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1-20 of 879 results with category "Critical Care"
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
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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.