Author Archives: CLIC-EM

07.07.12

by CLIC-EM

Validating the Select Use of ED Thoracotomy

ED thoracotomy  allows for evacuation of pericardial tamponade, direct control of intrathoracic hemorrhage, open cardiac massage, cross-clamping of the descending aorta, and is life-saving inselect patients.  

However, the procedure comes with serious risks including:

1)  Poor survival rates, reported as low as 2%.

2)  High risk exposure to blood borne pathogens.

3)  Commits the patient to an expensive and protracted hospital course.  

Needless to say, the decision to perform this procedure requires serious consideration of medical, social, ethical and economic issues.  

With these issues in mind, a clear clinical decision rule to initiate ED thoracotomy was published by Cothrenet al. based on 26 years of data (Table 1).

TABLE 1.  Indications & Contraindications for the use of ED thoracotomy in Penetrating Thoracic Trauma.

Indication

Witnessed cardiac arrest from penetrating thoracic trauma
+

Signs of Life in the field*

+

Less than 15 minutes of prehospital CPR

Contraindications

No signs of life in the field*

or

Signs of life in the field* + More than 15 minutes of prehospital CPR

*Signs of Life

Spontaneous respirations

Organized cardiac activity

Palpable pulse

Pupillary response

Mollberg et al. at the Mount Sinai Hospital in Chicago appliedthis clinical decision rule's ability to predict mortality after ED thoracotomy.  In 120 patients between 2003 and 2010, ED thoracotomies performed within the bounds of theCothren guidelines yielded 8.6% neurologically intact survivors, while thoracotomies performed outside the guidelines yielded 0% neurologically intact survivors (p=0.040).  

-- Peter Acker MD MPH

References:

Hunt PA, Greaves I, Owens WA.  "Emergency thoracotomy in thoracic trauma--a review." 

Injury, Int J Care Injured (2006) 37, 1--19.

Gomez et al.  "Outcomes in Emergency Room Thoracotomy." The American Surgeon (2010) 76, 406-410.

Mollberg et al. "Emergency Department Thoracotomy Guidelines." Annals of Thoracic Surgery (2011) 92:455-61.

Practice management guidelines for emergency department thoracotomy. Working Group, Ad Hoc Subcommittee on Outcomes, American College of Surgeons-Committee on Trauma.  J Am Coll Surg 2001;193:303-9.

Cothren CC, Moore E.  "Emergency department thoracotomyfor the critically injured patient: objectives, indications, and outcomes." World J Emerg Surg 2006;1:4.

07.07.12

by CLIC-EM

Validating the Select Use of ED Thoracotomy

ED thoracotomy  allows for evacuation of pericardial tamponade, direct control of intrathoracic hemorrhage, open cardiac massage, cross-clamping of the descending aorta, and is life-saving inselect patients.  

However, the procedure comes with serious risks including:

1)  Poor survival rates, reported as low as 2%.

2)  High risk exposure to blood borne pathogens.

3)  Commits the patient to an expensive and protracted hospital course.  

Needless to say, the decision to perform this procedure requires serious consideration of medical, social, ethical and economic issues.  

With these issues in mind, a clear clinical decision rule to initiate ED thoracotomy was published by Cothrenet al. based on 26 years of data (Table 1).

TABLE 1.  Indications & Contraindications for the use of ED thoracotomy in Penetrating Thoracic Trauma.

Indication

Witnessed cardiac arrest from penetrating thoracic trauma
+

Signs of Life in the field*

+

Less than 15 minutes of prehospital CPR

Contraindications

No signs of life in the field*

or

Signs of life in the field* + More than 15 minutes of prehospital CPR

*Signs of Life

Spontaneous respirations

Organized cardiac activity

Palpable pulse

Pupillary response

Mollberg et al. at the Mount Sinai Hospital in Chicago appliedthis clinical decision rule's ability to predict mortality after ED thoracotomy.  In 120 patients between 2003 and 2010, ED thoracotomies performed within the bounds of theCothren guidelines yielded 8.6% neurologically intact survivors, while thoracotomies performed outside the guidelines yielded 0% neurologically intact survivors (p=0.040).  

-- Peter Acker MD MPH

References:

Hunt PA, Greaves I, Owens WA.  "Emergency thoracotomy in thoracic trauma--a review." 

Injury, Int J Care Injured (2006) 37, 1--19.

Gomez et al.  "Outcomes in Emergency Room Thoracotomy." The American Surgeon (2010) 76, 406-410.

Mollberg et al. "Emergency Department Thoracotomy Guidelines." Annals of Thoracic Surgery (2011) 92:455-61.

Practice management guidelines for emergency department thoracotomy. Working Group, Ad Hoc Subcommittee on Outcomes, American College of Surgeons-Committee on Trauma.  J Am Coll Surg 2001;193:303-9.

Cothren CC, Moore E.  "Emergency department thoracotomyfor the critically injured patient: objectives, indications, and outcomes." World J Emerg Surg 2006;1:4.

06.12.12

by CLIC-EM

Bubble Test to Confirm Central Line Placement

One of the more serious complications of central venous catheter (CVC) placement involves arterial puncture and cannullation with a large caliber dialator and catheter.  This occurs in up to 5% of all CVC placement attempts.  

Depending on the location of  CVC placement, inadvertent arterial placement may lead to bleeding, embolism, neurologic injury, airway loss and even death.  Verifying venous placement prior to dilatation, cannulation and infusion of vasoactive agents is essential.

One method of doing so in situations where placement is equivocal by standard methods is with the less-publicized but highly useful bedside echocardiography bubble test.

In order to employ this method during CVC placement, after the target vessel has been entered with the finder needle, insert the finder needle catheter.  Have an assistant place the echo probe in a subcostal position.  Through the finder needle catheter rapidly flush 10cc sterile saline (both agitated and non-agitated have been shown to work).  If the catheter is in the venous system, the right atrium and right ventricle will opacify almost immediately on echo.  If the catheter is in the arterial system, there will be a delay, and then the left atrium and left ventricle will be noted to opacify.

This method can help differentiate between arterial and venous cannulations prior to dilatation and placement of large bore catheters.  It can also be used once a catheter has been placed, to confirm venous placement.  By doing so the user to may confidently identify venous catheter placement prior to chest x-ray.  

-- Peter Acker MD MPH

References:

Blaivas M.  "Video analysis of accidental arterial cannulation with dynamic ultrasound guidance for central venous access."  J Ultrasound Med 2009;28:1239-44.

Ghadiali N, Teo LM, Sheah K.  "Bedside confirmation of a persistent left superior vena cava based on aberrantly positioned central venous catheter on chest radiograph." Br J Anaesth 2006;96:53-6.

Prekker ME, Chang R, Cole JB, Reardon R.  "Rapid confirmation of central venous catheter placement using an ultrasonographic "Bubble Test." Acad Emerg Med 2010;17(7):e85-6.

Sacchetti A, Tapnio C.  "Confirmation of central venous catheter location."  Ann Emerg Med 1991;20(2):219.

Weingart S. "Central Lines." URL:<http://emcrit.org/central-lines>.  Accessed 04/26/12.

06.12.12

by CLIC-EM

Bubble Test to Confirm Central Line Placement

One of the more serious complications of central venous catheter (CVC) placement involves arterial puncture and cannullation with a large caliber dialator and catheter.  This occurs in up to 5% of all CVC placement attempts.  

Depending on the location of  CVC placement, inadvertent arterial placement may lead to bleeding, embolism, neurologic injury, airway loss and even death.  Verifying venous placement prior to dilatation, cannulation and infusion of vasoactive agents is essential.

One method of doing so in situations where placement is equivocal by standard methods is with the less-publicized but highly useful bedside echocardiography bubble test.

In order to employ this method during CVC placement, after the target vessel has been entered with the finder needle, insert the finder needle catheter.  Have an assistant place the echo probe in a subcostal position.  Through the finder needle catheter rapidly flush 10cc sterile saline (both agitated and non-agitated have been shown to work).  If the catheter is in the venous system, the right atrium and right ventricle will opacify almost immediately on echo.  If the catheter is in the arterial system, there will be a delay, and then the left atrium and left ventricle will be noted to opacify.

This method can help differentiate between arterial and venous cannulations prior to dilatation and placement of large bore catheters.  It can also be used once a catheter has been placed, to confirm venous placement.  By doing so the user to may confidently identify venous catheter placement prior to chest x-ray.  

-- Peter Acker MD MPH

References:

Blaivas M.  "Video analysis of accidental arterial cannulation with dynamic ultrasound guidance for central venous access."  J Ultrasound Med 2009;28:1239-44.

Ghadiali N, Teo LM, Sheah K.  "Bedside confirmation of a persistent left superior vena cava based on aberrantly positioned central venous catheter on chest radiograph." Br J Anaesth 2006;96:53-6.

Prekker ME, Chang R, Cole JB, Reardon R.  "Rapid confirmation of central venous catheter placement using an ultrasonographic "Bubble Test." Acad Emerg Med 2010;17(7):e85-6.

Sacchetti A, Tapnio C.  "Confirmation of central venous catheter location."  Ann Emerg Med 1991;20(2):219.

Weingart S. "Central Lines." URL:<http://emcrit.org/central-lines>.  Accessed 04/26/12.

05.29.12

by CLIC-EM

Affirming the Use of Early Narcotics for Acute Abdominal Pain

Acute abdominal pain accounts for 5-10% of all chief complaints to emergency departments.  There has long been debate regarding the role of analgesia in those presenting with acute abdominal pain.  Concerns of masking symptoms and less precise serial abdominal examinations feature prominently amongst those who advocate that aggressive analgesia is detrimental.  The humanistic desire to treat pain and the dearth of evidence implicating analgesia with decreased diagnostic certainty are frequently cited by those in favor of early analgesia.  Furthermore, newer imaging modalities have significantly altered traditional practice dogma as physical examination along with laboratory evidence suggestive of an acute abdomen are now followed by imaging to further clarify if patients are operative or non-operative candidates.

The Cochrane Review examined this issue in 2011.  Briefly, all randomized controlled trials that addressed adult (>14 years of age) patients presenting with non-traumatic, acute (<1 week duration) abdominal pain treated with opioid analgesics versus no analgesia were included in this meta-analysis (yielding eight trials with a cumulative total of 922 patients).  Six trials utilized morphine, one trial utilized tramadol, and the final employed papaveretum.  The pertinent findings are as follows:

1. Administration of opioid analgesics in patients with acute abdominal pain did not increase the risk of making unsuitable treatment decisions or diagnostic error.
2. Administration of opioid analgesics improved patient comfort compared to placebo.
3. No definitive determination could be made with respect to time-to-disposition.

In summary, there is evidence-based support for the early use of narcotic analgesia in adult patients presenting with non-traumatic, acute abdominal pain.  Further studies to distinguish the superiority of specific opioid analgesics compared to other opioids and non-opioids are needed.  Further research on traumatic abdominal pain would also be of utility.  Finally, further data on the time-to-disposition for patients who receive narcotic analgesia versus those who do not would make a compelling argument either for or against the use of narcotic analgesics.

-- Kunal Sharma MD

Reference:

Manterola C, Vial M, Moraga J, Astudillo P. Analgesia in patients with acute abdominal pain. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD005660. DOI: 10.1002/14651858.CD005660.pub3.

05.29.12

by CLIC-EM

Affirming the Use of Early Narcotics for Acute Abdominal Pain

Acute abdominal pain accounts for 5-10% of all chief complaints to emergency departments.  There has long been debate regarding the role of analgesia in those presenting with acute abdominal pain.  Concerns of masking symptoms and less precise serial abdominal examinations feature prominently amongst those who advocate that aggressive analgesia is detrimental.  The humanistic desire to treat pain and the dearth of evidence implicating analgesia with decreased diagnostic certainty are frequently cited by those in favor of early analgesia.  Furthermore, newer imaging modalities have significantly altered traditional practice dogma as physical examination along with laboratory evidence suggestive of an acute abdomen are now followed by imaging to further clarify if patients are operative or non-operative candidates.

The Cochrane Review examined this issue in 2011.  Briefly, all randomized controlled trials that addressed adult (>14 years of age) patients presenting with non-traumatic, acute (<1 week duration) abdominal pain treated with opioid analgesics versus no analgesia were included in this meta-analysis (yielding eight trials with a cumulative total of 922 patients).  Six trials utilized morphine, one trial utilized tramadol, and the final employed papaveretum.  The pertinent findings are as follows:

1. Administration of opioid analgesics in patients with acute abdominal pain did not increase the risk of making unsuitable treatment decisions or diagnostic error.
2. Administration of opioid analgesics improved patient comfort compared to placebo.
3. No definitive determination could be made with respect to time-to-disposition.

In summary, there is evidence-based support for the early use of narcotic analgesia in adult patients presenting with non-traumatic, acute abdominal pain.  Further studies to distinguish the superiority of specific opioid analgesics compared to other opioids and non-opioids are needed.  Further research on traumatic abdominal pain would also be of utility.  Finally, further data on the time-to-disposition for patients who receive narcotic analgesia versus those who do not would make a compelling argument either for or against the use of narcotic analgesics.

-- Kunal Sharma MD

Reference:

Manterola C, Vial M, Moraga J, Astudillo P. Analgesia in patients with acute abdominal pain. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD005660. DOI: 10.1002/14651858.CD005660.pub3.

04.30.12

by CLIC-EM

The Cunningham Technique for Reduction of Shoulder Dislocations

Dislocation of the shoulder joint is the most common major joint dislocation¹ and is a presenting complaint that every emergency physician must be familiar with.  The incidence of shoulder dislocations in the US has been estimated at 23.9 per 100,000 person-years² and of these, 95-97% are anterior dislocations.  Often procedural sedation is used to reduce shoulder dislocations which is not without its own risks, ties up nursing staff and increases length of stay in the Emergency Department³.   The Cunningham technique4 for shoulder reduction, described below, offers a method that does not require sedation and inflicts little to no pain on your patients.

Before getting started it should be noted that this technique works best with a calm, cooperative patient.  The reduction should be painless for the patient, however the patient has to believe you when you assure them of this and must be able to relax.

The first step is to get yourself and the patient into proper position.  Have the patient sit upright in a chair or on the side of the bed with their legs hanging off the side.  Position yourself directly opposite the patient by either kneeling alongside them if they are in a chair or standing if they are in the bed.  The patient should have the affected shoulder completely adducted.  This may by difficult in obese patients as their body habitus will not allow for complete adduction.  The patient should then rest their hand on your shoulder.  You should be close enough to the patient so they are not reaching for you.  You should then gently rest your wrist on the patient's forearm.  Avoid pulling down on the patient's arm as this will cause muscle spasm and pain.

The next step is to reduce spasm and relax the patient by massaging the shoulder muscles.  You can start by massaging the trapezius, moving to the deltoid and then massaging the biceps at the level of the mid humerus.  While massaging the shoulder muscles ask the patient to shrug their shoulders superiorly and posteriorly.  You can do this by asking them to sit up straight, push their chest out and shoulders back.  Remind the patient to try and stay as relaxed as possible and the humeral head should slide back into place.  Warn the patient that they may feel a strange sensation when the humeral head begins to slip into place but to try and stay relaxed and maneuver will be successful.  

Take a look at a few clips of Dr. Cunningham performing the technique:

http://www.youtube.com/watch?v=6h4-uBv27Vs


http://www.youtube.com/watch?v=jIVjVRXo79w

-Megan Stultz MD

References:

1. Westin CD, Gill EA, Noyes ME, Hubbard M. Anterior shoulder dislocation. A simple and rapid method for reduction. Am J Sports Med. May-Jun 1995; 23(3): 369-71.
2. Zacchilli MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010 Mar; 92(3): 542-9.
3. Jamali S. Anterior shoulder dislocation- seated versus traditional reduction technique. Aust Fam Physician. 2011 Mar; 40(3): 133-7.
4. http://shoulderdislocation.net

04.30.12

by CLIC-EM

The Cunningham Technique for Reduction of Shoulder Dislocations

Dislocation of the shoulder joint is the most common major joint dislocation¹ and is a presenting complaint that every emergency physician must be familiar with.  The incidence of shoulder dislocations in the US has been estimated at 23.9 per 100,000 person-years² and of these, 95-97% are anterior dislocations.  Often procedural sedation is used to reduce shoulder dislocations which is not without its own risks, ties up nursing staff and increases length of stay in the Emergency Department³.   The Cunningham technique4 for shoulder reduction, described below, offers a method that does not require sedation and inflicts little to no pain on your patients.

Before getting started it should be noted that this technique works best with a calm, cooperative patient.  The reduction should be painless for the patient, however the patient has to believe you when you assure them of this and must be able to relax.

The first step is to get yourself and the patient into proper position.  Have the patient sit upright in a chair or on the side of the bed with their legs hanging off the side.  Position yourself directly opposite the patient by either kneeling alongside them if they are in a chair or standing if they are in the bed.  The patient should have the affected shoulder completely adducted.  This may by difficult in obese patients as their body habitus will not allow for complete adduction.  The patient should then rest their hand on your shoulder.  You should be close enough to the patient so they are not reaching for you.  You should then gently rest your wrist on the patient's forearm.  Avoid pulling down on the patient's arm as this will cause muscle spasm and pain.

The next step is to reduce spasm and relax the patient by massaging the shoulder muscles.  You can start by massaging the trapezius, moving to the deltoid and then massaging the biceps at the level of the mid humerus.  While massaging the shoulder muscles ask the patient to shrug their shoulders superiorly and posteriorly.  You can do this by asking them to sit up straight, push their chest out and shoulders back.  Remind the patient to try and stay as relaxed as possible and the humeral head should slide back into place.  Warn the patient that they may feel a strange sensation when the humeral head begins to slip into place but to try and stay relaxed and maneuver will be successful.  

Take a look at a few clips of Dr. Cunningham performing the technique:

http://www.youtube.com/watch?v=6h4-uBv27Vs


http://www.youtube.com/watch?v=jIVjVRXo79w

-Megan Stultz MD

References:

1. Westin CD, Gill EA, Noyes ME, Hubbard M. Anterior shoulder dislocation. A simple and rapid method for reduction. Am J Sports Med. May-Jun 1995; 23(3): 369-71.
2. Zacchilli MA, Owens BD. Epidemiology of shoulder dislocations presenting to emergency departments in the United States. J Bone Joint Surg Am. 2010 Mar; 92(3): 542-9.
3. Jamali S. Anterior shoulder dislocation- seated versus traditional reduction technique. Aust Fam Physician. 2011 Mar; 40(3): 133-7.
4. http://shoulderdislocation.net

04.17.12

by CLIC-EM

Passive Leg Raise & Hemodynamics in the ED

Without adequate tissue delivery of oxygen, early shock states quickly progress to multi-organ dysfunction syndrome (MODS) in critically ill patients.  Early goal directed therapy (EGDT) with aggressive crystalloid resuscitation has been instrumental in halting and reversing a subset of distributive shock states.  

Adequate resuscitation is predicated on correct assessment of the patient's fluid status.  This routinely challenges ED clinicians evaluating patients early in the course of their illness - when they are without central lines and arterial lines, or when ultrasound is equivocal or technically limited.

Under-resuscitation may lead to inappropriate use of vasopressors, while over-resuscitation saddles the ICU team with extended hospital stays to remove volume once a distributive shock

state resolves.  

The shortcomings of central venous pressure (CVP) monitoring as a surrogate for preload are well-known and documented.   Studies have documented that CVP is about as good as a coin-flip with regard to assessing fluid status and responsiveness in the critically ill.

Other methods of measuring fluid-responsiveness have emerged and are seeing fair success.  These include pulse-pressure variation (PPV), bedside IVC ultrasound, plethysmography, and brachial artery peak velocity.  

One low-tech high-quality method to assess fluid responsiveness is the passive leg raise (PLR).  

Steps to performing PLR:

1. Seat the patient upright at 45 degrees with the legs flat.  
2. Hemodynamics are measured in this position (i.e., BP, PPV).  
3. Lie the patient's head flat and raise the legs to 45 degrees. 
4. Repeat hemodynamic measurements.  
5. If BP or PPV increase with the 2nd position, the patient is likely fluid responsive.

Image courtesy of  Hofer C, Cannesson M (9).

The idea behind the PLR is that, in effect, the patient is getting a reversible bolus, moving volume from their lower extremities to their thoracic compartment.  Preload is transiently increased and the Frank-Starling curve  is challenged.  

This test carries a number of characteristics that make it attractive to the ED clinician.  It may be used in patients with arrhythmias and spontaneously breathing patients (unlike pulse pressure variation).  It is reversible - patients who do not need volume will not become overloaded.  

Furthermore, it is easy to employ at the bedside, relatively inexpensive, reproducible by multiple caregivers, and retains an ability to be measured serially at any point in resuscitation.

Beyond the teleological argument, the literature seems to agree.  Changes in a large number of hemodynamic variables (aortic blood flow assessed by esophageal Doppler, continuous cardiac output monitoring, arterial pulse pressure variation) monitored during PLR correlate well with rapid fluid loading (3, 4, 5, 6, 8).

Unfortunately PLR is not usable in all patients.  In the severely hypovolemic, the volume of fluid in the lower extremities may not be adequate to have a measurable effect on preload and all related hemodynamic variables.  Likewise,PLR has also been shown to be a poor predictor of fluid responsiveness in patients with intra-abdominal hypertension (7).

-- Peter Acker MD MPH

References:

1) Marik P.  "Hemodynamic Parameters to Guide Fluid Therapy."  Transfusion Alternatives in Transfusion Med. 2010;11(3):102-112.

2) Marik PE, Baram M, Vahid B.  "Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares." Chest 2008 Jul;134(1):172-8.

3) Boulain T, Achard JM, Teboul JL, et al. "Changes in BP induced by passive leg raising predict response to fluid loading in critically ill patients." Chest 2002; 121:1245?1252.

4) Monnet X, Rienzo M, Osman D, et al. "Passive leg raising predicts fluid responsiveness in the critically ill." Crit Care Med 2006; 34:1402-1407.

5) Lafanechere A, Pene F, Goulenok C, et al. "Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients." Crit Care 2006; 10:R132.

6) Preau S, Saulnier F, et al. "Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis." Crit Care Med 2010 Mar;38(3):819-25.

7) Mahjoub Y, Touzeau J, et al. "The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension." Crit Care Med 2010 Sept; 38 (9): 1824-1829.

8) Maizel J, Airapetian N, Lorne E, et al.  "Diagnosis of central hypovolemia by using passive leg raising."  Intensive Care Med 2007; 33:1133-1138.

9) Hofer C, Cannesson M.  "Monitoring fluid responsiveness."  Acta Anaesthesiologica Taiwanica Volume 49, Issue 2, Pages 59-65.

04.17.12

by CLIC-EM

Passive Leg Raise & Hemodynamics in the ED

Without adequate tissue delivery of oxygen, early shock states quickly progress to multi-organ dysfunction syndrome (MODS) in critically ill patients.  Early goal directed therapy (EGDT) with aggressive crystalloid resuscitation has been instrumental in halting and reversing a subset of distributive shock states.  

Adequate resuscitation is predicated on correct assessment of the patient's fluid status.  This routinely challenges ED clinicians evaluating patients early in the course of their illness - when they are without central lines and arterial lines, or when ultrasound is equivocal or technically limited.

Under-resuscitation may lead to inappropriate use of vasopressors, while over-resuscitation saddles the ICU team with extended hospital stays to remove volume once a distributive shock

state resolves.  

The shortcomings of central venous pressure (CVP) monitoring as a surrogate for preload are well-known and documented.   Studies have documented that CVP is about as good as a coin-flip with regard to assessing fluid status and responsiveness in the critically ill.

Other methods of measuring fluid-responsiveness have emerged and are seeing fair success.  These include pulse-pressure variation (PPV), bedside IVC ultrasound, plethysmography, and brachial artery peak velocity.  

One low-tech high-quality method to assess fluid responsiveness is the passive leg raise (PLR).  

Steps to performing PLR:

1. Seat the patient upright at 45 degrees with the legs flat.  
2. Hemodynamics are measured in this position (i.e., BP, PPV).  
3. Lie the patient's head flat and raise the legs to 45 degrees. 
4. Repeat hemodynamic measurements.  
5. If BP or PPV increase with the 2nd position, the patient is likely fluid responsive.

Image courtesy of  Hofer C, Cannesson M (9).

The idea behind the PLR is that, in effect, the patient is getting a reversible bolus, moving volume from their lower extremities to their thoracic compartment.  Preload is transiently increased and the Frank-Starling curve  is challenged.  

This test carries a number of characteristics that make it attractive to the ED clinician.  It may be used in patients with arrhythmias and spontaneously breathing patients (unlike pulse pressure variation).  It is reversible - patients who do not need volume will not become overloaded.  

Furthermore, it is easy to employ at the bedside, relatively inexpensive, reproducible by multiple caregivers, and retains an ability to be measured serially at any point in resuscitation.

Beyond the teleological argument, the literature seems to agree.  Changes in a large number of hemodynamic variables (aortic blood flow assessed by esophageal Doppler, continuous cardiac output monitoring, arterial pulse pressure variation) monitored during PLR correlate well with rapid fluid loading (3, 4, 5, 6, 8).

Unfortunately PLR is not usable in all patients.  In the severely hypovolemic, the volume of fluid in the lower extremities may not be adequate to have a measurable effect on preload and all related hemodynamic variables.  Likewise,PLR has also been shown to be a poor predictor of fluid responsiveness in patients with intra-abdominal hypertension (7).

-- Peter Acker MD MPH

References:

1) Marik P.  "Hemodynamic Parameters to Guide Fluid Therapy."  Transfusion Alternatives in Transfusion Med. 2010;11(3):102-112.

2) Marik PE, Baram M, Vahid B.  "Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares." Chest 2008 Jul;134(1):172-8.

3) Boulain T, Achard JM, Teboul JL, et al. "Changes in BP induced by passive leg raising predict response to fluid loading in critically ill patients." Chest 2002; 121:1245?1252.

4) Monnet X, Rienzo M, Osman D, et al. "Passive leg raising predicts fluid responsiveness in the critically ill." Crit Care Med 2006; 34:1402-1407.

5) Lafanechere A, Pene F, Goulenok C, et al. "Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients." Crit Care 2006; 10:R132.

6) Preau S, Saulnier F, et al. "Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis." Crit Care Med 2010 Mar;38(3):819-25.

7) Mahjoub Y, Touzeau J, et al. "The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension." Crit Care Med 2010 Sept; 38 (9): 1824-1829.

8) Maizel J, Airapetian N, Lorne E, et al.  "Diagnosis of central hypovolemia by using passive leg raising."  Intensive Care Med 2007; 33:1133-1138.

9) Hofer C, Cannesson M.  "Monitoring fluid responsiveness."  Acta Anaesthesiologica Taiwanica Volume 49, Issue 2, Pages 59-65.

04.10.12

by CLIC-EM

Hands On Defibrillation

Only three interventions for cardiac arrest are backed by the literature: early high-quality chest-compressions, early defibrillation, and therapeutic hypothermia.

Wik et al. reported that chest compressions are not delivered for nearly half of the duration of out-of-hospital cardiac arrests, and when performed, compressions are delivered at suboptimal rates and depths.

The proportion of time spent compressing is an easily modified aspect of high-quality cardiopulmonary resuscitation (CPR) and may positively influence patient outcome independent of other known predictors of patient survival to discharge.

High-quality chest compression comprises:
- Appropriate rate (100 per minute)
- Appropriate depth (5 cm or 2 inches), allowing for complete chest wall recoil
- Minimizing periods of interruption

Continuous chest-compression CPR generates the necessary cardio-cerebral perfusion for return of spontaneous circulation (ROSC) and neurologically intact survival at discharge. Christenson et al. demonstrated that the "chest compression fraction" during cardiac arrest is highly prognostic - interruptions in chest compressions decreases the likelihood of survival.

Current recommendations are to stop compressions for no more than 10 seconds during pulse and rhythm check periods as well as for defibrillation if needed. This compression interruption for defibrillation can be decreased by charging the defibrillator during chest compression thereby decreasing "hands off" time required to deliver the defibrillation.

However, the necessity of "hands off" during defibrillation is being challenged. In fact, there is data to suggest current technology makes "hands on defibrillation" both safe and achievable. Biphasic defibrillators with real-time impedance monitoring, adhesive electrodes with more consistent electrode-skin coupling, ECG filtering, and continuous capnography all circumvent the need for rhythm checks and allow for uninterrupted chest compressions.

A 2008 study by Lloyd et al. measured leakage current through mock rescuers performing chest compressions on 43 patients receiving external, biphasic defibrillation. All rescuers were wearing a single pair of polyethylene medical gloves and standing on the patient's right side. Self-adhesive pads were placed in anteroposterior fashion. Shocks were given at 100J, 200J, and 360J. None of the 43 shocks delivered were perceptible to the mock rescuers. Leakage current for 1 of the 43 exceeded the maximum allowable leakage current for handheld equipment. Leakage current for all 43 was an order of magnitude below the allowable leakage current for non-handheld equipment. There were no adverse events.

There is a technical caveat to this promising practice. A response to this study published by an industry representative notes that while medical gloves do offer high insulation resistance, they are not designed for this purpose and cannot be guaranteed to reliably do so. Double gloving offers further protection but has not been studied.

In summary, for patients receiving external shocks from a biphasic defibrillator, there have been no documented adverse outcomes during continuous compressions provided by a healthcare provider wearing intact gloves. Wearing two sets of gloves likely confers additional protection.

While the presented evidence may convince only the most valiant amongst us to perform continuous compressions during defibrillation, it should assuage skepticism and challenge the notion that defibrillatory shocks cannot be administered simultaneously with chest compressions, possibly obviating the needs for "hands off" compressions altogether.

-- Kunal Sharma, MD and Eric Beck, DO, EMT-P


References:

Christenson J, Andrusiek D, Everson-Stewart S, et al. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation; 2009, 120(13):1241-7.

Lloyd MS, Heeke B, Walter PF, and Langberg JJ.  Hands-On Defibrillation : An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External Defibrillation.  Circulation; 2008, 117: 2510-2514.

Sullivan JL.  Letter by Sullivan Regarding Article, "Hands-On Defibrillation: An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External Defibrillation." Circulation; 2008, 118:e712.

Steen S, Liao Q, Pierre L, et al.  The critical importance of minimal delay between chest compressions
and subsequent defibrillation: a haemodynamic explanation.  Resuscitation; 2003, 58: 249-58.

Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA; 2005, 293(3):299-304.

04.10.12

by CLIC-EM

Hands On Defibrillation

Only three interventions for cardiac arrest are backed by the literature: early high-quality chest-compressions, early defibrillation, and therapeutic hypothermia.

Wik et al. reported that chest compressions are not delivered for nearly half of the duration of out-of-hospital cardiac arrests, and when performed, compressions are delivered at suboptimal rates and depths.

The proportion of time spent compressing is an easily modified aspect of high-quality cardiopulmonary resuscitation (CPR) and may positively influence patient outcome independent of other known predictors of patient survival to discharge.

High-quality chest compression comprises:
- Appropriate rate (100 per minute)
- Appropriate depth (5 cm or 2 inches), allowing for complete chest wall recoil
- Minimizing periods of interruption

Continuous chest-compression CPR generates the necessary cardio-cerebral perfusion for return of spontaneous circulation (ROSC) and neurologically intact survival at discharge. Christenson et al. demonstrated that the "chest compression fraction" during cardiac arrest is highly prognostic - interruptions in chest compressions decreases the likelihood of survival.

Current recommendations are to stop compressions for no more than 10 seconds during pulse and rhythm check periods as well as for defibrillation if needed. This compression interruption for defibrillation can be decreased by charging the defibrillator during chest compression thereby decreasing "hands off" time required to deliver the defibrillation.

However, the necessity of "hands off" during defibrillation is being challenged. In fact, there is data to suggest current technology makes "hands on defibrillation" both safe and achievable. Biphasic defibrillators with real-time impedance monitoring, adhesive electrodes with more consistent electrode-skin coupling, ECG filtering, and continuous capnography all circumvent the need for rhythm checks and allow for uninterrupted chest compressions.

A 2008 study by Lloyd et al. measured leakage current through mock rescuers performing chest compressions on 43 patients receiving external, biphasic defibrillation. All rescuers were wearing a single pair of polyethylene medical gloves and standing on the patient's right side. Self-adhesive pads were placed in anteroposterior fashion. Shocks were given at 100J, 200J, and 360J. None of the 43 shocks delivered were perceptible to the mock rescuers. Leakage current for 1 of the 43 exceeded the maximum allowable leakage current for handheld equipment. Leakage current for all 43 was an order of magnitude below the allowable leakage current for non-handheld equipment. There were no adverse events.

There is a technical caveat to this promising practice. A response to this study published by an industry representative notes that while medical gloves do offer high insulation resistance, they are not designed for this purpose and cannot be guaranteed to reliably do so. Double gloving offers further protection but has not been studied.

In summary, for patients receiving external shocks from a biphasic defibrillator, there have been no documented adverse outcomes during continuous compressions provided by a healthcare provider wearing intact gloves. Wearing two sets of gloves likely confers additional protection.

While the presented evidence may convince only the most valiant amongst us to perform continuous compressions during defibrillation, it should assuage skepticism and challenge the notion that defibrillatory shocks cannot be administered simultaneously with chest compressions, possibly obviating the needs for "hands off" compressions altogether.

-- Kunal Sharma, MD and Eric Beck, DO, EMT-P


References:

Christenson J, Andrusiek D, Everson-Stewart S, et al. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation; 2009, 120(13):1241-7.

Lloyd MS, Heeke B, Walter PF, and Langberg JJ.  Hands-On Defibrillation : An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External Defibrillation.  Circulation; 2008, 117: 2510-2514.

Sullivan JL.  Letter by Sullivan Regarding Article, "Hands-On Defibrillation: An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External Defibrillation." Circulation; 2008, 118:e712.

Steen S, Liao Q, Pierre L, et al.  The critical importance of minimal delay between chest compressions
and subsequent defibrillation: a haemodynamic explanation.  Resuscitation; 2003, 58: 249-58.

Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA; 2005, 293(3):299-304.

02.20.12

by CLIC-EM

Procalcitonin in Lower Respiratory Tract Infections

Community-Acquired Pneumonia (CAP) causes significant mortality in the developed world.  Though early treatment with antibiotics is essential, diagnosis is often difficult.  The current diagnostic algorithm relies heavily on non-specific symptoms (cough, fever, sputum) and insensitive tests (chest X-ray) before fully 75% of lower respiratory tract infections (LRTIs) are treated with antibiotics.

The obfuscating nature of this diagnosis and indiscriminate use of antibiotics has generated interest in biomarkers, of which one of the most promising is procalcitonin (PCT) -- a precursor to calcitonin, believed to be released by parenchymal cells in response to infection.

Evidence suggests that its release is either directly induced by microbial toxins, or indirectly by humoral factors in response to bacterial infection.  Alternatively, it is down-regulated in viral infections, attenuated by specific cytokines.  Taken together, these characteristics make it an attractive candidate for LRTI by aiding clinicians in determining which LRTIs are bacterial in nature, and possibly guiding appropriate usage of anti-microbials.  

Several small trials have shown promise forprocalcitonin in this application.  By using PCT levels to guide antibiotic use, overall decreases in antibiotic exposure have been achieved with similar clinical outcomes.  However, these studies have been poorly powered, and are likely not generalizable.

The largest trial to date of PCT as a guide to treatment of LRTI, was the ProHOSP randomized control trial.  This non-inferiority trial assessed primary endpoints of death, ICU admission and disease related complications, along with secondary endpoints of overall antibiotic exposure.  In this study the PCT group received antibiotics based on their PCT scores, while the control group received antibiotics based on predetermined practice guidelines.  

This trial showed no difference in the primary outcome measures (death, ICU admissions, complications) between the two arms.  However,  however this is a difficult conclusion to interpret as PCT-guided antibiotic selection could be suspended at clinician discretion in the sickest subset of the PCT arm (those needing ICU admission, those with hemodynamic and respiratory compromise).  Most of the extremely ill patients in the PCT group ended up receiving antitbiotics regardless of their PCT score, skewing the outcome data against PCT.

The ProHOSP trial also showed that the PCT group was exposed to significantly fewer days antibiotics than the control group (7 vs 10 days).  However antibiotic treatment duration in the control group was determined using outdated treatment guidelines, which preferred 7-10 days of treatment for CAP, while more up to date guidelines recommend a mere 5 days.  Thus patients in the control group were committed to significantly longer treatment periods, although clinical recovery (and in theory PCT decline) likely occurred much earlier.

There is need for a more sensitive and specific diagnostic testing algorithm for LRTIs, as our current practice patterns most certainly lead to overtreatment with antibiotics.  The jury is still out on procalcitonin, but the use of such biomarkers retains much potential in guiding rational diagnosis and treatment.   

-- Peter Acker MD MPH

References:

Christ-Crain M, Stolz D, Bingisser R, et al. Procalcitonin guidance of antibiotic therapy in community-acquired pneumonia: a randomized trial. Am J Respir Crit Care Med 2006; 174:84.

Gilbert D. Procalcitonin as a Biomarker in Respiratory Tract Infection.  Clinical Infectious Disease. 2011: 52; S346-350.

Mandell L, Wunderink R, Anzueto A, et al. IDSA/ATS Concensus Guidelines on the management of CAP in adults. Clinical Infectious Disease. 2007; 44: S27-72.

Schuetz P, Christ-Crain M, Muller B.  Pro-calcitonin and other biomarkers for the assessment of disease severity and guidance of treatment in bacterial infections.  Advances in Sepsis: 2008; 3: 82.

Schuetz P, Christ-Crain M, Thomann R, et al. Effect of procalcitonin-based guidelines vs standard guidelines on antibiotic use in lower respiratory tract infections: the ProHOSP randomized controlled trial. JAMA 2009; 302:1059.

Talan D, Procalcitonin: The Uber WBC Count? Emergency Medicine News. 2011; 33 (1): 16-17.

Woodhead M, Blasi F, Ewig S, et al. Guidelines for the management of adult lower respiratory tract infections. European Respiratory Journal. 2005; 26(6):1138-1180.

02.20.12

by CLIC-EM

Procalcitonin in Lower Respiratory Tract Infections

Community-Acquired Pneumonia (CAP) causes significant mortality in the developed world.  Though early treatment with antibiotics is essential, diagnosis is often difficult.  The current diagnostic algorithm relies heavily on non-specific symptoms (cough, fever, sputum) and insensitive tests (chest X-ray) before fully 75% of lower respiratory tract infections (LRTIs) are treated with antibiotics.

The obfuscating nature of this diagnosis and indiscriminate use of antibiotics has generated interest in biomarkers, of which one of the most promising is procalcitonin (PCT) -- a precursor to calcitonin, believed to be released by parenchymal cells in response to infection.

Evidence suggests that its release is either directly induced by microbial toxins, or indirectly by humoral factors in response to bacterial infection.  Alternatively, it is down-regulated in viral infections, attenuated by specific cytokines.  Taken together, these characteristics make it an attractive candidate for LRTI by aiding clinicians in determining which LRTIs are bacterial in nature, and possibly guiding appropriate usage of anti-microbials.  

Several small trials have shown promise forprocalcitonin in this application.  By using PCT levels to guide antibiotic use, overall decreases in antibiotic exposure have been achieved with similar clinical outcomes.  However, these studies have been poorly powered, and are likely not generalizable.

The largest trial to date of PCT as a guide to treatment of LRTI, was the ProHOSP randomized control trial.  This non-inferiority trial assessed primary endpoints of death, ICU admission and disease related complications, along with secondary endpoints of overall antibiotic exposure.  In this study the PCT group received antibiotics based on their PCT scores, while the control group received antibiotics based on predetermined practice guidelines.  

This trial showed no difference in the primary outcome measures (death, ICU admissions, complications) between the two arms.  However,  however this is a difficult conclusion to interpret as PCT-guided antibiotic selection could be suspended at clinician discretion in the sickest subset of the PCT arm (those needing ICU admission, those with hemodynamic and respiratory compromise).  Most of the extremely ill patients in the PCT group ended up receiving antitbiotics regardless of their PCT score, skewing the outcome data against PCT.

The ProHOSP trial also showed that the PCT group was exposed to significantly fewer days antibiotics than the control group (7 vs 10 days).  However antibiotic treatment duration in the control group was determined using outdated treatment guidelines, which preferred 7-10 days of treatment for CAP, while more up to date guidelines recommend a mere 5 days.  Thus patients in the control group were committed to significantly longer treatment periods, although clinical recovery (and in theory PCT decline) likely occurred much earlier.

There is need for a more sensitive and specific diagnostic testing algorithm for LRTIs, as our current practice patterns most certainly lead to overtreatment with antibiotics.  The jury is still out on procalcitonin, but the use of such biomarkers retains much potential in guiding rational diagnosis and treatment.   

-- Peter Acker MD MPH

References:

Christ-Crain M, Stolz D, Bingisser R, et al. Procalcitonin guidance of antibiotic therapy in community-acquired pneumonia: a randomized trial. Am J Respir Crit Care Med 2006; 174:84.

Gilbert D. Procalcitonin as a Biomarker in Respiratory Tract Infection.  Clinical Infectious Disease. 2011: 52; S346-350.

Mandell L, Wunderink R, Anzueto A, et al. IDSA/ATS Concensus Guidelines on the management of CAP in adults. Clinical Infectious Disease. 2007; 44: S27-72.

Schuetz P, Christ-Crain M, Muller B.  Pro-calcitonin and other biomarkers for the assessment of disease severity and guidance of treatment in bacterial infections.  Advances in Sepsis: 2008; 3: 82.

Schuetz P, Christ-Crain M, Thomann R, et al. Effect of procalcitonin-based guidelines vs standard guidelines on antibiotic use in lower respiratory tract infections: the ProHOSP randomized controlled trial. JAMA 2009; 302:1059.

Talan D, Procalcitonin: The Uber WBC Count? Emergency Medicine News. 2011; 33 (1): 16-17.

Woodhead M, Blasi F, Ewig S, et al. Guidelines for the management of adult lower respiratory tract infections. European Respiratory Journal. 2005; 26(6):1138-1180.

02.07.12

by CLIC-EM

The Mellick Method for Pediatric Laryngoscope Selection

Most emergency physicians (EPs) do not find themselves intubating sick children with any routine frequency.  However ,when faced with this critical situation, EPs often rely on the Broselow tape to assist with medication dosing and equipment sizing.  In some instances, a Broselow tape may not be readily available or the age/weight/height of the patient may be lacking.  In these circumstances, it is useful to have a method for rapid selection of the correct Mac or Miller blade to ensure successful intubation.

In an original article published in 2006 in Pediatric Emergency Care, Mellick and colleagues identified a novel technique to estimate pediatric blade sizing using facial landmarks that are easily accessible and adjust with age.  This method is analogous to the visual cues for selecting OP and NP airways with which we are quite familiar.  A 2-step summary of the method is listed below:

Step 1

Identify the lateral incisor and aim the pediatric blade toward the angle of mandible.

Measure from the base block of the blade to the tip of the blade.

Image Courtesy of Larry Mellick, MD

Step 2

The tip of the blade should be within 1 cm of the angle of the mandible.  

If it is too short, select the next longer blade size.  

If it is too long, select the next shorter blade size.

Image Courtesy of Larry Mellick, MD

This method was prospectively evaluated by Mellick et al. and the correct estimated blade size with this method was associated with fewer repeat attempts and fewer failed intubations.  In this study, the most common error resulting in multiple attempts or failed intubation was use of a blade sized shorter than necessary.

As a validated rapid assessment tool in the emergency physician's airway armamentarium, the Mellick method may make all the difference when seconds count.

-- Rohith Malya MD

Reference:

Mellick LB, Edholm T, and Corbett SW.  "Pediatric laryngoscope blade size selection utilizing facial landmarks."  Pediatric Emergency Care.  2006 Apr;22(4):226-9.

02.07.12

by CLIC-EM

The Mellick Method for Pediatric Laryngoscope Selection

Most emergency physicians (EPs) do not find themselves intubating sick children with any routine frequency.  However ,when faced with this critical situation, EPs often rely on the Broselow tape to assist with medication dosing and equipment sizing.  In some instances, a Broselow tape may not be readily available or the age/weight/height of the patient may be lacking.  In these circumstances, it is useful to have a method for rapid selection of the correct Mac or Miller blade to ensure successful intubation.

In an original article published in 2006 in Pediatric Emergency Care, Mellick and colleagues identified a novel technique to estimate pediatric blade sizing using facial landmarks that are easily accessible and adjust with age.  This method is analogous to the visual cues for selecting OP and NP airways with which we are quite familiar.  A 2-step summary of the method is listed below:

Step 1

Identify the lateral incisor and aim the pediatric blade toward the angle of mandible.

Measure from the base block of the blade to the tip of the blade.

Image Courtesy of Larry Mellick, MD

Step 2

The tip of the blade should be within 1 cm of the angle of the mandible.  

If it is too short, select the next longer blade size.  

If it is too long, select the next shorter blade size.

Image Courtesy of Larry Mellick, MD

This method was prospectively evaluated by Mellick et al. and the correct estimated blade size with this method was associated with fewer repeat attempts and fewer failed intubations.  In this study, the most common error resulting in multiple attempts or failed intubation was use of a blade sized shorter than necessary.

As a validated rapid assessment tool in the emergency physician's airway armamentarium, the Mellick method may make all the difference when seconds count.

-- Rohith Malya MD

Reference:

Mellick LB, Edholm T, and Corbett SW.  "Pediatric laryngoscope blade size selection utilizing facial landmarks."  Pediatric Emergency Care.  2006 Apr;22(4):226-9.

01.31.12

by CLIC-EM

Succinylcholine in Pediatric RSI

We pediatricians have been a little unfair to succinylcholine. As the sole depolarizing paralytic, and the one with the fastest on (30-60 seconds) and off (4-6 minutes) times, it is an essential medication to have in our RSI arsenal.  Many myths of its contraindications have been perpetuated.  When do we really need to avoid it in the pediatric patient?

Victims of crush or burn injuries?

The potential development of hyperkalemia with succinylcholine administration is not an acute concern for crush or burn injury victims.  Remember, the problem is that extensively damaged skeletal muscle responds by up-regulating its acetylcholine receptors, and it's the presence of these increased receptors that potentiates the release of intracellular potassium. However, the upregulation of these receptors is a process which takes hours - well over 24 hours - not minutes.  The injury victim in rehab who acutely decompensates and requires RSI should receive only non depolarizing paralytics, but succinylcholine can be safely used in the immediate resuscitation of victims of crush or burn injuries.

Children with head injury?

Pediatric trauma victims not uncommonly suffer head injury and the concern for potential increased intracranial pressure is high. Succinylcholine was found to increase the intracranial pressure of a few animal models and in some smaller studies looking at patients with known brain tumors - but this has not translated to the pediatric trauma bay very well. Unless there are other concerns about the use of succinylcholine for a particular patient, isolated head injury should not be a contraindication to its use.

Children with potential neuromuscular disorders?

The potential for developing malignant hyperthermia and/or hyperkalemia with succinylcholine is very real in these patients.  School-age children and older will already carry a known diagnosis (or at the very least, have an obvious neuromuscular abnormality) and it is a straightforward decision to avoid succinylcholine in this group.  Unfortunately, the diagnosis may not be known or suspected in the very young patient.  Caution should be exercised in young children (toddlers and under) who have any concern for developmental delay.  The most common muscular dystrophies - Duchenne and Becker - are X-linked recessive, by the way, so you could be fancy and use non depolarizing agents in all very young boys.

Myasthenic crisis?

The problem in myasthenia gravis is a little different than with other neuromuscular disorders, because rather than upregulating acetylcholine receptors, these patients have fewer receptors.  As a result, succinylcholine is difficult to use -- though it shouldn't cause hyperkalemia or cardiovascular instability, higher doses are required to achieve paralysis and the effect will be prolonged.  Given its unpredictability in this regard, use of a non depolarizing agent for RSI in the setting of myasthenic crisis makes the most sense.

-- Lisa McQueen MD

References:

Levitan R.  "Safety of succinylcholine in myasthenia gravis." Annals of Emergency Medicine 2005;45:225-56.

Walls, RM (ed).  Manual of Emergency Airway Management. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

Zelicof-Paul, A et al.  "Controversies in rapid sequence intubation in children."  Current Opinions in Pediatrics 2005;17:355-62.

01.31.12

by CLIC-EM

Succinylcholine in Pediatric RSI

We pediatricians have been a little unfair to succinylcholine. As the sole depolarizing paralytic, and the one with the fastest on (30-60 seconds) and off (4-6 minutes) times, it is an essential medication to have in our RSI arsenal.  Many myths of its contraindications have been perpetuated.  When do we really need to avoid it in the pediatric patient?

Victims of crush or burn injuries?

The potential development of hyperkalemia with succinylcholine administration is not an acute concern for crush or burn injury victims.  Remember, the problem is that extensively damaged skeletal muscle responds by up-regulating its acetylcholine receptors, and it's the presence of these increased receptors that potentiates the release of intracellular potassium. However, the upregulation of these receptors is a process which takes hours - well over 24 hours - not minutes.  The injury victim in rehab who acutely decompensates and requires RSI should receive only non depolarizing paralytics, but succinylcholine can be safely used in the immediate resuscitation of victims of crush or burn injuries.

Children with head injury?

Pediatric trauma victims not uncommonly suffer head injury and the concern for potential increased intracranial pressure is high. Succinylcholine was found to increase the intracranial pressure of a few animal models and in some smaller studies looking at patients with known brain tumors - but this has not translated to the pediatric trauma bay very well. Unless there are other concerns about the use of succinylcholine for a particular patient, isolated head injury should not be a contraindication to its use.

Children with potential neuromuscular disorders?

The potential for developing malignant hyperthermia and/or hyperkalemia with succinylcholine is very real in these patients.  School-age children and older will already carry a known diagnosis (or at the very least, have an obvious neuromuscular abnormality) and it is a straightforward decision to avoid succinylcholine in this group.  Unfortunately, the diagnosis may not be known or suspected in the very young patient.  Caution should be exercised in young children (toddlers and under) who have any concern for developmental delay.  The most common muscular dystrophies - Duchenne and Becker - are X-linked recessive, by the way, so you could be fancy and use non depolarizing agents in all very young boys.

Myasthenic crisis?

The problem in myasthenia gravis is a little different than with other neuromuscular disorders, because rather than upregulating acetylcholine receptors, these patients have fewer receptors.  As a result, succinylcholine is difficult to use -- though it shouldn't cause hyperkalemia or cardiovascular instability, higher doses are required to achieve paralysis and the effect will be prolonged.  Given its unpredictability in this regard, use of a non depolarizing agent for RSI in the setting of myasthenic crisis makes the most sense.

-- Lisa McQueen MD

References:

Levitan R.  "Safety of succinylcholine in myasthenia gravis." Annals of Emergency Medicine 2005;45:225-56.

Walls, RM (ed).  Manual of Emergency Airway Management. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

Zelicof-Paul, A et al.  "Controversies in rapid sequence intubation in children."  Current Opinions in Pediatrics 2005;17:355-62.

01.26.12

by CLIC-EM

Know Before You Push — Adenosine

This is the first in a series of articles focusing on important pharmacologic agents used in emergency medicine.  Key principles of dosing, administration, efficacy are reviewed in an evidenced based format.  Special attention is also given to the rare, uncommon, and/or under-appreciated effects of these medications.

Optimizing Vagal Maneuvers

Vagal maneuvers are recommended as an initial treatment of SVT, especially after immediate onset of tachycardia.  In a 1988 Lancet paper, vagal maneuvers were tested in 35 patients with SVT, with each maneuver used up to three times in an attempt to terminate tachycardia.  The Valsalva maneuver in the supine position was most effective, terminating SVT in 54% of cases.  Right carotid massage was only effective in 17% of cases, left carotid massage in 5% of cases, and the diving reflex in 17% of cases.  

Adenosine or CCB

When SVT is treated pharmacologically, adenosine and calcium channel blockers are frequently utilized to slow conduction for rate control and rhythm identification.  

A 2009 Cochrane Review found no significant difference in reversion or relapse rate betweenIV calcium channel blockers (CCB) and adenosine in the treatment of SVT. 

Time to reversion to sinus rhythm for verapamil was noted to be slower than adenosine in all studies reviewed.  Hypotension associated with verapamil use was more likely to be seen as a major adverse effect. However, side effects including nausea, chest tightness, dyspnea, and headache were more frequent with adenosine (10.8%) when compared with verapamil (0.6%).

Proarrhythmic Effects

Although widely used and generally safe, arrhythmias associated with the administration of adenosine have been well described.  Mallet reviewed the literature on the proarrhythmic effects of adenosine in 2004.  He noted that severe bradycardias and tachyarrhythmias induced by adenosine had been reported in over a decade of literature.

Enhanced effects of adenosine can be seen in the elderly, patients with sinus node dysfunction, patients taking dipyridamole, carbamazepine, digoxin, verapamil, and beta blockers.

Reduced efficacy of adenosine can be seen in patient taking theophylline and caffeine. Patients with a history of recurrent palpitations (suggesting possibility of latent pre-excitation or dual AV node physiology) should be monitored for the  induction of unstable tachydysrhythmias.

Dosing Considerations

Cairns et al. reported in 1991 that using an initial 12mg dose of IV adenosine increases the likelihood of conversion with a single dose without additional harm.  In contradistinction, dosing of adenosine should also be lowered in cardiac transplant patients to 1-3 mg IV, as these patients are particularly sensitive to adenosine.

-- Eric Beck, DO, EMT-P

References:

Mehta D, et al.  "Relative Efficacy of Various Physicial Manoeuvres in the Termination of Junctional Tachycardia." The Lancet, May 28, 1988, 1181-1185.

Cairns C, et al. "Intavenous Adenosine in the Emergency Department Mangement of Paroxysmal Supraventricular Tachycardia." Annals of Emergency Medicine. 1991;20:7, 717-721.

Mallet M.  "Proarrhythmic effects of adenosine: a review of the literature." Emerg Med J. 2004;21:408-410.

Holdgate A, Foo A.  "Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults (Review)."  The Cochrane Library. 2009:1.

01.26.12

by CLIC-EM

Know Before You Push — Adenosine

This is the first in a series of articles focusing on important pharmacologic agents used in emergency medicine.  Key principles of dosing, administration, efficacy are reviewed in an evidenced based format.  Special attention is also given to the rare, uncommon, and/or under-appreciated effects of these medications.

Optimizing Vagal Maneuvers

Vagal maneuvers are recommended as an initial treatment of SVT, especially after immediate onset of tachycardia.  In a 1988 Lancet paper, vagal maneuvers were tested in 35 patients with SVT, with each maneuver used up to three times in an attempt to terminate tachycardia.  The Valsalva maneuver in the supine position was most effective, terminating SVT in 54% of cases.  Right carotid massage was only effective in 17% of cases, left carotid massage in 5% of cases, and the diving reflex in 17% of cases.  

Adenosine or CCB

When SVT is treated pharmacologically, adenosine and calcium channel blockers are frequently utilized to slow conduction for rate control and rhythm identification.  

A 2009 Cochrane Review found no significant difference in reversion or relapse rate betweenIV calcium channel blockers (CCB) and adenosine in the treatment of SVT. 

Time to reversion to sinus rhythm for verapamil was noted to be slower than adenosine in all studies reviewed.  Hypotension associated with verapamil use was more likely to be seen as a major adverse effect. However, side effects including nausea, chest tightness, dyspnea, and headache were more frequent with adenosine (10.8%) when compared with verapamil (0.6%).

Proarrhythmic Effects

Although widely used and generally safe, arrhythmias associated with the administration of adenosine have been well described.  Mallet reviewed the literature on the proarrhythmic effects of adenosine in 2004.  He noted that severe bradycardias and tachyarrhythmias induced by adenosine had been reported in over a decade of literature.

Enhanced effects of adenosine can be seen in the elderly, patients with sinus node dysfunction, patients taking dipyridamole, carbamazepine, digoxin, verapamil, and beta blockers.

Reduced efficacy of adenosine can be seen in patient taking theophylline and caffeine. Patients with a history of recurrent palpitations (suggesting possibility of latent pre-excitation or dual AV node physiology) should be monitored for the  induction of unstable tachydysrhythmias.

Dosing Considerations

Cairns et al. reported in 1991 that using an initial 12mg dose of IV adenosine increases the likelihood of conversion with a single dose without additional harm.  In contradistinction, dosing of adenosine should also be lowered in cardiac transplant patients to 1-3 mg IV, as these patients are particularly sensitive to adenosine.

-- Eric Beck, DO, EMT-P

References:

Mehta D, et al.  "Relative Efficacy of Various Physicial Manoeuvres in the Termination of Junctional Tachycardia." The Lancet, May 28, 1988, 1181-1185.

Cairns C, et al. "Intavenous Adenosine in the Emergency Department Mangement of Paroxysmal Supraventricular Tachycardia." Annals of Emergency Medicine. 1991;20:7, 717-721.

Mallet M.  "Proarrhythmic effects of adenosine: a review of the literature." Emerg Med J. 2004;21:408-410.

Holdgate A, Foo A.  "Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults (Review)."  The Cochrane Library. 2009:1.

01.13.12

by CLIC-EM

Reversal of Novel Anticoagulants in the Bleeding Patient

In the last two years, two new oral anticoagulants have been introduced to the market. Despite advantages over their predecessors, these new agents have no proven reversal agent and limited data exists on how to potentially counteract the effects of these new drugs.  This poses a significant challenge to the physician faced with a bleeding patient on these anticoagulants.

        

Dabigatran (Pradaxa, Boehringer Ingelheim, Ridgefield CT), a direct thrombin inhibitor, was approved by the FDA in October of 2010 for prevention of stroke in patients with atrial fibrillation. 

Rivaroxaban (Xarelto, Jannsen, Titusville NJ), is a direct factor Xa inhibitor, was approved by the FDA for DVT prophylaxis in July of 2011 and also for stroke prevention in atrial fibrillation patients in November of 2011.  

Both are taken orally and offer several advantages over warfarin including:  less food and drug interactions, predictable pharmacokinetics, and no need for routine laboratory testing or dose adjustment.  

While PTT and INR assess the anticoagulant effect of heparin and warfarin, respectively, no laboratory test has been shown to adequately assess the levels or anticoagulation effect of the new drugs.  

Activated partial thromboplastin time (aPTT) and thrombin time (TT) are prolonged with these drugs but these tests underestimate drug effects at higher blood concentrations.  Therefore, a prolonged aPTT or TT indicates only that the drug is present but provides no information on how much is present or the extent of anticoagulation -- limiting these tests to qualitative roles only.

While there is no specific reversal agent for these new medications, there are potential management options for bleeding patients on these anticoagulants.  

PCC & FFP

Prothrombin complex concentrate (PCC) contains clotting factors II, IX, X, and thrombin (some also contain VII).

Eerenberg et al. evaluated the effects of PCC on 12 healthy male subjects who were treated with rivaroxaban then given PCC.  The study concluded there was complete reversal of rivaroxaban based on normalization of aPTT and endogenous thrombin potential following administration of PCC.  

This was then repeated with dabigatran and similar rates of reversal were not seen, leading the authors to conclude PCC would be effective in the reversal of rivaroxaban but not dabigatran.  

FFP contains many of the clotting factors in PCCs at a lower concentration, and may be of utility should PCCs be unavailable.

NovoSeven

Recombinant Factor VIIa (NovoSeven, Novo Nordisk, Princeton NJ) directly activates thrombin on the surface of platelets and has been shown to improve laboratory measures of clotting in rats.  Though theoretically useful, no case report or study has confirmed its therapeutic use in reversal of dabigatran or rivaroxaban.

Hemodialysis

There may also be a role for hemodialysis for removal of dabigatran.  Dabigatran has low protein binding, a moderate volume of distribution, and is a small molecule -- all properties making it amenable to dialysis.  

In one study where dabigatran was given to 6 patients with ESRD  on hemodialysis, it was estimated that 62% of the drug was removed by 2 hours and 68% by 4 hours of hemodialysis.  

Dialysis would not be an option for rivaroxaban as it is 95% protein bound.  

A simplified algorithm to managing bleeding patients on these anticoagulants is shown below:

Management of Dabigatran and Rivaroxaban Related Bleeding

Bleeding Severity	Management Recommendations
Mild	Delay next dose or discontinue dabigatran
Moderate to Severe	Symptomatic treatment Mechanical compression Surgical intervention Fluid replacement and hemodynamic support Blood product transfusion Oral charcoal (will adsorb drug if ingestion < 2 hours) Hemodialysis*
Life-threatening Bleeding	All the same treatment modalities as Moderate to Severe bleeding Consideration of PCC, rFVIIa, FFP Hemodialysis*

*Hemodialysis is not recommended for rivaroxaban

-- Megan Stultz MD

References:

Crowther MA. Managing bleeding in anticoagulated patients with a focus on novel therapeutic agents. J Thromb Haemost 2009; 7 (Suppl 1):107-110.

van Ryn J. Dabigatran etexilate - a novel, reversible, oral direct thrombin inhibitor: Interpretation of coagulation assays and reversal of anticoagulant activity. Thromb Haemost 2010; 103: 1116-1127.

Eerenberg ES et al. Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate. Circulation. 2011; 124: 1573-1579.

Stangier J, Rathgen K, Stahle H, Mazur D. Influence of renal impairment on the pharmacokinetics and pharmacodynamics of oral dabigatran etexilate: an open-label, parallel-group, single-centre study. Clin Pharmacokineti. 2010; 49: 259-268.

Hankey GJ, Eikelboom JW. Dabigatran etexilate: a new oral thrombin inhibitor. Circulation. 2010; 123: 1436-1450.

Perzborn E, Roehrig S, Straub A, Kubitza D, Mueck W, Laux V. Rivaroxaban: a new oral factor Xa inhibitor. Arterioscler Thromb Vasc Biol. 2010; 30: 376-381.

Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, Wang S, Alings M, Xavier D, Zhu J, Diaz R, Lewis BS, Darius H, Diener HC, Joyner CD, Wallentin L. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009; 361: 1139-1151.

01.13.12

by CLIC-EM

Reversal of Novel Anticoagulants in the Bleeding Patient

In the last two years, two new oral anticoagulants have been introduced to the market. Despite advantages over their predecessors, these new agents have no proven reversal agent and limited data exists on how to potentially counteract the effects of these new drugs.  This poses a significant challenge to the physician faced with a bleeding patient on these anticoagulants.

        

Dabigatran (Pradaxa, Boehringer Ingelheim, Ridgefield CT), a direct thrombin inhibitor, was approved by the FDA in October of 2010 for prevention of stroke in patients with atrial fibrillation. 

Rivaroxaban (Xarelto, Jannsen, Titusville NJ), is a direct factor Xa inhibitor, was approved by the FDA for DVT prophylaxis in July of 2011 and also for stroke prevention in atrial fibrillation patients in November of 2011.  

Both are taken orally and offer several advantages over warfarin including:  less food and drug interactions, predictable pharmacokinetics, and no need for routine laboratory testing or dose adjustment.  

While PTT and INR assess the anticoagulant effect of heparin and warfarin, respectively, no laboratory test has been shown to adequately assess the levels or anticoagulation effect of the new drugs.  

Activated partial thromboplastin time (aPTT) and thrombin time (TT) are prolonged with these drugs but these tests underestimate drug effects at higher blood concentrations.  Therefore, a prolonged aPTT or TT indicates only that the drug is present but provides no information on how much is present or the extent of anticoagulation -- limiting these tests to qualitative roles only.

While there is no specific reversal agent for these new medications, there are potential management options for bleeding patients on these anticoagulants.  

PCC & FFP

Prothrombin complex concentrate (PCC) contains clotting factors II, IX, X, and thrombin (some also contain VII).

Eerenberg et al. evaluated the effects of PCC on 12 healthy male subjects who were treated with rivaroxaban then given PCC.  The study concluded there was complete reversal of rivaroxaban based on normalization of aPTT and endogenous thrombin potential following administration of PCC.  

This was then repeated with dabigatran and similar rates of reversal were not seen, leading the authors to conclude PCC would be effective in the reversal of rivaroxaban but not dabigatran.  

FFP contains many of the clotting factors in PCCs at a lower concentration, and may be of utility should PCCs be unavailable.

NovoSeven

Recombinant Factor VIIa (NovoSeven, Novo Nordisk, Princeton NJ) directly activates thrombin on the surface of platelets and has been shown to improve laboratory measures of clotting in rats.  Though theoretically useful, no case report or study has confirmed its therapeutic use in reversal of dabigatran or rivaroxaban.

Hemodialysis

There may also be a role for hemodialysis for removal of dabigatran.  Dabigatran has low protein binding, a moderate volume of distribution, and is a small molecule -- all properties making it amenable to dialysis.  

In one study where dabigatran was given to 6 patients with ESRD  on hemodialysis, it was estimated that 62% of the drug was removed by 2 hours and 68% by 4 hours of hemodialysis.  

Dialysis would not be an option for rivaroxaban as it is 95% protein bound.  

A simplified algorithm to managing bleeding patients on these anticoagulants is shown below:

Management of Dabigatran and Rivaroxaban Related Bleeding

Bleeding Severity	Management Recommendations
Mild	Delay next dose or discontinue dabigatran
Moderate to Severe	Symptomatic treatment Mechanical compression Surgical intervention Fluid replacement and hemodynamic support Blood product transfusion Oral charcoal (will adsorb drug if ingestion < 2 hours) Hemodialysis*
Life-threatening Bleeding	All the same treatment modalities as Moderate to Severe bleeding Consideration of PCC, rFVIIa, FFP Hemodialysis*

*Hemodialysis is not recommended for rivaroxaban

-- Megan Stultz MD

References:

Crowther MA. Managing bleeding in anticoagulated patients with a focus on novel therapeutic agents. J Thromb Haemost 2009; 7 (Suppl 1):107-110.

van Ryn J. Dabigatran etexilate - a novel, reversible, oral direct thrombin inhibitor: Interpretation of coagulation assays and reversal of anticoagulant activity. Thromb Haemost 2010; 103: 1116-1127.

Eerenberg ES et al. Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate. Circulation. 2011; 124: 1573-1579.

Stangier J, Rathgen K, Stahle H, Mazur D. Influence of renal impairment on the pharmacokinetics and pharmacodynamics of oral dabigatran etexilate: an open-label, parallel-group, single-centre study. Clin Pharmacokineti. 2010; 49: 259-268.

Hankey GJ, Eikelboom JW. Dabigatran etexilate: a new oral thrombin inhibitor. Circulation. 2010; 123: 1436-1450.

Perzborn E, Roehrig S, Straub A, Kubitza D, Mueck W, Laux V. Rivaroxaban: a new oral factor Xa inhibitor. Arterioscler Thromb Vasc Biol. 2010; 30: 376-381.

Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, Wang S, Alings M, Xavier D, Zhu J, Diaz R, Lewis BS, Darius H, Diener HC, Joyner CD, Wallentin L. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009; 361: 1139-1151.

01.03.12

by CLIC-EM

Algorithm-based Treatment of Hidradenitis Suppurativa

Hidradenitis Suppurativa (HS) is a chronic, painful, debilitating disease that is poorly understood and with ill-defined treatment.  It affects approximately 4% of the US population, and frequently brings patients to the ER with pain and inflammation (1).  Due to the unclear nature and treatment, this condition is dealt with in many ways, some with poor outcomes, leading to increased morbidity and necessitating more radical treatments downstream.

The disease is diagnosed by the confluence of three criteria (2):

1. Typical lesions: multiple deep seated nodules and fibrosis
2. Typical locations (areas with apocrine glands): groin, axilla, perineal, peri-anal and infra-mammary regions
3. Chronicity and relapse

The underlying cause is debated but currently thought to be occlusion of the terminal follicular acro-infundibulum, which causes follicular duct expansion, wall rupture, antigen release and resulting inflammation (2).   Bacterial infection was long thought to be part of the disorder, leading to wide use of antibiotics for treatment (3,4).  

However approximately half of HS lesions are sterile upon culture (S. aureus and S. epidermidis being the most common isolates in non-sterile cultures),  indicating that other inflammatory processes are at work as well (4).  

Due to the unclear underlying etiology of HS, it has been difficult to target therapy for this disease process.  Numerous treatment modalities have been offered with varying success: antibiotics, immunosuppresants, anti-inflammatory medications, isotretinoins, surgical unroofing, classic I & D, and surgical excision (5).
 
Current treatment recommendations vary based on stage of the disease utilizing the Hurley Staging System (6):

Stage I: One or more abscesses with no sinus tract or scarring.
Stage II: One or more widely separated recurrent abscesses, with a tract and scarring.
Stage III: Multiple interconnected tracts and abscesses through the entire affected area.

After extensive research, a number of treatment modalities have proven themselves to be more efficacious, although none appear perfect.  Some are easily implemented in the ER, while others are better tolerated in the hands of a  specialist.  A treatment algorithm based on the Hurley Staging System is offered below.

Hurley Stage	ER Treatments
General (all stages)	-Minimize trauma, wear loose fitting clothes -Quit smoking (7) -Avoid anti-perspirants -Avoid high pH soaps -Do not shave affected areas
Stage I	Topical ABX8,9        -Clindamycin 1% BID X 12 weeks Topical ABX failures -> Oral antibiotics  X 7-10 days9,10       -Tetracycline 250-500 mg QID       -Doxycycline 100 mg BID       -Clindamycin 300 mg BID       -Augmentin 500 mg-1 g TID Dermatology referral       -Intra-lesional steroid injections       -Anti-androgen initiation
Stage II	Oral ABX (same as Stage I) Severe cases:       -Rifampin + Clindamycin combination therapy                     -Clindamycin 300 mg BID + Rifampin 300 mg BID X 3 months11,12 Referral to surgery for unroofing
Stage III	Employ same treatment principles from Stage I & II Surgical referral

Notably, classic incision and drainage is not a preferred treatment.  It may lead to short-term relief of symptoms but does not have any positive effects on the long-term progression of the disease.  It should be reserved for use in patients with tense abscesses creating unbearable pain (13).  If done, the wound should be packed, and patients should be given oral antibiotics with the first dose in the ER.

HS is a complicated, chronic disease, burdening patients with great pain and disability.  Much work remains to elucidate the exact underlying mechanisms and the most appropriate therapy.  However employment of uniform therapy tailored to severity stage appears to decrease symptoms, recurrence, and will ideally decrease the need for more radical interventions.  

-- Peter Acker MD MPH

References:

1.  Harrison BJ, Mudge M, Hughes LE. Recurrence after surgical treatment of hidradenitis suppurativa. Br Med J (Clin Res Ed) 1987; 294:487.

2.  Gordon SW. Hidradenitis suppurativa: a closer look. J Natl Med Assoc 1978; 70:339.

3.  Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol 1999; 140:90.

4.  Jemec GBE, Faber M, Gutschik E, Wendelboe P. The bacteriology of hidradenitis suppurativa. Dermatology 1996; 193:203-6.

5.  Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977-978.

6.  Hurley H. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa, and familial benign pemphigus. In: Roenigk RH, Roenigk HH Jr, eds. Dermatologic surgery: principles and practice. New York, NY: Marcel Dekker; 1989:729-739.

7.  Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. Br J Dermatol 2009; 161:831.

8.  Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol 1983; 22:325.

9.  Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol 1998; 39:971.

10.  Kaur MR, Lewis HM. Hidradenitis suppurativa treated with dapsone: A case series of five patients. J Dermatolog Treat 2006; 17:211.

11.   Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology 2009; 219:148.

12.   Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977-978.

13.   Lapins, J, Emtestam, L. Surgery. In: Hidradenitis Suppurativa, Jemec, GB, Revuz, J, Leyden, J (Eds), Springer, New York 2006. p.160.

01.03.12

by CLIC-EM

Algorithm-based Treatment of Hidradenitis Suppurativa

Hidradenitis Suppurativa (HS) is a chronic, painful, debilitating disease that is poorly understood and with ill-defined treatment.  It affects approximately 4% of the US population, and frequently brings patients to the ER with pain and inflammation (1).  Due to the unclear nature and treatment, this condition is dealt with in many ways, some with poor outcomes, leading to increased morbidity and necessitating more radical treatments downstream.

The disease is diagnosed by the confluence of three criteria (2):

1. Typical lesions: multiple deep seated nodules and fibrosis
2. Typical locations (areas with apocrine glands): groin, axilla, perineal, peri-anal and infra-mammary regions
3. Chronicity and relapse

The underlying cause is debated but currently thought to be occlusion of the terminal follicular acro-infundibulum, which causes follicular duct expansion, wall rupture, antigen release and resulting inflammation (2).   Bacterial infection was long thought to be part of the disorder, leading to wide use of antibiotics for treatment (3,4).  

However approximately half of HS lesions are sterile upon culture (S. aureus and S. epidermidis being the most common isolates in non-sterile cultures),  indicating that other inflammatory processes are at work as well (4).  

Due to the unclear underlying etiology of HS, it has been difficult to target therapy for this disease process.  Numerous treatment modalities have been offered with varying success: antibiotics, immunosuppresants, anti-inflammatory medications, isotretinoins, surgical unroofing, classic I & D, and surgical excision (5).
 
Current treatment recommendations vary based on stage of the disease utilizing the Hurley Staging System (6):

Stage I: One or more abscesses with no sinus tract or scarring.
Stage II: One or more widely separated recurrent abscesses, with a tract and scarring.
Stage III: Multiple interconnected tracts and abscesses through the entire affected area.

After extensive research, a number of treatment modalities have proven themselves to be more efficacious, although none appear perfect.  Some are easily implemented in the ER, while others are better tolerated in the hands of a  specialist.  A treatment algorithm based on the Hurley Staging System is offered below.

Hurley Stage	ER Treatments
General (all stages)	-Minimize trauma, wear loose fitting clothes -Quit smoking (7) -Avoid anti-perspirants -Avoid high pH soaps -Do not shave affected areas
Stage I	Topical ABX8,9        -Clindamycin 1% BID X 12 weeks Topical ABX failures -> Oral antibiotics  X 7-10 days9,10       -Tetracycline 250-500 mg QID       -Doxycycline 100 mg BID       -Clindamycin 300 mg BID       -Augmentin 500 mg-1 g TID Dermatology referral       -Intra-lesional steroid injections       -Anti-androgen initiation
Stage II	Oral ABX (same as Stage I) Severe cases:       -Rifampin + Clindamycin combination therapy                     -Clindamycin 300 mg BID + Rifampin 300 mg BID X 3 months11,12 Referral to surgery for unroofing
Stage III	Employ same treatment principles from Stage I & II Surgical referral

Notably, classic incision and drainage is not a preferred treatment.  It may lead to short-term relief of symptoms but does not have any positive effects on the long-term progression of the disease.  It should be reserved for use in patients with tense abscesses creating unbearable pain (13).  If done, the wound should be packed, and patients should be given oral antibiotics with the first dose in the ER.

HS is a complicated, chronic disease, burdening patients with great pain and disability.  Much work remains to elucidate the exact underlying mechanisms and the most appropriate therapy.  However employment of uniform therapy tailored to severity stage appears to decrease symptoms, recurrence, and will ideally decrease the need for more radical interventions.  

-- Peter Acker MD MPH

References:

1.  Harrison BJ, Mudge M, Hughes LE. Recurrence after surgical treatment of hidradenitis suppurativa. Br Med J (Clin Res Ed) 1987; 294:487.

2.  Gordon SW. Hidradenitis suppurativa: a closer look. J Natl Med Assoc 1978; 70:339.

3.  Lapins J, Jarstrand C, Emtestam L. Coagulase-negative staphylococci are the most common bacteria found in cultures from the deep portions of hidradenitis suppurativa lesions, as obtained by carbon dioxide laser surgery. Br J Dermatol 1999; 140:90.

4.  Jemec GBE, Faber M, Gutschik E, Wendelboe P. The bacteriology of hidradenitis suppurativa. Dermatology 1996; 193:203-6.

5.  Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977-978.

6.  Hurley H. Axillary hyperhidrosis, apocrine bromhidrosis, hidradenitis suppurativa, and familial benign pemphigus. In: Roenigk RH, Roenigk HH Jr, eds. Dermatologic surgery: principles and practice. New York, NY: Marcel Dekker; 1989:729-739.

7.  Sartorius K, Emtestam L, Jemec GB, Lapins J. Objective scoring of hidradenitis suppurativa reflecting the role of tobacco smoking and obesity. Br J Dermatol 2009; 161:831.

8.  Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol 1983; 22:325.

9.  Jemec GB, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol 1998; 39:971.

10.  Kaur MR, Lewis HM. Hidradenitis suppurativa treated with dapsone: A case series of five patients. J Dermatolog Treat 2006; 17:211.

11.   Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology 2009; 219:148.

12.   Mendonca CO, Griffiths CE: Clindamycin and rifampicin combination therapy for hi- dradenitis suppurativa. Br J Dermatol 2006; 154:977-978.

13.   Lapins, J, Emtestam, L. Surgery. In: Hidradenitis Suppurativa, Jemec, GB, Revuz, J, Leyden, J (Eds), Springer, New York 2006. p.160.

12.08.11

by CLIC-EM

2-Point Compression Ultrasound for DVT in the ED

The incidence of venous thromboembolism (VTE) in the US  approaches 600,000 patients with up to 100,000 deaths related to pulmonary embolus (PE).1,2  Fully 90% of PEs originate from deep venous thrombi (DVT) in the proximal vessels of the lower extremities, necessitating diagnostic skill in the emergency physician (EP) to clinch this diagnosis.

Unfortunately, signs and symptoms associated with DVT (palpable cord, ipsilateral edema, warmth, venous dilation) are insufficient to diagnose this condition.5  Ultrasound has replaced venography as the diagnostic study of choice in DVT, but the limited availability of this study outside banker's hours places the EP in a precarious position -- the presence of untreated DVTs and inappropriate anticoagulation pose separate and meaningful harm to the patient.

Recent data suggest that bedside ultrasonography performed by EPs may be adequate for diagnosis of DVT.  After a 30-hour training course for EPs in whole-leg ultrasound, sensitivity approaches 95%.6  However, a whole-leg study takes 13 minutes and the cost/benefit of this training course is unfeasible to many practitioners.

An alternative is the '2-point compression' exam that takes 3 minutes and requires far less training for EPs.  Crisp et al. found physicians with varying levels of ultrasound experience were able to diagnose proximal DVTs with 100% sensitivity and 99% specificity (using radiology performed proximal DVT scans as the gold standard) after a 10-minute training program detailing the 2-point compression technique.7 

This technique utilizes compression analysis of two sites with a 5-10 MHz linear-array probe:  

1.  Popliteal vein -- visualized with patient prone, probe in the mid-popliteal fossa.

2. Common femoral vein -- visualized with patient supine, probe at the inguinal ligament.

The exam is considered positive if the vessel is not compressible or a thrombus is visualized.8

The 2-point technique has been compared with whole-leg ultrasound for DVT, and rates of identifying proximal DVT were similar in randomized prospective studies.  The 2-point technique did miss isolated calf DVTs when compared with the whole-leg exam.  Yet, long-term clinical outcomes were equivalent between the two groups, questioning the clinical significance of anticoagulating calf DVTs.9

In conclusion, EPs are clearly capable of obtaining accurate results in the diagnosis of proximal DVT with bedside 2-point compression ultrasound after appropriate training.

-- Peter Acker MD MPH

References:

1) Cushman M, Tsai AW, White RH, et al. "Deep vein thrombosis and pulmonary embolism in two cohorts: the longitudinal investigation of thromboembolism etiology." Am J Med 2004; 117:19.

2) Beckman MG, Hooper WC, et al. " Venous Thromboembolism: A public Health Concern."  Am J Prev Med. 2010 Apr; 38 (4Suppl): S495-501.

3) Havig O. "Deep vein thrombosis and pulmonary embolism. An autopsy study with multiple regression analysis of possible risk factors." Acta Chir Scand Suppl 1977; 478:1.

4) Galanaud JP, Sevestre-Pietri MA, Bosson JL, et al. "Comparative study on risk factors and early outcome of symptomatic distal versus proximal deep vein thrombosis: results from the OPTIMEV study." Thromb Haemost. 2009; 102:493.

5)  Sandler DA, Duncan JS, Ward P, et al. "Diagnosis of deep-vein thrombosis: comparison of clinical evaluation, ultrasound, plethysmography, and venoscan with x-ray venogram." Lancet . 1984;2:716-18.

6)  Magazzini S, Vanni S, Toccafondi S, et al. "Duplex ultrasound in the emergency department for the diagnostic management of clinically suspected deep venous thrombosis." Acad Emerg Med. 2007;14:216-220.

7) Crisp JG, Lovato LM, Jan TB.  " Compression Ultrasonography of the Lower Extremity With Portable Vascular Ultrasonography Can Accurately Detect Deep Venous Thrombosis in the Emergency Department." Ann of Emerg Med. 2010; 56, 6: 601-610.

8) Cogo A, Lensing AWA, Koopman MMW, et al. "Compression ultrasonography for diagnostic management of patients with clinically suspected deep vein thrombosis: prospective cohort study." BMJ. 1998; 316(7124):17-20.

9)Bernardi E, Camporese G, Büller HR, et al. "Serial 2-point ultrasonography plus D-dimer vs whole-leg color-coded Doppler ultrasonography for diagnosing suspected symptomatic deep venous thrombosis: a randomized controlled trial." JAMA. 2008; 300:1653-1659.

12.08.11

by CLIC-EM

2-Point Compression Ultrasound for DVT in the ED

The incidence of venous thromboembolism (VTE) in the US  approaches 600,000 patients with up to 100,000 deaths related to pulmonary embolus (PE).1,2  Fully 90% of PEs originate from deep venous thrombi (DVT) in the proximal vessels of the lower extremities, necessitating diagnostic skill in the emergency physician (EP) to clinch this diagnosis.

Unfortunately, signs and symptoms associated with DVT (palpable cord, ipsilateral edema, warmth, venous dilation) are insufficient to diagnose this condition.5  Ultrasound has replaced venography as the diagnostic study of choice in DVT, but the limited availability of this study outside banker's hours places the EP in a precarious position -- the presence of untreated DVTs and inappropriate anticoagulation pose separate and meaningful harm to the patient.

Recent data suggest that bedside ultrasonography performed by EPs may be adequate for diagnosis of DVT.  After a 30-hour training course for EPs in whole-leg ultrasound, sensitivity approaches 95%.6  However, a whole-leg study takes 13 minutes and the cost/benefit of this training course is unfeasible to many practitioners.

An alternative is the '2-point compression' exam that takes 3 minutes and requires far less training for EPs.  Crisp et al. found physicians with varying levels of ultrasound experience were able to diagnose proximal DVTs with 100% sensitivity and 99% specificity (using radiology performed proximal DVT scans as the gold standard) after a 10-minute training program detailing the 2-point compression technique.7 

This technique utilizes compression analysis of two sites with a 5-10 MHz linear-array probe:  

1.  Popliteal vein -- visualized with patient prone, probe in the mid-popliteal fossa.

2. Common femoral vein -- visualized with patient supine, probe at the inguinal ligament.

The exam is considered positive if the vessel is not compressible or a thrombus is visualized.8

The 2-point technique has been compared with whole-leg ultrasound for DVT, and rates of identifying proximal DVT were similar in randomized prospective studies.  The 2-point technique did miss isolated calf DVTs when compared with the whole-leg exam.  Yet, long-term clinical outcomes were equivalent between the two groups, questioning the clinical significance of anticoagulating calf DVTs.9

In conclusion, EPs are clearly capable of obtaining accurate results in the diagnosis of proximal DVT with bedside 2-point compression ultrasound after appropriate training.

-- Peter Acker MD MPH

References:

1) Cushman M, Tsai AW, White RH, et al. "Deep vein thrombosis and pulmonary embolism in two cohorts: the longitudinal investigation of thromboembolism etiology." Am J Med 2004; 117:19.

2) Beckman MG, Hooper WC, et al. " Venous Thromboembolism: A public Health Concern."  Am J Prev Med. 2010 Apr; 38 (4Suppl): S495-501.

3) Havig O. "Deep vein thrombosis and pulmonary embolism. An autopsy study with multiple regression analysis of possible risk factors." Acta Chir Scand Suppl 1977; 478:1.

4) Galanaud JP, Sevestre-Pietri MA, Bosson JL, et al. "Comparative study on risk factors and early outcome of symptomatic distal versus proximal deep vein thrombosis: results from the OPTIMEV study." Thromb Haemost. 2009; 102:493.

5)  Sandler DA, Duncan JS, Ward P, et al. "Diagnosis of deep-vein thrombosis: comparison of clinical evaluation, ultrasound, plethysmography, and venoscan with x-ray venogram." Lancet . 1984;2:716-18.

6)  Magazzini S, Vanni S, Toccafondi S, et al. "Duplex ultrasound in the emergency department for the diagnostic management of clinically suspected deep venous thrombosis." Acad Emerg Med. 2007;14:216-220.

7) Crisp JG, Lovato LM, Jan TB.  " Compression Ultrasonography of the Lower Extremity With Portable Vascular Ultrasonography Can Accurately Detect Deep Venous Thrombosis in the Emergency Department." Ann of Emerg Med. 2010; 56, 6: 601-610.

8) Cogo A, Lensing AWA, Koopman MMW, et al. "Compression ultrasonography for diagnostic management of patients with clinically suspected deep vein thrombosis: prospective cohort study." BMJ. 1998; 316(7124):17-20.

9)Bernardi E, Camporese G, Büller HR, et al. "Serial 2-point ultrasonography plus D-dimer vs whole-leg color-coded Doppler ultrasonography for diagnosing suspected symptomatic deep venous thrombosis: a randomized controlled trial." JAMA. 2008; 300:1653-1659.

11.07.11

by CLIC-EM

Rethinking CVP in Distributive Shock

The need for accurate assessment of intravascular volume in shock states is critical.  Central venous pressure (CVP) is often cited as an essential parameter to institute aggressive resuscitation in distributive shock and to guide fluid therapy, based largely on its use in early goal directed therapy (EGDT).

As it turns out, high-quality evidence does not back continuous CVP monitoring in distributive shock.  A 2008 meta-analysis by Marik et al. in Chest addressed this very topic:  "Does Central Venous Pressure Predict Fluid Responsiveness, or A Systematic Review of the Literature and the Tale of Seven Mares."

In Marik's analysis (24 human studies with 803 patients total), the findings were remarkable:

1)  Initial CVP did not predict blood volume.

2)  Baseline CVP did not predict fluid responsiveness (per stroke index and cardiac index).

3)  The change in CVP did not predict fluid responsiveness.

Bottom line:  "The results from this study therefore confirm that neither a high CVP, a normal CVP, a low CVP, nor the response of the CVP to fluid loading should be used in the fluid management strategy of any patient."

In case you were wondering about the 'seven mares:'   This refers to the only study where CVP was shown to predict volume status - seven horses had blood removed (CVP decreased) and then reinfused (CVP then returned to initial value).

Over the past decade, CVP has assumed the role of the Swan-Ganz pulmonary capillary wedge pressure (PCWP) -- a theoretically useful surrogate for left-ventricle end-diastolic volume (LVEDV) not borne out by evidence.

Exactly how this happened is unclear, but it is important to note that CVP was not designed as an intervention in the original Rivers' EGDT study.  Rather, CVP monitoring was present in both the control and intervention arms of this study (thus making it impossible to isolate benefit due to CVP monitoring alone).

A current study seeks to rest the debate on CVP monitoring.  The Protocolized Care for Early Septic Shock (ProCESS) trial from Pittsburgh has three arms - EGDT, usual care, and protocolized standard care.  The protocolized standard care states that "Central venous catheters will only be used when standard IVs are unable to give the proper amount of fluid and medicines.  Blood transfusions will be given according to currently recommended guidelines."  Translation:  The 'no CVP' arm may be a game-changer if there is no validated benefit to CVP monitoring.

-- Jonathan Purcell, MD

11.07.11

by CLIC-EM

Rethinking CVP in Distributive Shock

The need for accurate assessment of intravascular volume in shock states is critical.  Central venous pressure (CVP) is often cited as an essential parameter to institute aggressive resuscitation in distributive shock and to guide fluid therapy, based largely on its use in early goal directed therapy (EGDT).

As it turns out, high-quality evidence does not back continuous CVP monitoring in distributive shock.  A 2008 meta-analysis by Marik et al. in Chest addressed this very topic:  "Does Central Venous Pressure Predict Fluid Responsiveness, or A Systematic Review of the Literature and the Tale of Seven Mares."

In Marik's analysis (24 human studies with 803 patients total), the findings were remarkable:

1)  Initial CVP did not predict blood volume.

2)  Baseline CVP did not predict fluid responsiveness (per stroke index and cardiac index).

3)  The change in CVP did not predict fluid responsiveness.

Bottom line:  "The results from this study therefore confirm that neither a high CVP, a normal CVP, a low CVP, nor the response of the CVP to fluid loading should be used in the fluid management strategy of any patient."

In case you were wondering about the 'seven mares:'   This refers to the only study where CVP was shown to predict volume status - seven horses had blood removed (CVP decreased) and then reinfused (CVP then returned to initial value).

Over the past decade, CVP has assumed the role of the Swan-Ganz pulmonary capillary wedge pressure (PCWP) -- a theoretically useful surrogate for left-ventricle end-diastolic volume (LVEDV) not borne out by evidence.

Exactly how this happened is unclear, but it is important to note that CVP was not designed as an intervention in the original Rivers' EGDT study.  Rather, CVP monitoring was present in both the control and intervention arms of this study (thus making it impossible to isolate benefit due to CVP monitoring alone).

A current study seeks to rest the debate on CVP monitoring.  The Protocolized Care for Early Septic Shock (ProCESS) trial from Pittsburgh has three arms - EGDT, usual care, and protocolized standard care.  The protocolized standard care states that "Central venous catheters will only be used when standard IVs are unable to give the proper amount of fluid and medicines.  Blood transfusions will be given according to currently recommended guidelines."  Translation:  The 'no CVP' arm may be a game-changer if there is no validated benefit to CVP monitoring.

-- Jonathan Purcell, MD

10.25.11

by CLIC-EM

IV Spike Cric

How do you improvise a cricothyrotomy with only IV supplies?  The answer is not a needle cric - it is the "IV Spike Cric."

This technique, oft cited as military invention, uses a 'high flow' IV tubing set either by itself or in conjunction with an ETT to create a cricothyrotomy device that provides for effective ventilation.  As with any cricothorotomy, this technique is only a temporizing measure.

Of note, the Baxter Clearlink System high-flow (10 gtt/mL) IV tubing spike and drip chamber have a design particularly favorable for this procedure.  

In a cadaveric model, the Baxter brand tubing was determined to be effective; other brands of tubing with different design features have not been specifically tested.

Technique:

1.            Cut 7-0 ETT tube at 4cm from BVM connector.

2.            Cut IV spike 3-4 cm from spike (in the middle of the drip chamber).

3.            Connect the cut ends of the ETT and drip camber (alternatively, the cut end of the IV spike can be used if no ETT is available).

4.            The nondominant hand is used to stabilize the trachea and stretch the overlying skin to maximize tension over the cricothyroid membrane and maximize the cutting advantage of the IV spike's edge.

The cricothyroid membrane should be palpated with the index finger of the dominant hand, and the improvised device is then introduced by puncturing the skin and cricothyroid membrane.

Orientation of the spike perpendicular to the membrane or angled slightly caudally affords the least resistance to tracheal entry.  

Once inserted, the device should be held firmly in place at all times and attached to the BVM for immediate ventilation.

5.            Stabilize the device with a bulky dressing.

As cricothyrotomy is typically unanticipated and rapid, considerable attention has focused on improvisational approaches.  The IV Spike Cric is one such important technique to keep in your airway armamentarium.

-- Eric Beck, DO, EMT-P


References


Platts-Mills TF, Lewin MR, Wells J, Bickler P; Improvised Cricothyrotomy Provides Reliable Airway Access in an Unembalmed Human Cadaver Model. Wilderness and Environmental Medicine, 17, 81-86 (2006).


Blanas N, Fisher JA; Letter to the Editor. Canadian Journal of Anesthesia, 46, 8, 809-810 (1999).

10.25.11

by CLIC-EM

IV Spike Cric

How do you improvise a cricothyrotomy with only IV supplies?  The answer is not a needle cric - it is the "IV Spike Cric."

This technique, oft cited as military invention, uses a 'high flow' IV tubing set either by itself or in conjunction with an ETT to create a cricothyrotomy device that provides for effective ventilation.  As with any cricothorotomy, this technique is only a temporizing measure.

Of note, the Baxter Clearlink System high-flow (10 gtt/mL) IV tubing spike and drip chamber have a design particularly favorable for this procedure.  

In a cadaveric model, the Baxter brand tubing was determined to be effective; other brands of tubing with different design features have not been specifically tested.

Technique:

1.            Cut 7-0 ETT tube at 4cm from BVM connector.

2.            Cut IV spike 3-4 cm from spike (in the middle of the drip chamber).

3.            Connect the cut ends of the ETT and drip camber (alternatively, the cut end of the IV spike can be used if no ETT is available).

4.            The nondominant hand is used to stabilize the trachea and stretch the overlying skin to maximize tension over the cricothyroid membrane and maximize the cutting advantage of the IV spike's edge.

The cricothyroid membrane should be palpated with the index finger of the dominant hand, and the improvised device is then introduced by puncturing the skin and cricothyroid membrane.

Orientation of the spike perpendicular to the membrane or angled slightly caudally affords the least resistance to tracheal entry.  

Once inserted, the device should be held firmly in place at all times and attached to the BVM for immediate ventilation.

5.            Stabilize the device with a bulky dressing.

As cricothyrotomy is typically unanticipated and rapid, considerable attention has focused on improvisational approaches.  The IV Spike Cric is one such important technique to keep in your airway armamentarium.

-- Eric Beck, DO, EMT-P


References


Platts-Mills TF, Lewin MR, Wells J, Bickler P; Improvised Cricothyrotomy Provides Reliable Airway Access in an Unembalmed Human Cadaver Model. Wilderness and Environmental Medicine, 17, 81-86 (2006).


Blanas N, Fisher JA; Letter to the Editor. Canadian Journal of Anesthesia, 46, 8, 809-810 (1999).