1-20 of 884 results with category "Critical Care"
While many intubations in critically ill patients go smoothly, they are a high risk procedure that EM and ICU physicians seek to continuously improve upon. Blade size is one aspect of the procedure that has received attention over the past several years. We don’t have prospective trials addressing this question, but there are several retrospective analyses that have investigated it.
- For Direct Laryngoscopy:
- The 2022 MacSize-ICU study and a 2023 study by Landefeld and colleagues with the Pragmatic Critical Care Research Group suggested that when using Macintosh geometry blades for direct laryngoscopy there was improved first pass success with size 3 blade. Secondary outcomes for these studies point to a worse glottic view with a size 4 blade.
- For Video Laryngoscopy:
- This finding did not hold up in video laryngoscopy. A 2023 study by Park et al. and now a 2026 retrospective study again by Landefeld et al. that looked at blade size for video laryngoscopy with Macintosh geometry blades found no difference in first pass success with size 3 vs size 4 blades.
Bottom Line: Continue to use your best clinical judgment when selecting a blade size, especially when performing video laryngoscopy. When performing direct laryngoscopy, if you are on the fence, consider using size 3 blade.
*These studies do not address intubation with hyperangulated designs
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Severe Community Acquired Pneumonia (SCAP) is broadly defined as CAP that requires ICU admission. Although MRSA pneumonia is overall quite rare (1), it is associated with a high mortality rate. Therefore, empiric MRSA coverage is commonly used for patients with SCAP. Common empiric agents include vancomycin and linezolid. Linezolid has both pharmacologic and clinical data that suggest it may be a preferred option for many patients.
When approaching a patient with SCAP, a key consideration is whether empiric MRSA coverage is needed. Risk factors for MRSA pneumonia include prior MRSA infection or colonization, recurrent skin infections, post-influenza pneumonia, recent hospitalization or antibiotic use (1).
If empiric MRSA coverage is determined to be needed, Linezolid offers several advantages for the treatment of SCAP. Highlights below:
- Linezolid has 100% oral bioavailability which can be especially useful for those patients with difficult IV access
- Linezolid has better lung epithelial lining penetration compared to vancomycin (6)
- In direct comparison between linezolid and vancomycin for confirmed MRSA pneumonia, linezolid was shown to have improved microbiologic cure rates without an improvement in mortality (2, 7)
- Linezolid was shown to have less nephrotoxicity than vancomycin (2, 7)
Side effects to consider with linezolid include:
- Serotonin syndrome, although extremely rare (5). May consider discussion with your pharmacist if taking additional serotonergic agents.
- Myelosuppression (typically thrombocytopenia), although usually with longer treatment courses. This study shows no significant difference in rates of thrombocytopenia compared to vancomycin (4).
If providing linezolid for treatment of SCAP:
- Dose: Linezolid 600mg IV or PO q12 hours
- Ideally should obtain blood cultures, sputum culture, MRSA nares prior to (or closely following) antibiotic administration
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Acute Hypoxemic Respiratory Failure (AHRF) is very common in the ED/ICU. In this multicenter cohort of 21,714 patients in a Canadian ICU registry (iCORE) receiving oxygen or respiratory support, 50% met criteria for acute hypoxemic respiratory failure within 24 hours of ICU admission, and 76% of those patients required invasive mechanical ventilation.
- AHRF severity was categorized using the same Pao2/Fio2 thresholds as the Berlin definition for ARDS: mild (201–300), moderate (101–200), and severe (<100).
- When Pao2/Fio2 ratios were unavailable, severity was assigned using Spo2/Fio2 thresholds: mild (236–315), moderate (149–235), and severe (< 148). One-third of patients were actually classified this way.
PaO2/FiO2 remains the conventional standard and is important for ARDS severity/prognosis, but SpO2/FiO2 is noninvasive, continuous, inexpensive, and showed good agreement with PaO2/FiO2-based severity classification. According to these authors, SpO2/FiO2 can be a practical substitute for PaO2/FiO2 when an ABG is unavailable.
- Important limitations are the reduced accuracy of SpO2 at high saturations and potential pulse-oximetry bias, including overestimation of oxygenation in patients with darker skin tones.
Worsened hypoxemia strongly tracked with worse outcomes. ICU mortality increased from 17% in mild AHRF to 26% in moderate and 44% in severe AHRF; severe disease was also associated with fewer ventilator-free days and a lower probability of ICU discharge.
- AHRF patients were often treated using ARDS-style lung-protective ventilation. Median tidal volume was about 6.5 mL/kg predicted body weight, and most measured plateau/driving pressures were within protective ranges. However, plateau pressure was infrequently documented.
- Among patients with severe AHRF, 26% received neuromuscular blockade, 13% received prone positioning, 12% received iNO, and 12% received ECLS within the first 30 days of ICU admission..
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Rarely do more than a few months go by without us posting yet another pearl about the dangers of hypoxemia or hyperoxemia. The data in general is strong that patients with significant exposure to either very high or very low oxygen levels do worse than patients with normoxia. But if the first step intervention is simple – if the SpO2/PaO2 is high, turn the oxygen support down, and if the SpO2/PaO2 is low, turn the oxygen support up - then in this day and age can we improve this with a closed-loop system? Click the Additional Information to find out!
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This trial showed that the percentage of mechanically ventilated patient post arrest who received conservative oxygen therapy (SaO2 90-95%) with favorable neurological outcomes was not significantly different compared to the percentage of patients who received liberal oxygen therapy (minimum FiO2 of 0.3, SaO2 > 90%). While avoiding hypoxemia along with hypercapnia remains a hallmark of post arrest care, exact oxygenation goals above SaO2 of 90% remain unclear.
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A multicenter double-blind RCT published in 2025 found that adult patients hospitalized with acute chest syndrome (ACS) who received 7 days of prophylactic therapeutic anticoagulation had a shorter time to ACS resolution (by approx 1 day) and reduced opioid consumption when compared to those receiving standard VTE prophylaxis.
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University of Maryland Medical Center is a referral center for patients with necrotizing fasciitis in the region, as we have a major hyperbaric chamber, and a specialized Soft Tissue Surgery team. Therefore, patients with soft tissue infection make up a group with frequent transferring to UMMC.
Some of the factors, from recent meta-analysis, suggest higher rate of mortality among this particular group of patients. When they display these factors, which are also consistent with our clinical observations, we should be more aggressive with their treatment:
Acute kidney injury OR 3.23 (2.76–5.04)
Bacteremia OR 3.89 (1.39–10.85)
Hypotension OR 1.97 (1.26–3.10)
Coagulopathy OR 2.81 (1.23–6.40)
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Taking a slight detour into the trauma critical care realm today…
BLUF: Favor aggressive calcium supplementation following trauma, especially when patient requires transfusion. Recent evidence is pointing towards a signal for improved outcomes.
Hypocalcemia in trauma is common. Roughly half to two-thirds of trauma patients are hypocalcemic on arrival, driven by both shock physiology and citrate chelation from blood products. Some authors advocate for hypocalcemia to be added as the fourth element of a "lethal diamond" alongside coagulopathy, acidosis, and hypothermia. See reference 1&2 for good discussions of this physiology.
Time for a grain of salt: A recent article in JTACS advocates for favoring calcium chloride during whole-blood or massive transfusion and was associated with improved early survival. Calcium chloride at a threshold of at least 1 g per 2 units of low-titer O whole blood was independently associated with an 84% (!) reduction in 24-hour mortality, with the benefit strongest at this 1:2 ratio and weaker at less aggressive thresholds. (LOTS of caveats with this finding, but interesting nonetheless).
Current major civilian guidelines say only that hypocalcemia should be prevented, with limited specificity on timing or dose, and the Joint Trauma System recommends 1 g calcium after the first unit and after every fourth unit thereafter. The current CAVALIER trial is evaluating prehospital calcium specifically. Those results and other recent literature could push major trauma organizations to update their recommendations in the near future.
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There were a handful of big name critical care studies published the last few weeks (LOGICAL, ARISE FLUIDS, SODa-BIC to name a few) but many of you probably already saw those so we're gonna stick with something a little more off the beaten path.
A retrospective observation trial was published recently by Gastanadui et al in Journal of Intensive Care looking at the mortality impact of corticosteroids in cardiogenic shock. They looked at 167,721 patients from the Vizient database admitted with cardiogenic shock (excluded patients with other indications for steroids). The unadjusted mortality was a whopping 48.8% in the steroid group and 29.6% in the non-steroid group. They did Inverse Probability Treatment Weighting (IPTW), which attempts (imperfectly, but best as you can retrospectively) to control for treatment selection bias, and still found a roughly 3% mortality increase in the steroid group.
Bottom Line: Corticosteroids were already controversial (at best) in cardiogenic shock, but this further adds to the reasons to avoid them in this condition. Of note, this trial excluded patients with classic hard-indications (e.g. adrenal insufficiency, COPD exacerbation, etc) and steroids should still be given to those groups, but in my opinion if you feel cardiogenic is the primary driver of the patient's shock and they do not have another indication, I would consider avoiding steroids solely for the shock.
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Bottom Line: Lactate is a useful but imperfect marker of critical illness. Below are some key points to consider when interpreting lactate.
- Lactated ringers should generally not significantly increase your measured lactate unless there is poor clearance (liver injury).
- Many medications can cause an elevation in lactate through multiple mechanisms that do not improve with fluid resuscitation.
- Lactate should be interpreted within the company it keeps (history, exam, vitals, urine output, hemodynamics).
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Sodium bicarbonate significantly reduced the need of renal replacement therapy (risk ratio [RR] 0.69; 95% CI, 0.61–0.78) but not mortality (RR, 0.84; 95% CI, 0.55–1.30). However, there was not enough sample size to support the outcome of mortality.
There was still significant heterogeneity between studies as the sources of metabolic acidosis were different between different studies in this meta-analysis study of randomized control trial. One study recruited patients with septic shock only, while other studies enrolled patients with different disease states.
There was also heterogeneity in the threshold for pH to enter the study.
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Not all patients with an acute PE will be crashing and critically ill, but it seemed worthwhile to remind everyone that there are new guidelines and recommendations from AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN/XYZLMNOP about the management of patients with acute pulmonary embolism in the 2026 AHA/ACC Joint Committee statement. A few key takeaways, with highlights for the sicker PE patients:
- New Classifications A through E for acute PE (see images below)
- Get familiar with the clinical scores! Hestia, PE Severity Index (PESI), simplified PESI (sPESI)
- ED discharge recommended for Category A and supported for Category B
- LMWH recommended over unfractionated heparin when parenteral AC is needed, unless contraindicated
- DOACs recommended over warfarin unless contraindicated
Highlights for the sicker PE patients, i.e. Categories C+:
- Get a look at the RV! (POCUS, CT, formal echo)
- Further stratify Category C patients/identify Category D earlier
- Find out how close to decompensation the patient might be
- Inform your management if the patient decompensates
- For PE patients with e/o RV strain (C2+ per this document; for me, particularly those C3+ with respiratory complaints as a marker of poor pulmonary perfusion, or Category D+), consider use of inhaled vasodilators
- Be careful with any sedation even if normotensive – decreasing preload / blunting the body's compensatory adrenergic response can be disastrous, have hemodynamic support available
- If you have to intubate, choose induction meds wisely and have hemodynamic support ready
- For patients with Category D-E acute PE:
- Norepinephrine = initial vasopressor of choice for hypotension due to modest inotropic effects; max at 15mcg/min due to effects on pulmonary vascular resistance at higher doses, if second vasopressor needed, reach for vasopressin
- Dobutamine as additional inotropic support OR for normotensive shock
- Avoid fluid boluses unless patient is also hypovolemic, and then give small boluses (250mL) only
- Consider advanced therapies for Category D and particularly E
- PE Response Team (PERT) Consultation recommended – and depending on where you practice, can help get the patient transferred if advanced therapies are an option
For a great breakdown and further discussion of the new guidelines, I recommend checking out the Life in the Fast Lane blogpost here.
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Should we give a dose of antibiotics after intubating to reduce risk of VAP down the line? A multicenter RCT conducted in 2024 - the PROPHY-VAP Trial - found that a single dose of 2g ceftriaxone administered within 12 hours of intubation reduced VAP within the first week of hospitalization for patients intubated for airway protection due to TBI, stroke or SAH, with a VAP rate of 14% in the CTX group vs 32% in the VAP group (HR 0.60; 95% CI 0.38-0.95).
Click the link below for details and additional discussion
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PaO2 to FiO2 (P:F) ratios, are often considered the gold standard in critical care for assessing the degree of oxygen-refractory hypoxia in various pathologies, particularly ARDS. P:F does have some limitations, including not accounting for the PEEP, but probably the most limiting is that it requires collecting an ABG, which is invasive and not always feasible or a top priority when resuscitating a critically ill hypoxic patient. On the other hand, SpO2 (pulse ox saturation) is routinely available, and of course the FiO2 should be known, so many have suggested perhaps using an SpO2 to FiO2 (S:F) ratio instead. But how S:F maps to P:F and how well they correlate is not fully known. Chaudhuri et al recently conducted a meta-analysis, published in Critical Care Medicine this month, which reviewed the literature on this.
Bottom Line: Yes, S:F ratios correlate well with P:F ratios, especially when the SpO2 is less than 97%, but you can't just substitute the S:F for P:F, you have to use one of the accepted formulas. See additional info on the website for the actual formula to apply and how a given S:F translates to P:F.
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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