Paralysis Analysis

Using Succinylcholine to Help, Not Harm

• Christopher Suprun, NREMT-P, CCEMT-P
• October 2008 JEMS Vol. 33 No. 10
• 2008 Oct 1

Paramedicine, the practice of emergency medicine in prehospital environments, owes a great deal to medicine of the past. Prehospital medicine has grown and flourished since its inception by Roman military medical units—known as the medicus legionis. But perhaps most important in its evolution is the Hippocratic Oath, because it established the standards a physician should maintain: to practice and prescribe to the best of my ability for the good of my patients, and to try to avoid harming them. 

However, we sometimes step away from this foundation in providing “advanced” care. As the following case study shows, when clinicians ignore the situational dangers of a go-to airway drug, and possess only what I recently heard referred to as a “thin veneer of competence” in dispensing it, they often do more harm than good.

Paralysis Gone Wrong
Family members find an 82-year-old male relative with significant difficulty breathing and call 9-1-1. Medic 1 arrives on scene at 1:30 a.m. The patient is breathing 28 times per minute, his oxygen saturation is less than 50% on room air, and he has absent lower lung sounds with only wheezing in the upper lobes. His GCS is 10 (spontaneous eye opening, incomprehensible verbal response and pain withdrawal). His HR is 130 and BP is 120/95. The patient has a history of asthma and previous myocardial infarction (MI). He denies allergies, but currently takes Klor-Con, furosemide, Prednisone, metoprolol, Levothyroid, Isosorbide and spironolactone.

The crew quickly places the patient on supplemental oxygen and prepares an albuterol updraft. An IV line is placed and electrodes are attached to the patient to monitor his cardiac rhythm. 

Both a three-lead and 12-lead ECG are performed, yielding sinus tachycardia at 130 without ST changes. During transport, the patient’s oxygen saturation increases to more than 80% and wheezing is noted throughout the lungs. An updraft of albuterol and Atrovent is administered, and the patient is transported to the local emergency department (ED). 

But here’s where the story really begins. Because of the patient’s continued respiratory distress and the likelihood for respiratory arrest, he’s of concern to the ED physician, who decides the patient should be pharmacologically paralyzed for intubation. Using the rapid sequence induction (RSI) method, the physician, with only a cursory review of the patient’s history, medications and vital signs, orders his nursing staff to administer etomidate and Versed to sedate the patient and succinylcholine to induce paralysis. Shortly thereafter, the patient suffers cardiac arrest and succumbs to undiagnosed hyperkalemia. 

Although this was an in-hospital situation, it could have easily happened to the EMS providers with whom the patient’s care originated—or any of us who utilize succinylcholine-based RSI methods. 

The Bigger Picture
Furosemide tends to cause hypokalemia, but the patient was taking potassium chloride (Klor-Con)  to counteract this tendency and normalize potassium levels. Further clues to the patient’s hyperkalemic history included the spironolactone, which is a weak diuretic, sometimes used in combination with other diuretics. Unlike Lasix, spironolactone doesn’t cause hypokalemia, but rather limits the excretion of potassium, potentially causing a “relative” hyperkalemia or at least a higher-than-normal potassium level.

There’s a common misconception that peaked T-waves will occur with hyperkalemia. In reality, they occur less than half the time. The lack of peaked, or tall, T-waves shouldn’t lead us to believe that hyperkalemia does or doesn’t exist. Hyperkalemia shouldn’t be assumed without either lab or field chemistry performed to confirm or rule out the condition using a lead II dynamic ECG tracing. There’s some evidence that peaked T waves in the precordial leads are more accurate.

In this case study, it was a physician who made the error in judgment on the patient’s airway, but EMS crews are often in the same situation, with too many decisions to make and too little time to manage a patient’s airway while preparing for transport to definitive care. 

Across the U.S., EMS organizations are using RSI to facilitate intubation in a host of patients, from trauma victims to those with congestive heart failure, and some field providers have called for using the procedure more frequently in the field. Consistently, systems use short-acting succinylcholine (Anectine, aka “suxx”) to induce paralysis in patients receiving the procedure, despite the inherent dangers of the medication.

And RSI use has increased dramatically in the past 10–15 years as more ground units attempt to use the same skill set as their flight colleagues, often without similar training requirements, such as mandatory operating room rotations or minimum successful intubations per month or quarter. These services have met with considerable criticism as repeated studies indicate that patients don’t fare better when intubated in the field, much less when paralyzed using RSI.15–19 

Multiple problems exist with RSI, including appropriate dosing of both sedatives and paralytics, patient selection into the RSI group and oversight of the procedure.   Hyperkalemia is just one of many negative interactions that succinylcholine has with other medications and with irregular patient medical conditions. Given the difficulties of this specific drug, it may make sense to eliminate this issue in the equation.

Suxx in Action
Many departments that utilize succinylcholine do so because of its short-acting nature. Whereas other paralytics can last for 45 minutes or longer, the depolarizing neuromuscular blocker succinylcholine lasts only five to 15 minutes.1–4 

Most paralytics are non-depolarizing; succinylcholine is the only polarizing one. It binds to muscarinic and nicotinic receptors and remains bound to the receptor site, causing muscle depolarization. Succinylcholine takes effect more quickly than non-depolarizing agents because pseudocholinesterase, an 
enzyme in the drug, causes natural degradation, but unlike acetylcholine (ACh), succinylcholine binds longer than ACh. 

Succinylcholine’s side effects include elevations in intracranial, intraocular and intragastric pressures; muscular fasciculation; rhabdomyolysis; and myoglobinuria.5–7 Additionally, negative inotropic and chronotropic effects may occur, and the drug has been associated with malignant hyperthermia, hyperkalemia, hypertension and dysrhythmias.8–11 Succinylcholine is also contraindicated in patients with crush injuries, glaucoma, penetrating eye injuries, neuromuscular disease, spinal trauma and patients who have experienced burns more than 24 hours earlier. 

Hyperkalemia, which often causes cardiac dysrhythmias, can occur when the patient treated with succinylcholine has an undiagnosed elevated potassium level. It can also cause certain hyperkalemia-related cardiac disturbances, even when initial serum potassium levels are normal.12 Moreover, repeated dosages of succinylcholine, required because of its short-acting nature, may precipitate ECG changes at the nodal level, causing bradycardias and periods of asystole.13 This is especially dangerous in pediatric patients, but given the fact that any patient who would require the RSI procedure is already seriously ill or injured, depressing cardiac output may not be appropriate either.

Rethinking RSI
Beyond the pharmacologic issues specific to the drug, there’s what I call the “blame-and-excuse” factors involved with RSI and succinylcholine. The American Heart Association (AHA) refers to intubation as definitive airway management, and it remains so in paramedic practice and training. RSI has created an opportunity for paramedics to place endotracheal (ET) tubes in patients who will require an airway prior to reaching a state of apnea, with the resulting acidosis and bradycardias likely to co-exist.

However, many EMS systems choose to do RSI because providers can take the risks associated with removing a patient’s ability to breathe and yet lower their responsibilitywith the short-acting nature of succinylcholine. Many medics think that if they miss the tube, it isn’t a big deal because anyone can bag for 10–15 minutes, but this misses the entire point of RSI. 

RSI intubation involves giving drugs that paralyze and then successfully placing the tube. It’s an issue of airway education and training, not which drugs are in the toolbox. RSI simply facilitates paralysis pharmacologically. Any paramedic can push drugs and create paralysis. Short-acting paralysis via succinylcholine is no better than rocuronium or any other non-depolarizing paralytic if the crew doesn’t successfully intubate the trachea. The difference is the patient regains muscle tone more quickly, but is still without a definitive airway and still severely ill or injured.

The follow-up argument in favor of short-acting paralysis is that the intubation itself doesn’t matter because of the availability of rescue airways (Combitube, LMA and King Airway). If the intubation doesn’t matter, the period of paralysis should be secondary. If an EMS crew decides to induce paralysis in a patient to facilitate intubation, they should be well-practiced in ET intubation (discussed in “Hall of Fame Skills,” July 2007 JEMS) with a strong understanding of the difficulty in the airway they’re planning to manage. 

Studies have shown that airway management should be focused on advanced training, regular experience and close monitoring of a limited group of providers to be successful—maximizing opportunities to perform the skill set.14 Difficult airways don’t always have to be managed with ET intubation, and perhaps it’s better to plan to use another airway management maneuver prior to compromising the patient’s ability to support their own effort at some level.

A final issue is the lack of understanding that RSI doesn’t involve just succinylcholine, but also powerful sedatives, which will add to the bradycardic nature of succinylcholine. Versed and Valium both have significant bradycardic and hypotensive effects in varying degrees and should also be an area of concern for providers.

One responder from a major metropolitan city told me, “I think RSI has its place, but there’s a complacency factor [on the part of my department regarding training]. We don’t have CE on the procedure; just a protocol. … We don’t get the training we need.”

His department recently had a case where a patient had fallen approximately 30 feet from an extension ladder and was intubated using short-acting etomidate and succinylcholine. The patient didn’t receive Versed, as required by protocol, and was awake as a flight crew placed his ET tube. Throughout the flight and transfer to the hospital, the patient was aware of his surroundings, but notsedated. Although this patient had an accelerated heart rate, RSI is a procedure that requires multiple medical calculations almost simultaneously to ensure safe, effective, sufficient paralysis.

Although RSI has its place in EMS, we must recognize the inherent dangers of the procedure and move toward a standard requiring organizations that perform RSI to have rigorous training programs associated with their protocols and pharmacologic agents.

Conclusion
Whenever possible, EMS should treat the patient’s condition. If we’re unable to treat the patient due to a lack of equipment or training, we should treat our patient’s pain. In all cases, though, we shouldn’t do harm. This ideal has nothing to do with negligence, but rather the fundamental tenet of doing what’s right for our patients. 

In multiple discussions, physicians have argued against field providers having such tools as RSI because they’re too dangerous. They spend a lot of time complaining of the danger; they should give equal time to training and remediation to ensure their EMS providers have both the tools and the training to do their job properly. No one should believe that RSI itself is dangerous, but like a 16-year-old driver, providers shouldn’t be given the keys to a Ferrari without proper training and experience. RSI is no different. Systems with a medical need for the procedure should approach it with similar awareness, understanding the fundamental implications that go along with removing a patient’s ability to breathe on their own. Add to that existing concern that the cocktail we’ve been using may not be appropriate.

For years, it’s been documented that succinylcholine has numerous disadvantages to non-depolarizing agents. EMS should demand better medications with which to treat illnesses and injuries, rather than risk further damage to our patients and to the reputation of prehospital providers everywhere. jems

Christopher Suprun, NREMT-P, CCEMT-P, is a frequent EMS and fire author and presenter at conferences across the country. He can be contacted through his Web site at www.consurgo.com.

References

1. Bean JD, Rogers MC: “Anesthetic considerations and pain management in the pediatric intensive care unit.” In Rogers MC (ed): Textbook of Pediatric Intensive Care. Williams & Wilkins: Baltimore, Md., 1987. pp. 1347–1381.

2. Glaser RB: “Sedation and rapid induction anesthesia for emergency intubation.” In Callahan ML (ed): Current Therapy in Emergency Medicine. BC Decker: Toronto, Ontario, 1987. pp. 21–26.

3. Leonard F: “Pain control: Anesthesia and analgesia.” In Rosen P, Baker FJ, Barkin RM, et al (eds): Emergency Medicine Concepts and Clinical Practice. Mosby: St. Louis, Mo., 1988. pp. 295–307.

4. Thompson JD, Fish S, Ruiz E: “Succinylcholine for endotracheal intubation.” Annals of Emergency Medicine. 11(10):526–529, 1982.

5. DeGarmo BH, Dronen S: “Pharmacology and clinical use of neuromuscular blocking agents.” Annals of Emergency Medicine. 12(1):48–55, 1983.

6. Dripps RD, Eckenhoff JE, Vandam LD: Introduction to Anesthesia: The Principles of Safe Practice. WB Saunders: Philadelphia, Pa.,1988. pp. 166–187.

7. Talucci RC, Shaikh KH, Schwab CW: “Rapid sequence induction with ortracheal intubation in the multiply injured patient.” The American Surgeon. 54(4):185–187, 1988.

8. Morris IR: “Techniques of endotracheal intubation and muscle relaxation.” In Rosen P, Baker FJ, Barkin RM, et al (eds): Emergency Medicine Concepts and Clinical Practice. Mosby: St. Louis, Mo.,1988. pp. 69–82.

9. Thompson MA: “Muscle relaxant drugs.” British Journal of Hospital Medicine. 23(2):153–168, 1980.

10. Miller RD, Savarese JJ: “Pharmacology of muscle relaxants and their antagonists.” In Miller RD (ed): Anesthesia. Churchill Livingstone: New York, N.Y., 1986. pp. 889–943.

11. Backofen JE, Rogers MC: “Emergency Management of the Airway.” In Rogers MC (ed): Textbook of Pediatric Intensive Care. Williams & Wilkins: Baltimore, Md., 1987. pp. 57–79.

12. Laurin EG, Sakles JC, Panacek EA, et al: “A comparison of succinylcholine and rocuronium for rapid sequence intubation of emergency department patients.” Academy of Emergency Medicine. 7(12):1362–1369, 2000.

13. Schoenstadt DA, CE Whitcher: “Observations on the mechanism of succinylcholine-induced cardiac arrhythmias.” Anesthesiology. 24:359–362, 1963.

14. Fakhry SM, Scanlon, JM, Robinson L, et al: “Prehospital rapid sequence intubation for head trauma: Conditions for a successful program.” Journal of Trauma. 60(5):997–1001, 2006.

15. Stockinger Z, McSwain N: “Prehospital endotracheal intubation for trauma does not improve survival over bag-valve-mask ventilation.” Journal of Trauma. 56(3):531–536, 2004.

16. David D, Peay J, Sise M, et al: “The impact of prehospital endotracheal intubation on outcome in moderate to severe traumatic brain injury.” Journal of Trauma. 58(5):933–939, 2005.

17. DiRusso S, Sullivan T, Risucci D, et al: “Intubation of pediatric trauma patients in the field: Predictor of negative outcome despite risk stratification.” Journal of Trauma. 59(1):84–91, 2005.

18. Wang HE, Peitzman A, Cassidey L, et al: “Out-of-hospital endotracheal intubation and outcome after traumatic brain injury.” Annals of Emergency Medicine. 44(5):439–450, 2004.

19. Wang HE, Kupas DF, Hostler D, et al: “Procedural experience with out-of-hospital endotracheal intubation.” Critical Care Medicine. 33(8):1864–1865, 2005.

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