as two lives and outcomes must be considered.

Some basic tenets of care, regardless of underlying issue, include:

• Obtain IV access above the diaphragm to avoid delay/prevention of administered products reaching central circulation due to compression of the IVC by the gravid uterus. 

• Provide supplemental oxygen as needed to maintain a saturation of >95% which corresponds to a PaO2 >70 mmHg. A PaO2 <60 mmHg is associated with fetal hypoxemia which will quickly lead to fetal acidosis and bradycardia. 

• Goal maternal PaCO2 is 28-32 mmHg; this respiratory alkalosis maintains a CO2 gradient to help shift offload fetal CO2 into the maternal circulation for clearance. 

• Hypotensive pregnant patients with a large uterus (20+ weeks) should be turned to the left lateral decubitus position or tilted leftward by at least 15 degrees to offload aortocaval compression and minimize secondary decrease in venous return) by the gravid uterus. 

• In cases of maternal cardiac arrest, the patient should be kept supine for chest compressions with the gravid uterus manually displaced to the left.

• Keeping the mother alive is the best way to keep the fetus alive. Standard sedatives, vasopressors, and inotropes are okay if they are needed. Exception for ketamine, which has mixed effects in existing studies and while low doses are probably safe if needed, use as a firstline agent is not recommended. Notify the NICU team of medications given to mother if there is a precipitous delivery.

• Fetal tococardiometry monitoring if available, or regular POCUS assessment of FHR, in all viable pregnancies.

Finally, once critical illness is identified the OB and NICU teams should be consulted immediately. Fetal distress in a viable pregnancy may be an indication for delivery, and initiation of the transfer process should occur if the supportive specialties are not in-house.

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When managing cardiac arrest, it is important to differentiate PEA, the presence of organized electrical activity without a pulse, from "pseudo-PEA,"where there is no pulse but there IS cardiac activity visualized on ultrasound. 

Why: 

• Pseudo-PEA is essentially a profound, low-flow shock state that often has reversible causes, such as hypovolemia, massive PE, tension pneumothorax, etcetera.
• Compared to PEA, with appropriate care patients with pseudo-PEA have a higher rate of ROSC as well as overall survival.

How: 

• POCUS during rhythm check in cardiac arrest. Be careful not to prolong the pause in compressions; acquire the US, if needed, for review once hands are back on the chest. 

What:

• In addition to searching for & addressing reversible causes of the pseudo-PEA, manage the profound shock state with pressors and/or inotropic support.
• In EDs where TEE is utilized during cardiac arrest resuscitations, strongly consider synchronization of external compressions with intrinsic cardiac activity to potentially improve ventricular filling and therefore coronary perfusion pressure.

Bottom Line: Pseudo-PEA is different from PEA. Utilize POCUS during your cardiac arrests to identify it and to help diagnose reversible causes, and treat it as a profound shock state with the appropriate supportive measures, i.e. pressors or inotropy. 

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