Category Archives: CLIC-EM

10.07.11
by

Resuscitation by Sublingual Injection

There are multiple routes of medication delivery for the critically ill patient. Commonly, these include the intravenous (IV) and intraosseous (IO) routes as well as the endotracheal tube, intramuscular, or clysis.  
But what can you do when the these routes are not feasible or desirable in a crashing patient?
Sublingual (SL) injection may provide an important route for drug administration.

This may be especially helpful for infants in cardiopulmonary arrest.  There is a high preshospital failure rate for IV access and ETT placement in this group, and the SL route originates from EMS providers.   
Rothrock et al. describe a case where paramedics were called to the scene of a witnessed cardiac arrest of a 7-month old child whose parents had started immediate CPR.  After multiple failed attempts at endotracheal intubation and IV access, the paramedics injected 1.5 mg epinephrine (0.2 mg/kg) followed by 0.15 mg atropine (0.02 mg/kg) sublingually.  Within 30 to 60 seconds, the child achieved return of spontaneous circulation (ROSC) with a palpable pulse and a heart rate of 180.
There is no standard technique for SL injection, however, the rich vascular plexus in the sublingual region allows for rapid uptake of injected medications.  Classically, SL injection is performed 1-2 cm from the midline of the frenulum into the sublingual vascular plexus.
Animal and human studies have shown that higher doses of medications must be administered SL in order to reach identical serum concentrations of peripherally administered medications.  More research is needed on dosing regimens via the SL route.
Regardless, EMS providers often utilize SL injections of 0.3-0.5mL of 1:1000 epinephrine for anaphylaxis patients where IV/IO access is unavailable.  Naloxone, flumazenil and ketamine have also been administered effectively via the SL route.
Next time you have a patient in extremis without vascular access, remember sublingual injection as a route for administration of initial resuscitative medications.
-- Megan Stultz, MD & Eric Beck, DO EMT-P
References:
Losek JD, Hennes H, Glaser P, et al: Prehospital care of the pulseless, nonbreathing pediatric patient.  Am J Emerg Med 1987; 5:370-374.
McIntyre KM (ed): Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). JAMA 1980; 244:453-509.
Ordog GJ, Wasserberger J, Jones J, et al: Efficacy of absorption of sublingual and intravenous Cardio-Green. Ann Emerg Med 1984; 13:426-428.
Rothrock SG, Green SM, Schafermeyer RW, Colucciello SA.  "Successful resuscitation from cardiac arrest using sublingual injection for medication delivery."  Ann Emerg Med 1993; 22:751-753.
10.07.11
by

Resuscitation by Sublingual Injection

There are multiple routes of medication delivery for the critically ill patient. Commonly, these include the intravenous (IV) and intraosseous (IO) routes as well as the endotracheal tube, intramuscular, or clysis.  
But what can you do when the these routes are not feasible or desirable in a crashing patient?
Sublingual (SL) injection may provide an important route for drug administration.

This may be especially helpful for infants in cardiopulmonary arrest.  There is a high preshospital failure rate for IV access and ETT placement in this group, and the SL route originates from EMS providers.   
Rothrock et al. describe a case where paramedics were called to the scene of a witnessed cardiac arrest of a 7-month old child whose parents had started immediate CPR.  After multiple failed attempts at endotracheal intubation and IV access, the paramedics injected 1.5 mg epinephrine (0.2 mg/kg) followed by 0.15 mg atropine (0.02 mg/kg) sublingually.  Within 30 to 60 seconds, the child achieved return of spontaneous circulation (ROSC) with a palpable pulse and a heart rate of 180.
There is no standard technique for SL injection, however, the rich vascular plexus in the sublingual region allows for rapid uptake of injected medications.  Classically, SL injection is performed 1-2 cm from the midline of the frenulum into the sublingual vascular plexus.
Animal and human studies have shown that higher doses of medications must be administered SL in order to reach identical serum concentrations of peripherally administered medications.  More research is needed on dosing regimens via the SL route.
Regardless, EMS providers often utilize SL injections of 0.3-0.5mL of 1:1000 epinephrine for anaphylaxis patients where IV/IO access is unavailable.  Naloxone, flumazenil and ketamine have also been administered effectively via the SL route.
Next time you have a patient in extremis without vascular access, remember sublingual injection as a route for administration of initial resuscitative medications.
-- Megan Stultz, MD & Eric Beck, DO EMT-P
References:
Losek JD, Hennes H, Glaser P, et al: Prehospital care of the pulseless, nonbreathing pediatric patient.  Am J Emerg Med 1987; 5:370-374.
McIntyre KM (ed): Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). JAMA 1980; 244:453-509.
Ordog GJ, Wasserberger J, Jones J, et al: Efficacy of absorption of sublingual and intravenous Cardio-Green. Ann Emerg Med 1984; 13:426-428.
Rothrock SG, Green SM, Schafermeyer RW, Colucciello SA.  "Successful resuscitation from cardiac arrest using sublingual injection for medication delivery."  Ann Emerg Med 1993; 22:751-753.
09.18.11
by

The Absolute Lymphocyte Count in Severe HIV


Have you ever wanted a rapid CD4 count on an HIV positive patient to help assess their risk for opportunistic or AIDS-defining infections?


Apart from large tertiary hospitals, the ability to obtain a lymphocyte subset remains limited and labor-intensive through traditional flow cytometry.  Resource-poor settings have encountered similar issues, and have looked for corollary markers for HIV progression.  One of them is the  absolute lymphocyte count (ALC).

Studies from South Africa and India have shown that the ALC correlates well with CD4 counts below 200 cells/mm3 with multiple studies confirming r values of 0.70 and greater.  

While not highly sensitive, the ALC appears to be a specific marker for severe immunocompromise.  There is an 80-95% specificity of an ALC<1200 cells/mm3 for a  CD4<200 cells/mm3.  

The value of the ALC lies in its presence as part of the standard CBC with differential.  While inadequate on its own to start HAART, the ALC may guide the EP to start early antimicrobials for opportunitistic infections consistent with the clinical presentation of the HIV positive patient.

-- Rohith Malya, MD

References:


Blatt SP, Lucey CR, Butzin CA, Hendrix CW, and Lucey DR.  "Total lymphocyte count as a predictor of absolute CD4+ count and CD4+ percentage in HIV-infected persons."  JAMA. 1993 Feb 3;269(5):622-6.


Crowe S, Turnbull S, Oelrichs R, and Dunne A.  "Monitoring of human immunodeficiency virus infection in resource-constrained countries."  Clin Infect Dis. 2003 Jul 1;37(Suppl 1):S25-35.


Srirangaraj Sreenivasan and Venkatesha Dasegowda.  "Comparing Absolute Lymphocyte Count to Total Lymphocyte Count, as a CD4 T Cell Surrogate, to Initiate Antiretroviral Therapy."  J Glob Infect Dis. 2011 Jul-Sep;3(3):265-268.


Srithanaviboonchai K, Rungruengthanakit K, Nouanthong P, Pata S, Sirisanthana T, and Kasinrerk W.  "Novel Low-Cost Assay for the Monitoring of CD4 Counts in HIV-Infected Individuals."  JAIDS. 2008 Feb 1; 47(2):135-9.

09.18.11
by

The Absolute Lymphocyte Count in Severe HIV


Have you ever wanted a rapid CD4 count on an HIV positive patient to help assess their risk for opportunistic or AIDS-defining infections?


Apart from large tertiary hospitals, the ability to obtain a lymphocyte subset remains limited and labor-intensive through traditional flow cytometry.  Resource-poor settings have encountered similar issues, and have looked for corollary markers for HIV progression.  One of them is the  absolute lymphocyte count (ALC).

Studies from South Africa and India have shown that the ALC correlates well with CD4 counts below 200 cells/mm3 with multiple studies confirming r values of 0.70 and greater.  

While not highly sensitive, the ALC appears to be a specific marker for severe immunocompromise.  There is an 80-95% specificity of an ALC<1200 cells/mm3 for a  CD4<200 cells/mm3.  

The value of the ALC lies in its presence as part of the standard CBC with differential.  While inadequate on its own to start HAART, the ALC may guide the EP to start early antimicrobials for opportunitistic infections consistent with the clinical presentation of the HIV positive patient.

-- Rohith Malya, MD

References:


Blatt SP, Lucey CR, Butzin CA, Hendrix CW, and Lucey DR.  "Total lymphocyte count as a predictor of absolute CD4+ count and CD4+ percentage in HIV-infected persons."  JAMA. 1993 Feb 3;269(5):622-6.


Crowe S, Turnbull S, Oelrichs R, and Dunne A.  "Monitoring of human immunodeficiency virus infection in resource-constrained countries."  Clin Infect Dis. 2003 Jul 1;37(Suppl 1):S25-35.


Srirangaraj Sreenivasan and Venkatesha Dasegowda.  "Comparing Absolute Lymphocyte Count to Total Lymphocyte Count, as a CD4 T Cell Surrogate, to Initiate Antiretroviral Therapy."  J Glob Infect Dis. 2011 Jul-Sep;3(3):265-268.


Srithanaviboonchai K, Rungruengthanakit K, Nouanthong P, Pata S, Sirisanthana T, and Kasinrerk W.  "Novel Low-Cost Assay for the Monitoring of CD4 Counts in HIV-Infected Individuals."  JAIDS. 2008 Feb 1; 47(2):135-9.

09.10.11
by

Double Down for Persistent Refractory Ventricular Fibrillation


No doubt you have encountered a patient in persistent ventricular fibrillation (VF) cardiac arrest and have run out of options.  Beyond high quality uninterrupted CPR, biphasic defibrillation, pressors, and antiarrhythmics, therapy remains limited.

Enter double sequential defibrillation for the refractory VF cardiac arrest patient.  First described by Dr. David Hoch in 1994, this concept utilizes two defibrillators set up to provide sequential shocks seconds apart for patients with refractory VF during routine electrophysiology (EP) testing.

Hoch et al. found that 5 out of 2990 consecutive patients undergoing 5450 routine EP studies in a 3-year period experienced refractory VF (estimated incidence of 0.1%).  These 5 patients received multiple single transthoracic defibrillatory shocks (initial shock at 200J, subsequent shocks at 360J monophasic) without success.  

This was followed by double sequential shocks, delivered externally at 0.5-4.5 seconds apart by means of two defibrillators (each set at 360J monophasic) with separate pairs of electrodes.  All 5 patients were successfully cardioverted with their first double sequential shock.

To perform double sequential defibrillation in your ED, attach a second set of pads placed just left of the patient's existing pads, creating a new vector.  At the time of defibrillation, both shock buttons are depressed as near-simultaneously as possible - delivering as much as 720J monophasic -- resulting in a delay between the shocks from each defibrillator.  This is consistent with the sequential description by Hoch.

I have had personal success with double sequential defibrillation for persistent refractory ventricular fibrillation, with one ROSC using 720J and one nonresponder using 400J.

EMS Systems in Fort Worth, TX, Wake County, NC and New Orleans, LA have presented good data on this method.  At the 2011 EMS State of Sciences Conference in Dallas, TX, Dr. Juliette Saussy, former EMS Medical Director of New Orleans, shared that 4 of 16 deployments of double sequential defibrillation for refractory VF in New Orleans resulted in ROSC.  One of the four was a 64  year-old female who went home neurologically intact.  Reports from Wake County have been similar with good rhythm conversion by double sequential defibrillation and mixed success in achieving ROSC and neurologic preservation at discharge.

Lessons learned from the street are invaluable for practice in the ED.  Next time you have a patient in refractory ventricular fibrillation and have exhausted the algorithm, consider using a second defibrillator.


-- Eric Beck, DO, EMT-P


References:
Hoch DM, WP Batsford, SM Greenberg, CM McPherson, LE Rosenfeld, M Marieb, and JH Levine.  "Double sequential external shocks for refractory ventricular fibrillation."  Journal of the American College of Cardiology.  April 1994.  23(5): 1141-5.

Saussy JM.  "A Shocking Two-some!  The Big Easy Experience with Big Difficult VF."  Presented at EMS State of Science:  Gathering of the Eagles XIII.  25 February 2011.  Dallas, TX.
09.10.11
by

Double Down for Persistent Refractory Ventricular Fibrillation


No doubt you have encountered a patient in persistent ventricular fibrillation (VF) cardiac arrest and have run out of options.  Beyond high quality uninterrupted CPR, biphasic defibrillation, pressors, and antiarrhythmics, therapy remains limited.

Enter double sequential defibrillation for the refractory VF cardiac arrest patient.  First described by Dr. David Hoch in 1994, this concept utilizes two defibrillators set up to provide sequential shocks seconds apart for patients with refractory VF during routine electrophysiology (EP) testing.

Hoch et al. found that 5 out of 2990 consecutive patients undergoing 5450 routine EP studies in a 3-year period experienced refractory VF (estimated incidence of 0.1%).  These 5 patients received multiple single transthoracic defibrillatory shocks (initial shock at 200J, subsequent shocks at 360J monophasic) without success.  

This was followed by double sequential shocks, delivered externally at 0.5-4.5 seconds apart by means of two defibrillators (each set at 360J monophasic) with separate pairs of electrodes.  All 5 patients were successfully cardioverted with their first double sequential shock.

To perform double sequential defibrillation in your ED, attach a second set of pads placed just left of the patient's existing pads, creating a new vector.  At the time of defibrillation, both shock buttons are depressed as near-simultaneously as possible - delivering as much as 720J monophasic -- resulting in a delay between the shocks from each defibrillator.  This is consistent with the sequential description by Hoch.

I have had personal success with double sequential defibrillation for persistent refractory ventricular fibrillation, with one ROSC using 720J and one nonresponder using 400J.

EMS Systems in Fort Worth, TX, Wake County, NC and New Orleans, LA have presented good data on this method.  At the 2011 EMS State of Sciences Conference in Dallas, TX, Dr. Juliette Saussy, former EMS Medical Director of New Orleans, shared that 4 of 16 deployments of double sequential defibrillation for refractory VF in New Orleans resulted in ROSC.  One of the four was a 64  year-old female who went home neurologically intact.  Reports from Wake County have been similar with good rhythm conversion by double sequential defibrillation and mixed success in achieving ROSC and neurologic preservation at discharge.

Lessons learned from the street are invaluable for practice in the ED.  Next time you have a patient in refractory ventricular fibrillation and have exhausted the algorithm, consider using a second defibrillator.


-- Eric Beck, DO, EMT-P


References:
Hoch DM, WP Batsford, SM Greenberg, CM McPherson, LE Rosenfeld, M Marieb, and JH Levine.  "Double sequential external shocks for refractory ventricular fibrillation."  Journal of the American College of Cardiology.  April 1994.  23(5): 1141-5.

Saussy JM.  "A Shocking Two-some!  The Big Easy Experience with Big Difficult VF."  Presented at EMS State of Science:  Gathering of the Eagles XIII.  25 February 2011.  Dallas, TX.
09.02.11
by

Apneic Oxygenation during RSI


Endotracheal intubation is a high-risk procedure routinely performed by emergency physicians. Approximately 8% of all emergency airway management cases require more than one one attempt, and about 8% will result in esophageal intubation.  To minimize hypoxic time, EPs traditionally employ preoxygenation with high-flow O2 via NRB for adequate nitrogen washout.  Apneic oxygenation is an additional tool for prolonging time to critical desaturation through passive insufflation of non-respirating airways with high FIO2 air.

During apnea, oxygen is absorbed from alveoli across the pulmonary vasculature.  This absorption depletes the alveoli of O2 and leaves behind an area of relative low O2 concentration.  In order to re-establish this equilibrium, oxygen from the proximal portions of the airway (nasopharynx through bronchi) flows down a gradient to replenish the O2-depleted alveoli.

Rapid induction and paralysis closes the upper airway secondary to laxity of soft tissue structures.  At this time, a finite amount of oxygen is trapped in the airways that will be available for passive absorption through the non-respiring lungs.  In order to capitalize on the principle of apneic oxygention, insufflation of O2 to the nasopharynx (i.e.,  nasal cannula +/- nasal trumpet, jaw thrust and face mask O2) significantly prolongs time to desaturation, and thus extends the window of safe intubating conditions.

Identifying this principle in 1959, Frumin et al. provided 100% FIO2 to apneic intubated volunteers and then measuring arterial oxygen saturation.  Healthy subjects sustained normoxia (98% O2 saturation and up) for greater than 50 minutes.  Taha et al. concurred in a later 2006 study, finding that nasopharyngeal O2 insufflation significantly prolongs time to desaturation prior to intubation for elective surgical procedures.  More recently, Baraka et al. applied this principle and proved its efficacy in the morbidly obese population.  

Multiple studies confirm this principle as safe and effective.  Its use should become routine practice for patients at high-risk for oxygen desaturation.

-- Peter Acker MD MPH

References:

Engstrom J, Hedenstierna G, Larsson A. "Pharyngeal oxygen administration increases the time to serious desaturation at intubation in acute lung injury: an experimental study." Crit Care. 2010; 14(3): R93.

Schwartz DE, Matthay MA, Cohen NH. "Death and other complications of emergency airway management in critically ill adults." Anesthesiology. 1995;82:367-376.

Weingart SD. "Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department." J. Emerg. Med. 2010 Apr 7.

Taha SK, Siddik-Sayyid SM, El-Khatib MF, Dagher CM, Hakki MA, Baraka AS.  "Nasopharyngeal oxygen insufflation following pre- oxygenation using the four deep breath technique." Anaesthesia 2006;61:427-30.

Frumin MJ, Epstein RM, Cohen G. "Apneic oxygenation in man." Anesthesiology 1959; 20: 789-98.

Baraka AS, Taha SK, Siddik-Sayyid SM, et al. "Supplementation of pre-oxygenation in morbidly obese patients using nasopharyngeal oxygen insufflation." Anaesthesia 2007; 62: 769-73.
09.02.11
by

Apneic Oxygenation during RSI


Endotracheal intubation is a high-risk procedure routinely performed by emergency physicians. Approximately 8% of all emergency airway management cases require more than one one attempt, and about 8% will result in esophageal intubation.  To minimize hypoxic time, EPs traditionally employ preoxygenation with high-flow O2 via NRB for adequate nitrogen washout.  Apneic oxygenation is an additional tool for prolonging time to critical desaturation through passive insufflation of non-respirating airways with high FIO2 air.

During apnea, oxygen is absorbed from alveoli across the pulmonary vasculature.  This absorption depletes the alveoli of O2 and leaves behind an area of relative low O2 concentration.  In order to re-establish this equilibrium, oxygen from the proximal portions of the airway (nasopharynx through bronchi) flows down a gradient to replenish the O2-depleted alveoli.

Rapid induction and paralysis closes the upper airway secondary to laxity of soft tissue structures.  At this time, a finite amount of oxygen is trapped in the airways that will be available for passive absorption through the non-respiring lungs.  In order to capitalize on the principle of apneic oxygention, insufflation of O2 to the nasopharynx (i.e.,  nasal cannula +/- nasal trumpet, jaw thrust and face mask O2) significantly prolongs time to desaturation, and thus extends the window of safe intubating conditions.

Identifying this principle in 1959, Frumin et al. provided 100% FIO2 to apneic intubated volunteers and then measuring arterial oxygen saturation.  Healthy subjects sustained normoxia (98% O2 saturation and up) for greater than 50 minutes.  Taha et al. concurred in a later 2006 study, finding that nasopharyngeal O2 insufflation significantly prolongs time to desaturation prior to intubation for elective surgical procedures.  More recently, Baraka et al. applied this principle and proved its efficacy in the morbidly obese population.  

Multiple studies confirm this principle as safe and effective.  Its use should become routine practice for patients at high-risk for oxygen desaturation.

-- Peter Acker MD MPH

References:

Engstrom J, Hedenstierna G, Larsson A. "Pharyngeal oxygen administration increases the time to serious desaturation at intubation in acute lung injury: an experimental study." Crit Care. 2010; 14(3): R93.

Schwartz DE, Matthay MA, Cohen NH. "Death and other complications of emergency airway management in critically ill adults." Anesthesiology. 1995;82:367-376.

Weingart SD. "Preoxygenation, reoxygenation, and delayed sequence intubation in the emergency department." J. Emerg. Med. 2010 Apr 7.

Taha SK, Siddik-Sayyid SM, El-Khatib MF, Dagher CM, Hakki MA, Baraka AS.  "Nasopharyngeal oxygen insufflation following pre- oxygenation using the four deep breath technique." Anaesthesia 2006;61:427-30.

Frumin MJ, Epstein RM, Cohen G. "Apneic oxygenation in man." Anesthesiology 1959; 20: 789-98.

Baraka AS, Taha SK, Siddik-Sayyid SM, et al. "Supplementation of pre-oxygenation in morbidly obese patients using nasopharyngeal oxygen insufflation." Anaesthesia 2007; 62: 769-73.
08.25.11
by

Management of Laryngospasm: The Laryngospasm Notch


A rare though serious potential adverse event during procedural sedation is the development of laryngospasm.  Most often cited in association with ketamine sedation, multiple attempts to identify risk factors (URI symptoms, adjunctive medications, depth of sedation) have failed to identify strong predictors. Since it appears to be idiosyncratic, and since its occurrence requires immediate action, anticipation and advanced preparation for managing laryngospasm is key.

Standard management includes airway repositioning and using a bag-valve-mask device to apply positive pressure ventilation.  If positive pressure fails to break the laryngospasm, the next step in most standard treatment protocols is paralysis with continued positive pressure ventilation.  

Though not formally studied in clinical trials, pressure on the "laryngospasm notch" has been described in the anesthesia literature as a strategy for breaking laryngospasm without the use of paralytics.  

The "laryngospasm notch" described by Philip Larson is located behind the ear between the mastoid process and the mandible. Firm pressure on both sides not only results in jaw thrust, but also causes periosteal pain at the styloid process, resulting in breaking of the laryngospasm.

I have not tried this myself (yet) and beyond the anesthesia anecdotes could find nothing in the medical literature describing its use during procedural sedation. If anyone tries it - let us know!  

-- Lisa McQueen, MD

References:

Green SM, Roback MG, Krauss B. "Laryngospasm during emergency department ketamine sedation: a case - control study." Pediatric Emergency Care 2010;26:798-802.

Johnstone RE. "Laryngospasm treatment - an explanation." Anesthesiology  1999;91:581-2.

Larson PC. "Laryngospasm - the best treatment." Anesthesiology 1998;89:1293-4.
08.25.11
by

Management of Laryngospasm: The Laryngospasm Notch


A rare though serious potential adverse event during procedural sedation is the development of laryngospasm.  Most often cited in association with ketamine sedation, multiple attempts to identify risk factors (URI symptoms, adjunctive medications, depth of sedation) have failed to identify strong predictors. Since it appears to be idiosyncratic, and since its occurrence requires immediate action, anticipation and advanced preparation for managing laryngospasm is key.

Standard management includes airway repositioning and using a bag-valve-mask device to apply positive pressure ventilation.  If positive pressure fails to break the laryngospasm, the next step in most standard treatment protocols is paralysis with continued positive pressure ventilation.  

Though not formally studied in clinical trials, pressure on the "laryngospasm notch" has been described in the anesthesia literature as a strategy for breaking laryngospasm without the use of paralytics.  

The "laryngospasm notch" described by Philip Larson is located behind the ear between the mastoid process and the mandible. Firm pressure on both sides not only results in jaw thrust, but also causes periosteal pain at the styloid process, resulting in breaking of the laryngospasm.

I have not tried this myself (yet) and beyond the anesthesia anecdotes could find nothing in the medical literature describing its use during procedural sedation. If anyone tries it - let us know!  

-- Lisa McQueen, MD

References:

Green SM, Roback MG, Krauss B. "Laryngospasm during emergency department ketamine sedation: a case - control study." Pediatric Emergency Care 2010;26:798-802.

Johnstone RE. "Laryngospasm treatment - an explanation." Anesthesiology  1999;91:581-2.

Larson PC. "Laryngospasm - the best treatment." Anesthesiology 1998;89:1293-4.
08.17.11
by

Making a Difference in Acute Hyperkalemia

Part 2 of 3:  Taking Beta-Agonists to the Next Level
Since the 1930s, physicians have been aware of the ability of beta-agonists to lower serum potassium.  Early studies with epinephrine's nonselective beta-agonism gave way to the beta-2 receptor specificity of albuterol (salbutamol) through a mechanism of cyclic AMP stimulation, activation of the Na+/K+ pump, and flux of potassium into the intracellular compartment.  

High-Dose Albuterol
Multiple studies have confirmed the ability of nebulized albuterol to lower serum potassium within 30 minutes.  However, what is less well-known is the existence of a dose-response curve for nebulized albuterol.  High-dose albuterol (15-20 mg/hour) given for 2 hours effectively doubles the potassium-lowering (1 mmol/L vs 0.6 mmol/L) when compared with conventional-dose albuterol (10 mg/hour).  This potassium-lowering effect has been shown to persist for at least 3 hours (and often up to 6 hours) after cessation of the nebulized albuterol.
Traditional concerns that higher doses of albuterol lead to increased side effects (tremor, tachycardia, anxiety) have not borne out.  While tachycardia is noted more frequently, studies have noted the absence of clinically significant events and the consistence of patient tolerance between conventional-dose and high-dose albuterol.
Albuterol Non Responders
A caveat to albuterol use for hyperkalemia is the presence of 'non-responders.'  Between 20% and 40% of patients do not achieve a serum decrease in potassium of 0.5 mmol/L.  While this remains to be be confirmed in larger studies, the simple presence of 'non-responders' in small cohort studies precludes the use of albuterol as single therapy for hyperkalemia.
Terbutaline
Terbutaline, a beta2-agonist well-known to our nephrology colleagues, has been shown to be equally efficacious through a subcutaneous route of administration.  Administering 7 micrograms/kg SQ, Sowinskiet al. noted an average potassium decrease of 1.34 mmol/L with maximal effect at 60 minutes persistent through 300 minutes.  
Dialysis Patients
Quite often, hyperkalemia presents in patients who have missed dialysis.  When these patients present to the ED, they universally receive albuterol as part of a potassium-lowering cocktail.  
However, as Allon et al. point out, the patients who receive albuterol 30 minutes prior to dialysis have less removal of potassium (up to 40% less).  Given that albuterol shifts potassium to the intracellular compartment, it is inaccessible by dialysis and puts the patient at risk for 'rebound hyperkalemia' several hours post-dialysis -- when the albuterol has worn off and potassium floods the extracellular compartment.  Emergency physicians should be aware of this special situation and consider the timing of albuterol with relation to emergent dialysis.  
-- Jonathan Purcell, MD
References:
Allon M, Dunlay R, Copkney C. "Nebulized albuterol for acute hyperkalemia in patients on hemodialysis." Ann Intern Med 1989;110:426-429.
Allon M, Copkney C. "Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients." Kidney Int 1990;38:869-872.
Allon M, Shanklin N. "Effect of albuterol treatment on subsequent dialytic potassium removal." Am J Kidney Dis 1995;26:607-613.
Jonkers R, Van Boxtel CJ, Oosterhuis B. "Beta-2-adrenoceptor-mediated hypokalemia and its abolishment by oxprenolol." Clin Pharmacol Ther 1987;42(6):627-33.
Montoliu J, Lens XM, Revert L. "Potassium-lowering effect of albuterol for hyperkalemia in renal failure." Arch Intern Med 1987;147:713-717.
Montoliu J, Almirall J, Ponz E, et al. "Treatment of hyperkalaemia in renal failure with salbutamol inhalation." J Intern Med 1990;228:35-37.
Shingarev R, Allon M. "A physiologic-based approach to the treatment of acute hyperkalemia." Am J Kidney Dis 2010;56:578-584.
Sowinski KM, Cronin D, Mueller BA, et al. "Subcutaneous terbutaline use in CKD to reduce potassium concentrations." Am J Kidney Dis 2005;45:1040-1045.
08.17.11
by

Making a Difference in Acute Hyperkalemia

Part 2 of 3:  Taking Beta-Agonists to the Next Level
Since the 1930s, physicians have been aware of the ability of beta-agonists to lower serum potassium.  Early studies with epinephrine's nonselective beta-agonism gave way to the beta-2 receptor specificity of albuterol (salbutamol) through a mechanism of cyclic AMP stimulation, activation of the Na+/K+ pump, and flux of potassium into the intracellular compartment.  

High-Dose Albuterol
Multiple studies have confirmed the ability of nebulized albuterol to lower serum potassium within 30 minutes.  However, what is less well-known is the existence of a dose-response curve for nebulized albuterol.  High-dose albuterol (15-20 mg/hour) given for 2 hours effectively doubles the potassium-lowering (1 mmol/L vs 0.6 mmol/L) when compared with conventional-dose albuterol (10 mg/hour).  This potassium-lowering effect has been shown to persist for at least 3 hours (and often up to 6 hours) after cessation of the nebulized albuterol.
Traditional concerns that higher doses of albuterol lead to increased side effects (tremor, tachycardia, anxiety) have not borne out.  While tachycardia is noted more frequently, studies have noted the absence of clinically significant events and the consistence of patient tolerance between conventional-dose and high-dose albuterol.
Albuterol Non Responders
A caveat to albuterol use for hyperkalemia is the presence of 'non-responders.'  Between 20% and 40% of patients do not achieve a serum decrease in potassium of 0.5 mmol/L.  While this remains to be be confirmed in larger studies, the simple presence of 'non-responders' in small cohort studies precludes the use of albuterol as single therapy for hyperkalemia.
Terbutaline
Terbutaline, a beta2-agonist well-known to our nephrology colleagues, has been shown to be equally efficacious through a subcutaneous route of administration.  Administering 7 micrograms/kg SQ, Sowinskiet al. noted an average potassium decrease of 1.34 mmol/L with maximal effect at 60 minutes persistent through 300 minutes.  
Dialysis Patients
Quite often, hyperkalemia presents in patients who have missed dialysis.  When these patients present to the ED, they universally receive albuterol as part of a potassium-lowering cocktail.  
However, as Allon et al. point out, the patients who receive albuterol 30 minutes prior to dialysis have less removal of potassium (up to 40% less).  Given that albuterol shifts potassium to the intracellular compartment, it is inaccessible by dialysis and puts the patient at risk for 'rebound hyperkalemia' several hours post-dialysis -- when the albuterol has worn off and potassium floods the extracellular compartment.  Emergency physicians should be aware of this special situation and consider the timing of albuterol with relation to emergent dialysis.  
-- Jonathan Purcell, MD
References:
Allon M, Dunlay R, Copkney C. "Nebulized albuterol for acute hyperkalemia in patients on hemodialysis." Ann Intern Med 1989;110:426-429.
Allon M, Copkney C. "Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients." Kidney Int 1990;38:869-872.
Allon M, Shanklin N. "Effect of albuterol treatment on subsequent dialytic potassium removal." Am J Kidney Dis 1995;26:607-613.
Jonkers R, Van Boxtel CJ, Oosterhuis B. "Beta-2-adrenoceptor-mediated hypokalemia and its abolishment by oxprenolol." Clin Pharmacol Ther 1987;42(6):627-33.
Montoliu J, Lens XM, Revert L. "Potassium-lowering effect of albuterol for hyperkalemia in renal failure." Arch Intern Med 1987;147:713-717.
Montoliu J, Almirall J, Ponz E, et al. "Treatment of hyperkalaemia in renal failure with salbutamol inhalation." J Intern Med 1990;228:35-37.
Shingarev R, Allon M. "A physiologic-based approach to the treatment of acute hyperkalemia." Am J Kidney Dis 2010;56:578-584.
Sowinski KM, Cronin D, Mueller BA, et al. "Subcutaneous terbutaline use in CKD to reduce potassium concentrations." Am J Kidney Dis 2005;45:1040-1045.
08.03.11
by

Maximizing LP Success: The Early Stylet Removal Technique.

Have you ever tapped a baby and ended up with bloody CSF that was non-interpretable? Have you ever tapped a baby but haven't felt the "pop"?

Classically, lumbar puncture is performed by advancing a spinal needle through the skin and soft tissues until a "pop" is felt by puncturing the dura.  At this point the stylet is removed and CSF collected.  The elusive "pop" may not be felt, however, so the operator is forced to make an educated guess as to when to remove the stylet to check for CSF flow.  All of us have had the experience of multiple attempts resulting in little or no CSF, or only bloody CSF.

Try this trick next time:  Once through the skin and soft tissues, remove the stylet and advance slowly.  As you penetrate the dura, you will immediately see CSF even if you don't feel the "pop," and can then stop advancing the needle and collect the fluid.  

This technique of early stylet removal has been shown to increase procedure success, with fewer attempts needed and increased yield of interpretable fluid.

Replace the stylet before removing the spinal needle, however, to avoid the theoretical creation of a persistent CSF leak by strands of arachnoid that may find their way into your needle hub.

-- Lisa McQueen, MD

References:

Baxter AL, Fisher RG, Burke BL, et al.  "Local anesthetic and stylet styles: factors associated with resident lumbar puncture success." Pediatrics.  2006; 117:876-881.

Mellick L and Vining M.  "Maximizing infant spinal tap success."  Pediatric Emergency Care.  
2010; 26:687-8.

Nigrovic LE, Kuppermann N, Neuman MI.  "Risk factors for traumatic or unsuccessful lumbar punctures in children."  Annals of Emergency Medicine.  2007; 49:762-71.
08.03.11
by

Maximizing LP Success: The Early Stylet Removal Technique.

Have you ever tapped a baby and ended up with bloody CSF that was non-interpretable? Have you ever tapped a baby but haven't felt the "pop"?

Classically, lumbar puncture is performed by advancing a spinal needle through the skin and soft tissues until a "pop" is felt by puncturing the dura.  At this point the stylet is removed and CSF collected.  The elusive "pop" may not be felt, however, so the operator is forced to make an educated guess as to when to remove the stylet to check for CSF flow.  All of us have had the experience of multiple attempts resulting in little or no CSF, or only bloody CSF.

Try this trick next time:  Once through the skin and soft tissues, remove the stylet and advance slowly.  As you penetrate the dura, you will immediately see CSF even if you don't feel the "pop," and can then stop advancing the needle and collect the fluid.  

This technique of early stylet removal has been shown to increase procedure success, with fewer attempts needed and increased yield of interpretable fluid.

Replace the stylet before removing the spinal needle, however, to avoid the theoretical creation of a persistent CSF leak by strands of arachnoid that may find their way into your needle hub.

-- Lisa McQueen, MD

References:

Baxter AL, Fisher RG, Burke BL, et al.  "Local anesthetic and stylet styles: factors associated with resident lumbar puncture success." Pediatrics.  2006; 117:876-881.

Mellick L and Vining M.  "Maximizing infant spinal tap success."  Pediatric Emergency Care.  
2010; 26:687-8.

Nigrovic LE, Kuppermann N, Neuman MI.  "Risk factors for traumatic or unsuccessful lumbar punctures in children."  Annals of Emergency Medicine.  2007; 49:762-71.
07.26.11
by

Novel Approaches in the Management of DKA

Part 1:  Skipping the Insulin Bolus

This is the first in a 3-part series on the modern ED treatment of DKA.  The second part will focus on 'Skipping the Insulin Drip,' while the third part will discuss the 'Irrelevance of Type I and Type II.'

Early studies from the 1920s through the 1950s on DKA relied on multiple push-doses of IV insulin at predetermined intervals to overcome the insulin-resistant or insulin-deficient state of DKA.  At a time when the mortality of DKA remained high (often due to sudden hypoglycemia or persistent hyperglycemia), these studies rarely used insulin in continuous infusion.  

Physiologically, the administration of bolus IV insulin results in major shifts in serum potassium, glucose, and osmolarity.  Our pediatric colleagues are well-aware of the dangers of cerebral edema from the initial bolus dose of insulin in DKA.  Taken together, these risks question the utility of the initial insulin bolus in adults presenting in DKA.  

In a retrospective review of 157 ED patients treated for DKA at Henry Ford in Detroit, Goyal et al. examined this very question.  Half the patients received an initial insulin bolus followed by infusion, and half were started on an insulin infusion alone.  Their results and analysis confirmed that there was no statistical difference between the two groups in:  ED length of stay, hospital length of stay, or most notably in the average glucose change per hour (both groups were in the 50-60 mg/dL/h range).

Dr. Abbas Kitabchi at the University of Tennessee, a legend in DKA research and the lead author of the ADA consensus statement on the treatment of DKA, agrees with the idea that the initial bolus dose may be bypassed entirely.  In a prospective randomized study of 37 patients assigned to the same groups (bolus/infusion vs. infusion alone), he concluded:

"Times to reach glucose <or=250 mg/dl, pH >or=7.3, and HCO(3)(-) >or=15 mEq/l did not
differ significantly ... [and] use of a bolus or priming dose of insulin is not necessary when an adequate continuous insulin infusion such as 0.14 units/kg/hr (or 10 units/h in a 70-kg patient) is used."
 
Both these studies confirm what many of us already suspected --that the risks of the insulin bolus in DKA outweigh all potential benefit.  Now, we have real-world ER data and a randomized study from the lead author of the ADA consensus statement on DKA to back this practice change.

-- Rohith Malya, MD

References:

Black AB and JM Malins.  "Diabetic Ketosis.  A Comparison of Results of Orthodox and Intensive Methods of Treatment Based on 170 Conscecutive Cases."  Lancet.  8 January 1949; 253(6541):56-9.

Goyal N, JB Miller, SS Sankey, and U Mossallam.  "Utility of initial bolus insulin in the treatment of diabetic ketoacidosis."  Journal of Emergency Medicine.  2010 May; 38(4):422-7.

Kitabchi AE, MB Murphy, J Spencer, R Matteri, and J Karas.  "Is a Priming Dose of Insulin Necessary in a Low-Dose Insulin Protocol for the Treatment of Diabetic Ketoacidosis?"  Diabetes Care.  2008 Nov; 31(1
07.26.11
by

Novel Approaches in the Management of DKA

Part 1:  Skipping the Insulin Bolus

This is the first in a 3-part series on the modern ED treatment of DKA.  The second part will focus on 'Skipping the Insulin Drip,' while the third part will discuss the 'Irrelevance of Type I and Type II.'

Early studies from the 1920s through the 1950s on DKA relied on multiple push-doses of IV insulin at predetermined intervals to overcome the insulin-resistant or insulin-deficient state of DKA.  At a time when the mortality of DKA remained high (often due to sudden hypoglycemia or persistent hyperglycemia), these studies rarely used insulin in continuous infusion.  

Physiologically, the administration of bolus IV insulin results in major shifts in serum potassium, glucose, and osmolarity.  Our pediatric colleagues are well-aware of the dangers of cerebral edema from the initial bolus dose of insulin in DKA.  Taken together, these risks question the utility of the initial insulin bolus in adults presenting in DKA.  

In a retrospective review of 157 ED patients treated for DKA at Henry Ford in Detroit, Goyal et al. examined this very question.  Half the patients received an initial insulin bolus followed by infusion, and half were started on an insulin infusion alone.  Their results and analysis confirmed that there was no statistical difference between the two groups in:  ED length of stay, hospital length of stay, or most notably in the average glucose change per hour (both groups were in the 50-60 mg/dL/h range).

Dr. Abbas Kitabchi at the University of Tennessee, a legend in DKA research and the lead author of the ADA consensus statement on the treatment of DKA, agrees with the idea that the initial bolus dose may be bypassed entirely.  In a prospective randomized study of 37 patients assigned to the same groups (bolus/infusion vs. infusion alone), he concluded:

"Times to reach glucose <or=250 mg/dl, pH >or=7.3, and HCO(3)(-) >or=15 mEq/l did not
differ significantly ... [and] use of a bolus or priming dose of insulin is not necessary when an adequate continuous insulin infusion such as 0.14 units/kg/hr (or 10 units/h in a 70-kg patient) is used."
 
Both these studies confirm what many of us already suspected --that the risks of the insulin bolus in DKA outweigh all potential benefit.  Now, we have real-world ER data and a randomized study from the lead author of the ADA consensus statement on DKA to back this practice change.

-- Rohith Malya, MD

References:

Black AB and JM Malins.  "Diabetic Ketosis.  A Comparison of Results of Orthodox and Intensive Methods of Treatment Based on 170 Conscecutive Cases."  Lancet.  8 January 1949; 253(6541):56-9.

Goyal N, JB Miller, SS Sankey, and U Mossallam.  "Utility of initial bolus insulin in the treatment of diabetic ketoacidosis."  Journal of Emergency Medicine.  2010 May; 38(4):422-7.

Kitabchi AE, MB Murphy, J Spencer, R Matteri, and J Karas.  "Is a Priming Dose of Insulin Necessary in a Low-Dose Insulin Protocol for the Treatment of Diabetic Ketoacidosis?"  Diabetes Care.  2008 Nov; 31(1
07.21.11
by

Picking Up the Subtle Right Ventricular MI


Right ventricular myocardial infarction (RVMI) is thought to occur in up to 50% of inferior wall infarcts.  Its early recognition and treatment is important because it retains a unique hemodynamic response profile with high risk for decompensated cardiogenic shock.

There are three currently accepted methods to clinching the diagnosis of RVMI.  Their origin and significance are discussed below.   
1.  ST elevation in lead III > lead II
The first pathologic report of RVMI in 1930 in the American Heart Journal noted that ST elevation was higher in lead III than lead II in the setting of a patient with an inferior wall infarct.  In Einthoven's triangle, Lead II is positioned at +60 degrees and Lead III is positioned at +120 degrees (a quick primer:  the 3 o'clock position is 0 degrees and clockwise rotation is positive).  Given it's vector directly over the RV, lead III crosses the main RV axis more so than lead II.

 A 2001 retrospective review of 175 patients by Saw et al. examined the 'lead III greater than lead II' criterion against isolated elevation in V4R for diagnosis of RVMI.  The former criterion was noted to be more sensitive (97% vs 65%) but less specific (56% vs 78%).
2.  ST elevation greater than 1 mm in V1
ST elevation in lead V1 greater than 1 mm is highly suggestive of RVMI.  First described in 1981 by Chou et al., this sensitive finding was present in 8 of 11 cases of right ventricular infarction confirmed by hemodynamic data or autopsy.
3.  ST elevation greater than 1 mm in right-sided leads (V4R, V5R, and V6R)
Right-sided precordial leads commonly involve V4R, V5R, and V6R.  Multiple studies concur that ST elevation greater than 1 mm lead in V4R is the most sensitive single finding for RVMI and may even be used alone as the only right precordial lead.  Correct placement of lead V4R (the axial reflection of V4) occurs when the lead is located at the right mid-clavicular fifth intercostal space.
In patients with concern for RVMI (documented inferior ST elevation, or chest pain with a drop in BP after nitrates/opiates), the standard 12-lead EKG should be meticulously examined for all three of these findings:  ST elevation in lead III greater than lead II, ST elevation greater than 1 mm in V1, and ST elevation in dedicated right-sided leads (at least V4R).  
-- Jonathan Purcell, MD
References:
Chou TC, J Van der Bel-Kahn, J Allen, L Brockmeier, and NO Fowler.  "Electrocardiographic diagnosis of right ventricular infarction."  American Journal of Medicine.  1981 Jun; 70(6):1175-80.

Saw J, C Davies, A Fung, JJ Spinelli, and J Jue.  "Value of ST elevation in lead III greater than lead I in inferior wall acute myocardial infarction for predicting in-hospital mortality and diagnosing right ventricular infarction."  American Journal of Cardiology.  2001 Feb 15; 87(4):448-50, A6.




07.21.11
by

Picking Up the Subtle Right Ventricular MI


Right ventricular myocardial infarction (RVMI) is thought to occur in up to 50% of inferior wall infarcts.  Its early recognition and treatment is important because it retains a unique hemodynamic response profile with high risk for decompensated cardiogenic shock.

There are three currently accepted methods to clinching the diagnosis of RVMI.  Their origin and significance are discussed below.   
1.  ST elevation in lead III > lead II
The first pathologic report of RVMI in 1930 in the American Heart Journal noted that ST elevation was higher in lead III than lead II in the setting of a patient with an inferior wall infarct.  In Einthoven's triangle, Lead II is positioned at +60 degrees and Lead III is positioned at +120 degrees (a quick primer:  the 3 o'clock position is 0 degrees and clockwise rotation is positive).  Given it's vector directly over the RV, lead III crosses the main RV axis more so than lead II.

 A 2001 retrospective review of 175 patients by Saw et al. examined the 'lead III greater than lead II' criterion against isolated elevation in V4R for diagnosis of RVMI.  The former criterion was noted to be more sensitive (97% vs 65%) but less specific (56% vs 78%).
2.  ST elevation greater than 1 mm in V1
ST elevation in lead V1 greater than 1 mm is highly suggestive of RVMI.  First described in 1981 by Chou et al., this sensitive finding was present in 8 of 11 cases of right ventricular infarction confirmed by hemodynamic data or autopsy.
3.  ST elevation greater than 1 mm in right-sided leads (V4R, V5R, and V6R)
Right-sided precordial leads commonly involve V4R, V5R, and V6R.  Multiple studies concur that ST elevation greater than 1 mm lead in V4R is the most sensitive single finding for RVMI and may even be used alone as the only right precordial lead.  Correct placement of lead V4R (the axial reflection of V4) occurs when the lead is located at the right mid-clavicular fifth intercostal space.
In patients with concern for RVMI (documented inferior ST elevation, or chest pain with a drop in BP after nitrates/opiates), the standard 12-lead EKG should be meticulously examined for all three of these findings:  ST elevation in lead III greater than lead II, ST elevation greater than 1 mm in V1, and ST elevation in dedicated right-sided leads (at least V4R).  
-- Jonathan Purcell, MD
References:
Chou TC, J Van der Bel-Kahn, J Allen, L Brockmeier, and NO Fowler.  "Electrocardiographic diagnosis of right ventricular infarction."  American Journal of Medicine.  1981 Jun; 70(6):1175-80.

Saw J, C Davies, A Fung, JJ Spinelli, and J Jue.  "Value of ST elevation in lead III greater than lead I in inferior wall acute myocardial infarction for predicting in-hospital mortality and diagnosing right ventricular infarction."  American Journal of Cardiology.  2001 Feb 15; 87(4):448-50, A6.




07.14.11
by

Revisiting the Golden Hour in Trauma

The first 60 minutes after a traumatic injury is oft referred to as the "Golden Hour." Through education, practice and promulgation, the Golden Hour has become a fundamental axiom of EMS and trauma care.  The concept that definitive care must be initiated within a 60 minute window - that injury outcomes improve with reduced transport times - is used to justify EMS and trauma systems in the United States and many other countries.

Unlike the cardiac arrest literature, where multiple high-quality studies associate prolonged out-of-hospital time with poor outcomes, trauma transport lacks this scientific data set.  A recent 2010 study by the Resuscitation Outcomes Consortium, an epidemiologic out-of-hospital trauma registry, tells us that transport time may be far less important than widely believed.  

Data from 146 US and Canadian ground and air EMS transport agencies over a 16 month period from 2005 to 2007 analyzed 806 trauma deaths in a pool of 3656 patients (22% mortality).  After multivariate, subgroup, and instrumental analyses, no significant association was found between time and mortality for any EMS interval (activation, response, on-scene, transport, and total time) among injured patients with physiologic abnormalities.

This data confirms what was noted in a Dutch single-center prospective study in 2007 by Lichtveld et al.  Among other conclusions, this study noted "the time interval between the accident and arrival at the hospital does not appear to affect the risk of death."

A landmark paper by Lerner and Moscati in 2001 looked at the medical literature behind the "Golden Hour" concept.  The authors were unable to find a single scientific article to support (or refute) the Golden Hour concept.  Indeed, many articles that discussed the Golden Hour referenced other articles that had no mention of the Golden Hour whatsoever.  
In sum, Lerner and Moscati traced the origin of the Golden Hour concept to famed trauma surgeon R. Adams Cowley of the Shock Trauma Center at the University of Maryland in Baltimore, writing:

"The intuitive nature of the concept and the prestige of those who originally expressed it resulted in its widespread application and acceptance.  Despite the lack of definitive scientific evidence, numerous research studies and requests for research funding are based on achieving the golden hour for all trauma patients and take for granted that time always matters."

Despite our intuition that less time is better for trauma patients, there are risks and costs involved in attempting to deliver patients to trauma centers within 60 minutes.  These risks and costs may be justified if there is a definite and substantial benefit (even in limited circumstances) to the Golden Hour, but this remains heretofore unproven.

-- Eric Beck, DO EMT-P

References:

Lerner EB and RM Moscati.  "The Golden Hour: Scientific Fact or Medical 'Urban Legend'?"  Academic Emergency Medicine.  2001 July; 8(7):758-60.

Lichtveld RA, IF Panhuizen, RBJ Smit, HR Holtslag, and C van der Werken.  "Predictors of Death in Trauma Patients who are Alive on Arrival to Hospital."  European Journal of Trauma and Emergency Surgery.  2007; 33: 46-51.

Newgard CD, RH Schmicker, JR Hedges, JP Trickett, DP Davis, EM Bulger, TP Aufderheide, JP Minei, JS Hata, KD Gubler, TB Brown, JD Yelle, B Bardarson, and G Nichol (Resuscitation Outcomes Consortium Investigators).  "Emergency Medical Service Intervals and Survival in Trauma:  Assessment of the 'Golden Hour' in a North American Prospective Cohort."  Annals of Emergency Medicine.  2010 March; 55(3):235-246.
07.14.11
by

Revisiting the Golden Hour in Trauma

The first 60 minutes after a traumatic injury is oft referred to as the "Golden Hour." Through education, practice and promulgation, the Golden Hour has become a fundamental axiom of EMS and trauma care.  The concept that definitive care must be initiated within a 60 minute window - that injury outcomes improve with reduced transport times - is used to justify EMS and trauma systems in the United States and many other countries.

Unlike the cardiac arrest literature, where multiple high-quality studies associate prolonged out-of-hospital time with poor outcomes, trauma transport lacks this scientific data set.  A recent 2010 study by the Resuscitation Outcomes Consortium, an epidemiologic out-of-hospital trauma registry, tells us that transport time may be far less important than widely believed.  

Data from 146 US and Canadian ground and air EMS transport agencies over a 16 month period from 2005 to 2007 analyzed 806 trauma deaths in a pool of 3656 patients (22% mortality).  After multivariate, subgroup, and instrumental analyses, no significant association was found between time and mortality for any EMS interval (activation, response, on-scene, transport, and total time) among injured patients with physiologic abnormalities.

This data confirms what was noted in a Dutch single-center prospective study in 2007 by Lichtveld et al.  Among other conclusions, this study noted "the time interval between the accident and arrival at the hospital does not appear to affect the risk of death."

A landmark paper by Lerner and Moscati in 2001 looked at the medical literature behind the "Golden Hour" concept.  The authors were unable to find a single scientific article to support (or refute) the Golden Hour concept.  Indeed, many articles that discussed the Golden Hour referenced other articles that had no mention of the Golden Hour whatsoever.  
In sum, Lerner and Moscati traced the origin of the Golden Hour concept to famed trauma surgeon R. Adams Cowley of the Shock Trauma Center at the University of Maryland in Baltimore, writing:

"The intuitive nature of the concept and the prestige of those who originally expressed it resulted in its widespread application and acceptance.  Despite the lack of definitive scientific evidence, numerous research studies and requests for research funding are based on achieving the golden hour for all trauma patients and take for granted that time always matters."

Despite our intuition that less time is better for trauma patients, there are risks and costs involved in attempting to deliver patients to trauma centers within 60 minutes.  These risks and costs may be justified if there is a definite and substantial benefit (even in limited circumstances) to the Golden Hour, but this remains heretofore unproven.

-- Eric Beck, DO EMT-P

References:

Lerner EB and RM Moscati.  "The Golden Hour: Scientific Fact or Medical 'Urban Legend'?"  Academic Emergency Medicine.  2001 July; 8(7):758-60.

Lichtveld RA, IF Panhuizen, RBJ Smit, HR Holtslag, and C van der Werken.  "Predictors of Death in Trauma Patients who are Alive on Arrival to Hospital."  European Journal of Trauma and Emergency Surgery.  2007; 33: 46-51.

Newgard CD, RH Schmicker, JR Hedges, JP Trickett, DP Davis, EM Bulger, TP Aufderheide, JP Minei, JS Hata, KD Gubler, TB Brown, JD Yelle, B Bardarson, and G Nichol (Resuscitation Outcomes Consortium Investigators).  "Emergency Medical Service Intervals and Survival in Trauma:  Assessment of the 'Golden Hour' in a North American Prospective Cohort."  Annals of Emergency Medicine.  2010 March; 55(3):235-246.