UMEM Educational Pearls - Critical Care

Category: Critical Care

Title: Avoid Over-Sedation of Intubated ED Patients

Keywords: analgosedation, sedation, intubation, (PubMed Search)

Posted: 8/23/2022 by Kami Windsor, MD
Click here to contact Kami Windsor, MD

 

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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Category: Critical Care

Title: We should give some calcium... right??? ---- Part 2

Keywords: Calcium, Cardiac Arrest, ACLS, Code Blue (PubMed Search)

Posted: 8/16/2022 by Mark Sutherland, MD
Click here to contact Mark Sutherland, MD

We previously posted on the COCA trial, which looked at empiric calcium administration in cardiac arrest.  They studied 391 adult Danish cardiac arrest patients.  The immediate and 30 day outcomes showed no benefit, and in fact strongly trended towards calcium being WORSE than placebo.  This article provides the 6 month and 1 year follow up data.  Surprise, surprise... calcium is still not looking good.  

At 6 months survival non-significantly favored the placebo group, and at 1 year it significantly favored the placebo group.  Neurologic outcome for those who survived was also no better, and perhaps slightly worse, in the calcium group. 

Importantly, the trial excluded patients with "traumatic cardiac arrest, known or suspected pregnancy, prior enrollment in the trial, adrenaline prior to possible enrollment, and clinical indication for calcium at the time of randomization."

Bottom Line:  The evidence continues to not support the routine empiric administration of calcium in cardiac arrest.  Patients in whom there is an indication to give calcium (e.g. known ESRD, suspected hyperkalemia, etc) are excluded from these trials, and should likely still receive empiric calcium, but in undifferentiated cardiac arrest you can probably skip the calcium.

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Diastolic Blood Pressure

  • The diastolic blood pressure (DBP) is determined by vascular tone and remains relativley constant throughout the arterial system.
  • A low DBP (< 50 mm Hg) suggests vasodilation and may be associated with an increased risk of myocardial ischemia and left ventricular dysfunction.
  • In a recent trial, Ospina-Tascon and colleagues described the diastolic shock index (heart rate/DBP) and found that a DSI > 2.2 was associated with higher mortality in patients with septic shock.
  • Take Home Point: pay attention to the DBP and, when low, consider initiation of vasopressors concomitant with fluid resuscitation.

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Hemodynamic instability and cardiac arrest are major complications following endotracheal intubation.  The mantra “resuscitate before you intubate” has prompted several studies of how to prevent this.

The PREPARE II trial is a multicenter ICU-based trial studying the effect of 500cc of crystalloid versus no crystalloid pre-emptively to prevent hypotension following endotracheal intubation. The study enrolled 1067 critically ill patients in United States ICUs. Some 60% of patient were intubated for respiratory failure and 20% were already on vasopressor.  The primary induction drugs we etomidate and rocuronium. Importantly, urgent intubation was an exclusion. There were no differences in multiple endpoints including hypotension, new need for vasopressors, cardiac arrest, or 28-day mortality. 

This was in some ways this in not unexpected and patients already in an ICU setting have typically received some form of fluid loading already. Being ICU based and primarily a more smoldering medical population this has limited application to more emergent and undifferentiated settings, but study underscores the need for a broad and nuanced view of what “resuscitate” means. Positive pressure may exacerbate hypovolemia, but the patient’s underlying disease, the effect of anesthetic drugs both by direct action via relief of pain, discomfort, or dyspnea may predominate if you think the patient is euvolemic.

Remember to dose anesthetics/sedatives/RSI drugs with an eye toward hemodynamics and consider starting vasopressors prior to intubation

Bottom Line:

-In a broad well-conducted ICU-based study a 500cc peri-intubation bolus doesn’t prevent hypotension

-Have a broad view of what resuscitation for intubation might entail

-Having fluid ready for intubation is helpful, hemodynamic dosing of drugs and having a plan for vasopressors might be even more helpful

-Applicability to ED environments is limited in this ICU-based trial

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Category: Critical Care

Title: Awareness With Paralysis Among Critically Ill Emergency Department Patients: A Prospective Cohort Study

Keywords: Awareness, mechanical ventilation, Emergency Department, Rocuronium (PubMed Search)

Posted: 7/26/2022 by Quincy Tran, MD (Updated: 3/5/2024)
Click here to contact Quincy Tran, MD

Have you ever wonder what patients feel after being intubated in the ED?

The study " Awareness With Paralysis Among Critically Ill Emergency Department Patients: A Prospective Cohort Study" aimed at answering just that.

Settings: Emergency Departments from 3 hospitals; This was a secondary analysis of a prospective trial.

Patients:

Patients who received neuromuscular blockade in ED

Intervention: None.

Comparison: None.

Outcome: Primary outcome was Awareness while paralyzed, secondary outcome was Perceived threat, which is considered the pathway for PTSD.

Study Results:

The study evaluated 388 patients.  There were 230 (59%) patients who received rocuronium.

Patients who received rocuronium (5.5%, 12/230) were more likely to experience awareness than patients receiving other neuromuscular blockade (0.6%, 1/158).

Patients who experienced awareness during paralysis had a higher threat perception score that those who did not have awareness (15.6 [5.8] vs. 7.7 [6.0], P<0.01).

A multivariable logistic regression, after adjustment for small sample size, showed that Rocuronium in the ED was significantly associated with awareness (OR 7.2 [1.39-37.58], P = 0.02). 

Discussion:

With the increasing use of rocuronium for rapid sequence intubation in the ED, clinicians should start to pay more attention to the prevalence of awareness during paralysis.  According to the study, patients reported pain from procedures, being restrained, and worst of all feelings of impending death.

One of the risk factors for awareness during paralysis would be the long half-life of rocuronium, compared to that of succinylcholine.  Therefore, clinicians should consider prompt and appropriate dosage of sedatives for post-intubation sedation.  Previous studies showed that a mean time from intubation till sedatives was 27 minutes (2), and propofol was started at a low dose of 30 mcg/kg/min for ED intubation (3). 

 

Conclusion:

Approximately 5.5% of all patients or 4% of survivors of patients who had invasive mechanical ventilation in the ED experienced awareness during paralysis.  They also were at high risk for PTSD.

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Tachyarrhythmias in the setting of high-dose vasopressors due to septic shock are not uncommon. Aside from amiodarone, some providers may not know of alternative therapeutic options in the setting of septic shock. In addition, some may view the use of a beta-blocker as counter-intuitive or counter-productive in the setting of norepinephrine usage.

However, there have been multiple smaller studies evaluating using esmolol (and other short-acting beta-blockers) in the setting of tachycardia, septic shock and pressors. Outcomes regarding the theoretical benefits of beta-blockade in sepsis (i.e. decreased mortality/morbidity 2/2 decreased sympathetic innervation, inflammation, myocardial demand etc.) have been varied. However, esmolol has been demonstrated multiple times to be effective at reducing heart rate without significant adverse outcomes (i.e. no sig diff in mortality, refractory shock, or time on vasopressors).  

 

Caveats/pitfalls

-most of the studies discuss “adequate resuscitation” prior to initiation of esmolol

-not studied in patients that also had significant cardiac dysfunction 

-be aware that esmolol gtts can be a lot of volume and pts can become volume overloaded if boarding in the ED for an extended period of time

 

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Category: Critical Care

Title: Dodging DKA Dogma with Subcutaneous Insulin

Keywords: Insulin infusion, diabetes mellitus, diabetic ketoacidosis, DKA, subcutaneous, long-acting (PubMed Search)

Posted: 6/29/2022 by Kami Windsor, MD (Updated: 9/21/2022)
Click here to contact Kami Windsor, MD

Question

 

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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Category: Critical Care

Title: Multimodal strategies for vasopressor administration

Keywords: Vasopressors, Hypotension, Shock, Sepsis (PubMed Search)

Posted: 6/21/2022 by Mark Sutherland, MD (Updated: 3/5/2024)
Click here to contact Mark Sutherland, MD

Although it is well-documented that there is no true "maximum" dose of vasopressor medications, further blood pressure support as doses escalate to very high levels tends to be limited.  As such, debate has raged in Critical Care as to when is the "right" time to start a second vasoactive medication.  The VASST trial (Russell et al, NEJM, 2008) is considered to be the landmark trial in this area, and found a trend towards improvement with early addition of vasopressin to norepinephrine, but no statistically significant difference, and may have been underpowered.  

Partly as a result of VASST, the pendulum has tended to swing towards maximizing a single vasoactive before adding a second over the past decade.  The relatively high cost of vasopressin in the US has also driven this for many institutions.  However, more recently a "multi-modal" approach, emphasizing an earlier move to second, or even third, vasoactive medication, is increasingly popular.  Although cost is often prohibitive for angiotensin-2 given controversial benefits, many now advocate for targeting adrenergic receptors (e.g. with norepinephrine or epinephrine), vasopressin receptors (e.g. with vasopressin or terlipressin) and the RAAS system (e.g. with angiotensin 2) simultaneously in patients with refractory shock.  A recent review by Wieruszewski and Khanna in Critical Care (see references) outlines this approach well. 

Bottom Line: When to add a second vasoactive medication (e.g. vasopressin) for patients with refractory shock after a first vasoactive is controversial and not known.  Current practice is trending towards earlier addition of a second (or third) agent, especially if targeting different receptors, but there is limited high-quality evidence to support this approach.  Many practicioners (including this author) still follow VASST and consider vasopressin once doses of around 5-15 micrograms/min (non-weight based) of norepinephrine are reached.

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Vasopressor Tips in the Critically Ill

  • Critically ill patients often require the administration of vasopressors to maintain adequate organ perfusion.
  • A few tips to consider when administering vasopressors include:
    • Titrate to mean arterial blood pressure (MAP) or diastolic blood pressure goals.  Systolic blood pressure (SBP) is not a key driver of perfusion pressure.
    • As vasopressors also result in venoconstriction and can increase venous return, early initation may limit the need for overly aggressive fluid resuscitation.
    • Vasopressors can be safely administered through an appropriately placed peripheral venous catheter.
    • There is no maximal dose of vasopressors.
    • Consider vasopressors with a different mechanism of action in patients with persistent shock refractory to the initial vasopressor agent.

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Background:

Lung-protective ventilation with low-tidal volume improves outcome among patients with Acute Respiratory Distress Syndrome.  The use of low tidal volume ventilation in the Emergency Departments has been shown to provide early benefits for critically ill patients.

Methodology:

A systemic review and meta-analysis of studies comparing outcomes of patients receiving low tidal volume ventilation vs. those who did not receive low tidal volume ventilation.

The authors identified 11 studies with approximately 11000 patients.  The studies were mostly observational studies and there was no randomized trials.

The authors included 10 studies in the analysis, after excluding a single study that suggested Non-low tidal volume ventilation was associated with higher mortality than low tidal volume ventilation (1).

Results:

Comparing to those with NON-Low tidal volume ventilation in ED, patients with Low-Tidal volume ventilation in ED were associated with:

  • Significant lower risk of death (OR 0.80, 95% CI 0.72-0.88, I2 = 0%),
  • Lower risk of ARDS (OR 0.57, 95% CI 0.44-0.75, I2 = 21%),
  • Shorter ICU length of stay (Mean Difference -1.19 days [-2.38, -0.11]),
  • Shorter ventilator-free days (-1.03 days, [-1,74, -0.32]).

Discussion:

  • If the outlying study by Prekker et al was included, there as no significant difference in mortality.
  • Tidal volume in ED has been steadily decreased.  It was approximately 9 ml/kg of predicted body weight when reported in 2009, and was approximately 6.5 mg/kg PBW in 2018.
  • Most ventilator settings in the ED would be continued in the ICU.

Conclusion:

Although there was low quality of evidence for low tidal volume ventilation in the ED, Emergency clinicians should continue to consider this strategy.

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-If the patient is able to maintain mentation/airway/SpO2/hemodynamics and cough up blood, intubation is not immediately necessary

  • an ETT will actually reduce the diameter of the airway and can impede clearance and precipitate respiratory failure

-If you do intubate, intubate with the largest ETT possibly to faciliate bronchoscopic interventions and clearance of blood

  • Men: 8.5 or above; Women: 8.0 or above

-The CT scan that typically needs to be ordered is a CTA (not CTPA) with IV con

  • 90% of life-threatening hemoptysis from the bronchial arteries

-See if you can find prior/recent imaging in the immediate setting (e.g. pre-existing mass/cavitation on R/L/upper/lower lobes) 

  • having a level of suspicion for location/lateralization is helpful for the performing bronchoscopist to allow them to empirically occlude a location with an endobronchial blocker in a crashing hypoxemic patient if visualization is difficult 2/2 blood

-Get these meds ready before the bronchoscopist gets to the bedside to expedite care: 

  • iced/cold saline, thrombin, code-dose epi (which will be diluted)
  • there is also some (not great) data for intravenous TXA and improved outcomes

-If the pt's vent suddenly has new high peak pressures or decreased volumes after placement of endobronchial blocker, be concerned that the blocker has migrated

  • this can happen even with 1 cm movement of the ETT or blocker, or extension of the patient's neck
  • know where the ETT is secured as well as the endobronchial blocker (analagous to locking of a transvenous pacer)
  • pts with endobronchial blockers should also be on continuous neuromuscular blockade

 

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Encountered a situation in CCRU where we needed to prepare for a patient exsanguinating from gastric varices, and found a great summary of the different types of gastroesophageal balloons from EMRAP.

 

Summary: https://www.youtube.com/watch?v=Yv4muh0hX7Y

More in depth video on the Minnesota tube: https://www.youtube.com/watch?v=4FHIiA_doWU

Nice review article: https://www.sciencedirect.com/science/article/abs/pii/S0736467921009136



Category: Critical Care

Title: Adding Vasopressin and Steroids to the Code Cocktail? Not so fast...

Keywords: in-hospital cardiac arrest, IHCA, resuscitation, code, epinephrine, vasopressin, methylprednisolone (PubMed Search)

Posted: 5/2/2022 by Kami Windsor, MD (Emailed: 5/3/2022)
Click here to contact Kami Windsor, MD

Question

 

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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ED Low-Tidal Volume Ventilation

  • Low-tidal volume ventilation (LTVV) reduces mortality in patients with ARDS and may reduce mortality in patients without ARDS.
  • Recent literature has highlighted the importance of initial ED ventilator settings, as these often persist for many hours after ICU admission.
  • But..does the use of LTVV in the ED really make a difference?
  • A recent systematic review and meta-analysis sought to evaluate the use of LTVV in the ED and the impact upon clinical outcomes.
  • In short, the use of LTVV in the ED was associated with an increase in the use of LTVV in the ICU, decreased occurrence of ARDS after admission, shorter ICU and hospital lengths of stay, decreased duration of mechanical ventilation, and decreased mortality.
  • Take Home Point:  The use of LTVV in the ED makes a difference!

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Category: Critical Care

Title: APRV or Low Tidal Volume Strategy for patients with COVID-19

Keywords: APRV, low tidal volume, COVID-19 (PubMed Search)

Posted: 4/5/2022 by Quincy Tran, MD (Updated: 3/5/2024)
Click here to contact Quincy Tran, MD

During the height of the pandemic, a large proportion of patients who were referred to our center for VV-ECMO evaluation were on Airway Pressure Release Ventilation (APRV).  Does this ventilation mode offer any advantage?  This new randomized control trial attempted to offer an answer.

---------------

1.Settings: RCT, single center

2. Patients: 90 adults patients with respiratory failure due to COVID-19

3. Intervention: APRV with maximum allowed high pressure of 30 cm H20, at time of 4 seconds.  Low pressure was always 0 cm H20, and expiratory time (T-low) at 0.4-0.6 seconds. This T-low time can be adjusted upon analysis of flow-time curve at expiration.

4. Comparison: Low tidal volume (LTV)  strategy according to ARDSNet protocol.

5. Outcome: Primary outcome was Ventilator Free Days at 28 days.

6.Study Results:

  • Baseline characteristics were similar. At randomization, PF ratio for APRV group = 140 (SD 42) vs. 149 (SD 50) for LTV group.
  • Median Ventilator Free Day for APRV group: 3.7 [0-15] days vs. 5.2 [0-19] for LTV group ( P = 0.28)
  • APRV group had higher PaO2/FiO2 ratio during first 7 days (mean difference = 26, P<0.001)
  • ICU length of stay for APRV group: 9 [7-16] vs. 12 [8-17] days (P = 0.17)
  • Severe hypercapnia (Pco2 at ≥ 55 along with a pH < 7.15): APRV group = 19 (42%) vs. LTV = 7 (15%), P = 0.009.
  • Death at 28 days: 35 (78%) for APRV group, vs. 27 (60%) for LTV group ( P = 0.07)

7.Discussion:

  • Hypercapnea was transient and was mostly due to implementation of the ventilator settings.  The protocol recommended reduction of T-high to allow more ventilation, but most clinicians did not want to shorten the T-High, but instead opted for higher T-low.
  • Although the number of barotrauma were similar in both group, all 4 cases of barotrauma in the APRV group occurred within a very short period of time (3 weeks), prompted the safety monitoring board to recommend stopping recruitment for COVID-19 patients.

8.Conclusion:

APRV was not associated with more ventilator free days or other outcomes among patients with COVID-19, when compared to Low Tidal Volume strategies in this small RCT.

 

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Category: Critical Care

Title: Epinephrine versus norepinephrine in cardiac arrest patients with post-resuscitation shock

Keywords: OHCA, shock, epinephine, norepinephrine, cardiac arrest (PubMed Search)

Posted: 3/23/2022 by William Teeter, MD (Updated: 3/5/2024)
Click here to contact William Teeter, MD

The use of catecholamines following OHCA has been a mainstay option for management for decades. Epinephrine is the most commonly used drug for cardiovascular support, but norepinephrine and dobutamine are also used. There is relatively poor data in their use in the out of hospital cardiac arrest (OHCA). This observational multicenter trial in France enrolled 766 patients with persistent requirement for catecholamine infusion post ROSC for 6 hours despite adequate fluid resuscitation. 285 (37%) received epinephrine and 481 (63%) norepinephrine.

Findings

  • Deaths from refractory shock (35% vs. 9%, P<0.001) and Recurrent cardiac arrest (9% vs. 3%, P<0.001) were higher in the epinephrine group
  • In both univariate/multivariate analyses, use of epinephrine was significantly associated with:
    • All-cause mortality during the hospital stay (83% vs. 61%, P<0.001) / (OR 2.6, 95%CI 1.4–4.7, P=0.002)
    • Cardiovascular-specific mortality (44% vs. 11%, P<0.001) / (aOR 5.5, 95%CI 3.0–10.3, P<0.001)
    • Frequency of unfavorable neurological outcomes (37% vs. 15%, P<0.001) / (aOR 3.0, 95%CI 1.6–5.7, P=0.001)
  • While propensity scoring and match analysis largely confirmed these findings, further regression did not associate epinephrine with all-cause mortality.

Limitations:

  • Epinephrine arm: significantly longer time to ROSC, lower blood pH at admission, higher rates of unshockable rhythm, higher levels of arterial lactate at admission, lower LV ejection fraction, and higher levels of myocardial dysfunction.
  • Propensity matching always has the potential for confounders.

Summary:

Norepinephrine may be a better choice for persistent post-arrest shock. However, this study is not designed to sufficiently address confounders to recommend abandoning epinephrine altogether, but it does give one pause. 

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Category: Critical Care

Title: Acute liver failure

Posted: 3/15/2022 by Duyen Tran, MD (Updated: 3/5/2024)
Click here to contact Duyen Tran, MD

Acute liver failure is defined as new and rapidly evolving hepatic dysfunction associated with neurologic dysfunction and coagulopathy (INR >1.5). Most common cause of death in these patients are multiorgan failure and sepsis. Drug-induced liver injuy most common cause in US, with viral hepatitis most common cause worldwide.

Management of complications associated with acute liver failure

  • Hepatic encephlopathy: Administer lactulose orally or via enema if risk of aspiration. Goal is to slow progression to severe encephalopathy and minimize development of cerebral edema.
  • Coagulopathy: Reverse if significant bleeding or if patient needs to have invasive procedure. FFP and 4-factor PCC not indicated in absence of bleeding. Additionally these patients may be vitamin-K deficient for which vitamin K can be given.
  • Consider empiric antibiotics due to increased susceptibility to infection.
  • Renal dysfunction: correct hypovolemia with fluid resuscitation. May require RRT, continuous preferred for hemodynamic stability.
  • If persistent hypotension despite adequate volume resuscitation and pressors, IV hydrocortisone indicated as adrenal insufficiency is common in these patients.
  • Early consultation with liver transplant center. King's College Criteria and MELD score are most commonly used prognostic tools.

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How to set the correct PEEP remains one of the most controversial topics in critical care.  In fact, just on UMEM Pearls there are 55 hits when one searches for PEEP, including this relatively recent pearl on PEEP Titration.  

A recent Systematic Review and Network Meta-Analysis looked at existing trials on this issue.  They found that:

1) Higher PEEP strategies were associated with a mortality benefit compared to lower PEEP strategies

2) Lung Recruitment Maneuvers were associated with worse mortality in a dose (length of time of the maneuver) dependent fashion.

This fits with recent literature and trends in critical care and bolsters the feeling many intensivists are increasingly having that we may be under-utilizing PEEP in the average patient.  

Bottom Line: As an extremely broad generalization, we would probably benefit the average patient by favoring higher PEEP strategies, and avoiding lung recruitment maneuvers.  Do keep in mind that it is probably best to continue lower PEEP strategies in patient populations at high risk of negative effects of PEEP (e.g. COPD/asthma, right heart failure, volume depleted with hemodynamic instability, bronchopleural fistula) until these groups are specifically studied.

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Hyperglycemic Hyperosmolar State (HHS)

  • Though less common, HHS has a mortality rate that is 10x greater than DKA.
  • The hallmark features of HHS include severe hyperglycemia (> 600 mg/dL), hyperosmolality (> 320 mOsm/kg), minimal to no ketosis, and severe dehydration.
  • Though the management of HHS is similar to DKA and includes fluid resuscitation, correction of hyperglycemia, and correction of electrolyte abnormalities, it is important to also monitor serum osmolality.
  • Too rapid correction of serum osmolality can cause cerebral edema and worsen patient outcomes.
  • Current recommendations are to monitor serum osmolality every 1-2 hours with a correction of no more than 3 mOsm/kg/hr.

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Category: Critical Care

Title: Balanced Multielectrolyte Solution versus Saline in Critically Ill Adults

Keywords: Saline, balanced fluid, critically ill, mortality (PubMed Search)

Posted: 2/8/2022 by Quincy Tran, MD (Updated: 3/5/2024)
Click here to contact Quincy Tran, MD

The debate is still going on: Whether we should give balanced fluids or normal saline.  

Settings: PLUS study involving 53 ICUs in Australia and New Zealand. This was a double-blinded Randomized Control trial.

  • Patients: A total of 5037 adults who were admitted to any ICU.
  • Intervention: Balanced multielectrolyte solutions (BMES). Once patient is outside the ICU, the type of fluid was decided by the treating physicians.
  • Comparison: Normal saline
  • Outcome: 90-day all cause mortality.

Study Results:

  • Patient characteristics:
    • 2515 patients in BMES group vs. 2522 in Saline group.  Characteristics were similar in both groups.
    • Median fluid amount = 3.9L (BMES group) vs. 3.7L (Saline group).
  • Primary outcome:
    • Mortality = 21.8% (BMES group) vs. 22.0 (Saline), (OR 0.99, 95% CI 0.86-1.14)
  • Secondary outcomes:
    • Requiring Dialysis: OR 0.98 (95% CI 0.83-1.16)
    • Requiring vasopressor: OR 0.92 (95% CI 0.78-1.09)
    • Maximum creatinine level: similar between groups (155.5 umol/L for BMES vs. 154.5 umol/L for Saline group)

Discussion:

  • Treatment with saline increased serum chloride, and lower pH than BMES, but kidney function was not affected.
  • An updated meta-analysis including this trial was also published in January 2022. This updated meta-analysis showed that the risk ratio for 90-day mortality for BMES was 0.96 (95% CI 0.91-1.01).  This data suggested that using BMES could reduce risk of death (up to 9%) or increase risk of death (up to 1%).
  • Appropriate volume resuscitation is still more important than the type of fluid.

 

Conclusion:

 

  • BME treatment was not associated with improved mortality.

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