The Easy IJ: Another Option for Difficult IV Access in Stable Patients?

Background: We have all taken care of patients in whom IV access is difficult due to a multitude of reasons including repeated prior IV access, advanced vascular disease and shock. This often creates delays in patient care, increases ED length of stay, and uses up ED staff that have other patients to care for. Many providers have resorted to using IO access, particularly in critically ill patients due to speed of establishing access.  In stable patients, however, this may be a less desirable.  Ultrasound guidance has been a great addition in these patients.  Ultrasound guided peripheral IVs and external jugular access would probably be the next “go to options” in these patients. The authors of this paper evaluate yet another option: The Easy IJ. 

What They Did:

  • Multicenter, prospective observational study to evaluate the efficacy and safety of the easy IJ in stable ED patients with difficult intravenous access

Definition:

  • Easy Internal Jugular (IJ) Access: Placement of an 18 gauge, 4.8 cm, single-lumen catheter (the same catheter used for peripheral access) in the IJ with ultrasound guidance

Materials Required:

  • Ultrasound machine with high-frequency linear transducer
  • Chlorhexidine
  • 4.8cm, 18-gauge single-lumen catheter
  • 2 bio-occlusive adherent dressings
  • Sterile ultrasound gel
  • Loop catheter extension
  • Saline flush

Outcomes:

  • Initial success rate
  • Mean procedure time
  • Average pain score
  • Number of Skin punctures
  • Complications

Inclusion:

  • Patients requiring IV access
  • Failed attempts at establishing peripheral or external jugular vein access (Including attempts using ultrasound)
  • Ability to dilate IJ with Valsalva maneuver
  • Ability to sign written consent

Exclusion:

  • Hemodynamic instability (HR >150BPM, or MAP <60mmHg)
  • Untreated pneumothorax
  • Clinical need for triple-lumen venous catheter

Results:

  • 83 attempts in 74 patients
  • Median body mass index (BMI): 27kg/m2
  • Initial success rate: 88% (95% CI 79 – 94)
  • Mean procedure time: 4.4 min (95% CI 3.8 – 4.9)
  • Average pain score 3.9 out of 10 (95% CI 3.4 – 4.5)
  • Number of Skin Punctures:
    • One: 75%
    • Two: 19%
    • Three – Five: 6%
  • Complications:
    • Pneumothorax: 0/83 (0%)
    • Line Infection: 0/83 (0%)
    • Arterial Puncture: 0/83 (0%)
    • Loss of Patency: 10/73 (14%) successful lines

Strengths:

  • Only multicenter study to date to evaluate the Easy IJ
  • Absence of pneumothorax was confirmed by either CXR (82/83) or CT scan (1/83)
  • This is an increasing dilemma in the care of EM patients, and gives a nice simple solution, that does not take as long as Central venous access or the discomfort associated with IO in stable awake patients
  • No major patient-centered adverse events
  • Time of procedure recorded as time from skin prep to confirmation of IV. Many studies start time from when the needle hits the skin.

Limitations:

  • Absence of line infection determined by chart review in 55 out of 83 patients. If patients sought care at other facilities this would underestimate the incidence of line infection
  • All attempts at access were performed by physicians with >20 previous ultrasound guided line placements, may reduce generalizability if provider is not well versed with ultrasound
  • Primary outcome not clearly stated
  • Confidence intervals are wide relative to complication rates for the Easy IJ
  • Easy IJ catheters were left in for ≤24hrs in this study, therefore infection risk beyond 24 hours cannot be ascertained from this study
  • Unstable patients were excluded in this study, therefore cannot draw conclusions of the Easy IJ in unstable patients

Discussion:

  • The authors of the paper state that in the limited literature available on this procedure there are no documented cases of pneumothorax, neck hematoma, inadvertent arterial placement, line infection, or site infection
  • The procedure itself takes about 5 minutes which is a significantly shorter time than central line placement

Author Conclusion: “The Easy IJ was inserted successfully in 88% of cases, with a mean time of 4.4 min. Loss of patency, the only complication, occurred in 14% of cases.”

Clinical Take Home Point: In stable patients, who have had failed attempts at establishing peripheral or external jugular vein access, the Easy IJ is a rapid method of achieving short-term IV access with no major adverse patient oriented outcomes.

References:

  1. Moayedi S et al. Safety and Efficacy of the “Easy Internal Jugular (IJ)”: An Approach to Difficult Intravenous Access. JEM 2016. 51(6): 636 – 42. PMID: 27658558

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

The post The Easy IJ: Another Option for Difficult IV Access in Stable Patients? appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Post Intubation Hypotension: The AH SHITE mnemonic

You have just secured the endotracheal tube following an uneventful intubation of a moderately ill  patient in your emergency department. They had a normal pre-intubation blood pressure.  As you are calling the admit in to the ICU the patient’s nurse tells you that the BP is now in the 70’s.

NOW WHAT?

  1. Blindly give a half gallon of saline and stay in your seat.
  2. Get up, walk to the patient’s room, and consider the possible causes of post intubation hypotension.

There is a laundry list of potential pathologies in play, some of which require time critical interventions. Option 2 is the only acceptable option for evaluating a patient with post intubation hypotension.

Here is a  crowd sourced approach that will allow most etiologies of post intubation hypotension to be identified: The AH SHITE mnemonic is something that you can quickly run through en route to the patient’s room, or at the bedside. This is intended as a starting point to the evaluation of the patient with post intubation hypotension.

Treatment of these issues will not be discussed in detail. Thanks to @precordialthump and @pbsherren for helping me  fine tune the list and force the mnemonic.

A Acidosis

Patients with profound metabolic acidosis typically have a high minute ventilation, until they become fatigued and then their pH can drop. Post intubation ventilator settings need to provide minute ventilation that approximates pre-intubation levels. One way of ensuring this is to check a pre-intubation ETCO2 and to then aim for this number with a well planned post intubation ventilation strategy. 8cc/kg tidal volume (upper range of ARDSNET vent strategy) and a high RR (30’s) with close attention to post intubation gases is a good start.

Does giving bicarb to profoundly acidotic patients on the vent help?

 Henderson Hasselbalch equation:

H+ + HCO3- <—> H2O + CO2

This equation is an equilibrium, any increase in H+ concentration will tip the equation to the right, and generate more CO2. This will typically cause tachypnea, unless the patient is profoundly fatigued. Adding bicarb will produce more CO2, if the patient is already being ventilated at a maximum minute ventilation this will not be able to be increased, and without removing the CO2 from the system, the pH will not change.

Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations.

  • Anesthesiology. 1990 Jun;72(6):1064-76. PMID: 2161621
  • When isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCO2 increased and pH was unchanged. pH only rises when CO2 is eliminated.
  • If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.

Sodium Bicarbonate for the treatment of Lactic Acidosis.

  • Chest 2000; 117(1): 260 – 7. PMID: 10631227
  • 18 animal studies: no improvement with bicarb
  • 2 human studies, average lactates 7-8mmol/l
  • pH improved by 0.14, and 0.05
  • No improvement in hemodynamic parameters / response to pressors.

Giving bicarb does pose a risk of impaired oxygen delivery via an increased hemoglobin affinity for oxygen. This is seen in studies on healthy volunteers. A downstream effect from this is that lactate concentrations can increase. This has been seen in studies on animals with hypoxic lactic acidosis.

A Anaphylaxis

Ketamine and Etomidate do not typically cause allergic reactions. There are no case reports of anaphylaxis to Etomidate. Neuromuscular blocking agents are divalent molecules that make it easier for anaphylaxis to occur, even in the setting of no previous exposure. (See REBEL EM post in Anaphylaxis to NMB agents)

Anaphylaxis is more common with rocuronium and succinylcholine than with atracurium.

  • Anesthesiology. 2015 Jan;122(1):39-45. PMID:25405395
  • This was a retrospective, observational cohort study of intraoperative anaphylaxis to NMBDs at two Auckland, NZ hospitals between 2006 and 2012.
  • All cases of suspected perioperative anaphylaxis were referred to the same allergy clinic. These were high grade anaphylaxis events, including profound hypotension, and intraoperative cardiac arrest.
  • 92,858 anesthetic cases involving new exposures to NMB’s. 21 patients with anaphylaxis were confirmed out of 89 patients referred to the allergy clinic.
  • Rates:
    • Sux: 1:2080
    • Roc: 1:2499
    • Atracurium: 1:22451

H Heart:Tamponade

Consider cardiac tamponade in both traumatic and medical presentations. Penetrating chest trauma should be an obvious trigger to perform bedside cardiac ultrasound. Elderly patients on anticoagulants with minor falls, and end stage renal disease patients may have occult / borderline tamponade that only declares itself after a change to positive pressure ventilation.

Timing of tracheal intubation in traumatic cardiac tamponade: a word of caution.

  • Resuscitation 2009 Feb;80(2):272-4 PMID: 19059695
  • Authors suggest raising the threshold for intubation, and preparing for immediate relief of tamponade after intubation. Consider awake intubation strategy without interrupting spontaneous ventilation. 

H Heart: Pulmonary Hypertension

Patients with known severe pulmonary hypertension are a nightmare to intubate. Hypervolemia, hypoxia, and hypercarbia are known to worsen their right heart function. Fluid boluses are unlikely to help an overloaded, distended right ventricle, and may worsen LV impingement.

Pulmonary Hypertension and right ventricular failure in emergency medicine.

  • Annals of Emergency Medicine Dec 2015; 66(6):619-28 PMID:26342901
  • Give norepinephrine, and treating whatever worsened the Pulmonary Hypertension may help.

S Stacked breaths / Autopeep

Patients with obstructive lung pathology who are not completely exhaling prior to the next breath being initiated can progressively develop air trapping, this can lead to increased intrathoracic pressure that can decrease venous return overtime, and cause hypotension, and eventual arrest.

Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect.

  • Am Rev Respir Dis. 1982 Jul;126(1):166-70. PMID: 7046541
  • Alveolar pressure can remain positive throughout the ventilatory cycle of intubated patients with airflow obstruction. Abnormally compliant lungs transmit a high fraction of alveolar pressure to intrathoracic vessels so these effects may be exaggerated in patients with chronic obstructive pulmonary disease.
  • Failure to recognize the hemodynamic consequences of auto-PEEP may lead to inappropriate fluid restriction or unnecessary vasopressor therapy.

H Hypovolemia

Hypovolemia from profound shock states such as hemorrhage, sepsis, and anaphylaxis should be reasonably easy to identify. Occult hypovolemia can be unmasked by the physiologic insult that occurs when patients are switched from spontaneous ventilation to positive pressure ventilation. With the increase in intrathoracic pressure that accompanies positive pressure ventilation any patient with low venous pressures / low pre-load may develop hypotension. Adjusting PEEP settings, and giving a bolus of an appropriate resuscitative fluid will help.

I Induction Agent

Propofol gets a bad rap for being blamed as the only agent capable of causing post intubation collapse. Any sedative agent that takes away an individual’s conscious drive to survive could potentially result in post intubation collapse; Weingart has described this as the ‘nine inch nails to Bob Marley transformation’. (See intubating the patient in shock from SMACC 2013). Decreasing the dose of sedative, and having pressors / push dose pressors ready could help to mitigate this.

T Tension Pneumothorax

Consider tension pneumo in any patient with obstructive lung disease that has increased airway pressures. Rather that blindly needling the chest of these patients, use ultrasound to confirm whether a pneumothorax is present. This will avoid inadvertently causing a pneumothorax in a patient with normal lungs that may have an alternative explanation for their hypotension.

E Electrolytes

Succinylcholine has a well known set of contraindications due to the risk of succinylcholine associated hyperkalemia. Major burns, crush injuries, and end stage renal disease patients are typically rather obvious. Occult contraindications include those patients with histories of malignant hyperthermia, previous stroke / spinal cord injuries, or those with prolonged ICU stays. Several case reports exist of patients who have had profound hyperkalemia without obvious risk factors. In the absence of an alternative explanation for hypotension, and especially in the setting of any rhythm change consider checking a potassium level, or empirically treating with Calcium.

Cardiac Arrest From Succinylcholine-Induced Hyperkalemia

Summary:

Anticipate that intubation can worsen underlying physiologic parameters, and can cause some intubation specific causes of hypotension. Anticipating post intubation hypotension and being ready to correct specific causes is an essential part of any intubation.

Transform your mantra for post intubation hypotension evaluation from Resuscitate, Intubate, Panic like #$@#, to Resuscitate, Intubate, Anticipate.

Remember this sage advice from Louis Pasteur: ‘Fortune favors the prepared mind’.  The better you plan your intubation (see Salim’s HOP killer series) the less likely you will be dealing with post intubation hypotension.

Post Peer Reviewed By: Salim Rezaie (Twitter: @srrezaie)

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Episode 36 – Resuscitate Before You Endoscopate?

Background: Upper gastrointestinal hemorrhage (UGIH) is a commonly seen complaint in the ED.  Currently, endoscopy is the standard therapy shown to not only help with diagnosis, but also risk stratify patients and potentially offer effective hemostatic treatment of acute nonvariceal UGIH.  What is frequently an area of debate, is the optimal timing of endoscopy. Even more frustrating is the different definitions of early endoscopy ranging anywhere from 1hr up to 24hrs after initial presentation.

Now on one hand, earlier timing of endoscopy could be associated with suboptimal resuscitation and potential hemodynamic instability.  On the other hand, delayed endoscopy delays hemostasis from endoscopic therapy and increases the risk of rebleeding and need for surgery.  I think we all agree that we should resuscitate our patients before endoscopy (or as I like to say resuscitate before you endoscopate), but is there a population of patients with UGIH that require sooner than later endoscopy? To talk about this topic we have a special guest Rory Spiegel.  You can find Rory on twitter as @EMNerd_ or on the EMCrit blog where he discusses methodological issues with studies

Episode 36: Resuscitate Before You Endoscopate?

Click here for Direct Download of Podcast

Special Guest: Rory Spiegel
Twitter: @EMNerd_

Clinical Question:  Is there a population of patients with Nonvariceal UGIH that require sooner (<6hrs) than later (>6hrs) endoscopy?

Time to Endoscopy Paper #1 [1]

What They Did:

  • A systematic review of English language citations from 1980 – 2000

Outcomes:

  • Tried to Answer 3 Questions:
    • Does early endoscopy allow for safe and prompt discharge of low-risk patients with acute nonvariceal UGIH?
    • Does early endoscopy improve patient outcomes vs delayed endoscopy in high risk patients with acute nonvariceal UGIH?
    • Does early endoscopy reduce resource utilization vs delayed endoscopy for all comers with acute nonvariceal UGIH? 

Inclusion:

  • Studies including information regarding the effectiveness of early endoscopy determined by patient outcomes (mortality, rebleeding, transfusion requirements, need for emergency surgery, endoscopic complications, and readmission)
  • Studies including economic outcomes (length of stay and direct costs)

Exclusion:

  • Not written in English
  • Non-human studies
  • Not related to UGIH or lesions that can cause UGIH
  • Solely related to variceal bleeding or other complications of portal hypertension
  • Solely related to non-endoscopic interventions or complications

Results:

  • 23 studies met inclusion criteria
  • Does Early Endoscopy Allow for Safe and Prompt Discharge of Low-Risk Patients with Acute Nonvariceal UGIH?
    • Only 3 Controlled Trials [2 – 4] evaluated early endoscopy vs “usual care”: All Trials with ≤110patients (Total Number of Patients = 213)
    • Largest Trial (110 patients) [2] Compared Endoscopy <2hours vs “usual care” (24 – 48hours): 46% of patients with <2hour endoscopy avoided hospitalization and no complications or readmissions at 30days
  • Does Early Endoscopy Improve Patient Outcomes vs Delayed Endoscopy for High-Risk Patients with Acute Nonvariceal UGIH?
    • Only 1 RCT [5] with 124 patients compared Early Endoscopy (<12hrs) vs Delayed Endoscopy (12 – 24hrs): Early endoscopy resulted in decreased transfusion requirement only for patients with bloody NGL aspirate but had no effect on mortality or need for surgery
  • Does Early Endoscopy Improve Utilization Outcomes vs Delayed Endoscopy (1 – 2days) for All Comers with Acute Nonvariceal UGIH?
    • Only 2 RCTs: One with low risk patients and the other with high risk patients
      • Low Risk Patients [2]: 110 patients; Mean hospital stay decreased by 1 day and cost savings of $1594 per patient in the early endoscopy group compared to the delayed endoscopy group (1d vs 2d and $2068 vs $3662 respectively)
      • High Risk Patients [5]: Early endoscopy saved 10.t days per patient compared with delayed endoscopy (4.0 +/- 3.5d vs 14.5d +/- 10.8d respectively) in patients with bloody aspirates but no effect on LOS in patients with coffee ground aspirates

Author Conclusion: “The overwhelming majority of existing data suggest that early endoscopy is safe and effective for all risk groups.  The clinical and economic outcomes of early endoscopy should be confirmed in additional well-designed randomized controlled trials.  Given the strength of evidence, efforts to develop a more standardized and time-sensitive approach to acute nonvariceal upper gastrointestinal tract hemorrhage should be undertaken.”

Time to Endoscopy Paper #2 [6]

What They Did:

  • Nationwide cohort study based on a database of consecutive patients admitted to the hospital with PUB in Denmark
  • Patients were stratified according to the presence of hemodynamic instability at presentation and American Society of Anesthesiologists (ASA) score
  • Used descriptive statistics and logistic regression analyses to identify optimal time frames for endoscopy 

Outcomes:

  • Primary Outcome: In-hospital mortality
  • Secondary Outcome: 30d mortality

Results:

  • >12,000 patients analyzed
  • Stable Patients with ASA score of 1 – 2: No association between increased mortality and timing of endoscopy
  • Stable Patients with ASA score 3 – 5: Endoscopy 12 – 36 hours after admission to the hospital was associated with lower in-hospital mortality (OR 0.48) compared to endoscopy outside this time frame
  • Hemodynamic instability and ASA score of 1 – 5: Endoscopy at 6 – 24 hours after admission to hospital was associated with lower in-hospital mortality (OR 0.73) compared with endoscopy outside this time frame

Author Conclusion: “Timing of endoscopy is associated with mortality in patients with PUB and an ASA score of 3 – 5 or hemodynamic instability. Our findings suggest that in these patients, a period of time to optimize resuscitation and manage comorbidities before endoscopy may improve outcome.”

Issues Discussed with Rory:

  • Patients Enrolled in Studies are Often Not Unstable: There is often a discrepancy between the patients we are thinking of when debating the timing of endoscopy and the patients these trials examine. In the first paper the patients deemed “high risk” were semi-stable patients. As a matter of fact, patients experiencing massive bleeds, variceal bleeds, or “could not participate in endoscopy” were excluded. It is difficult to consent unstable patients and therefore they are often not well represented or accounted for at all in research studies. The majority of patients evaluated in the first study are “low risk” patients (i.e. some sequelae of UGIH, not actively bleeding or hemodynamically stable). Only one RCT evaluated “high risk” patients defined as having a bloody aspirate on NG lavage.
  • What is Meant by “Early” Endoscopy: There is a big discrepancy about what we mean by early endoscopy and what the literature defines as early endoscopy. In the first trial, early endoscopy is defined as within the first 24hours.  What we often mean by early endoscopy is “get here as fast as you can.” It’s not surprising that these studies find very little difference between groups (i.e. <12hrs vs 12 – 24hrs).
  • Sicker Patients Typically Get Earlier Endoscopy, But do Worse (i.e increased mortality) Because They are Just Sicker
  • Nonvariceal UGIH Can Be Divided into Sick and Not Sick: Another way to say this is hemodynamically stable and hemodynamically unstable. The sick patients should really be subdivided further sick and really sick. Those patients who respond to resuscitation and those who either transiently respond or don’t respond at all.
    • Hemodynamically Stable: In patients without significant comorbid conditions and not actively bleeding one could argue scoping early (<6hrs) could afford early discharge and reduce costs but with no improvements in mortality. In patients with comorbid conditions or actively bleeding (i.e. melena, hematochezia) optimizing chronic and acute medical conditions is probably warranted with a delayed endoscopy (12 – 24hrs). The bottom line here is the timing of endoscopy for these patients is probably dependent on the time they arrive to the emergency department.
    • Hemodynamically Unstable: First and foremost, these patients should get adequate resuscitation. Some patients will be responders and some patients will be transient responders or won’t stabilize at all.  The patients that stabilize will most likely be admitted to the ICU and should probably get an endoscopy sooner than later, but one could argue 12 – 24 hours would be acceptable.  There is a lot of grey area here where some patients who do stabilize for whatever reason may need endoscopy sooner than the next day.  For the patients that transiently stabilize or don’t stabilize at all despite maximal medical therapy, what is the optimal time for endoscopy: <6hrs, <3hrs, or maybe <2hrs?  There is very scant evidence evaluating this population.  Our GI colleagues will say there is a high mortality associated with doing endoscopy in these patients early, but then again, these patients probably have a higher mortality despite the endoscopy itself. There is no real clinical evidence or physiological reason why sick patients will become more unstable during endoscopy.  If they already survived the hemodynamic turmoil of intubation then endoscopy shouldn’t add any further serious stress to their compromised system.  In the sickest of the sick, there really should be no time period of optimal endoscopy other than “as soon as GI can get there.”

Clinical Take Home Point:

In HD unstable patients the triage point to deciding on how early to perform endoscopy is response to resuscitation. If they stabilize, they can go to the ICU with frequent assessments with a courtesy call to our GI colleagues.  The patients who transiently stabilize or don’t stabilize at all despite resuscitation (i.e. Already doing everything that we can from a medical standpoint: blood products, pressors, intubation, PPI, Octreotide, etc.) need hemostasis and the only way this is going to happen is with endoscopy.  For these patients, we need to get GI in at whatever time of the day it is.  So you still resuscitate before endoscopy (or as I like to say resuscitate before you endoscopate), but the response to that resuscitation is what determines who should get scoped sooner (i.e <2hrs, <3hrs, <6hr etc…)

References:

  1. Spiegel BMR et al. Endoscopy for Acute Nonvariceal Upper Gastrointestinal Tract Hemorrhage: Is Sooner Better? Arch Intern Med 2001. 161 (11): 1393 – 404. PMID: 11386888
  2. Lee JG et al. Endoscopy-Based Triage Significantly Reduces Hospitalization Rates and Costs of Treating Upper GI Bleeding: A Randomized Controlled Trial. Gastrointest Endosc 1999. 50(6): 755 – 61. PMID: 10570332
  3. Campo et al. Safety of Out-Patient Management of Nonvariceal Upper Gastrointestinal Bleeding: Preliminary Results of a Randomized Study [Abstract] Gastrointest Endosc 1998; 47: AB81. Abstract 228
  4. Brullet et al. Outpatient vs. Hospital Care After Endoscopic Injection in Selected patients leeding From Peptic Ulcers: Preliminary Results of a Randomized study [Abstract] Gastrointest Endosc 1998; 47: AB81. Abstract 227
  5. Lin HJ et al. Early or Delayed Endoscopy for Patients with Peptic Ulcer Bleeding. A Prospective Randomized Study. J Clin Gastroenterol 1996. 22(4): 267 – 71. PMID: 8771420
  6. Laursen SB et al. Relationship Between Timing of Endoscopy and Mortality in Patients with Peptic Ulcer Bleeding: A nationwide Cohort Study. Gastrointest Endosc 2016. S0016-5107(16):30555-7. PMID: 27623102

The post Episode 36 – Resuscitate Before You Endoscopate? appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Are we Missing Acute MIs with Clinical Risk Scores?

Background: In 2011, we saw 7 million patients in the emergency department (ED) complaining of chest pain. Most of these patients did NOT have an acute coronary syndrome (ACS) or an acute myocardial infarction (AMI). Missing an AMI is one of the biggest fears we have in the ED. By using validated risk scores, we can help decrease the risk of missing AMI and the resultant adverse events. There are multiple scores available for our use. Thrombolysis in Myocardial Infarction (TIMI) predicts risk of adverse outcomes in the next 14 days. Global Registry of Acute Coronary Events (GRACE) predicts outcomes at 6 months. ED specific scores include HEART and Emergency Department Assessment of Chest Pain (EDACS). But, how well do these scores actually perform? Are we missing AMIs by using these clinical risk scores?

What They Did:

  • This study was part of a larger, multicenter, prospective observational study. The original study was looking to validate a novel cardiac troponin for ED use in patients suggestive of ACS.
    • 7 geographically different academic US EDs
    • Inclusion: patients age 21 or older with symptoms suggestive of ACS
    • Exclusion: implanted defibrillator discharge < 24 hours, cardiac procedure or bypass < 30 days, recent chest trauma
    • Recorded: clinical gestalt, TIMI, GRACE, HEART-1, HEART-2, and EDACS to separate into low, intermediate, and high risk. EDACS only uses low and not low risk classifications. (Difference between HEART-1 and HEART-2 was using one or two troponins.)
  • Cutoffs used: HEART 0-3, TIMI = 0, GRACE < 50, EDACS < 16

Outcomes:

  • Primary—presence or absence of AMI. Final diagnosis was determined by a committee of 3 (2 cardiologists, 1 ED), blinded to each other’s determination. The ESC/ACCF/AHA/WHR 3rd Universal definition of MI was used.

Results:

  • 434 patients included in the final analysis
    • Median Age: 57 years (Range: 49 – 64)
    • Diagnosis of AMI: 18.4%
    • Median Time Between Serial cTn: 4.1 hr (Range 2.7 – 7.8hr)

Strengths:

  • Adequate enrollment: Study needed at least 45 patients with AMI and assumed a 10% prevalence for AMI. They would need 450 patients enrolled in the study (They enrolled 459 of which 434 were included in the final analysis).
  • Use of all major risk assessment scores at recommended cutoffs

Limitations:

  • Only 82 patients had confirmed AMI: This is a small sample size
  • Possible selection bias, excluded many patients due to incomplete data: This could lead to under- or over-estimation of clinical risk scores
  • Only used AMI, likely missed other ACS and longer-term major adverse cardiac events (MACE)
  • Each hospital troponin was different, with variable cutoffs. This may have caused variability in the results of the prediction scores this study
  • Half of the false negative cases involved point of care assays. The high rate of missed AMI in patients classified as low risk may be due to using older, less sensitive cTn assays, which have high coefficients of variation
  • Some facilities used POC cTnI as their initial test and laboratory cTnI as their follow up test, which makes it difficult to evaluate rise and fall as two different assays were used

Discussion:

  • Of all the symptoms described diaphoresis was much more common in patients diagnosed with an AMI vs patients without AMI (43.8% vs 5.4%). Take diaphoresis seriously.
  • All assessments were within statistical variability, but high miss rates were noted in all except TIMI, and gestalt + troponin.
  • Reducing score cutoffs would result in zero misses, but much fewer patients would be classified as low risk. The lower cut-offs were defined as:
    • HEART-1 = 1
    • GRACE </= 48
    • TIMI= 0
    • HEART-2 </= 2
    • EDACS </= 11
  • The percentage of patients that would be considered low risk with these lower cut offs come at the price of less patients identified as low risk:
    • HEART-1: 1%
    • GRACE: 3.3%
    • TIMI: 7%
    • HEART-2: 19.5%
    • EDACS: 33.6%
  • It is important to note that the original HEART score and EDACS score have had prospective evaluation. Most of the HEART score studies are performed in European populations and the EDACS score was derived and validated in New Zealand but used hs cTnI. The findings of this study may simply be due to different populations (European vs US) or the use of hs cTnI (which until recently was not available in the US). Even so, due to the smaller population of this study, 95% CIs were very wide.
  • Just a little discussion point about risk scores. Risk scores are tools to help clinicians have a standardized approach to patient complaints. There will always be exceptions to the tools. Not to pick on anyone one score, but lets talk about the HEART-2 score as an example. It is possible that someone could have a low risk score (0 – 3) and not truly be low risk.
    • Lets start with risk factors. If a patient doesn’t go to see a doctor, then they won’t have any past medical history, when in fact they may. This will grossly underestimate their risk.
    • Although only one ECG is required for the HEART-2 score, there is something to be said for multiple ECGs. Be sure to look at pre-hospital ECGs, old ECGs in your EMR, and for god’s sake, get serial ECGs in patients you are concerned about. Remember, a single ECG is one point in time. We don’t want to miss dynamic changes and the best way to find these subtle changes may be looking at pre-hospital ECGs, old ECGs, and serial ECGs.
    • What about troponins? It is very possible that you could have a patient that doesn’t go to doctors, and therefore has no risk factors, a normal ECG and have a positive troponin. By definition, this would still be low risk if you use the HEART-2 score at face value. I think most of us would agree that positive troponins are not low risk. Even if it is not ACS that is causing the elevation, there maybe another pathology at play. This is not a low risk patient, and should not be sent home without further risk stratification or workup.

Author Conclusion: “Using their recommended cutpoints and non-high sensitivity cTn, TIMI and unstructured clinical impression were the only scores with no missed cases of AMI. Using lower cutpoints (GRACE ≤48, TIMI = 0, EDACS ≤11, HEART ≤2) missed no case of AMI, but classified less patients as low-risk.”

Clinical Take Home Point: Clinical gestalt remains the most useful tool for assessment of risk of ACS/AMI. The use of risk assessment tools should be regarded as just that, tools. Keep in mind the limitations of each as you are taking care of patients.

References:

  1. Singer AJ et al. Missed Myocardial Infarctions in ED Patients Prospectively Categorized as Low Risk by Established Risk Scores. Am J Emerg Med 2017. [Epub Ahead of Print] PMID: 28108220

Post Peer Reviewed By: Salim Rezaie (Twitter: @srrezaie)

The post Are we Missing Acute MIs with Clinical Risk Scores? appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.

Low-Dose Ketamine for Acute Pain in the ED: IV Push vs Short Infusion?

Background: Ketamine’s role in the ED has expanded in recent years.  The clinical reasons for this make it easy to understand why, and include analgesia, amnesia, and anesthesia. Amazingly, ketamine does not only reduce acute pain, but it also decreases persistent chronic and neuropathic pain as well. More importantly, use of low-dose ketamine (0.1 – 0.3 mg/kg IV) has been demonstrated to be opioid sparing.  Some of the major issues with IV push low-dose ketamine include its adverse effects, such as feelings of unreality, nausea/vomiting, and dizziness. Many emergency medical providers have anecdotally noticed a decrease in adverse effects when ketamine is given slowly. In the paper we are reviewing today, the authors tried to see if increasing the duration of the ketamine from IV push (3 – 5 min) to a slow infusion (10 – 15 min) could mitigate some of these effects, while maintaining analgesic efficacy.

What They Did:

  • Randomized patients presenting to the ED with acute abdominal, flank, or musculoskeletal pain with an initial pain score of ≥5 to: Ketamine 0.3mg/kg by either IV Push (over 5min) or Short Infusion (0.3mg/kg mixed in 100mL normal saline solution over 15min) with Placebo Double-Dummy (both groups got an iv push, and an infusion).

Outcomes:

  • Primary Outcome: Safety Efficacy at 5, 15, 30, 60, 90, and 120 min post administration
    • Side Effects Rating Scale of Dissociative Anesthetics (SERSDA): Measures the severity of nine adverse effects with a score of 0 – 4 for each adverse effect. 0 = side effects absent and 4 = adverse effect is bothersome
    • Richmond Agitation-Sedation Scale (RASS): A score of -4.0 – 4.0 with -4 = deeply sedated, 0 = alert and calm, and 4 = combative
  • Secondary Outcomes:
    • Analgesic Efficacy via Numerical Pain Rating Scale (NRS): A score of 0 – 10
    • Changes in Vital Signs
    • Need for Rescue Analgesia

Inclusion:

  • Adults 18 – 65 years of age presenting to the ED
  • Primary complaint for management of acute abdominal, flank, back, traumatic chest or musculoskeletal pain
  • Intensity of pain ≥5 on the Numeric Pain Rating Scale
  • Able to Consent

Exclusion:

  • Pregnancy
  • Breast Feeding
  • Altered Mental Status
  • Allergy to Ketamine
  • Weight <46kg or >115kg
  • Unstable vital signs (SBP <90 or >180mmHg, Pulse rate <50 or >150bpm, and RR <10 or >30 BPM)
  • Medical history of acute head or eye injury
  • Seizure
  • Intracranial hypertension
  • Renal or hepatic insufficiency
  • Alcohol or drug abuse
  • Psychiatric Illness
  • Recent (4h before) analgesic use

Results:

  • 48 patients enrolled in the study

  • Median Severity of Feeling of Unreality on SERDSA at 5 min
    • IVP: 3.0
    • SI: 0.0
    • P=0.001
  • Median RASS Scale at 5 min
    • IVP -2.0
    • SI: 0.0
    • P = 0.01
  • Decrease in Mean Pain Scores from Baseline to 15 min
    • IVP: 5.2 +/- 3.53
    • SI: 5.75 +/- 3.48
  • No Statistical Differences with Respect to Changes in Vital Signs and Need for Rescue Medication
  • There was no statistical difference on the SERSDA scale for 8 of the variables measured: headache, fatigue, dizziness, hearing, vision, mood change, discomfort, hallucination.

Strengths:

  • Double dummy design: All participants received a corresponding placebo in order to keep patients and providers blinded
  • Dummy IV push or Slow infusion given simultaneously to maintain blinding
  • Treating providers, patients and the data collecting research team blinded to medication route received
  • No difference in baseline pain

Limitations:

  • Convenience Sample: Patients not enrolled consecutively (Only Monday – Friday 8a – 8p)
  • Single center study
  • Small sample size did not allow for assessment of variance in safety profiles of the two routes of administration (i.e. statistical significance) or for possible differences in the other SERSDA assessed adverse effects.

Discussion:

  • If patients required additional pain medication 30 min after study drug administration, 0.1mg/kg IV morphine was offered as a rescue analgesic.
  • Several studies have shown a correlation to side effects of low-dose ketamine with rapid rates of infusion. The pharmacologic reason for this is ketamine’s lipophilicity allows for rapid penetration of the blood-brain barrier and rapid saturation of the NMDA/glutamate receptors.
  • Excluded head / eye injured patients despite ample evidence that ketamine is safe in these populations.
  • The authors note that in their institution a 15 min infusion is billed the same as an IV push.
  • One issue with slow infusion would be the availability of an infusion pump, however the authors discuss hanging the infusion, and running over approximately 15 min, without using an infusion pump. This saves time setting up the pump, and saves the issue of running out of pumps. We emailed the lead author Sergey Motov about this and his response was as follows:

“In my ED, we do not routinely use an IV infusion pump for a short infusion of SDK. After 6 years of doing so we have had no major adverse effects. Our nurses and ED pharmacists are very comfortable with a no pump approach by adjusting the flow rate to a 15 min time frame. Furthermore, we cap the max dose at 30 mg even if patient’s weight exceeds 100 kg which adds additional safety/comfort to our staff. This only applies to short infusion. For continuous drips we use IV infusion pumps. ”

Author Conclusion: “Low-dose ketamine given as a short infusion is associated with significantly lower rates of feeling of unreality and sedation with no difference in analgesic efficacy in comparison to intravenous push.”

Clinical Take Home Point: Low dose ketamine of 0.3mg/kg, mixed into 100mL of Normal Saline given over slow infusion (15 minutes) has a decreased side effect (i.e hallucinations or dizziness) and equal analgesic profile when compared to IV push (5 minutes) low dose ketamine.

References:

  1. Motov S et al. A Prospective Randomized, Double-Dummy Trial Comparing Intravenous Push Dose of Low Dose Ketamine to Short Infusion of Low Dose Ketamine for Treatment of Moderate to Severe Pain in the Emergency Department. AJEM 2017; S0735 – 6757(17): 30171 – 7.  PMID: 28283340

For More Thoughts on This Topic Checkout:

Post Peer Reviewed By: Rob Bryant (Twitter: RobJBryant13)

The post Low-Dose Ketamine for Acute Pain in the ED: IV Push vs Short Infusion? appeared first on R.E.B.E.L. EM - Emergency Medicine Blog.