UMEM Educational Pearls - Critical Care

When managing a hypotensive patient who may have some element of cardiogenic shock, it has long been debated whether it is better to start an inodilator like dobutamine, and use a true vasopressor like norepinephrine to offset the vasodilation, or start an inopressor like epinephrine.  Currently, this is largely a practice pattern issue, with different providers and specialties tending to make different choices (in my anecdotal experience, medical intensivists tend to do norepi+dobutamine, whereas cardiac surgeons and intensivists tend to use epi).  

Banothu et al recently studied this question in children with "cold" septic shock (they do not specify how this was defined) and found quicker time to resolution of shock with norepi+dobutamine vs epinephrine.  It should be noted that this was a secondary outcome, was a small study, was in children (who I'm told are not just little adults), and no difference in mortality or patient oriented outcomes was found.  However, this is a good opportunity to review what is known on this topic:

-A small RCT in Lancet 2007 by Annane et al found no difference

-A very small RCT in Acta Pharmacologica Sinica 2002 by Zhou et al suggested norepi-dobutamine has favorable effects on gastric mucosa and tissue oxygenation relative to epi or dopamine

-A small RCT in Intensive Care Medicine 1997 similarly suggested that oxygenation in the splanchnic circulation may be better with norepi+dobut than epi.

Take Home: There is very limited evidence in either direction when choosing between an inodilator + vasopressor (e.g. norepi + dobutamine) vs single inopressor (e.g. epi) strategy for a hypotensive patient in which inotropy is desired.  There is some weak evidence that norepi + dobutamine may be better for maintaing gut oxygenation and may resolve shock faster.  Personally, I would weakly recommend norepi + dobutamine over epinephrine, but continuing to follow provider preference and go with the agent(s) you're most comfortable with is also very reasonable.  If using the inodilator/vasopressor combination, it is recommended to titrate the vasopressor (e.g. norepi) to MAP and inodilator (e.g. dobutamine) to a measure of cardiac function such as CO/CI.  

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An Uncommon Cause of Shock

• Sepsis is the most common cause of distributive shock encountered in the emergency department and intensive care unit.
• Notwithstanding, it is important to consider other etiologies of shock, especially when the patient is not responding to resuscitation.
• Adrenal crisis is one uncommon etiology of distributive shock whereby the diagnosis is often delayed.
• Risk factors for adrenal crisis can include recent GI illness, thyrotoxicosis, recent surgery, and physical or psychological stress.
• Patients often have nonspecific symptoms of generalized weakness, abdominal pain, vomiting, fever, and altered mental status.
• Current guidelines recommend the administration of 100 mg of hydrocortisone in adults suspected of having adrenal crisis.   

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Title:

The Impact of Thoracic Ultrasound on Clinical Management of Critically Ill Patients (UltraMan): An International Prospective Observational Study

Settings: 4 hospitals (3 in Netherlands and 1 in Italy)

Participants: All adults patients who were admitted to the ICU but patients who died within 8 hours of thoracic ultrasound were excluded.

Thoracic ultrasound procedure: cardiac, lung, diaphragm, inferior vena cava. The main indicators were Respiratory, Cardiac and Volume status.

Study Results:

725 thoracic ultrasound examinations and 534 patients.  Clinical management occurred in 247 (88.5%) patients within 8 hours of ultrasound.

Thoracic ultrasound was performed by 111 operators, ranging from inexperienced to very experienced.

Common findings from thoracic ultrasound among these ICU patients.

• Atelectasis 233 (32.1%)
• Pleural effusion 221 (30.5%)
• Pulmonary edema 120 (16.6%)
• Pneumonia 107 (14.8%)

Discussion:

• There was a major impact in fluid management.
  • Patients who needed more fluid (N=63) would have a balance of +907 ml within 8 hours.
  • Patients who need euvolemia (N = 28) would have a balance of +80ml within 8 hours.
  • Patients who need less fluid (N=45) would have a balance of -411ml within 8 hours.
• There was no information regarding management change according the experience of the operators.
• The authors did not assess patient-centered outcomes from these management changes.

Conclusion: Thoracic ultrasound provided a significant change in management of critically ill patients.

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Thrombolytic-induced angioedema is a known complication of alteplase or tenecteplase administration, occurring in 0.9-5.1% of patients who received thrombolytics due to ischemic stroke. Angioedema occurs due to activation of the kinin and complement pathway by plasminogen, leading to both bradykinin and histamine release.

Swelling most commonly occurs acutely while the t-PA is infusing, but can have a delayed presentation up to 24 hours post administration. It normally has an orolingual distribution, although in severe cases there can be laryngeal involvement as well. There is a 4-fold-increase occurrence in patients who take ACE inhibitor medications ^[1] with some studies noting a high prevalence in strokes involving the right insular brain region ^[2].

Once identified, the t-PA infusion should be immediately discontinued. As there may be histamine involvement in angioedema formation, patients are initially treated with steroids, H1, and H2 blockers with as needed epinephrine injections.

Given the orolingual predominance, airway obstruction must be ruled out and the patient closely monitored with emergent intubation performed if necessary.

As the kinin pathway (bradykinin) appears to play the largest role in angioedema formation, C1 esterase inhibitors and bradykinin inhibitors can be used in severe or refractory cases ^[3,4].

However, most cases are mild and resolve with t-PA discontinuation and the initial steroid and histamine blockade.

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Although extubation has historically been the purview of critical care, as ED lengths of stay continue to worsen, and as we see more and more rapidly reversible respiratory failure (e.g. opioid overdose), it is valuable for ED providers to be facile in extubating patients.  In addition, a longstanding debate in critical care has revolved around the proper device to extubate patients to, specifically: regular nasal cannula (NC) vs high flow nasal cannula (HFNC) vs noninvasive positive pressure ventilation (NIPPV).  Although data are mixed, the literature suggests extubation to HFNC or NIPPV may reduce risk of reintubation, esspecially in patients at a high risk of reintubation, but doesn't show a clear difference between HFNC and NIPPV.  

Hernandez et al recently conducted an RCT in two Spanish ICUs looking at HFNC vs NIPPV upon extubation for high risk patients.  NIPPV was associated with a lower reintubation rate (23%) as opposed to HFNC (39%).  Hospital LOS was also shorted in the NIPPV group, but no other differences were observed.  

It should be noted that this study, and pretty much the entirety of this literature base, is in ICU patients.  In fact, in this study, patients were excluded if they were intubated less than 24 hours.  Generally speaking, patients with shorter intubation tend to be lower risk for reintubation and other post-extubation negative outcomes, so I would use caution extrapolating this too much to the ED.  Unfortunately however, there is very limited literature to guide ED extubation practices.  

Bottom Line:

1) Know how to assess readiness for extubation and consider extubation in the ED if they meet  criteria

2) For patients at higher risk of reintubation (older, sicker, CHF, COPD, obesity, airway issues) who you are considering extubating, you may wish to extubate them to Noninvasive Positive Pressure Ventilation, even though there is little solid literature showing best practices in terms of post-extubation respiratory support in the ED.

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Transcutaneous Cardiac Pacing

• Transcutaneous cardiac pacing (TCP) is often attempted while preparing for transvenous cardiac pacing in critically ill patients with symptomatic bradycardia unresponsive to medical therapy.
• For TCP, pacer pads can be placed in either the anterolateral (AL) or anteroposterior (AP) positions.  
• Current resuscitation guidelines from the American Heart Association and the European Resuscitation Council do not identify a preferred pacer pad placement for TCP.
• In a recent study of patients who received TCP following cardioversion from atrial fibrillation or flutter, Moayedi and colleagues found that pacer pads placed in the AP position required less mA to capture and chest wall contractions were less severe when compared to the AL position.
• In fact, capture was approximately 80% more likely with pacer pads placed in the AP position compared to the AL position.
• Take Home Point: Consider placing the pacer pads in the AP position the next time you need to initiate TCP.

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This was a cross-sectional survey for the Diversity-Related Research Committee of the Women in Critical Care (WICC) Interest Group of the American Thoracic Society.

Settings: 62 sites in Canada and the US

Participants: Attending physicians who worked in ICUs

Questionaire:

·         Measure of Moral Distress for healthcare professionals (27 items),

·         Maslach burnout inventory (2 items),

·         Stanford Professional Fulfilment Index (14-items), Brief Cope scale (14-items)

Study Results:

1.       Demographics:

·         431 participants (approximately 43.3% response rate).

·         334 (65%) participants worked at University-affiliated hospitals

·         387 (89.0%) worked in Adult ICUs.

·         Pre-pandemic, clinical days/months was 10.1 (± 14) days, and increased to 13.1 (± 16) days during the pandemic.

2.       Measure of moral distress: Average score 95.6 ± 66.9 (maximum 417).

·         The highest score (mean 8.5 ± 4.8), for distress, came from the item: “Follow the family insistence to continue aggressive treatment even though it is not in the best interest of the patient.” ((Family wanted to do everything).

3.       Stanford Fulfillment Index:

·         387 (91.9%) intensivists found their work meaningful and 365 (86.5%) felt worthwhile at work, although most felt physically (297, 71.6%), emotionally (266 [63.8%]) exhausted.

4.       Coping strategies:

·         Participants resorted to a wide variety of scoping strategies ranging from Acceptance (90%), Self-distraction (85%) to Substance abuse (32%) and Denial (18%).

·         Most physicians (231 [55.9%]) reported that their coping remained the same before and during the pandemic.

Discussion:

·         Physicians are quite resilient. The authors found that physicians who worked more days experienced significantly more moral distress but with similar Stanford Professional Fulfillment score.

·         This finding was similar to an exploratory analysis from a meta-analysis that showed physicians, among other healthcare workers, were less likely to have severe symptoms of PTSD (2).

·         Women and physicians who were persons of color experienced significantly higher moral distress and burn-out.

Conclusion:

There was moderate moral distress and burn-out, although physicians who worked in ICUs still achieved moderate professional fulfillment.  Up to 20% of ICU physicians used a maladaptive coping strategy

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DOSE VF (DOuble SEquential External Defibrillation for Refractory VF) Trial 

Background - High quality data regarding the use of double sequential external defibrillation (DSED) and vector-change (VC) defibrillation in refractory vfib is limited

Study

-Three-group, cluster-randomized, controlled trial in six Canadian paramedic services

-Study population: 

-OHCA with refractory vfib (initial presenting rhythm of vfib or pulseless VT that was still present after three consecutive rhythm analyses and standard defibrillations separated by 2 minute intervals of CPR) of presumed cardiac etiology (405 patients)

-Some notable exclusion criteria: 

-suspected drug overdose, hypothermia, traumatic cardiac arrest

-Protocol:

-First 3 defib attempts in the standard (anterior-lateral) position

-If remained in vfib after three consecutive shocks randomized to one of:

1. Standard defib for all subsequent attempts (136 pts)

2. VC defib (all subsequent attempts in anterior-posterior position) (144 pts)

3. DSED (applied second set of pads in AP position) with near simultaneously (<1 sec) defib shocks (125 pts)

Results

-Primary outcome: survival to hospital discharge

-38 patients (30.4%) in the DSED group vs. 18 (13.3%) in the standard group (RR 2.21; 95% CI, 1.33 to 3.67) (Fragility index of 9)

-31 patients (21.7%)  in the VC group (RR [vs. standard], 1.71; 95% CI, 1.01 to 2.88) (Fragility index of 1)

-Notable secondary outcome: survival with a good neurologic outcome

-34 patients (27.4%) who received DSED vs. 15 patients (11.2%)  with standard defibrillation (RR, 2.21; 95% CI, 1.26 to 3.88)

Takeaways/Caveats:

-68% of arrests witnessed, 58% received bystander CPR, median response time of 7.4-7.8 min

-Did not reach planned sample size 2/2 COVID pandemic

-No reporting of post-arrest care (e.g. TTM, PCI)

-Overall rates of survival and good neuro outcome on the higher side even with standard of care

-More/larger studies needed, but can consider DSED for refractory vfib, particularly if you are in a setting without more advanced circulatory support/resources

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Airway Pressure Release Ventilation (APRV) is an "advanced" mode of mechanical ventilation that has long been considered a "rescue" mode of ventilation and has recently garnered much more attention during the COVID pandemic.  Given the long boarding times of critical care patients in the ED with widespread improvement in sight, I wanted to send out some great resources that have come out recently delineating the difference in thought process between APRV as a "rescue" mode and as a "primary" mode.

Rory Spiegel of EMNerd and former UMMC CCM fellow has recently given a great talk on APRV and its use as a rescue mode of ventilation. See also Phil Rola's recent paper listed on that webpage.

https://emcrit.org/emcrit/aprv-for-lung-rescue/

APRV as a primary mode of ventilation has been used in the STC for years and is often referred to in the literature according to the basic ventilatory philsophy called Time Controlled Adaptive Ventilation. I realize this may be heresy to some and perhaps a curiousity to others. I recommend you take some time to peruse the following resources:

1. Dr. Habashi has done a great deal of work in the basic and translation literature on APRV and TCAV. His recent review dispels many myths and concerns surrounding APRV

Myths and Misconceptions of Airway Pressure Release Ventilation: Getting Past the Noise and on to the Signal - https://www.frontiersin.org/articles/10.3389/fphys.2022.928562/full

2. The TCAV Network has great resources for those who want to do a deeper dive into this topic. 

https://www.tcavnetwork.org/

(Can also find their recommended protocols at the Multi Trauma Critical Care education website: https://stcmtcc.com/handouts/)

Attachments

2211021655_fphys-13-928562_(2).pdf (5,575 Kb)

2211021655_Standard_Settings_for_APRV_using_the_TCAV_Method.pdf (1,525 Kb)

2211021655_APRV_TCAV_Rescue_Strategy_Strategy_Guidelines_2020.pdf (1,614 Kb)

Question

Arterial line waveform interpretation and troubleshooting are essential skills for any physician caring for critically ill patients. Overdamping and underdamping of the arterial line waveform leads to inaccurate systolic and diastolic blood pressure readings which can lead to unidentified hypertension or hypotension. In addition to scrutiny of the arterial waveform pattern, the square-wave test is a tool to identify overdamped or underdamped arterial lines. 

Overdamped arterial waveforms will underestimate systolic blood pressure and overestimate diastolic blood pressure. Underdamping will have the opposite effect and overestimate systolic blood pressure and underestimate diastolic blood pressure. In both cases, the mean arterial pressure (MAP) often remains the same.  

The square-wave test is a rapid flush that is applied to the arterial line for approximately 1 second. This rapid high-pressure surge results in vibration and oscillation of the arterial catheter. These oscillations are then read by the pressure transducer and the number and amplitude of these oscillations can be measured. 0 or 1 oscillations is suggestive of overdamping. 3 or more oscillations is suggestive of an underdamped system. 

Major causes of an overdamped arterial line waveform include low infusion bag pressure, loose connectors, air bubbles in the tubing, blood clot in the circuit, or kinking of vascular catheter. An underdamped arterial line, however, is caused by overly stiff circuit tubing or a defective transducer.   

Scrutiny of the arterial waveform and utilization of the square-wave test can be helpful to both identify erroneous arterial line blood pressure readings as well as suggest likely corrective measures.  

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Attachments

2210242137_Arterial_line_overdamped_and_underdamped_examples.jpg (112 Kb)

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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Needless to say, therapeutics for COVID-19 pneumonia have been controversial.  From hydroxychloroquine to ivermectin to remedesivir to steroids to bleach (sorry, but it had to be said...),  it depends on who you ask whether medications make a difference in COVID, how much of a difference, when they should be given, and what the correct dose is. 

Dexamethasone, however, ala the RECOVERY trial, is one of the relatively few therapies supported by the majority of the literature and guidelines, and generally is recommended when respiratory support is required for COVID-19 pneumonia.  Further add to this that steroids for ARDS is a long-running point of critical care controversy (e.g. DEXA-ARDS, Meduri, etc), and all you need to say to an intensivist is "how much steroid should I give this patient?" and you can walk away and come back 10 minutes later to find them having not noticed you had ever left.

Wu et all did a fairly small (n=107) single-centered RCT looking at dexamethasone 6 mg daily vs dexamethasone 20 mg daily for COVID-19 requiring O2.  There are several notable limitations to this study, but in short it did NOT add support to the notion that higher dose dexamethasone is a good thing for COVID-19 pneumonia.  In fact, the 20 mg group trended towards worse outcomes.  Small sample size, single-center, limited follow up, variable use of biologics between the groups, and failure to investigate intermediate doses between 6 and 20 are all significant limitations of this trial. Of note, DEXA-ARDS, which was conducted before COVID (2013-2018), looked at 20 mg x 5 days followed 10 mg x 5 days and DID find a significant benefit, as well as pretty darn good NNT and p values (and was a higher quality trial), so in my opinion it is also not unreasonable to use DEXA-ARDS dosing if the patient meets moderate-severe ARDS (P:F < 200) criteria, even though of course DEXA-ARDS was before COVID and Wu et al slightly contradicts it. 

When faced with a very sick COVID-19 pneumonia patients many intensivists will do either RECOVERY or DEXA-ARDS dexamethasone (with relatively limited basis to choose one vs the other), and some will do Meduri protocol methylprednisolone (1-2 mg/kg/day).  Relatively few nowadays will omit steroids unless there's a contraindication.

Bottom Line: It probably remains a good idea to give dexamethasone to your COVID-19 pneumonia patients with hypoxia, but you can probably stick to RECOVERY (see reference below; 6 mg daily x 10 days) dosing as opposed to higher doses.  If they're REALLY sick (P:F < 200), consider DEXA-ARDS (20 mg x 5 days followed by 10 mg x 5 days) dosing.

Optimal Timing of Source Control in Sepsis

• Sepsis is the most common critical illness encountered in the emergency department.
• Much of the resuscitation of patients with sepsis is focused on early and appropriate antibiotic administration, appropriate fluid resuscitation, vasopressor support, and continued hemodynamic monitoring.
• Another critical pillar in sepsis resuscitation is source control.  To date, there is varying literature on the optimal timing of source control in sepsis.
• In a recent cohort study of approximately 5,000 patients with community-acquired sepsis, Reitz and colleagues report a 29% reduction in risk-adjusted odds of 90-day mortality for patients who had early source control (< 6 hours) compared to those with late source control (6-36 hours).
• The greatest reduction in risk-adjusted 90-day mortality with early source control occurred in patients with gastrointestinal/abdominal and soft-tissue sources of infection.
• Take Home Pearl: Early source control matters in sepsis resuscitation, especially in sicker patients with a GI or soft-tissue source of infection.

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Enter the WATERFALL trial into the present flood of fluid strategy trials, a multi-country (primarily Spain) open-label RCT of “Aggressive” versus “Moderate” fluid resuscitation with lactated ringers for early mild acute pancreatitis.

Population: 249 adults (1/3 of the planned enrollment) presenting to the ED within 24hrs hours of abdominal pain onset diagnosed with mild acute pancreatitis. Numerous exclusions for local pancreatic complications, acute or chronic organ dysfunction (including CHF and CKD), among many others. Average age of 57, 51% female, 61% due to gallstones, median Charleson index of 2, median BISAP of 1, and 52% clinically judged hypovolemic on enrollment.

Interventions: 1:1 randomization to two complex protocols, both with time points every 48 hours and same criteria for initiating oral diet.

• “Aggressive”: Immediate 20ml/kg bolus of LR hours with repeat 20ml/kg boluses for hypoperfusion followed by 3ml/kg/hr infusion for 12hrs, then 1.5-3ml/kg/hr for at least 36hrs
• “Moderate”: 10ml/kg bolus only if hypovolemic with repeat 10ml/kg boluses for hypoperfusion followed 1.5 ml/kg/hr infusion for 20hrs

Outcomes/Results: Primary outcome was development of moderate of severe pancreatitis with no difference found between the two strategies. Median fluid at 72 hours was 8.3L (IQR 7.1- 10.8) in the aggressive arm and 6.6L (IQR 4.1 - 8.0) in the moderate arm.  Several point estimates favor the moderate group, but none statistically significant and there was not a difference in symptom or SIRS improvement at 72 hours.  The trial was stopped after 1/3 enrollment when the monitoring board noted a significantly increased rate of fluid overload in the aggressive arm (20.5%) versus the moderate arm (6.6%). 

Discussion:

-Aggressive fluids for mild acute pancreatitis didn’t show benefit over a moderate strategy and showed some harms in contrast to previous smaller studies and some guideline recommendations in mild disease

-Only reached 1/3 of target enrollment significantly limiting analysis

-This was by design not a trial of severe or critical disease

-The open label nature may have affected some endpoints, including safetly endpoints

-Another trial to shift our thinking a bit about how to use and safely limit fluid resuscitation

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Have you ever encountered an ESRD patient who missed dialysis because the patient "felt too sick to go to dialysis"? The patient then had hypotension from an infected catheter line? Do we give 30 ml/kg of balanced fluid now?

__________________________

Title: Outcomes of CMS-mandated ?uid administration among ?uid-overloaded patients with sepsis: A systematic review and meta-analysis.

Settings: This is a meta-analysis

Patients: Septic patients who have underlying fluid overload conditions (CHF or ESRD).

Intervention: intravenous fluid administration according to the mandate by the Center for Medicare/Medicaid as 30 ml per kilograms of bodyweight.

Comparison: fluid administration at less than 30 ml/kg of body weight.

Outcome: 30-day mortality, rates of vasopressor requirement, rates of invasive mechanical ventilation

Study Results:

• Random-effects meta-analysis of 5 studies, including 5804 patients.  There were 5260 (91%) patients receiving non-aggressive IVF at < 30 ml/kg versus 544 (9%) patients received aggressive IVF at rates > 30 ml/kg.
• Patients who received aggressive IVF > 30 ml/kg were associated with 30-day all-cause mortality OR 1.42 (95% CI 0.88-2.3, P = 0.15, I² =35%).
• The need for vasopressor during stay was similar: OR 0.69 (95%CI 0.42-1.15, P=0.21, I² = 33%)
• The need for invasive mechanical ventilation during hospitalization was similar: OR 0.85 (95% CI 0.57-1.26, P = 0.42, I² = 0)
• Both groups had similar ICU length of stay: Standard Difference in Means -0.002 (Very small magnitude), 95% CI -0.35 to 0.34, P= 0.99, I² = 53)
• Similar hospital length of stay: Standard Difference in means -0.11 (small magnitude), 95% CI -0.62 to 0.38), P= 0.67, I²=77%

Discussion:

• All studies were retrospective studies, as it’s hard to do RCT when the treatment is required by guidelines.  Although the studies were graded as high quality but there was still risk of bias.
• Until there is significant evidence to change the guidelines, please document thoroughly in your charts if you do not give sepsis patients who have fluid overload the required volume of IVF at 30 ml/kg.
• Consider early vasopressor.

Conclusion:

• Patients who have fluid overload and sepsis had similar outcomes when they were given IVF at rates < 30 ml/kg, compared to those given IVF > 30 ml/kg as required by CMS.

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Point-of-care ultrasound compression of the carotid artery for pulse determination in cardiopulmonary resuscitation

Background:

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Take Home:

This is essentially a secondary analysis of a previous prospective observational cohort study with high quality methods. The authors have an excellent discussion of the previous studies on this topic (which for those with an interest I highly recommend you read). They conclude that this study supports previous literature which I would think would be seemingly obvious, which is that those who are more ill to begin with have less tolerance of propofol (in a dose-independent relationship) in this and previous studies. Their use of IPTW extends the analysis on this large international population by addressing confounders in a novel way.

Their overall conclusion is that propofol is bad for the critically ill, and especially bad for those with pre-existing risk factors for intubation complications. I agree: This study suggests in even stronger terms that propofol should be used carefully and probably only in unhealthy patients when other options are unavailable.

Study Background and Characteristics

• INTUBE study¹ was a prospective cohort study conducted from October 1, 2018, to July 31, 2019
• Enrolled consecutive “critically ill” patients over 8 week period at 197 clinical sites from all over the world. Critically ill was defined as those with “an underlying life-threatening condition causing cardio–respiratory failure or neurologic impairment”.
• Outcome of “cardiovascular instability/collapse” as one or more of the following events within 30 minutes of intubation start: (1199 of 2760 enrolled patients; 43.4%)
  • systolic arterial pressure <65 mm Hg recorded at least once (collapse criteria) – 12.8%
  • cardiac arrest (collapse criteria) – 7.8%
  • systolic arterial pressure <90 mm Hg for >30 minutes – 24%
  • new requirement or increase of vasopressors – 87.8%
  • fluid bolus >15 ml/kg to maintain the target blood pressure – 13.2%
• STROBE Compliant

Findings

• CV-instability group were significantly older, high SOFA scores, and higher rates of ischemic heart disase, NYHA 3/4 heart failure, poor oxygenation (SPO2/FIO2 ration), pressors, fluid bolus/total, systolic/diastolic BP, and more commonly respiratory failure and cardiovascular instability as the reason for intubation.
• CV-stability group was less likely to receive propofol and at lower doses and more likely receive ketamine.
• Notably, CV-instability patients were less likely to be intubated by emergency physicians versus anesthesiology.
• Anesthesiologists were more likely to use propofol and more emergency medicine physicians using ketamine.
• Higher incidence of CV-instability in ischemic heart disease and heart failure, noninvasive ventilation and apneic oxygenation, and in the 30–45° head-up position.
• ICU mortality associated with:
  • vasopressors/fluids without hypotension (OR, 1.47; 95% CI, 1.21–1.79)
  • systolic blood pressure <90 mm Hg for >30 min despite vasopressors (OR, 2.65; 95% CI, 1.87–3.75)
  • systolic blood pressure <65 mm Hg (OR, 1.89; 95% CI, 1.31–2.71)
  • cardiac arrest (OR, 8.79; 95% CI, 5.46–14.7)
• Inverse Probability Treatment Weighting² (IPTW) analysis found that the only treatment effect with significance associate with the entire CV-instability group was propofol usage (OR, 1.23; 95% CI, 1.02–1.49).
  • No treatment effect, including propofol use or dosage, was associated with those meeting cardiovascular collapse criteria.

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Question

Traditionally, internal jugular and subclavian central line placement has required chest x-ray confirmation of correct placement (venous cavoatrial junction placement) as well as demonstrating lack of complication (no pneumothorax) prior to use of that central line. However, current evidence supports similar if not superior complication identification and placement confirmation with ultrasound,^(1-7) allowing for a much quicker confirmation time than traditional chest x-ray, which can be vital in critically ill patients who need immediate medication administration.

Venous placement is confirmed with prompt visualization of microbubbles in the right atrium and ventricle with a rapid flush of 5-10 ml of agitated saline via the distal central line port. Additionally, if the opacification occurs <2 seconds after injection then the catheter tip is sufficiently distal in the central venous system to not require additional verification. Additional confirmation of lung sliding in both lung apices will rule out pneumothorax.

Some authors recommend checking the contralateral internal jugular vein to ensure that the central line catheter has not traveled up the internal jugular towards the head, however this may be redundant as long as the time from agitated saline injection to right atrial visualization of microbubbles is clearly less than 2 seconds.

Bottom Line: Utilization of ultrasound for central line placement confirmation is a relatively simple, rapid, safe, and accurate means of confirmation of venous catheter placement and catheter tip location, as well as ruling out pneumothorax complications.

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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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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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