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Background: Management and workup of fever in the neonate has been a long-standing challenge. This unique age group is particularly susceptible to serious bacterial infections (SBI’s) despite their clinical “well” appearance. Newborns, specifically those < 60 days of age are considered high risk for SBI’s (urinary tract infections, bacteremia, bacterial meningitis) primarily due to an underdeveloped immune system. As fragile hosts, simple bacterial infections are easily communicated via hematogenous spread, from one system to another. Once bacteremic, spread of infection through their permeable blood-brain barriers is relatively easy. Through a cascade of cellular events, bacteria are able to easily penetrate the CNS, leading to overwhelming meningitis &/or death.[1] Confounding their vulnerability, is the lack of immunizations in the first month of life. If you recall, at birth, newborns are given just their first hepatitis B vaccine. The remainder of baseline immunizations (Pneumococcal, Haemophilus influenzae type b [Hib], Rotavirus, Diphtheria, tetanus & acellular Pertussis [DTap], and Polio) are traditionally not given until 6 weeks – 2 months of age.[2] Thus infants in the < 60 day age range are dependent on their mothers’ antibodies for protection. Lastly as any clinician who has taken care of a sick newborn can attest, babies at this age rarely manifest an “ill-appearance” until they are critically ill, making their exam in the early stages of bacteremia falsely reassuring. Collectively this makes the workup of fever (38 ℃/100.4 ℉) in this age group particularly challenging.

REBEL Cast Episode 64: A Clinical Prediction Rule for Febrile Infants ≤60 Days at Low Risk for Serious Bacterial Infections

For the last few decades we have relied on not just one, but a combination of clinical tools to help us risk stratify patients and determine what workup is needed. Boston, Rochester, Philadelphia criteria to name a few. However many of these rules were not statistically derived and therefore lack a balance of test sensitivity (avoiding missed SBIs) and specificity (preventing overcasting and over treating patients without SBIs). The Step-by-Step approach published in 2016 [3], was a step forward in an algorithmic approach of delineating low risk patients for SBI with higher sensitivity than Rochester, however it also had its limitations. Thus most clinicians remain appropriately conservative particularly in the <60 day age group, and continue to perform comprehensive workups. Being mindful however of potential unnecessary invasive testing (i.e. lumbar punctures) in addition to high costs associated with testing, treatment and hospitalizations, it is a worthy ongoing investigation to find a better approach.

In February 2019, significant strides were made for this neonatal age group in a study published by Nathan Kuppermann and his colleagues in the Febrile Infant Working Group of the Pediatric Emergency Care Applied Research Network (PECARN) group. They published an observational study in JAMA Pediatrics, “A Clinical Prediction Rule to Identify Febrile Infants 60 Days and Younger at Low Risk for Serious Bacterial Infections”. This is perhaps the most exciting study to have been published in the last decade, as they set out to derive and validate a clinical prediction rule to identify febrile infants 0- 60 days who are at low risk for SBIs.

What they did:
    • A large, prospective observational, multi-center study, using RNA microarray analysis to detect bacteria of SBIs, on data collected from 2011-2013.
    • SBI was defined as: bacterial meningitis, bacteremia, &/or urinary tract infection.  
    • Fever was defined by rectal temperature of at least 38 ℃ in the ED, in a prior health care setting, or at home within 24 hours.
    • All patients had blood and urine cultures obtained.
    • Cerebrospinal fluid (CSF) testing was performed only at the discretion of the treating clinician. To verify that patients whom did not undergo CSF testing, did not ultimately develop bacterial meningitis, families were contacted 8-14 days after discharge for follow-up data collection.
  • Data was then divided into a derivation set and a validation set in attempt to create a clinical prediction rule that could predict the presence of a SBI.
  • Primary: Serious bacterial infection (SBI) defined as:
      • UTI: catheterized specimen with growth of a single pathogen (50,000 cfu/ml or 10,000-50,000 cfu/ml + abnormal UA); suprapubic catheterized specimen (with > 1000 cfu/ml).
      • Bacteremia: defined by growth of a single bacterial pathogen in the blood.
    • Bacterial meningitis: defined by growth of a single bacterial pathogen in CSF.
  • 1896 febrile infants were initially enrolled (1821 with procalcitonin data analyzable and complete assessments for SBI) were included.
      • 908 randomly allocated into a derivation set
    • 913 randomly allocated into a validation set

Any infant who:

    • Appeared critically ill (determined by the treating clinician)
    • Who received antibiotics in the preceding 48 hours
    • Premature birth history (<36 weeks gestation)
    • Had pre-existing medical conditions
    • Had indwelling devices
  • Had soft tissue infections
    • 1896 febrile infants were enrolled (1821 with procalcitonin data analyzable and complete assessments for SBI)
  • 1399 (76.8%) of infants had a lumbar puncture (LP) performed (including 871/1266 infants aged 29 – 60 days [68.8%])
  • Serious bacterial infections were diagnosed in 170 infants (9.3%)*
      • 151 (8.3%) with UTIs
      • 26 (1.4%) with bacteremia
      • 10 (0.5%) with bacterial meningitis
      • 16 (0.9%) had concurrent bacterial infections
          • 10 of these had UTI + bacteremia
          • 5 of these had meningitis + bacteremia
        • 1 of these had bacteremia + meningitis + UTI
      • 4 patients had HSV infections, of which 3 were younger than 28 days and had HSV in their CSF
      • No patients who did not have CSF cultures obtained were later found to have bacterial meningitis.
    • *Remainder of patients were excluded as procalcitonin was not obtained.

    • Procalcitonin results were not available to the treating clinicians, which minimizes potential bias of clinician assessment.
    • Patients who had procalcitonin levels measured were randomly divided into derivation and validation sets, strengthening their overall results.
    • Authors also performed a sub-cohort analysis of patients ≤ 28 days vs >28 days, allowing them to look at how their rule applied within age-specific parameters.
    • Given the fact that bacteremia and bacterial meningitis are more invasive SBI’s than UTIs, the authors also performed a sub-analysis to evaluate the rule accuracy, to identify patients with infections (including patients with concurrent UTI and bacteremia or meningitis).
    • The prediction rule is simple and requires only: Urinalysis (UA), Absolute neutrophil count (ANC), and serum procalcitonin making it easy to use in clinical practice.
    • The prediction rule had high sensitivity for identifying SBI’s and high negative predictive value, while maintaining high specificity.
  • The rule does not require CSF data, potentially obviating the need for routine LPs for many young febrile infants, though further confirmation of this is still needed.
    • This study focused only on serious bacterial infections and did not include serious viral infections (ie: herpes simplex virus encephalitis, enterovirus). Viral panels or seasonally appropriate viral tests (RSV, influenza) were also not included, hence other potentially serious non-bacterial sources of fever were not considered.
    • Did not include infants 61-90 days.
    • Convenience samples were obtained on patients only during times when research staff was available.
    • CSF testing was performed at the discretion of the treating clinician, however to verify that patients discharged from the ED without CSF testing did not have bacterial meningitis, families were contacted by telephone 8 – 14 days after index ED visit.
    • The lower end of the confidence interval of the Negative Predictive Value in the validation group was 98.4%, leaving a small potential false-negative rate.
    • No other biomarkers outside of procalcitonin were evaluated.
  • In total, only a very small number of patients actually had bacteremia or bacterial meningitis, therefore validation of these findings on cohorts with greater numbers of invasive infections will be needed before implementation.

The PECARN clinical prediction rule is promising in that it demonstrates high sensitivity and specificity for identifying infants with SBIs, while retaining a high negative predictive value, with only a small potential false-negative rate. The rule is relatively simple and easy to use, mandating only three objective data points: UA, ANC, serum procalcitonin. As compared to previous rules, these investigators rounded the numerical cut-offs of ANC (rounded to 4000/uL) and procalcitonin (to 0.5 ng/mL) to make these variables even easier to apply clinically, while still retaining the same sensitivities and only slightly lower specificities.[4]  

The most notable factor in this prediction rule is the fact the rule does not require CSF data. A similar prospective study was done also omitting CSF in 2016, referred to as the “Step-by-step” approach. [3] This approach differentiated low/intermediate/high risk infants 22- 90 days by using both objective data [leukocyturia,  procalcitonin (> 0.5 ng/ml) ANC (>10,000 mm3) or CRP (>20 mg/L)] as well as the subjective assessment of “ill appearance” using the Pediatric Assessment triangle.[3]  Though this was a well conducted multi-center prospective study, that demonstrated high sensitivities (98.9% to detect all SBIs; 92% to detect invasive infections) and proved to have higher negative predictive values than Rochester criteria and the Lab-score outcomes, this study also had its limitations. Primarily its use of subjective criteria of “abnormal pediatric assessment triangle” makes it less reliable to apply clinically. Together with the age range that it was limited to (22 days – 90 days), leaves the youngest of infants (0-21 days) automatically “high risk”, hence not obviating the need for a full septic workup in this cohort.

Neither the Step-by-step approach or the PECARN Clinical prediction rules addressed serious viral etiologies, and HSV encephalitis and enterovirus are certainly not benign. In the PECARN rule, the fact that 0.2% of patients were noted to be positive for HSV infections, and all 3 infants were <28 days of age highlights the continued need for extreme caution in this very young age group.[4]   Although this clinical prediction rule seems to be the most straightforward and promising algorithm yet, the decision to omit lumbar puncture needs further external validation.

Authors Conclusions:

Kupperman et al states “We derived and validated an accurate prediction rule to identify febrile infants 60 days and younger at low risk for SBI’s using urinalysis, ANC, and procalcitonin levels. Once further validated on an independent cohort, clinical application of the rule has the potential to decrease unnecessary lumbar punctures, antibiotics and hospitalizations”. [4]

Rebel Take Home Points:
    • The PECARN Clinical Prediction rule shows future promise to help risk stratify low-risk patients for SBI. The following variables in particular (if negative or low valued) were associated with a low risk for SBI.
        • Urinalysis
        • Absolute Neutrophil Count
      • Serum procalcitonin
    • However further independent validation is still needed before it is reliably applied.
  • Until further validation, clinicians need to remain cautious with this age group, particularly conservative in the <28 day olds in whom risks of SBI and severe viral infections are greatest.
  1. Doran K, Fulde M. et al. Host–pathogen interactions in bacterial meningitis. Acta Neuropathol. 2016; 131: 185–209. PMID:26744349
  2. Recommended Child and Adolescent Immunization Schedule for ages 18 years or younger, United States, 2019. [CDC Website]
  3. Gomez B et al. Validation of the “Step-by-Step” Approach in the Management of Young Febrile Infants. Pediatrics 2016; 138(2). PMID: 27382134
  4. Kuppermann N, et al. A Clinical Prediction Rule to Identify Febrile Infants 60 Days and Younger at Low Risk for Serious Bacterial Infections. JAMA Pediatr. 2019 Feb 18. PMID: 30776077
For More on This Topic Checkout:

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post REBEL Cast Episode 64: A Clinical Prediction Rule for Febrile Infants ≤60 Days at Low Risk for Serious Bacterial Infections appeared first on REBEL EM - Emergency Medicine Blog.

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Background:Tracheal intubation is a common procedure performed on critically ill patients. In these patients, there is a high risk of life-threatening complications associated with the procedure, with severe hypoxemia being one of the more common. Development of severe hypoxemia, in turn, increases the risk of post-intubation cardiac arrest. Therefore, optimal preoxygenation is an essential part of tracheal intubation to help stave off subsequent complications.

Both NIV and HFNC can provide a higher fraction of inspired oxygen than standard oxygen therapies.  HFNC can provide continuous oxygen up to 70L/min via nasal prongs with the potential advantage of remaining in place for apneic oxygenation. NIV can also provide high flow oxygen but must be removed during the apneic phase of intubation.  To date there has not been a study comparing NIV vs HFNC to reduce the incidence of severe hypoxemia during intubation until now; the FLORALI-2 trial.

What They Did: 

  • Determine if preoxygenation with NIV is better than HFNC in reducing risk of severe hypoxemia during intubation
  • Multicenter, open-label, non-blinded, parallel-group randomized clinical trial done in 28 ICUs in France


  • Primary: Occurrence of severe hypoxemia (i.e. Pulse oximetry <80%) for  ≥5sec from beginning of RSI (end of preoxygenation) to 5min after confirmation of tracheal intubation via capnography
  • Secondary:
    • Value of pulse oximetry at end of preoxygenation and lowest value during intubation
    • Feasibility of preoxygenation evaluated by a four-point scale (easy, quite easy, quite difficult, difficult)
    • Cormack grade
    • Immediate complications (arterial hypotension, sustained cardiac arrhythmia, bradycardia, cardiac arrest, death, esophageal intubation, regurgitation, gastric distension, dental injury, and new infiltrate on CXR)
    • Late complications (occurrence of ventilator-associated pneumonia, worsening of SOFA score from days 1 – 7, duration of mechanical ventilation, length of stay in ICU, and mortality at day 28)


  • Consecutive adult patients aged >18 years, admitted to the ICU, undergoing tracheal intubation for acute hypoxemic respiratory failure:
    • Respiratory rate >25 breaths per min OR
    • Signs of respiratory distress OR
    • PaO2/FiO2 ratio of ≤300mmHg


  • Cardiac arrest
  • GCS <8
  • Intubated prior to ICU admission
  • Other contraindications to NIV (recent laryngeal, esophageal, or gastric surgery and substantial facial fractures)
  • Pulse oximetry not available
  • Pregnancy or breastfeeding
  • Refusal to participate


  • Preoxygenation done in a semi-recumbent position at 30 degrees for 3 – 5 minutes
  • NIV group = preoxygenation delivered via a face mask connected to an ICU ventilator with pressure support ventilation to obtain an expired TV between 6mL/kg and 8mL/kg of predicted bodyweight with a PEEP of 5cmH20 and FiO2 of 1.0
    • NIV provide oxygenation and ventilation during preoxygenation and between induction and laryngoscopy, but neither oxygenation nor ventilation during laryngoscopy
  • NFNC group = preoxyenation delivered by applying oxygen continuously via binasal prongs with a gas flow of 60L/min through a heated humidifier and an FiO2 1.0
    • Jaw thrust was performed to maintain patent upper airway
    • HFNC continued during laryngoscopy until endotracheal tube placed into trachea
    • HFNC therefore provided oxygenation but little ventilation during preoxygenation between induction and laryngoscopy, and also during laryngoscopy


  • 322 patients enrolled
  • 313 patients in the intention-to-treat analysis
    • Severe Hypoxemia:
      • NIV preoxygenation: 23%
      • HFNC preoxygenation: 27%
      • 95% CI -13.7 to 5.5
      • P = 0.39
  • 242 patients with moderate to severe hypoxemia (PaO2/FiO2 ≤200mmHg)
    • Severe Hypoxemia:
      • NIV preoxygenation: 24%
      • HFNC preoxygenation: 35%
      • aOR 0.56
      • 95% CI 0.32 – 0.99
      • P = 0.459
  • No difference in serious immediate or late adverse events between groups
    • Most common immediate complication was arterial pressure <90mmHg in ≈50% of intubations


  • Multicenter, randomized controlled trial comparing NIV vs HFNC as preoxygenation for hypoxemic respiratory failure
  • 1ststudy to compare effects of HFNC to NIV for pre-oxygenation
  • Consecutive patients from 28 ICUs in France randomized
  • Blinded review board checked data and decided which patients could be included in the intention-to-treat analysis
  • An adjudication committee, who was unaware of study groups, reviewed all the data on pulse oximetry that were recorded and stored to analyze the events occurring during intubation
  • Used the same make of pulse oximetry monitor and single-use digital sensors at all participating centers to ensure pulse oximetry was monitored equivalently
  • Baseline characteristics of patients did not significantly differ between two groups with the exception of:
    • More shock in HFNC group vs NIV group (25% vs 17%)
    • Less PaO2/FiO2 ≤200 in HFNC group vs NIV group (73% vs 82%)
  • Complete follow up at 28 days
  • Randomization properly done with computer-generated blocks


  • Physicians could not be blinded to individual patient assignments, but the coordinating center and all the investigators remained unaware of the outcomes of each study group until data were locked
  • HFNC group had jaw thrust maneuver performed to ensure a patent airway and it is not clear if the NIV also got this maneuver
  • Statistical analysis assumed there would be a 15% difference in severe hypoxemia between NIV and HFNC which is a big number.  A more realistic difference may have been 5 – 10%
  • Some episodes of severe hypoxemia may have been missed which could underestimate severe hypoxemia events
  • Unfair comparisons of pre-oxygenation in patients with lung shunt physiology
  • Large exclusion of patients that were intubated in ICU not included in this study making it difficult to draw conclusions on patients without hypoxemia, urgent intubation, cardiac arrest, or in a coma
  • Primary outcome was a monitor-oriented outcome and not a patient-oriented outcome such as mortality
  • Non-blinded study as treatment allocation could not be concealed which could bias results


  • Difficult to draw conclusions about ED patients as 1697 patients excluded from this study as they were intubated prior to ICU admission
  • Intubation medications included:
    • Etomidate 0.2 – 0.3mg/kg or Ketamine 1.5 – 3.0mg/kg
    • Rocuronium 0.6 – 1.0mg/kg or Succinylcholine 1.0mg/kg
      • The dosing for rocuronium should be 1.2mg/kg and for succinylcholine should be 1.5mg/kg
  • Pulse oximetry values, duration of laryngoscopy, and procedure of intubation did not differ between two groups

Author Conclusion:“In patients with acute hypoxaemic respiratory failure, preoxygenation with non-invasive ventilation or high-flow oxygen therapy did not change the risk of severe hypoxaemia. Future research should explore the effect of preoxygenation method in patients with moderate-to-severe hypoxaemia at baseline.” 

Clinical Take Home Point: It’s hard to know what to take away from this study, as the comparisons were far from fair or even optimal.  As a matter of fact, we are comparing apples to oranges. In a population of patients with severe shunt physiology we are comparing NIV (increased alveolar recruitment through higher levels of PEEP and no nasal/apneic oxygenation) to HFNC (a lower magnitude of alveolar recruitment with lower levels of PEEP + nasal/apneic oxygenation) during laryngoscopy.  Essentially, less than optimal pre-oxygenation (NIV alone) with even worse pre-oxygenation (HFNC alone).

In patients with shunt physiology we must optimize pre-oxygenation by recruiting atelectatic alveoli with the best tools we have available:

  1. Increasing PEEP via BVM + PEEP valve with flush rate oxygen AND
  2. Nasal/Apneic oxygenation


  1. Frat JP et al. Non-Invasive Ventilation Versus High-Flow Nasal Cannula Oxygen Therapy with Apnoeic Oxygenation for Preoxygenation Before Intubation of Patients with Acute Hypoxaemic Respiratory Failure: A Randomised, Multicentre, Open-Label Trial. Lancet Respir Med 2019. PMID: 30898520

Post Peer Reviewed By: Anand Swaminathan, MD (Twitter: @EMSwami)

The post FLORALI-2: Non-Invasive Ventilation (NIV) vs High-Flow Nasal Cannula (HFNC) as Pre-Oxygenation Prior to Intubation appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL EM has been committed to critical appraisal of current research with application at the bedside to improve patient care. The constant influx of new published research makes it difficult to stay current with the latest and greatest. We had our 2nd annual Rebellion in EM conference from June 28th – 30th, 2019 in San Antonio, TX.  The opening keynote on day 3 of the conference was given by Anand Swaminathan, MD on the most powerful words in medicine.

As emergency clinicians, our words matter. Some words, though, matter more than others. Here we explore the most powerful words in medicine, why they are so powerful and how understanding their power can help us develop and grow.

Rebellion in EM 2019: The Most Powerful Words in Medicine via Anand Swaminathan, MD

Rebellion in EM 2019 - The Most Powerful Words in Medicine by Anand Swaminathan - YouTube

Also Be Sure to Checkout our YouTube Channel

Critical Point #1: Medical Professionals are Uncomfortable Saying “I Don’t Know” but, it is Vital to our Development
  • Medical professionals are often “over-achievers” and often have enjoyed uninterrupted success academically
  • Medical culture has a pervasive aversion to admitting the limits of one’s abilities and skills.

Critical Point #2: The Ability to Say, “I Don’t Know”, is Governed by Three General Principles in Cognitive Psychology

  • The Dunning-Kruger Effect: We tend to overestimate our abilities and we are unaware, especially as novices, that we are doing it.
  • Mindset: Saying “I don’t know” isn’t an admission of failure but rather should be recognized as an opportunity for growth.
  • Resilience: Passionate perseverance is critical for development but re- quires us to admit and be comfortable with “I don’t know.”

Critical Point #3: Incorporation of These Psychological Principles into our Daily Lives Allows us to Improve as Medical Professionals and Human Beings

Anand Swaminathan MD, MPH
Assistant Professor of Emergency Medicine
St. Joseph’s Regional Medical Center
Twitter: @EMSwami

  1. Kruger J, Dunning D. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. J Pers Soc Psychol. 1999;77(6): 1121. PMID: 10626367
  2. Dweck CS. Mindset: The new psychology of success. New York, NY: Ballantine Books: 2006.
    Dweck CS. Motivational processes affecting learning. Am Psychol. 1986; 41(10): 1040– 1048.
  3. Duckworth A. Grit: The power of passion and perseverance. New York, NY: Scribner; 2016.
  4. ICE Blog: The Most Powerful Words in Medicine: “I Don’t Know”

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Rebellion in EM 2019: The Most Powerful Words in Medicine via Anand Swaminathan appeared first on REBEL EM - Emergency Medicine Blog.

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REBEL EM has been committed to critical appraisal of current research with application at the bedside to improve patient care. The constant influx of new published research makes it difficult to stay current with the latest and greatest. We had our 2nd annual Rebellion in EM conference from June 28th – 30th, 2019 in San Antonio, TX.  The opening keynote on day 2 of the conference was given by myself, on the impact we have on our patients & the impact they have on us.

We see thousands of patients a year…we are kind, professional, and get the job done. But every once in a while, perhaps only a couple times a year…there is a patient, or family that we really connect with. There’s no real “science” behind what selects out some people from the flocks of other patients that we see. For me, the story I’m about to share with you is about a patient that I personally connected with. He and his family opened up my eyes about the importance of human connection. He reminded me why we do what we do, and it’s important to learn from the patients’ perspective…that our interaction with them can also leave a long lasting impact.”

Rebellion in EM 2019: The Impact We Have on Patients & The Impact they Have on Us via Salim R. Rezaie, MD

Rebellion in EM 2019: The Impact We Have on Patients - YouTube

Also Be Sure to Checkout our YouTube Channel

Critical Point #1: Everyone gets jaded, but it is important to remember patients are not just symptoms. Treat others how you would treat your own family.

Critical Point #2: The decision to call a code is multifactorial.  Trust your gut and think about all the factors that can affect prognosis before making a decision.

Critical Point #3: Relationships with patients and their families reminds us why the job is so important and it is ok to open up and have those relationships.

Post Peer Reviewed By: Mizuho Morrison, DO (Twitter: @mizuhomorrison)

The post Rebellion in EM 2019: The Impact We Have on Patients & The Impact They Have on Us appeared first on REBEL EM - Emergency Medicine Blog.

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EMS rolls in with a 28 year-old male brought in for severe agitation after being found smashing glass bottles in the street. As police approached him, he cut himself with the broken glass and was bleeding significantly, though they could not fully evaluate his wounds due to his agitation. He was restrained by 6 officers and brought to you without IV access. He is thrashing around on the gurney in 4-point restraints, with blood soaking through the gauze bandages on his arms. What do you do?

Excited Delirium Syndrome:

Best defined as “delirium associated with excited behavior or agitation.”[1] it is a dangerous, high‐morbidity, and high‐mortality condition that requires immediate and aggressive management.

No single comparative study has been performed to conclude whether one treatment approach is preferable to another in the management of excited delirium. Because patients with excited delirium can develop hyperthermia, hypoxia, acidosis, hypovolemia, rhabdomyolysis, hyperkalemia, traumatic injuries (including intracranial), seizures, coma, and death, the need for sedation to rapidly gain control of the patient is paramount. When the patient is covered in a spit-mask, with 900lbs of security guards holding him down, every minute that the patient is uncontrolled can lead to increased temperature, worsening acidosis, worsening of traumatic injuries, and progression toward seizure, coma, or death.

Benzodiazepines and antipsychotics such as haloperidol, the most commonly used sedative agents, have limitations including slow onset, respiratory depression, and variability in clinical response.[2-3] As such, there is a need for a rapid acting agent that can safely sedate patients with excited delirium.  

Prehospital Studies:

The prehospital community led the way in reporting on ketamine for sedation of acutely agitated patients. One of the original case reports was of a suicidal patient considering jumping off a bridge. Police on the opposite side of a fence held the patient until he was sedated by ketamine and a fire crew could extricate him.[4]

A few years later authors from the Israeli military published their experience with using ketamine in combative trauma patients, as well as a proposed algorithm using ketamine to sedate agitated trauma patients.[5]

Fast forward to 2012 and we get data about ketamine to sedate severely agitated patients in the aeromedical setting and in 2015 within a fire-fighter based EMS system.[6-7]

These studies, and several others, set the stage for two prospective studies on ketamine in the pre-hospital setting, one in 2016 and one in 2018, both from the same group in Minnesota. In the 2016 study Cole, et al found that ketamine was significantly faster at inducing sedation compared with haloperidol (5 min vs 17 min, respectively) and patients who received ketamine required less redosing.[8] In the 2018 study, Cole, et al found the median time to adequate sedation with ketamine was 4.2 min and 90% of patients had adequate sedation prehospital. However, 57% (28/ 49) of patients were intubated.[9]  

Whoa, what? 57% intubated? Yikes. This number was higher than other pre-hospital studies reporting intubation rates of 23% , 26% , 29%, 39%, and 63%.[7,10,11,8,12]

While the pre-hospital intubation rate with ketamine has been the source of much debate[13-15], it was clear that ketamine worked quickly in the prehospital setting.

Emergency Department Studies:

These pre-hospital studies paved the way for several recent studies of emergency department ketamine use. Hopper published a retrospective review in 2015 that described the use of ketamine to treat acute agitation in 27 patients. They found ketamine had few major adverse effects on vital signs in a population with almost 22% alcohol intoxication. No patients were intubated. However, a high proportion (62.5%) of patients required additional pharmacologic treatment for agitation, suggesting that ketamine was useful only for initial control of severe agitation.[16]

The following year a group from Australia published their experience using ketamine as a rescue treatment for patients who had already failed previous sedation attempts.[17] 49 patients were administered rescue ketamine. Five patients (10%) were not sedated within 2 hours or required additional sedation within 1 hour, and the median time to sedation post-ketamine was 20 minutes. No patients were intubated. The authors concluded that ketamine appeared effective and did not cause obvious harm in a small sample and is a potential option for patients who have failed previous attempts at sedation. They recommended ketamine doses of 4-5 mg/kg IM to achieve sedation.

In 2017 we published the first prospective study of ketamine as a first-line agent for sedating acutely agitated emergency department patients.[18] We compared time-to-sedation in patients receiving ketamine, midazolam, haloperidol, lorazepam, and the combination of a benzodiazepine and haloperidol given together. 24 patients were given ketamine and their mean time to sedation was 6.5 minutes, compared with 13 minutes for Haldol, 15 minutes for midazolam, almost 18 minutes for lorazepam, and 23 minutes for the combination treatment. Significantly fewer patients receiving ketamine as a first line sedating agent were agitated at 5-, 10-, and 15-minutes. 8% of patients were intubated.

Another 2017 manuscript highlighted the use of ketamine in the sedation of agitated pediatric patients.[19] Kowalski et al present the successful use of ketamine in 5 agitated adolescent patients with underlying psychiatric disease and/or drug intoxication.

There is little doubt that ketamine is faster than traditional medications in achieving sedation of severely agitated emergency department patients. The questions that remain involve the side effects and risk profile of using ketamine in a population that often has underlying psychiatric disease and/or polysubstance abuse.

Adverse Events:

The high intubation rate seen in prehospital studies does not seem to correlate to the use of ketamine in the emergency department. A meta-analysis (that did not include the Heydari study) found the rate of intubation of agitated ED patients receiving ketamine was 1.8%.[20]

Some have argued that comparing pre-hospital intubation rates to those from the use of ketamine in the ED is an “apples and oranges” [13] comparison. It is important to note though that just because some studies found a high intubation rate, it does not necessarily mean that the patients intubated in those studies absolutely required endotracheal intubation. It is likely that some providers are uncomfortable with dissociated patients and may have chosen to intubate on EMS arrival for unfamiliarity with a “GCS 3K.”[15]

Another lingering concern revolves around the use of ketamine in patients with a history of psychiatric illness. Some fear that the N-methyl-D-aspartic acid (NMDA) receptor antagonist properties of ketamine can cause decompensation of psychiatric illness. The American College of Emergency Physicians Clinical Policy even lists psychiatric illness as an absolute contraindication for procedural sedation with ketamine.[21] While this contraindication has been questioned, a 2019 study by Lebin et al. was the first to provide evidence of psychiatric outcomes in emergency department patients who received pre-hospital ketamine for acute agitation.[22]  Compared to patients who received benzodiazipines in the pre-hospital setting, those who were given ketamine had no statistically significant differences for psychiatric inpatient admission or ED psychiatric evaluation. Patients with schizophrenia who received ketamine did not require psychiatric inpatient admission or ED psychiatric evaluation significantly more than those who received benzodiazepines. It appears that in undifferentiated, highly agitated patients, receiving ketamine rather than benzodiazepines for sedation has a minimal impact on meaningful psychiatric outcomes. Our psychiatry colleagues, however, may still disagree.[23] See REBEL EM for a deeper discussion of this phenomenon.

We look forward to the results of an ongoing randomized control trial by a group in Vancouver, B.C. comparing intramuscular ketamine to a combination of intramuscular midazolam and haloperidol with regards to the time required for adequate behavioral control in agitated emergency department patients.[24]

Treatment Algorithm:

While we do not recommend ketamine as a first line agent for the treatment of mild to moderate agitation, it does have a role in the treatment of the combative excited delirium patient. In patients for whom rapid sedation is imperative, consider giving at least 1 mg/kg IV or 5 mg/kg IM of ketamine according to the following algorithm: [25]

It is important to note that IV/IO access need not be established for the purposes of administering the initial dose of a calming medication. After administration, maintain appropriate oxygen saturation, monitor for side effects, treat injuries, and explore/treat the underlying cause of the patient’s severe agitation.

Guest Post Written By:

Jeff Riddell, MD
Assistant Professor of Clinical Emergency Medicine
Co-Director, Medical Education Fellowship
LA County + USC Emergency Medicine Residency
Department of Emergency Medicine
Keck School of Medicine of the University of Southern California
Los Angeles, CA
Twitter: @jeff__riddell

Expert Peer Review By:

Reuben J. Strayer, MD FRCPC FAAEM
Associate Medical Director
Department of Emergency Medicine
Maimonides Medical Center
Brooklyn, NY
Twitter: @emupdates

  1. Gonin P, Beysard N, Yersin B, Carron PN. Excited delirium: a systematic review. Acad Emerg Med 2018;25:552–65. PMID: 28990246
  2. Rossi J, Swan MC, Isaacs ED. The violent or agitated patient. Emerg Med Clin North Am 2010;28(1):235–56. PMID: 19945609
  3. Battaglia J, Moss S, Rush J, et al. Haloperidol, lorazepam, or both for psychotic agitation? A multicenter, prospective, double-blind, emergency department study. Am J Emerg Med 1997;15(4):335–40. PMID: 9217519
  4. Hick JL, Ho JD. Ketamine chemical restraint to facilitate rescue of a combative “jumper.” Prehosp Emerg Care 2005;9(1):85–9. PMID: 16036834
  5. Melamed E, Oron Y, Ben-Avraham R, Blumenfeld A, Lin G. The combative multitrauma patient: a protocol for prehospital management. Eur J Emerg Med 2007;14(5):265–8. PMID: 17823561
  6. Le Cong M, Gynther B, Hunter E, Schuller P. Ketamine sedation for patients with acute agitation and psychiatric illness requiring aeromedical retrieval. Emerg Med J 2012;29(4):335–7. PMID: 21565879
  7. Keseg D, Cortez E, Rund D, Caterino J. The use of prehospital ketamine for control of Agitation in a metropolitan firefighter-based EMS system. Prehosp Emerg Care 2015;19:110–5. PMID: 25153713
  8. Cole JB, Moore JC, Nystrom PC, et al. A prospective study of ketamine versus haloperidol for severe prehospital agitation. Clin Toxicol 2016;54(7):556–62. PMID: 27102743
  9. Cole JB, Klein LR, Nystrom PC, Moore JC, Driver BE, Fryza BJ, Harrington J, Ho JD. A prospective study of ketamine as primary therapy for prehospital profound agitation. Am J Emerg Med. 2018 May;36(5):789-796. PMID: 29033344
  10. Hollis GJ, Keene TM, Ardlie RM, Caldicott DG, Stapleton SG. Prehospital ketamine use by paramedics in the Australian Capital Territory: A 12 month retrospective analysis. Emerg Med Australas. 2017 Feb;29(1):89-95. PMID: 27699989
  11. Burnett AM, Peterson BK, Stellpflug SJ, Engebretsen KM, Glasrud KJ, Marks J, Frascone RJ. The association between ketamine given for prehospital chemical restraint with intubation and hospital admission. Am J Emerg Med. 2015 Jan;33(1):76-9. PMID: 25455046
  12. Olives TD, Nystrom PC, Cole JB, Dodd KW, Ho JD. Intubation of Profoundly Agitated Patients Treated with Prehospital Ketamine. Prehosp Disaster Med. 2016 Dec;31(6):593-602. PMID: 27640730
  13. Cole JB, Driver BE, Klein LR, Moore JC, Nystrom PC, Ho JD. In reply: Ketamine is an important therapy for prehospital agitation – Its exact role and side effect profile are still undefined. Am J Emerg Med. 2018 Mar;36(3):502-503. PMID: 29229535
  14. Miner JR. Ketamine is a good first-line option for severely agitated patients in the prehospital environment. Am J Emerg Med. 2018 Mar;36(3):501-502. PMID: 29329930
  15. Strayer R. https://emupdates.com/jon-cole-on-ketamine-for-agitation/ Emergency Medicine Updates blog. Nov 2, 2017.
  16. Hopper AB, Vilke GM, Castillo EM, Campillo A, Davie T, Wilson MP. Ketamine use for acute agitation in the emergency department. J Emerg Med. 2015 Jun;48(6):712-9. PMID: 25843924
  17. Isbister GK, Calver LA, Downes MA, Page CB. Ketamine as Rescue Treatment for Difficult-to-Sedate Severe Acute Behavioral Disturbance in the Emergency Department. Ann Emerg Med. 2016 May;67(5):581-587. PMID: 26899459
  18. Riddell J, Tran A, Bengiamin R, Hendey GW, Armenian P. Ketamine as a first-line treatment for severely agitated emergency department patients. Am J Emerg Med. 2017 Jul;35(7):1000-1004. PMID: 28237385
  19. Kowalski JM, Kopec KT, Lavelle J, Osterhoudt K. A Novel Agent for Management of Agitated Delirium: A Case Series of Ketamine Utilization in the Pediatric Emergency Department. Pediatr Emerg Care. 2017 Sep;33(9):e58-e62. PMID: 26466151
  20. Mankowitz SL, Regenberg P, Kaldan J, Cole JB. Ketamine for Rapid Sedation of Agitated Patients in the Prehospital and Emergency Department Settings: A Systematic Review and Proportional Meta-Analysis. J Emerg Med. 2018 Nov;55(5):670-681. PMID: 30197153
  21. Green SM, Roback MG, Kennedy RM, Krauss B. Clinical practice guideline for emergency department ketamine dissociative sedation: 2011 update. Ann Emerg Med. 2011 May;57(5):449-61. PMID: 21256625
  22. Lebin JA, Akhavan AR, Hippe DS, Gittinger MH, Pasic J, McCoy AM, Vrablik MC. Psychiatric Outcomes of Patients With Severe Agitation Following Administration of Prehospital Ketamine. Acad Emerg Med. 2019 Mar 15. doi: 10.1111/acem.13725. [Epub ahead of print] PMID: 30873690
  23. Tian LL, Newman WJ. Psychiatric Considerations Regarding Prehospital Administration of Ketamine for Agitation. J Nerv Ment Dis. 2019 Jan;207(1):43-44. PMID: 30575708
  24. Barbic D, Andolfatto G, Grunau B, Scheuermeyer FX, MacEwan W, Honer WG, Wong H, Barbic SP. Rapid agitation control with ketamine in the emergency department (RACKED): a randomized controlled trial protocol. Trials. 2018 Nov 26;19(1):651. PMID: 30477544
  25. Linder LM, Ross CA, Weant KA. Ketamine for the Acute Management of Excited Delirium and Agitation in the Prehospital Setting. Pharmacotherapy. 2018 Jan;38(1):139-151. PMID: 29136301

The post The Evolution of Ketamine for Severe Agitation appeared first on REBEL EM - Emergency Medicine Blog.

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Acute respiratory failure has many causes which can affect the ability to either take up oxygen (hypoxemic), eliminate carbon dioxide (hypercapnia), or both. Acute respiratory failure has many possible causes and in this post/video we will name the causes of acute respiratory failure and describe lung shunt physiology.

Critical Care Fundamentals: Acute Respiratory Failure via Frank Lodeserto, MD - YouTube

Also Be Sure to Checkout our YouTube Channel

4 Main Causes of Acute Respiratory Failure:
  1. Increased Work of Breathing: Look for the triad of Tachypnea(short shallow tidal volumes), Tachycardia and Diaphoresis (↑Catecholamine surge)
  2. Refractory Hypoxemia: SHUNT physiology!!
  3. Airway Protection: Look for the pooling of secretions in the airway
  4. Apnea/Hypopnea: Think of reversible causes first like hypoglycemia, opiates and benzodiazepines
  • ↑WOB & Refractory hypoxemia: Depending on clinical situation, the use of NIPPV (BPAP,BiPAP) or Heated Humidified High Flow Nasal Cannula can be attempted
  • Airway Protection & Apnea/Hypopnea: Typically will not be able to use NIPPV or HiFlow, but move to intubation

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Critical Care Fundamentals: Approach to Acute Respiratory Failure appeared first on REBEL EM - Emergency Medicine Blog.

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Take Home Points on SVT
  • Superficial venous thrombosis refers to a clot and inflammation in the larger, or “axial” veins of the lower extremities and superficial thrombophlebitis refers to clot and inflammation in the tributary veins of the lower extremities. While we previously thought of this as a benign entity, we actually found the superficial venous thrombosis has been associated with concomitant DVT and PE.
  • Small, superficial clots can be treated with compression, NSAIDs, and elevation. These patients should be seen for follow up within 7-10 days to make sure the clot has not progressed.
  • Clots that are longer than 5 cm should be treated with prophylactic dosing of anticoagulation: fondaparinux 2.5mg subq once daily for 45 days or enoxaparin 40 mg subq once daily for 45 days. 
  • Clots that are within 3 cm of the sapheno-femoral junction should be treated the same as a DVT. 
  • A superficial thrombus could mean there is a deeper clot elsewhere, even in the other leg! Take a good history, perform a thorough physical exam and consider a bilateral lower extremity DVT study in concerning patients.

REBEL Core Cast 14.0 – Superficial Venous Thrombosis Shownotes


  • The term superficial phlebitis is used if the patient has pain and inflammation involving a vein but ultrasound shows no evidence of thrombus. 
  • Superficial thrombophlebitis is generally used if the patient has pain, inflammation and thrombus in the tributary veins of the lower extremities. 
  • Superficial venous thrombosis is used when the clot and inflammation are in the larger, or “axial” veins of the lower extremities and this is done really to help communicate that these are serious clots that have the potential to cause complications similar to deep vein thrombosis. 

Cause for Concern:

  • Patients at risk of complications of their superficial venous thrombosis  include: male gender, history of VTE, cancer, SVT in a non-varicose vein, large SVT >5 cm, or SVT involving the sapheno-femoral junction (SFJ).
  • Studies within the last 5 years showing that 25% of patients with a superficial thrombus also had a DVT and 5% of patients had a concomitant PE. (Frappe 2014, Cosmi 2015)
  • 17% of the DVTs were found in the contralateral limb. (Cosmi 2015)


  • Patients will present with pain and redness in the distribution of a superficial vein.
  • D-dimer has been shown to have high false negative rate for superficial venous thrombosis.  (Cosmi 2015)
  • The diagnostic test of choice is ultrasound as this helps assess the length of the thrombus and evaluates for extension deeper veins.
  • Consider bilateral ultrasound as DVT may be found in concomitant extremity.


  • Small, superficial clots can be treated with compression, NSAIDs, and elevation. These patients should be seen for follow up within 7-10 days to make sure the clot has not progressed.
  • Clots that are longer than 5 cm should be treated with prophylactic dosing of anticoagulation: fondaparinux 2.5mg subq once daily for 45 days or enoxaparin 40 mg subq once daily for 45 days. 
  • Clots that are within 3 cm of the sapheno-femoral junction should be treated the same as a DVT. 
For More on This Topic Checkout:
  • Core EM: Superficial Venous Thrombosis
  • EM Cases: Episode 88 – DOACs Part 1: Use and Misuse
  • LITFL: Venous Thromboembolism (VTE) Prophylaxis
  • Cosmi B. Management of superficial vein thrombosis. Journal of thrombosis and haemostasis : JTH. 13(7):1175-83. 2015. PMID: 25903684
  • Frappe P, et al the STEPH Study Group. Annual diagnosis rate of superficial-vein thrombosis of the lower limbs: the STEPH community-based study. J Thromb Haemost 2014; 12: 831–8. PMID: 24679145
  • Guyatt GH et al. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 141(2 Suppl):7S-47S. 2012. PMID: 22315257

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post REBEL Core Cast 14.0 – Superficial Venous Thrombosis appeared first on REBEL EM - Emergency Medicine Blog.

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Shock is one of the most important problems with which physicians will contend with.  The magnitude of the problem is illustrated by the high mortality associated with shock.  Assessment of perfusion is independent of arterial pressure, in that hypotension does not always need to be present to define shock.  Emphasis in defining shock is based on tissue perfusion in relation to cellular function. In this post, the basics of shock, we will define shock, discuss the causes of lactate elevation, and review the main categories of shock.

Critical Care Fundamentals: The Basics of Shock via Frank Lodeserto, MD - YouTube

Also Be Sure to Checkout our YouTube Channel

Shock occurs when supply does not meet demands and NOT defined by a blood pressure (patients may be normotensive, or even hypertensive in shock)

Lactate: Usually elevated in shock, but the classic belief that lactate is elevated because of anaerobic metabolism and tissue hypoxia is not the main reason. Lactate is produced in shock under aerobic conditions due to B2 adrenergic stimulation from elevated epinephrine levels. Lactate elevation doesn’t always mean a patient is in shock or has sepsis (although lactate is elevated in these conditions), but you must have a broad differential as lactate can be elevated for many additional reasons.

Cold Shock: Low SV state

Systolic Blood Pressure correlates with stroke volume


Determinants of SV: Preload, Contractility, and Afterload

Characterized by:

  • Tachycardia
  • Narrow Pulse Pressure (compensation by vasoconstriction and ↑SVR)
  • Cold to touch
  • ↓peripheral pulses (later stages,↓ central pulses)
  • Delayed capillary refill

Categories of Cold Shock:

  1. Cardiogenic
  2. Hypovolemic
  3. Obstructive
Warm Shock:↓Systemic vascular Resistance (ie Vasodilatory Shock)


Characterized by:

  • Tachycardia
  • Wide Pulse Pressure
  • Warm to touch
  • Bounding peripheral pulses
  • Brisk capillary refill

Categories of Warm Shock: Just 1 Distributive Shock, but 5 main causes of Distributive Shock

  1. Sepsis: Sepsis is unique and patients have components of hypovolemic shock and cardiogenic shock (Myocardial depression from circulating cytokines)
  2. Adrenal Insufficiency:↓Cortisol (up-regulates vascular tone ↓ catecholamine release)
  3. Anaphylaxis
  4. Hepatic failure: ↑ endogenous Nitric Oxide which is a potent vasodilator
  5. Neurogenic:↓ sympathetic output, and may have bradycardia due to unopposed vagal tone

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Critical Care Fundamentals: The Basics of Shock appeared first on REBEL EM - Emergency Medicine Blog.

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Mechanical Ventilation is a modality commonly used in the critically ill, but many providers, may not have a strong understanding of the basics of mechanical ventilation. Emergency Medicine and Critical Care Physicians need to have a firm grasp of the basic concepts of mechanical ventilation because without it, we can do serious harm to our patients. Airway management is not complete once the endotracheal tube is placed through the cords, and the proper selection of both the ventilator mode and initial settings is essential to ensure your patient has the best possible outcomes. You should not simply rely on the respiratory therapist to know your patients physiology. Clear communication with your therapist about the patient’s physiology and initial ventilator setting is crucial.

Mechanical Ventilation Basics Part 2 by Frank Lodeserto, MD - YouTube

Also Be Sure to Checkout our YouTube Channel

3 Types of Breaths
  1. Controlled Breath: Fully controlled by the ventilator
  2. Assisted Breath: Patient can trigger a breath, but once triggered, the ventilator will do all the work
  3. Supported/Spontaneous Breath: Patient triggers the breath, and does much of the work during the breath
2 Ways Breaths are Delivered
  1. Volume Delivered: Predetermined volume is delivered to patient (Pressure needed to give this breath depends on the compliance)
  2. Pressure Delivered: Predetermined pressure given to patient (Tidal volume is unknown and depends on compliance)

Compliance = Δ Volume/ΔPressure

Volume Delivered Breath
  • Advantage: Control Minute Ventilation (can set RR and Tidal Volume)
  • Disadvantage: Square/Constant flow delivery which is not physiologic, Higher PIP compared to Pressure
Pressure Delivered Breath
  • Advantage: Decelerating flow waveform-physiologic, and mimics normal inspiration, Higher Mean Airway Pressure allows more homogenous gas distribution
  • Disadvantage: Loose direct control of minute ventilation (Can set RR, but must watch tidal volume closesly as compliance changes)

↑Peak Inspiratory Pressure & ↑ Plateau Pressure= Compliance issue

↑Peak Inspiratory Pressure & ↓ Plateau Pressure= Resistance Issue

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Critical Care Fundamentals: Basics of Mechanical Ventilation Part 2 appeared first on REBEL EM - Emergency Medicine Blog.

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Background Information:

Syncope is defined as a sudden transient loss of consciousness (LOC) followed by complete resolution. It represents 1-3% of all emergency department (ED) visits. 1 1% of all hospitalizations are due to syncope as it may have resulted from a serious underlying condition, such as arrhythmia, acute cardiac ischemia, pulmonary embolism or internal hemorrhage. 2,3 Prior studies have demonstrated that up to a half of these serious conditions, particularly arrhythmias, are missed during ED evaluation and become evident after disposition. 1 Several risk stratification tools, such as the Canadian Syncope Risk Score (CSRS; Figure 1) and the San Francisco Syncope Rule (SFSR; Figure 2) have been developed to help identify serious outcomes. 4,5 The authors of this study sought to describe the time to occurrence of serious arrhythmias relative to when the patient arrived in the ED and based on their CSRS risk category. Furthermore, their goal was to use the results of this study to provide guidance for decision making regarding duration and location of cardiac monitoring.

Clinical Question:
  • To describe the incidence and time to arrhythmia occurrence following syncope and to inform decisions regarding duration of monitoring based on ED risk stratification using CSRS
What They Did:
  • An observational prospective cohort study of all adult patients across 6 EDs who presented within 24 hours of a syncopal episode
Inclusion Criteria:
  •  Adult ED patients (over the age of 16)
Exclusion Criteria:
    • Prolonged LOC (>5 minutes)
    • Obvious witnessed seizure
    • Mental status changes from baseline
    • Head trauma causing LOC
    • Major trauma
    • Unable to obtain history (ie. Language barrier, intoxication with drugs or alcohol)
  • Primary Outcome:
    • Time occurrence of serious arrhythmia relative to ED arrival time based on CSRS risk category
    • The detection or occurrence of Serious Outcome within 30 days of syncope
      • Serious Outcome was defined as: Death, arrhythmia, MI, serious structural heart disease, aortic dissection, PE, severe pulmonary HTN, significant hemorrhage, SAH, and other serious condition causing syncope, or procedural interventions for treatment of syncope
  • Secondary Outcome:
    • Optimal duration of cardiac monitoring and location of such monitoring

Patient enrollment:

  • 5581 patients were analyzed of the total 5719 enrolled with the mean age being 53.4 years
  • 6% hospitalization rate, one that is much lower compared to the United States’ 32% of ED admissions6
  • Timing: Median time to ED after syncopal episode was 1.1 hours
  • Risk Stratification
    • 4123 (or 73.9% of total patients) = Low Risk
    • 1062 (or 19%) = Medium Risk
    • 396 (7.1%) = High Risk
    • Low Risk -> 15 had the following arrhythmic outcomes described below, and of them, 6 within 2 hours of ED arrival.
      • 6 had sinus node dysfunction
      • 4 patients with new or uncontrolled atrial fibrillation
      • 2 patients with supraventricular tachycardia
      • The remaining 3 out of the 15 had high risk issues characterized by 2 having a high degree atrioventricular (AV) block and one requiring pacemaker placement
  • Medium Risk -> 92 had arrhythmic outcomes, 45 within 6 hours of ED arrival
  • High Risk -> 100 had arrhythmic outcomes, 47 within 6 hours of ED arrival
  • Based on the 30-day follow-up data:
    • 0.2% of the low risk patients experienced an arrhythmic outcome after the cardiac monitoring cutoff point of 2 hours. In the medium and high-risk groups, that proportion of patients was 5.0% and 18.1%, respectively.

Critical Results:

Serious outcomes:

  • Only 12 (or 0.2%) patients suffered death from an unknown cause.
  • It is important to know that of the 30 patients (or 0.6%) who had an arrhythmia only 14 of them (0.3% of enrolled patients) would have benefited from an immediate intervention:
      • 5 High-grade AV block
      • 4 ventricular arrhythmias
      • 4 requiring pacemaker/AICD insertion
  • 505 of the arrhythmic outcomes were identified within 2 hours of ED arrival in low risk patients and within 6 hours in medium and high-risk patients
  • Of all the 417 serious outcomes (or 7.5% of enrolled patients) 161 were arrhythmias which consisted of:
      • 61 were sinus node dysfunction
      • 43 had new or uncontrolled atrial fibrillation
      • 30 High-grade AV blocks
      • 19 Ventricular arrhythmias
      • 8 Supraventricular Tachycardias
  • There was a subgroup of 30 patients who had a pacemaker/implantable cardio-verter-defibrillator placed within 30 days. Since the authors confirmed device insertion over telephone follow-up they listed several reasons as to not being able to identify the arrhythmia:
      • No medical records available for review
      • Arrhythmia was not documented or captured on a rhythm strip
      • Device was inserted at the discretion of the treating electrophysiologist
  • Of the 161 patients with arrhythmias, 63 had pacemakers inserted, 8 had internal cardiac defibrillators implanted, 5 underwent cardioversion, 3 had ablations performed and the remainder were managed medically.
  • Overall, 91.7% of arrhythmic outcomes among medium and high-risk patients were identified within 15 days.
  • ZERO low risk patients experienced ventricular arrhythmias or unexplained death whereas 0.9% of medium risk patients and 6.3% of high-risk patients experienced them

  • Multicenter study over 6 different EDs where patients were consecutively enrolled and not a convenience sample
  • Emergency department-based study on a common ED chief complaint
  • List of serious outcomes and list of prespecified serious arrhythmias was selected by an “international panel of experts” as conditions that needed to be identified during the patients ED visit or identified in the short term
  • Utilized an already developed clinical decision tool to risk stratify syncope patients that expands beyond CHESS (CHF, Hematocrit, Electrocardiogram, Shortness of breath, Systolic blood pressure).
  • Collected data on various phases of the patient’s care (ie. Pre-hospital, inpatient and discharge)
  • Four-step structured review of all available medical records:
    1. Reviewed not just this ED visit but ones after, hospitalizations & outpatient visits
    2. Scripted telephone interview 30-days following
    3. Looked at all local hospitals within the province of Ontario and Alberta using a national database
    4. For patients unable to be reached by phone they looked at provincial coroner’s office (as all sudden and unexpected deaths have to be reported)
  • 2-Blinded physicians reviewed all the serious outcomes and disagreements were dealt with by a third physician if needed
  • Only 6% of the total enrolled were lost to follow up
  • Since this study was embedded within a larger study and performed as a secondary analysis, there was no a priori sample size calculated before hand.
  • When a troponin was not obtained it was counted as normal. This may be a bit pre-emptive, just because a lab value was not obtained does not mean it’s normal.
  • In over 1500 patients, or a quarter of those analyzed, time of syncope was not recorded
  • 20% of eligible patients were not enrolled and uncertain cases were coded as missed
  • 261 patients who were younger with low prevalence of comorbidities, didn’t have an ECG performed because the treating emergency physician at the time thought they were low risk
  • All hospitals were Canadian and their ability to easily obtain medical records using a more unified health system makes this a confounding factor to external validity
  • Decision to perform outpatient cardiac monitoring was left up to treating EM physician
  • The authors do not define exactly what they mean by a “short term hospitalization” when talking about admitting those high-risk patients.
  • All the study centers were urban locations and the authors recognize that longer prehospital times may resulted in missed transient arrhythmias.
  • Furthermore, since transport times were short and unaccounted for, this may further decrease this study’s reproducibility in the community settings.
  • The authors report the prevalence of their findings as in line with a 1.6% overall 30-day mortality reported in a meta-analysis  and the 30-day rate of ventricular arrhythmias found in the validation phase of the San Francisco Syncope Rule.4, 7
  • Among patients with moderate- and high-risk CSRS scores, the vast majority of the arrhythmic serious conditions occurred within 15 days of the index syncope
  • The authors state that as long there is no suspected evolving non-arrhythmic serious condition (ie. Sepsis), and after appropriate work-up, medium risk patients can be discharged after 6 hours with consideration for an outpatient cardiac monitoring device. This is too much of a broad and generalized statement and instead should emphasize the importance incorporating the overall patient’s clinical picture in their disposition.
  • In regard to an outpatient cardiac monitoring device, this is not something routinely done upon discharge from most ED in the United States, especially in large urban academic centers. This may play into a benefit of a more unified Canadian health care system may better facilitate outpatient follow-up.
  • It is important to note that this study applies to a very narrow subset of patients with serious outcomes. While the other causes of syncope are equally important and should not be missed, they were not the focus of this study.
  • Always remember that no matter the risk score used (CSRS, SFSR, etc), the management and disposition of each patient should be tailored to their particular clinical picture. Clinical decision tools should not supersede one’s physical exam skills and clinical gestalt.
Author’s Conclusions:
  • The authors found that 2 hours for low-risk patients and 6 hours for medium- and high-risk patients were the optimal cut points for ED monitoring. The authors add that a 15-day outpatient monitoring for medium and high risk patients should be considered. They lastly state that high-risk patients may benefit from a short hospitalization.
Our Conclusion:
  • When using the Canadian Syncope Risk Score to identify low risk patients, without obvious serious condition, consider discharging them with outpatient follow up after 2 hours of observation in the ED. While medium risk patients can likely be discharged following 6 hours of cardiac monitoring, there should be a low-threshold for admission based on their overall clinical picture. High risk patients may benefit from a hospital admission for further evaluation, establishment of follow-up after discharge, and a needs assessment for outpatient cardiac monitoring.
Potential to Impact Current Practice:
  • Only 0.6% of all medium or high-risk patients on the CSRS score had ventricular arrhythmias and died of an unknown cause. All ventricular arrhythmias were identified within 15 days of index syncope presentation. The decision to discharge a patient with outpatient cardiac monitoring depends on several factors which includes but is not limited to: Access and/or ability to follow-up outpatient, physician-patient preference, local practice environment and medicolegal considerations
Clinical Bottom Line:
  • Cardiac monitoring cutoff periods based on patient risk for adverse outcomes are not only clinically sensible but also serve to balance over-testing vs benefit of diagnostic yield. While the risk factors, times and recommended dispositions based off this study are derived below, it is important to recognize that various clinicians in different healthcare systems may have dissimilar thresholds
    • Low Risk (2-hour observation) = Residual 0.2% risk of serious arrhythmic outcome (ZERO of the low risk cohort were ventricular arrhythmias or death) and can be discharged home
    • Medium Risk (6-hour observation) = Residual 5.0% risk of serious arrhythmic outcome (0.9% of the medium risk cohort were ventricular arrhythmias or death) and can most likely be discharged home but requires follow-up within 24-48hours
    • High Risk (6-hour observation) = Residual 18.1% risk of serious arrhythmic outcome (6.3% of the high risk cohort were ventricular arrhythmias or death) and likely need to be admitted if follow-up cannot be arranged before 24-48 hours
For more on this topic, check out these other FOAMed Resources: REFERENCES:
  1. Thiruganasambandamoorthy V, et al. Duration of Electrocardiographic Monitoring of Emergency Department Patients With Syncope. Circulation. 2019; PMID: 30661373
  2. Thiruganasambandamoorthy V, et al. Emergency department management of syncope: need for standardization and improved risk stratification. Intern Emerg Med. 2015; PMID: 25918108
  3. Thiruganasambandamoorthy V, et al. Outcomes in Canadian emergency department syncope patients: are we doing a good job? J Emerg Med. 2013 PMID: 23218198
  4. Quinn J, et al. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006; PMID: 16631985
  5. Thiruganasambandamoorthy V, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ. 2016; PMID: 27378464
  6. Sun BC, Emond JA, Camargo CA., Jr Characteristics and admission patterns of patients presenting with syncope to US Emergency departments, 1992–2000. Acad Emerg Med. 2004 PMID: 15466144
  7. Solbiati M, et al. Syncope recurrence and mortality: a systematic review. Europace. 2015; PMID: 25476868

Figure 2: San Francisco Syncope Rule (SFSR). Image from Medicalchemy Acute Medicine

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

The post Duration of Electrocardiographic Monitoring of Emergency Department Patients with Syncope appeared first on REBEL EM - Emergency Medicine Blog.

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