Let It Flow! Intraosseous Flow Rates by Insertion Site

Intraosseous (IO) access has become increasingly popular as a ‘safety net’ for failed IV access and has become a go-to procedure in pre-hospital cases of rapidly decompensating patients. Think of the cardiac arrest patient or the hemodynamically unstable trauma patient. The IO has proven a quick and reliable way to gain access to medullary venous plexuses in long bones, which drain into systemic venous circulation. We can basically think of the bone marrow as a vein that will not collapse on us that can be accessed very rapidly, with very little training. We have infused fluids, medications, and blood products successfully through the IO. And now that increased support has grown for the use of IOs prehospitally, the question has become which site is best: Tibia (which many people seem to be most comfortable with due to prominent landmarks and distance from resuscitative efforts), humerus, or sternum. There is literature supporting, and widespread consensus for, proximal tibia as the optimal insertion site in children, but this consensus does not exist in adults. Choice often depends on comfort level of the operator and convenience of the location, but we should also consider the difference in flow rates between sites.

There are few studies comparing IO placement sites but the ones that exist compare proximal to distal tibia, tibia to humerus, and one study which compared IO infusion rates between tibia, humerus and sternum in cadavers. The first study found that IO flow rates in the proximal tibia were significantly faster with and without use of a pressure bag than flow rates the in the distal tibia. The drawback of this study was its small sample size of only 22 patients. Pasley et al did a cadaver study published 1 year ago which utilized 16 cadavers to compare flow rates and found that the sternal site had the highest and most consistent flow rate compared to the humerus and tibia. In fact the average flow rate in the sternum according to this study was 1.6x higher than the humerus and 3.1x higher than the tibia. Additionally, this study showed that the tibia had the greatest number of insertion difficulties (In 3 out of the 16 cadavers, infusion was unsuccessful after insertion and alternate tibia had to be used.) Ong et al did a study in 2009 which had very different results. This study recruited 24 patients who presented to an ED in Singapore, all patients received a tibial IO, and those who needed a second access point were given a humeral IO (which 11 patients received). This study found no significant difference between the flow rates at the tibial and humeral site in contrast to Pasley’s study which did show a significant difference between humerus and tibia with the humeral site achieving a 1.8x greater volume on average than the tibia. Small sample size is an issue in all articles existing on this subject.

It seems that there have been no conclusive studies in human or cadaver studies on best IO insertion site, but, if we believe the most recent study by Pasley et al, the sternal and humeral IO sites, in that order, have better flow rates compared to tibial placement. This higher flow rate could make a difference when rapid fluid resuscitation is imperative and could lead to better survival of our patients. A new device called the FASTResponder was released by Pyng Medical in 2013 to make the sternal IO concept easier. This device is safe on ages 12 years and older and makes site identification easy. Another benefit of the device is, unlike the IO drill system, it requires no batteries, and, anecdotally, there is less pain on fluid delivery compared to other sites. One factor we are still unclear about is if the sternal IO could pose a problem if cervical immobilization is being used in trauma patients, with chest compressions, and for some airway procedures. Pyng Medical advertises on their website that it is “safe” to use in conjunction with cervical immobilization devices and CPR. However, the drill-based EZ-IO is approved for all ages, and many providers are already comfortable with it. According to Pasley’s study, the humeral placement is second best in terms of flow rates and had less insertional difficulties. He also notes that the humeral site had the greatest variability in volumes infused from subject to subject. There doesn’t seem to be enough evidence yet to draw firm conclusions; more studies are needed with a greater number of test subjects to increase reliability.  Furthermore, outcome measures, though often difficult to study, would be nice.

References

Carness J, Russell J, Rodrigo M, et al. Fluid Resuscitation Using the Intraosseous Route: Infusion with Lactated Ringer’s and Hetastarch. Military Medicine 2012; 2:222.

Ong M, Chan Y, Jen J, Ngo A. An observation prospective study comparing tibial and humeral intraosseous access using the EZ-IO. Amer Journal of Emergency Medicine 2009; 27, 8-15. 

Pasley J, Miller C, Dubose J, et al. Intraosseous Infusion Rates under High Pressure: A Cadaveric Comparison of Anatomic Sites. Distribution A: Approved for Public Release 2014: Case Number 88ABW-2014-1139.

Tan B, Chong S, Koh Z, Ong M. EZ-IO in the ED: an observational, prospective study comparing flow rates with proximal and distal tibia intraosseous access in adults. Amer Journal of EM 2012;30(8):1602-6.

Permissive Hypotension

You are dispatched to a scene where a 21 year old male has been shot in the chest by an unknown caliber handgun. On exam, you note a single GSW to the chest inferior to the left nipple. His VS are: BP 62/48, HR 138/min, RR 36 and labored. He is agitated and diaphoretic, but is AAOx4. You establish peripheral access and begin administering crystalloid fluid as a bolus. Your transport time to the trauma center is 20 minutes, due to road closures.

How much fluid should you administer en route to the trauma center?

            Captain Walter Cannon introduced the world to the concept of permissive hypotension in penetrating trauma back in 1918 during World War I. Cannon was an Army surgeon who witnessed the poor outcomes of patients who were “resuscitated” to “normal” blood pressures and developed the idea of the tenuous clot.  In 1994, Bickel and colleagues compared low volume resuscitation (300-340 ml) with standard ATLS volumes of 2400 ml.  In a randomized prospective trial, Bickel demonstrated a change in mortality of almost 7% in the low volume resuscitation group. This group also had less complications (ICU length of stay, development of acute respiratory distress syndrome, and abdominal compartment syndrome) compared with the standard resuscitation group.

            This practice of permissive hypotension in penetrating chest trauma is now widely accepted and practiced. The idea of the tenuous clot is real. Increased fluid volumes raise the blood pressure to levels higher than required, resulting in dilution of clotting factors and increased bleeding. The majority of these injuries are in non-compressible sites. Hence, patients end up bleeding more than they would have if we had never touched them in the first place.

            Therefore, consider resuscitating penetrating chest trauma patients to normal mental status.  This holds true for other trauma patients where bleeding is felt to be the cause of hypotension. The vast majority of people will retain normal mental status around 90 mmHg SBP. If the SBP is at least 90 mmHg, consider giving no fluids at all.

Boswell, K.  Menaker, J. Assessment and Treatment of the Trauma Patient in Shock, 2014-11-01Z, Volume 32, Issue 4, Pages 777-795, 

2015: The Death of Longboards (Hopefully)

Myths in medicine take too long to go away.  Longboards are yet another modality that serve no purpose except to harm our patients.  Luckily this unnecessary tool used by EMS is going away around the world.  Many states and cities have completely stopped using longboards for ALL patients.  These places include areas within Connecticut, Los Angeles, Kansas, Oregon, Missouri, Houston, New Mexico,.etc.  No matter what your injuries are, in many regions throughout the world, you will not be placed on a longboard, because they are not being used at all.

These devices have hurt our patients since they offer no benefit, yet we continue to use them in our region.  The misconceptions about these devices are enormous, yet the science tells us the following...

Longboards:

1.      Worsen the pain of patients resulting in more unnecessary imaging tests and more radiation exposure.

2.      Cause respiratory compromise/decreased pulmonary function by lying patients flat.

3.      Delay on-scene time for trauma patients.

4.      Result in pressure sores for patients by rapid tissue breakdown from the board.

5.      Increase the risk of aspiration.

Unfortunately, we continue to have folks who spread misconceptions about these devices, which prevent us from moving forward with evidence based medicine.  Luckily, a lot of places are ignoring these folks and moving forward.  Some of the incorrect EMS statement that we have heard are:

1.      The DOT makes me put everyone on a longboard.

2.      I will get my license/certification taken away if I don’t use a longboard.

3.      The DHSS does not allow patients to be brought to hospitals without a longboard.

4.      If someone else puts a patient on a longboard, I cannot take the patient off.

5.      It splints the back.  (No, in fact it was only designed to help extricate patients.)

6.      I will get sued if I don’t put someone on a longboard

These are all ridiculous, and it is great that many places around the country are moving forward with the science.  Lets make 2015 the year we get rid of these terrible devices in New Jersey and around the country.

Following the science, in January 2015, we will be telling EMS providers that they do not need to place anyone on a longboard that is brought into our hospital.  Please join us in getting rid of this outdated modality and provide the same information to EMS.

References:

1. Chan D, Goldberg R, Tascne A, et al. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994;23:48-51.

2. March JA, Augband SC, Brown LH. Changes In Physical Examination Caused By Use Of Spinal Immobilation. Prehospital Emerg Care. 2002; 6: 421-424.

3. Schriger DL, Larmon B, LeGarrick T, et al. Spinal immobilization on a flat backboard: Does it result in neutral position of the cervical spine? Am J Emerg Med. 1991;20:878-81.

4. Schafermeyer RW, Ribbeck BM, Gaskins J, et al. Respiratory effects of spinal immobilization in children. Ann Emerg Med. 1991;20:1017-1019.

5. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy nonsmoking man. Ann Emerg Med.-1988; 17:915-8.

6. Barney RN, Cordell WH, Miller E. Pain associated with immobilization on rigid spine boards (Abstract). Ann Emerg Med.1989; 18:918.

 7. Chan D, Goldberg, RM,  Jennifer Mason, J et al., Backboard Versus Mattress Splint:  A Comparison Of Symptoms. The Journal of Emergency Medicine. 1996. 14:193-298.

8. Totten VY, Sugarman DB, Respiratory Effects Of Spinal Immobilization. Prehosp Emerg Care 1999;3:347-352

9.  Hauswald M,  McNally T. Confusing Extrication with Immobilization: The Inappropriate Use of Hard Spine Boards for Interhospital Transfers. Air Med J. 2000; 19: 126-127

10. Hauswald M,Braude D.Spinal immobilization in trauma patients: is it really necessary?_Current Opinion in Critical Care 2002;8:566–70.

11. Hauswald M,Ong G,Tandberg D,Omar Z. Out-of-hospital spinal immobilization:  its effect on neurologic injury.  Academic Emergency Medicine 1998;5:214-219.

12. S. Abram S, Bulstrode C. Routine spinal immobilization in trauma patients: What are the advantages and disadvantages? The Surgeon. 2010;8:218–222.

13. Connell RA, Graham CA, Munro PT. Is spinal immobilization necessary for all patients sustaining isolated penetrating trauma? Injury. 2003;34: 912–914.

14. Kaups KL, Davis JW. Patients With Gunshot Wounds To The Head Do Not Require Cervical Spine Immobilization And Evaluation. J Trauma. 1998; 44:865– 867.

15. Haut ER,  Efron DT,  Adil H, Haider AH et al. Spine Immobilization in Penetrating Trauma: More Harm Than Good? The Journal of Trauma. 2010;  68.

16. Cornwell EE, Chang DC, Bonar JP, et al. Thoracolumbar immobilization for trauma patients with torso gunshot wounds: is it necessary? Arch Surg. 2001;136:324 –327.

17. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998;5:214 –219.

18. Kaups KL, Davis JW. Patients with gunshot wounds to the head do not require cervical spine immobilization and evaluation. J Trauma. 1998;44:865–867.

19. Mark Hauswald, MD, Darren Braude, MD, MPH .Diffusion of Medical Progress: Early Spinal Immobilization in the Emergency Department. Academic Emergency Medicine 2007; 14:1087–1089.

Intubation in Head Trauma

You arrive on scene of a 17 year old male pedestrian struck, unknown medical history.  A friend who was with the patient reports that they were returning from getting dinner when he was struck by a vehicle while riding his bicycle.  The friend denies any alcohol or other intoxicating substances.  The patient is combative, fighting with rescuers, and pulling at his cervical collar.  He has evidence of head trauma externally with scalp bleeding controlled with direct pressure.  You suspect that this patient has a traumatic brain injury and needs airway management to assist in his care.  You administer 4 mg midazolam intranasal to obtain mild sedation to assist with patient care.  Approximately two minutes later, the patient is more amenable to patient care efforts.  You establish IV access, place the patient on high-flow nasal cannula, and call medical control for rapid sequence intubation orders for this approximately 70 kg patient.  The physician orders 150 mcg fentanyl IVP, 100 mg ketamine IVP, and 100 mg succinylcholine IVP.  What about lidocaine?  What about defasciculating doses of a non-depolarizing paralytic?  What about the contraindication for ketamine in head trauma?

For decades, physicians and prehospital providers have been taught many myths about intubation and intracranial pressures:  Give lidocaine prior to intubation, don’t give succinylcholine without a defasciculating dose, and never give ketamine for a head injury. 

What about pretreatment for the adrenergic response to intubation?  Clinical pearl #25 addresses the use of lidocaine as pretreatment in trauma airways.  The bottom line is that some studies show that it blunts the adrenergic response to intubation and others show no significant difference.  In fact, many of the studies were actually focused on deep tracheal suctioning of already-intubated patients.  For this reason, it is not routinely recommended that lidocaine be given prior to RSI in head injury. 

If attempting to decrease intracranial pressure (ICP) and the adrenergic response to intubation (including increased HR and BP), the better medications to use are opioids, such as fentanyl 2-3 mcg/kg, or esmolol 2 mg/kg, a short-acting beta-blocker.  Fentanyl was superior to lidocaine or placebo in blunting the increase in blood pressure but not the heart rate from intubation.  In these same studies, esmolol was found to significantly blunt the increase in blood pressure and heart rate.^1–3  However, esmolol is not a typical pre-hospital medication, but it can be considered in the emergency department.  Furthermore, blunting the heart rate is typically not as critical as the blood pressure except in cases of great vessel dissection, in which the tachycardia may cause increasing shear forces on the dissection flaps.  Fentanyl also provides analgesia, which is not provided in the majority of intubations using only etomidate.

Should we be giving defasciculating doses of a non-depolarizing paralytic prior to succinylcholine?  The theory behind this stems from the mechanism of action of succinylcholine.  In order to achieve paralysis, succinylcholine activates the receptors at the neuromuscular junction, hence causing the fasciculations, and does not allow them to “reset” for the next nerve impulse.  These fasciculations are theorized to cause an increase in ICP by having many large muscle groups suddenly contracting, increasing systemic vascular resistance.  However, these fasciculations, as you know, are transient and short-lived.  In some small scale studies, succinylcholine does raise ICP in surgical patients, and a defasciculating dose does seem to block the increase.  However, this increase is transient, and the clinical significance is not known.  Furthermore, the addition of another medication for RSI results in more work for the intubating crew, especially if the non-depolarizing paralytic is vecuronium and requires dissolution in sterile water prior to drawing it up.  As a result, defasciculating doses of non-depolarizing paralytics are not routinely recommended.^4,5

Isn’t ketamine contraindicated for head trauma?  Decades ago, animal models were noted to have increased ICP when administered ketamine, and it was consequently contraindicated for years on the basis that it would decrease cerebral perfusion.  However, this is not the only variable when it comes to cerebral blood flow.  The more important number is the cerebral perfusion pressure (CPP), which is the difference between the mean arterial pressure (MAP) and the ICP à CPP = MAP – ICP.  If the MAP remains unchanged and the ICP increases, the CPP goes down, which is bad.  However, ketamine also increases MAP, and more recent studies actually show that CPP increases with ketamine.  In one study, ketamine actually decreased ICP in children.⁶  If combined with other sedatives, particularly GABA-agonists, it may also improve the post-trauma metabolism of the brain.⁷

Once again, something that has been taught for years as dogma has been based on weak, often conflicting, evidence.^8,9  Ketamine, in contrast to years of teaching, is actually an ideal induction agent for RSI in head trauma, providing analgesia and improving CPP in many instances.  However, it should be avoided in patients who are already markedly hypertensive.

References

1.                 Feng CK, Chan KH, Liu KN, Or CH, Lee TY. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin. 1996;34(2):61-7. Available at: http://www.ncbi.nlm.nih.gov/pubmed/9084524. Accessed August 31, 2014.

2.                 Gupta S, Tank P. A comparative study of efficacy of esmolol and fentanyl for pressure attenuation during laryngoscopy and endotracheal intubation. Saudi J Anaesth. 2011;5(1):2-8. doi:10.4103/1658-354X.76473.

3.                 Pouraghaei M, Moharamzadeh P, Soleimanpour H, et al. Comparison between the effects of alfentanil, fentanyl and sufentanil on hemodynamic indices during rapid sequence intubation in the emergency department. Anesthesiol pain Med. 2014;4(1):e14618. doi:10.5812/aapm.14618.

4.                 Minton MD, Grosslight K, Stirt JA, Bedford RF. Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade. Anesthesiology. 1986;65(2):165-9. Available at: http://www.ncbi.nlm.nih.gov/pubmed/2874752. Accessed August 31, 2014.

5.                 Clancy M. In patients with head injuries who undergo rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome? A literature review. Emerg Med J. 2001;18(5):373-375. doi:10.1136/emj.18.5.373.

6.                 Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN. Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension. J Neurosurg Pediatr. 2009;4(1):40-6. doi:10.3171/2009.1.PEDS08319.

7.                 Sehdev RS, Symmons DAD, Kindl K. Ketamine for rapid sequence induction in patients with head injury in the emergency department. Emerg Med Australas. 2006;18(1):37-44. doi:10.1111/j.1742-6723.2006.00802.x.

8.                 Bourgoin A, Albanèse J, Léone M, Sampol-Manos E, Viviand X, Martin C. Effects of sufentanil or ketamine administered in target-controlled infusion on the cerebral hemodynamics of severely brain-injured patients. Crit Care Med. 2005;33(5):1109-13. Available at: http://www.ncbi.nlm.nih.gov/pubmed/15891344. Accessed August 31, 2014.

9.                 Schmittner MD, Vajkoczy SL, Horn P, et al. Effects of fentanyl and S(+)-ketamine on cerebral hemodynamics, gastrointestinal motility, and need of vasopressors in patients with intracranial pathologies: a pilot study. J Neurosurg Anesthesiol. 2007;19(4):257-62. doi:10.1097/ANA.0b013e31811f3feb.