Brought in By Ambulance #5: Chemical Takedown - IM Ketamine for Prehospital Restraint

Clinical scenario: You are working the overnight shift in the Emergency Department (ED) when a pre-arrival for "agitation" pops up on the board.  You see EMS roll by with several police officers and decide that you should follow.  On the stretcher lies a partially clothed, basically unresponsive patient who is maintaining a respiratory rate of 10 and oxygen saturation of 88% on room air.  As you quickly slap on the oxygen, check the patient's response to pain with a sternal rub, see an end-tidal CO2 reading of 35, and contemplate intubation, EMS starts to provide their signout.  The paramedics responded to a call for "altered behavior" and were confronted with a psychotic, agitated, diaphoretic patient who would likely fit the description of Excited Delirium Syndrome (ExDS).  The patient quickly ran at and jumped on a paramedic.  The paramedics, fire department, and police restrained the patient who required multiple doses of Haldol and Ativan to facilitate transport.  As you further assess the patient, you wonder, "is there a better way to chemically restrain a patient that maximizes the safety of EMS providers and patients?".  As the patient's sats improve to 98%, you realize that you have some time to think. You have recently heard about prehospital use of IM ketamine for just this purpose and decide to review the evidence.

Practical exercise:  Calculate the IM Ketamine dose to takedown the Incredible Hulk.

Literature Review:
In 2011, the term "Excited Delirium Syndrome (ExDS)" was coined to describe the clinical syndrome referred to in different venues as "agitated delirium", "excited delirium", or "Sudden Death in Custody Syndrome".   The American College of Emergency Physicians (ACEP) convened a task force to define the spectrum of the syndrome which has the following clinical features [1,2]:

                   - hyper-aggressive or bizarre behavior, including lack of clothing
                   - lack of sensitivity to pain
                   - hyperthermia
                   - diaphoresis
                   - attraction to light or shiny objects

The exact etiology of ExDS is unknown, but there is a strong association with pre-existing psychiatric disease (in particular, schizophrenia) and drugs of abuse (cocaine, methamphetamine, and PCP) [2].

Most importantly,  ExDS conveys a high risk of mortality, in the realm of 10% [1,2].  The exact cause of death is not completely clear, but is thought to arise from severe acidosis or hyperkalemia, and is usually the end result of physical struggle or restraint.  Agitated, combative patients also pose a risk to prehospital providers.  Follow this link to watch a video of ExDS from presentation to death. 

Multiple pharmacologic therapies for chemical restraint of patients with ExDS have been suggested, from anti-psychotics, to benzodiazepines to the dissociative drug, ketamine:
Table 2 from Vilke et. al (Ref 3).

Anti-psychotics and benzodiazepines have long delays to peak effect when given via the IM route, in the realm of 15-30 minutes.  Because of its relatively rapid onset,  there has more widespread  prehospital of IM ketamine for chemical restraint of ExDS.

Several studies have attempted to examine the efficacy of ketamine for prehospital management of ExDS.  Anecdotal evidence for the effectiveness of prehospital ketamine came from initial case series and has been adopted into EMS protocols for extreme agitation [4,5].  These initial case series also highlighted the potential adverse effects of the drug, including hypersalivation, laryngospasm, and hypoxia (at least in the doses used ~ 5 mg/kg IM).

After the initial case series were reported, a pilot, retrospective study of prehospital ketamine for ExDS was published in the Western Journal of Emergency Medicine [6].  In this study, the authors reviewed the paramedic run sheets for 52 violent and agitated patients who were given a single 4 mg/kg dose of IM ketamine  The average time to sedation and medical control was approximately 2 minutes. At the 4 mg/kg IM dosage,  3/52 patients developed respiratory depression, two of whom were intubated.  In each of these cases, the patients had received IV midazolam in conjunction ketamine to prevent emergence reaction.  The authors concluded that "ketamine may be safely and effectively used by trained paramedics following a specific protocol."  A major caveat to this study is that the authors did not examine what happened later in the emergency department.  Interestingly, a previously published case series of 13 patients found that of the three patients who developed respiratory distress, two did so only after arrival to the ED while one patient arrived with ventilation being assisted by EMS [5].  In none of these cases was the impending respiratory distress documented in the prearrival note, suggesting that 6% may be a gross underestimation of the true incidence of respiratory complications. 

Another outcome measure for respiratory complication is by examining incidence of intubation after the patients arrive in the emergency department.  A recent retrospective study published in the American Journal of Emergency Medicine examined the correlation between ketamine dosage and need for intubation [7].  They reviewed the prehospital and emergency department records for 51 consecutive patients who were administered ketamine for prehospital chemical restraint.  Fourteen (29%) of patients required intubation.  Of note, none of these patients were intubated in the field.  Patients who were intubated were administered a significantly higher ketamine dose (6.16 +/- 1.62 mg/kg) than those who were not (4.90 +/- 1.54 mg/kg).  It is not clear what proportion of patients were intubated as a side-effect of the ketamine as opposed to facilitation of  medical care in the emergency department.  It was specifically noted that two of the patients were intubated because of "recurrent agitation and need for additional sedation" and one patient was intubated to facilitate medical workup (a lumbar puncture).  The mortality rate for these patients was not documented, but 71% of the patients were admitted to the hospital, primarily on medical (55%) rather than psychiatric (14%) services.

A final consideration is whether ketamine interacts at all with the psychiatric disorders that underlie some cases of ExDS.  Ketamine acts as an NMDA-receptor antagonist, thereby causing a deficiency in glutamate-mediated
Ketamine chemical structure (wiki)


neurotransmission [8] .   Because PCP and ketamine-abuse can model some aspects of schizophrenia, some have postulated that some aspects of schizophrenia are due to defects in glutamate-mediated neurotransmission.  Indeed, in one study they found that CSF from schizophrenic patients had lower glutamate content when compared with controls [9].  While the "glutamate hypothesis of schizophrenia" remains controversial, because a subset of ExDS syndrome patients have psychotic disorders, one might be concerned that ketamine could have an adverse effect on the underlying psychiatric disease, although this does not appear to have been directly studied anywhere and there are no reports in the limited literature regarding ketamine administration for chemical restraint.

Take Home Points:  ExDS is a syndrome with a high rate of mortality. IM Ketamine is a promising treatment for the prehospital realm because of its rapid time of onset (~2-5 min).  Providers administering ketamine need to have heightened awareness and ability to handle potential respiratory complications, including respiratory depression and laryngospasm.  The long-term effects of single dose ketamine administration in patients with underlying psychiatric diagnoses is unclear.

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by H. Phil Moy

References:
1. Vilke, G. M., DeBard, M. L., Chan, T. C., Ho, J. D., Dawes, D. M., Hall, C., ... & Bozeman, W. P. (2012). Excited delirium syndrome (ExDS): defining based on a review of the literature. The Journal of emergency medicine, 43(5), 897-905.
2. Vilke, G. M., Payne-James, J., & Karch, S. B. (2012). Excited delirium syndrome (ExDS): redefining an old diagnosis. Journal of forensic and legal medicine, 19(1), 7-11.
3. Vilke, G. M., Bozeman, W. P., Dawes, D. M., DeMers, G., & Wilson, M. P. (2012). Excited delirium syndrome (ExDS): treatment options and considerations. Journal of forensic and legal medicine, 19(3), 117-121.
4. Ho, J. D., Smith, S. W., Nystrom, P. C., Dawes, D. M., Orozco, B. S., Cole, J. B., & Heegaard, W. G. (2013). Successful management of excited delirium syndrome with prehospital ketamine: two case examples. Prehospital Emergency Care, 17(2), 274-279.
5.Burnett, A. M., Salzman, J. G., Griffith, K. R., Kroeger, B., & Frascone, R. J. (2012). The emergency department experience with prehospital ketamine: a case series of 13 patients. Prehospital Emergency Care, 16(4), 553-559.
6. Scheppke, K. A., Braghiroli, J., Shalaby, M., & Chait, R. (2014). Prehospital use of IM ketamine for sedation of violent and agitated patients. Western Journal of Emergency Medicine, 15(7), 736.
7. Burnett, A. M., Peterson, B. K., Stellpflug, S. J., Engebretsen, K. M., Glasrud, K. J., Marks, J., & Frascone, R. J. (2014). The association between ketamine given for prehospital chemical restraint with intubation and hospital admission. The American journal of emergency medicine.
8. Murray, R. M., Paparelli, A., Morrison, P. D., Marconi, A., & Di Forti, M. (2013). What can we learn about schizophrenia from studying the human model, drug‐induced psychosis?. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 162(7), 661-670.
9.  Kim, J. S., Kornhuber, H. H., Schmid-Burgk, W., & Holzmüller, B. (1980). Low cerebrospinal fluid glutamate in schizophrenic patients and a new hypothesis on schizophrenia. Neuroscience letters, 20(3), 379-382.

Brought in by Ambulance, #4: Pour Some Sugar on Me

Case Scenario: 
Your unit is responding on the quiet to a 36 year-old F with chief complaint of “sick.”  You arrive to find a cachectic woman (BMI 16) who suffers from lifelong anorexia. She complains of shortness of breath, abdominal pain and general malaise. She walks herself to the ambulance and after her vitals are taken, a FSBS is 56.  According to your protocol, this should be treated in the following manner: the EMT-B administers 15 gm oral glucose solution and repeat as needed, while the EMT-P administers 25 gm D50W IV/IO or D10W IV/IO, or glucagon 1 mg IM if no IV/IO access available.  The medic asks your opinion and as the patient was symptomatic, you suggested starting with oral glucose solution. However, this made her feel nauseated. Once again, the medic asks you whether to give D10W or D50W. You elected for D10W, but you admittedly have no evidence for doing so. After an uneventful ride to the hospital, the patient’s repeat blood glucose was 254 mg/dL.

Clinical Question:
What is the best way to treat hypoglycemia in the prehospital environment?

Literature Review:  
Most common sources define hypoglycemia as less than 60-70 mg/dL. According to the Endocrine Society’s Clinical Practice Guidelines, hypoglycemia should only be treated and investigated in patients showing signs of "Whipple’s triad" -- signs and symptoms of hypoglycemia, a low plasma glucose reading, and resolution of symptoms with elevation of plasma glucose concentration [1]. The signs and symptoms of hypoglycemia are quite vague and nonspecific; they can include shakiness, anxiety, headaches, and weakness, progressing to seizures and unconsciousness [2]. Severe symptoms typically occur with serum glucose values less than 40 mg/dL [3]. It seems obvious that seizures and unconsciousness attributed to hypoglycemia should be treated, but any of the minor signs and symptoms could easily be appreciated on almost any primary scene response. Therefore the vast majority of hypoglycemic patients encountered by EMS providers are most likely going to be treated.

Once we have decided to treat prehospital hypoglycemia, we must determine the optimum modality for doing so. We could find no published work doing a heads-up comparison of oral versus intravenous carbohydrate administration, but there has been work related to D10W versus D50W. An EMS system in California published data from their experience replacing 50mL D50W with 100mL D10W as the standard treatment for hypoglycemia [7]. In 164 treated patients, the median pretreatment glucose was 38 mg/dL, and at 8 minutes after treatment was 98 mg/dL.Twenty-nine patients required an additional dose, and one patient required a third. There were no adverse events reported. The authors conclude these results demonstrate the feasibility, safety, and efficacy of D10 as an alternative to D50.

One unblinded randomized controlled trial compared D10W to D50W in prehospital hypoglycemic patients with GCS < 15 (approx. 25 pts in each group) with regards to the ability of the solutions to raise glucose to normal values and the time to reach a GCS of 15 [4]. The mean repeat glucose value in these groups was 112 and 169 in the D10W and D50W groups, respectively (p = 0.003). The authors note that the average D10 given was 10g (100 mL) and D50 given was 25g (50 mL) (p < 0.001). There were no significant differences between the groups in median time to recovery, median post-treatment GCS, or number of patients experiencing another hypoglycemic episode within 24 hours. The authors conclude that due to the efficacy of treatment with lower risk of hyperglycemia, D10 should be the preferred agent.
   
Not only is D50 more likely to cause hyperglycemia after administration, but it also carries with it the risk of hypertonicity and tissue necrosis. D50 has an osmolarity of 2,525 mOsm/L and a pH between 3.5 and 6.5. This is in contrast to D10 which has an osmolarity of 506 mOsm/L and is pH neutral. Usual IV therapy recommendations state that solutions with osmolarity greater than 900 mOsm/L should be administered through central access. There have also been several case reports of extremity amputation after dextrose extravasation [5,8].

To illustrate the difficulty in administering D50, one of our toxicology faculty compared the injection of D50 to injecting maple syrup. This is not a facetious analogy, as a simple look at the nutrition label of a bottle of syrup reveals:



Note that D50 = 50g of sugar per 100mL of soluion. Each "amp" of D50 contains 25g of sugar in 50mL. Compare that to Aunt Jemima's, which contains 32g of sugar in 60mL solution.

The primary EMS agency bringing patients to our facility recently updated their protocols to make D10 the preferred agent for treating hypoglycemia prehospital. The Medical Director of this agency reiterated the preferable safety profile of D10 compared with D50, and remarked on another important advantage of D10 -- it does not need to be diluted for use in pediatric patients.

In the absence of IV/IO access, evidence exists for the efficacy of IM glucagon in treating prehospital hypoglycemia [9]. The response to glucagon may take longer than when oral or IV glucose solutions are used [10, 11], though may cause a greater increase in blood glucose levels than 10g of glucose solution [12].
   
Take-home:
- If mental status allows, hypoglycemic patients should first be offered oral glucose -- preferably 15gm of a standard glucose formula, but syrup, juice, or honey can also be used. (Note that honey has a lower glycemic index than most juices or glucose solution and thus theoretically may not be as effective.) 
- The next line of therapy should probably be IV D10, as there is good evidence to suggest efficacy on par with that of D50 but with a more favorable safety profile.
- If no IV/IO access is available and oral glucose is unable to be administered, it is reasonable to administer 1mg IM glucagon.

References:
[1] Evaluation and management of adult hypoglycemic disorders.  J Clin Endocrinol Metab, 2009, 94(3), 709.
[2] American Diabetes Association.  Diabetes.org
[3] National Diabetes Information Clearinghouse.  Diabetes.niddk.nih.gov
[4] Moore and Woolard. Emerg Med J, 2005, 22, 512-515.
[5] Kumar et al. ANZ Journal of Surgery, 2001, 71, 285-289.
[6] Is D50 Too Much of a Good Thing?  Stephen Wood, 2007, m.jems.com/article/patient-care
[7] Kiefer et al. Prehosp Disaster Med2014, 29(2), 190-194.
[8] Lawson et al. Am J Emerg Med, 2013, 31(5), 886:e3-5.
[9] Vukmir et al. Ann Emerg Med, 1991, 20(4), 375-9.
[10] Howell et al. J Accid Emerg Med, 1997, 14(1), 30-2.
[11] Carstens and Sprehn. Prehosp Disaster Med, 1998, 13(2-4), 44-50.
[12] Vermeulen et al. Diabetes Care, 2003, 26(8), 2472-3.

Submitted by Chris Miller, PGY-2.
Edited by C. Sam Smith (@CSamSmithMD), PGY-3.
Faculty reviewed by Hawnwan P. Moy.

Brought in by Ambulance, #3: My leg hurts! Well, here's your C-collar...

Case Scenario:
You are doing your second supervisor ride along and hoping that your white cloud of peace will disperse so you can see some St. Louis action. You are called emergently to MVC vs. two pedestrians. On arrival to the scene, you find one patient on the ground with an open fracture of his leg.  ABC’s are fine. The patient notes the car came around the corner and hit his leg. He remembers everything, and complains only of his leg hurting. A quick examination of his neck reveals no midline tenderness and no pain with range of motion. However, secondary to his distracting injury a C-collar was placed. As the ambulance drives away with the patient, you wonder what the evidence behind C-collar use is, and if it was really necessary to place a collar in this gentleman without any neck pain.



Current EBM evidence:
Most of the recommendations on c-collar use are based on opinion and tradition. The American Association of Neurological Surgeons and the Congress of Neurological Surgeons Joint Commission have made recommendations; however, most of these recommendations are based on Level III evidence. Unfortunately, there is a paucity of evidence for the implementation and continued use of C-spine collars. In fact, a Cochrane review in 2007 noted there wasn’t a single prospective RCT on c-collar use.

Currently, most of the validated evidence we have for spinal cord protection is in terms of imaging. Both the NEXUS criteria and the Canadian C-spine rules have been validated, and are used by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons Joint Commission on their official recommendations on the management of acute spinal cord injury. The NEXUS criteria and the Canadian C-spine rules have been applied in the pre-hospital setting; those who will require imaging should therefore be placed in a cervical collar for C-spine stabilization.

Nexus Criteria:
No imaging if all of the following are true:
●No posterior midline cervical tenderness
●Normal level of alertness
●No evidence of intoxication
●No abnormal neurologic findings
●No painful distracting injuries

There has never been any control trial on patients examining if C-collars actually stabilize the spine. There have been a multitude of trials on volunteers and models, many of which have contradicting results. While some studies show that C-collars do stabilize the neck, others show that collars may actually increase neck movement. In a controversial study done by Hauswald et.al, un-immobilized patients in Malaysia had better neurological outcome than similar patients who were immobilized in New Mexico. While this study compared no immobilization to full spinal immobilization (and therefore flawed in the analysis), the overall philosophy that second injury due to transport is rare as the forces are weak compared to the force required to injure the spinal cord may still hold true.

While the evidence to support the use of C-collars is weak, there is an increasing amount of evidence noting potential risks and morbidity associated with C-collar use. While the goal of C- collars is to reduce movement of the cervical spine and protect the spinal cord, a few case studies have shown that forcing a neck into “anatomical position” can actually cause spinal cord injury, particularly in patients with ankylosing spondylitis. A study on cadavers noted that extrication collars caused an increased degree of separation between vertebrae when there is a dissociative injury.

In a systematic review done by Sparke et. al, there have been a few studies noting an increase of ICP pressure with the placement of C-collar. It is estimated that risk of increased ICP is 35.8%. It is thought that the increased ICP is secondary to pressure placed on the jugular veins (causing venous congestion); however there is no real knowledge of the etiology of the increased ICP. Sparke et. al also did a review of the risk of tissue ulcerations secondary to C-collar placement. A review of 14 studies showed the incidence of hospital acquired pressure ulcers from a C-collar range from 23.9-44%. While the review noted that the measurement of pressure from the C-collars was highly variable between studies, pressures from C-collars can be quite elevated (up to 150mmgHg). The review also notes that none of the studies examined in the review were randomized control trials.

The immobilization of the neck can cause increased difficulty in airway management and protection. It is often much more difficult to intubate a patient that has been placed in a C-collar. Patients who do not require intubation are at an increased risk of aspiration with vomiting.

Additionally, once a C-collar has been placed, the patient may be more likely to undergo imaging to have his C-spine cleared. In a study done by Kim et. al., children who were placed in a C-collar were much more likely to undergo imaging to clear the c-spine (56.6 vs 13.4%) and were much more likely to be admitted to the hospital 41.6 vs 14.3%). This can have serious implications on the length of stay on the patient, as well as overall cost to the patient and the hospital.

While the evidence supporting C-collars is minimal, the potential consequence of movement causing additional spinal cord injury is so severe that much better evidence will be required before a change can occur. However, there is the potential to try and reduce the number of C-collars placed, especially on low-risk individuals. In a prospective study done by Rose et. al, it was found that physical exam (no neuro deficit and no midline tenderness or pain with range of motion) was over 99% sensitive with a 99% negative predictive value. In this study, all patients with GCS greater than or equal to 14 were attempted to be clinically cleared regardless of ethanol level or presence of distracting injuries. All patients received CT imaging of their spine, even if they were clinically cleared. Of the 464 patients with distracting injuries that were clinically cleared, only one was found to have C-spine fracture (C2 lateral mass). It should be noted that of the 544 patients without distracting injury that were cleared clinically, one was also found to have a C-spine injury (C6 lamina and C7 superior facet).

Take Home:
-No prospective randomized study on use of c-collars
-There are possible adverse outcomes with use of c-collars (eg increased ICP, pressure ulcers)
-There is evidence supporting clearing c-collar clinically, even with distracting injuries

References:
1. Walters BC, Hadley MN, Hurlbert RJ, Aarabi B, Dhall SS, Gelb DE, Harrigan MR, Rozelle CJ, Ryken TC, Theodore N; American Association of Neurological Surgeons; Congress of Neurological Surgeons. Guidelines for the management of acute cervical spine and spinal cord injuries: 2013 update. Neurosurgery. 2013 Aug;60 Suppl 1:82-91.
2. Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K.. Prehospital Use of Cervical Collars in Trauma Patients: A Critical Review. J Neurotrauma. 2014 Mar 15;31(6):531-40.
3. Hauswald M, Ong G, Tandberg D, Omar Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998 Mar;5(3):214-9.
4. Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010 Aug;69(2):447-50.
5. Papadopoulos MC, Chakraborty A, Waldron G, Bell BA. Lesson of the week: exacerbating cervical spine injury by applying a hard collar. BMJ. 1999 Jul 17;319(7203):171-2.
6. Sparke A, Voss S, Benger J. The measurement of tissue interface pressures and changes in jugular venous parameters associated with cervical immobilisation devices: a systematic review. Scand J Trauma Resusc Emerg Med. 2013 Dec 3;21:81.
7. Leonard J, Mao J, Jaffe DM. Potential adverse effects of spinal immobilization in children. Prehosp. Emerg. Care 16, 513-518.
8. Rose MK, Rosal LM, Gonzalez RP, Rostas JW, Baker JA, Simmons JD, Frotan MA, Brevard SB. Clinical clearance of the cervical spine in patients with distracting injuries: It is time to dispel the myth. J Trauma Acute Care Surg. 2012 Aug;73(2):498-502.

Submitted by Melissa Kroll, PGY-2.
Faculty Reviewed by Phil Moy.

Brought In By Ambulance, #2: Needle Decompression

You are on your first ride along of your EMS rotation. The first couple of trips are low acuity patients. While hanging out in the captain's chair in the darkened back of the truck as your unit patrols the streets, the steady rocking back and forth begins to lull you to sleep...

Tones drop. The call comes in, and seconds later the lights and sirens are at full blare. A few minutes of tense waiting as the ambulance courses through the neighborhood and then the rig screeches to a halt. You hear the EMS providers get out of the cab and raised voices outside. You mobilize the monitor and supply bag and wait for the back doors to open to jump out. However, when they do open, the medics & first responders quickly load up a 20-something female who reportedly was shot in the chest.

Once loaded, the EMT calls out vitals -- HR 60, BP 70/40, RR 22, O2 sat 99%. You begin your ATLS exam. Airway: midline, patent. Breathing: clear on the left, no appreciable breath sounds on the right. You palpate weak pulses in the bilateral radial wrists. You remove the patient’s undergarments and note a gunshot wound to the right parasternal area. The paramedic confirms your findings and instructs you to needle decompress the chest. “You know where to do it, right? Second intercostal space, mid-clavicular line. Here is the needle.” As you are about to impale the patient with a 14-gauge angiocatheter, you can't help but wonder why we place a needle in the anterior chest, but place the definitive treatment (a thoracostomy tube) in the lateral chest.

Clinical Question:

What is the optimal location for needle decompression of traumatic pneumothorax?

Literature Review:

For the majority of EMS agencies, it has long been standard practice to needle decompress those patients with a tension pneumothorax to allow air to evacuate -- effectively converting a tension pneumothorax to an open pneumothorax and thereby restoring respiratory and circulatory function. Currently, ATLS guidelines call for a 5cm angiocatheter device to be inserted at the second intercostal space, mid-clavicular line (2-MC). There are no validated studies supporting this practice as the optimal management. Failure is commonly reported, with published failure rates anywhere from 25-50% in cadaveric, radiologic, and clinical studies. In these studies, the vast majority of failures were attributed to excessive chest wall thickness, user error (including failure to identify to proper anatomic site), and catheter malfunction or obstruction. 

Several lines of questioning are currently being pursued in the EMS, trauma, and EM literature. As our population becomes more obese and thus the distance the needle/catheter must traverse before entering the pleural space becomes longer, can a 5cm catheter reliably reach the pleural space along the 2-MC? Does decompression at this site lead to excessive risk of damaging vital underlying structures? Is there a more appropriate site for needle decompression? Specifically, should more consideration be given to performing needle decompression at a similar site to that used during tube thoracostomy, roughly the 5th intercostal space, anterior axillary line (5-AA)?

Before beginning any such discussion, it must be noted that although a provider may know the proper site, that does not mean he/she can find it. This unfortunate fact was confirmed in a 2005 study by Ferrie et al that included 25 emergency medicine physicians, 21 of whom were ATLS certified. Twenty-two (88%) EP’s named the standard location (2-MC), but only 15 (60%) were able to accurately identify it on a human volunteer.

This is particularly worrisome given the high density of physiologically relevant and sensitive structures found in close proximity to the 2-MC. In 2003, Rawlins published a case series of 3 patients who presented with pneumothorax and were needle decompressed in the 2-MC which subsequently lead to life threatening intra-thoracic hemorrhages. The concern was that this location is very close to the subclavian vessels and internal mammary artery with its medial branches, and thus the 5-AA may be a safer approach. However, Wax et al conducted a study in which CT scans of 100 patients were reviewed and distances from potential needle insertion points to proximate soft tissue and vascular structures were calculated. They concluded the safer site was actually the anterior chest, not the lateral chest.

A further concern is that as patients become larger, the standard catheter length may longer be adequate to ensure entry into the pleural space. A study by Stevens in 2009 calculated chest wall thickness at the 2-MC in 110 trauma patients using CT scans. They concluded that using a standard 4.4cm angiocatheter would result in unsuccessful needle decompression in 50% of trauma patients in their cohort. Inaba et al took this idea one step further, comparing chest wall thickness at the 2-MC to the 5-AA. Using a 5cm needle, 42.7% of needle decompressions would be expected to fail at the 2-MC compared to 16.7% at the 5-AA. There was, on average, 1.3cm less tissue to penetrate at the 5-AA site before reaching the pleural cavity. Unfortunately, the evidence is again conflicting. Another study of chest wall thickness using CT scan data was published by Sanchez et al in 2011. A review of CT scans from 159 patients revealed potential failure rates of 33.6% at 2-MC, 73.6% at the 4th intercostal space, mid-axillary line (4-MA), and 55.3% at the 5th intercostal space, midaxillary line (5-MA), assuming a 5cm device was used. 

If switching from the anterior chest to the lateral chest would not be expected to improve success of decompression based on radiographic studies, perhaps the answer is using a longer device. A study by Chang et al in 2014 again used retrospectively-obtained CT data from a trauma cohort to estimate success of a 5cm angiocatheter versus an 8cm device, based on measured chest wall thickness as well as distance to the closest vital structure. They compared the 2-MC to the 4th intercostal space, anterior axillary line (4-AA). The chest wall thickness at the 4-AA was significantly thinner than that at the 2-MC, though in their study this did not lead to significantly different theoretical rates of success. The 8cm device was theoretically capable of reaching the pleural cavity in 96% of subjects at either location, and the 5cm device was gauged to have 66% success at the 2-MC and 81% at the 4-AA (a nonsignificant difference in this cohort). Interestingly, these authors also looked at theoretical chance of the angiocath reaching a sensitive anatomic structure. They even tried to take into account improper insertion technique by measuring distance from the chest wall to the nearest anatomic structure, even if this was not expected to be injured if the needle followed the proper course perpendicular to the chest wall. They found a relatively high theoretical risk (32%) of striking a vital structure when using the 8cm catheter at the 4-AA location -- even more concerning that this structure is actually the left ventricle. This rate fell to 9% if the distance was measured perpendicular to the chest wall, though this is still a worryingly high chance of hitting the LV even if your catheter is inserted correctly. 

All of these studies have significant limitations, most notably that their calculated success and failure rates are purely theoretical, based on idealized calculations using CT measurements of tissue depth in which "correct" anatomic positioning is assured. Thus validity of their conclusions for a provider caring for a crashing penetrating trauma patient in the chaotic prehospital environment is minimal. There is a distinct lack of real-world data regarding the practice of needle decompression. No randomized controlled trials or even prospective observational studies appear to exist in the literature.

Even taking this into account, the documented high rates of failure of "traditional" needle decompression and the theoretical advantage -- or at the least, viability -- of a lateral approach have prompted several organizations to specifically list it in their recommendations as an "alternate" site for needle decompression. Most notably, the Committee for Tactical Combat Casualty Care (TCCC), authors of guidelines for trauma care of US servicemen and women injured in combat, adopted the 4/5-AA as an alternate site in their manuals beginning in 2012. The Tactical Emergency Casualty Care (TECC) guidelines, which were created to adapt to the TCCC guidelines to tactical EMS care in the civilian realm, share this recommendation.

Take home:

- There is no validated study to support the use of the 2-MC as the optimal location for needle decompression.
- Needle decompression at the 2-MC is associated with a high failure rate, 25-50% in some studies.
- Radiologic studies confirm the viability of needle decompression using a lateral approach.
- Lack of real-world studies of needle decompression limit application of radiologic conclusions to prehospital care.
- Several trauma organizations have adopted a lateral approach for needle decompression into their guidelines and manuals.
- Use of an 8cm rather than the standard 5cm catheter may improve chance of reaching the pleural cavity, but may also increase chance of injuring vital structures such as the left ventricle.
- Prehospital providers likely need more education, preferably with high-fidelity simulators, to ensure proper understanding of anatomic positioning in both anterior and lateral approaches.

References:
1) Emerg Med J. 2003 Jul;20(4):383-4.
2) Anesth Analg. 2007 Nov;105(5):1385-8.
3) Prehosp Emerg Care. 2009 Jan-Mar;13(1):14-7.
4) Arch Surg. 2012 Sep;147(9):813-8.
5) Acad Emerg Med. 2011 Oct;18(10):1022-6.
6) J Trauma Acute Care Surg. 2014 Apr;76(4):1029-34.
7) Needle Decompression of Tension Pneumothorax Tactical Combat Casualty Care Guidelines Recommendation 2012-05. July 6, 2012.
8) J Special Operations Medicine. 2011 Summer/Fall;11(3):104-22.

Submitted by Daniel Kolinsky, PGY-2 with additions from C. Sam Smith, PGY-3.

Brought In By Ambulance, #1: Vagal maneuvers in SVT

In this section, we will highlight EBM queries targeted to the prehospital care of patients.


Without further ado...
You respond to a call-out for "palpitations." You arrive on-scene to find a middle-age female patient who is awake, well-oriented, and talking to you in complete sentences. She is complaining of her heart "fluttering," and reports feeling somewhat short of breath and anxious. She reports a prior history of palpitations without a clear working diagnosis. Cardiac leads are placed, and the monitor shows a well-organized narrow-complex rhythm with rate in the 160s. Her BP is stable. Her skin appears warm and well-perfused. As the EMT's are working on establishing IV access, you wonder how effective vagal maneuvers are in terminating SVT.

Clinical Question:

Which vagal maneuver, if any, should be used to terminate SVT?

Literature:

In two studies, the authors found that the valsalva maneuver was more successful in terminating SVT than carotid massage or ice-to-face. In one case series, valsalva was able to terminate SVT in 54% of patients. These study authors also found that a right carotid massage was slightly more efficacious than a left carotid massage in terminating SVT (17% vs 5%). Attempting to provoke the diving reflex with ice had the same efficacy as the right carotid massage (17%)1.

A second study of prehospital treatment of SVT found that valsalva was more efficacious if the patient was supine, the maneuver was sustained for 15 seconds, and a pressure of 40mm Hg was obtained. The study again found that valsalva was more successful than carotid sinus massage and the ice-to-the face technique2.

In a third study, there was a trend toward valsalva being more effective than carotid sinus massage.  Valsalva had a success rate of 19.4% vs 10.5% for carotid sinus massage, though these figures did not reach statistical significance. When initial carotid massage did not resolve the SVT, valsalva was able to convert in 16.9% cases, versus 14% when carotid massage was used after failed valsalva.  Overall, the conversion rate was 27.7%3.

Valsalva maneuver is inherently safer than a carotid massage, as there is no risk of causing decreased carotid perfusion or dislodging clot. The most difficult part is ensuring full patient participation, especially in pediatric patients. One method that has been suggested to promote valsalva in pediatric patients is asking the child to blow through a straw. Several reports also suggest that valsalva maneuver is more efficacious than carotid massage in terminating SVT. There is also limited data to suggest that a right carotid massage is better than a left carotid massage. Given that Valsalva is safer and may be more efficacious, attempts at terminating SVT should begin with Valsalva.

Take home points:

- In available reports, valsalva maneuver appears to be the most efficacious of vagal maneuvers in terminating SVT. It may be effective anywhere from 20-50% of the time.

References:
1. Mehta D, Wafa S, Ward DE, Camm AJ. Relative efficacy of various physical manoeuvres in the termination of junctional tachycardia. Lancet. 1988;1(8596):1181.
2. Smith G, Morgans A, Boyel M. Use of the Valsalva manoeuvre in the prehospital setting: a review of the literature. Emerg Med J. 2009 Jan;26(1):8-10
3. Lim SH, Anantharaman V, Teo WS, Goh PP, Tan AT. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998 Jan;31(1):30-35

Contributed by Steven Hung, PGY-2

Rigid Backboard for Spinal Immobilization?

You are working a busy overnight shift when you see EMS bring in a “trauma packaged” patient – a young, healthy-appearing female, on a hard backboard and with a C-collar in place. Per their report, she was the restrained driver of a vehicle struck from behind at a low rate of speed while stopped at a red light. The patient denies LOC, but is endorsing pain in her neck and all the way down her back. She is complaining that the backboard is uncomfortable and making her back pain worse.

Clinical Question: 


What are the indications for prehospital rigid spine immobilization? Could it have been deferred in this patient?

Literature:


Despite the dogmatic and traditional use of rigid backboards for extrication and transport of patients with possible blunt traumatic injury of the spine, it is not an altogether benign intervention. The discomfort associated with bumpy ambulance rides while secured to a rigid board may worsen a patient’s initial presentation to the ED providers such that unnecessary spinal imaging is ordered. Prolonged transport times on rigid boards have been associated with pressure sore formation and respiratory compromise.

The use of rigid spine immobilization by prehospital providers has become based largely on mechanism of injury and concern for possible spinal cord compromise, rather than being based on signs or symptoms of spinal injury itself. This is the opposite of how diagnosis of such injuries is handled once the patient arrives to the ED. As the validation studies of the NEXUS and Canadian C-spine rules have shown, the risk of a C-spine fracture in a patient with normal mental status and without clinical signs or symptoms of spinal cord injury or distracting injury is vanishingly small.

With this in mind, the National Association of EMS Physicians (NAEMSP) and the American College of Surgeons Committee on Trauma published a position paper in the journal Prehospital Emergency Care entitled “Indications for Prehospital Spinal Immobilization.” This paper (and the accompanying resource document) outlines who should and should not be immobilized based on best evidence.

To begin, patients must first be assessed for a mechanism of injury capable of causing spinal cord injury. This is somewhat open to interpretation by EMS providers, and can vary for different patient populations (i.e., a fall from standing would be a very low-risk mechanism for healthy young adult male but much higher risk in an elderly, frail female). The document specifically addresses penetrating wounds, based on evidence published in a paper in the Journal of Trauma in 2010. Basically, if a penetrating wound to the head, neck, or torso does not obviously affect the area of the spine and is not associated with evidence of spinal injury (including focal neurologic deficits), there is no need for rigid immobilization.

If the mechanism is determined to be a risk for spinal cord injury, the EMS provider must then perform a spinal assessment, which is largely derived from the NEXUS and Canadian rules for C-spine imaging. The spinal assessment is “positive” if there is any midline tenderness, palpable/visible midline deformity, or a new neurologic deficit. Immobilization must also be considered for those in which a spinal assessment is unreliable. This includes patients with altered mental status, who are intoxicated with alcohol or drugs, who have a painful distracting injury (by NAESMP criteria, a long bone fracture proximal to the wrists or ankles), or who are otherwise unable to fully participate in the exam due to a language barrier or due to age (i.e., pre-verbal pediatric patients).

If this assessment is negative, NAESMP recommends a C-collar should still be placed if the patient is over 65 (due to increased risk of C-spine injury in this population), but the patient does not require further spinal immobilization and can be transported in position of comfort. Obviously, a C-collar should be placed on any patient if there is midline tenderness in the C-spine.

Interestingly, a study from the Journal of Emergency Medicine published in 2013 reported data from a high-speed infrared motion analysis of healthy volunteers that showed those who extricated themselves with a C-collar in place had less spinal motion than those who were told to hold still while EMS crews attempted extrication themselves. Thus, if the patient is able to extricate themselves and able to ambulate, they should be allowed to do so. If their spinal assessment is positive, they can then be secured to the stretcher with seatbelts, which has been shown to be as effective at immobilizing the T- and L-spine as a rigid backboard. If the patient cannot self-extricate, they can be extricated using standard equipment and transported to the stretcher via a hard backboard. However, he or she should be logrolled off the backboard once reaching the stretcher to minimize time spent on the hard board. The safety of this approach is reinforced by data from other studies which have shown an extremely remote risk of significant (i.e., surgical) T- or L-spine injury in restrained persons in low-risk MVCs.

Take home: 


Remember that securing to the stretcher is an effective mode of spinal immobilization. Rigid backboards should probably be reserved for transfer of a nonambulatory patient from the scene to the stretcher, and should be removed as soon as possible.

References:

1) Prehosp Emerg Care. 2014;18(2):306-14.
2) J Trauma. 2010;68(1):115-20.
3) J Emerg Med. 2013;44(1):122-7.
4) Spine J. 2014. PMID 24486471 [EPub].
5) J Emerg Med. 2006;31(4):403-5.
6) Injury. 2006;36(4):519-25.


Kindly contributed by Sam Smith, PGY-3.