NFL player recovery, hyperkalemia from SUX not likely here

IVAN HRONEK ih7 at msn.com
Sat Sep 15 04:42:29 BST 2007






Anesthesiology - Volume 104, Issue 1 (January 2006)


 

Review ArticleSuccinylcholine-induced Hyperkalemia in Acquired Pathologic States: Etiologic Factors and Molecular Mechanisms J.A. Jeevendra Martyn, M.D., F.R.C.A., F.C.C.M. a, *Martina Richtsfeld, M.D. bDavid O. Warner, M.D., Editor



a  Professor, Harvard Medical School; Director, Clinical and Biochemical Pharmacology Laboratory, Massachusetts General Hospital; and Anesthetist-in-Chief, Shriners Hospital for Children, Boston b  Research Fellow, Massachusetts General Hospital, Harvard Medical School, and Shriners Hospital for Children, Boston 
 
ONSET AND DUATION OF SUSCEPTIBILITY TO HYPERKALEMIA WITH SUCCINYLCHOLINE
 
The up-regulation of AChRs at the muscle membrane has been demonstrated within hours of denervation, the most severe form of immobilization. Even in the absence of denervation, immobilization with and without the use of muscle relaxants can lead to redistribution from the NMJ and up-regulation of AChRs in the extrajunctional areas as early as 6–12 h.33, 34 This up-regulation is not high enough to cause hyperkalemia with succinylcholine even at 24–48 h of immobilization/denervation. Persistence of the perturbation, however, will lead to further up-regulation. In a study of denervation of a single limb, hyperkalemia was observed as early as 4 days after injury, but the potassium levels did not reach lethal levels, probably related to the duration and limited (single limb) nature of the denervation.69 The concomitant presence of a pathologic state (e.g., meningitis, head injury) together with immobilization has been reported to cause hyperkalemic cardiac arrest as early as 5 days.15 Use of nondepolarizing muscle relaxants, clostridial infections, major burns, and quadriplegia are conditions involving many muscle fibers. These pathologic states associated with immobilization may be sufficient to up-regulate receptors to critical levels to cause hyperkalemia even earlier. Therefore, it may seem wise to avoid the use of succinylcholine beyond 48–72 h of denervation/immobilization or any other pathologic state where AChRs are known to increase.70 Whether severe infection alone, in the absence of confinement in bed, is a contraindication to succinylcholine, is unknown. It should be noted, however, that hyperkalemia to succinylcholine has not been reported in patients with acquired pathologic states of less than 4 days' duration.
The up-regulation of AChRs can persist as long as the condition that induced it continues to be present. Quadriplegics and paraplegics with persistent paralysis, therefore, could have the potential for succinylcholine hyperkalemia throughout life. Succinylcholine hyperkalemia has been seen 8 weeks after recovery from a transient stroke.71 Hence, the hyperkalemic response to succinylcholine after even transient stroke or denervation may last even after recovery of muscle power. In another patient, cardiac arrest after succinylcholine administration was seen weeks after mobilization and “resolution” of Guillain-Barré syndrome.72 A pathologic state causing direct damage or inflammation to muscle (e.g., radiation to muscles, or metastatic rhabdomyosarcoma) may cause sufficient up-regulation of AChRs to cause hyperkalemia after succinylcholine.73, 74 Rhabdomyosarcoma is a muscle tumor expressing high quantities of AChRs. Compared with simple immobilization, the use of muscle relaxants will cause more profound increases in AChRs.26, 75 It is also unknown, however, when this AChR up-regulation, in critically ill intensive care unit patients who have had critical illness neuropathy/myopathy and/or muscle relaxants, reverts to normal. The recovery of muscle dysfunction can be delayed as long as 1–5 yr after critical illness and prolonged stay in the intensive care unit.76, 77 The relation of this muscle dysfunction to AChR number is unclear. Therefore, it seems prudent to avoid succinylcholine in patients who have recovered recently from critical illness, particularly if muscle function is still abnormal. Our experience with burned patients suggests that AChRs return to normal levels when wounds are healed, protein catabolism has subsided, and the patient is mobile. This healing process may take well over 1–2 yr after wound coverage in patients with major (80% body surface area) burns. If immobilization persists as a result of severe contractures or other reasons, the up-regulation will not be abated. We have observed resistance to nondepolarizers as long as 1 yr after complete healing of a 35% body surface area burn and discharge from the hospital.78 This would suggest that the chance for hyperkalemia may still be present, although the potassium levels may or may not reach lethal levels at this late stage.
 
 
Succinylcholine IS one of the medications with a potential to cause malignant hyperthermia as are all the potent anesthetic gases. The induced therapeutic hypothermia really has nothing to do with that.
Ivan, LA



> From: roydanks at hotmail.com> To: trauma-list at trauma.org> Date: Fri, 14 Sep 2007 22:09:29 -0500> Subject: RE: NFL player recoverey> > I think you have your meds confused. With some anesthetics we worry about malignant HYPERthermia. Succinylcholine is not one (I don't think, but I'm not in anesthesia). But you don't give succs to spinal cord injuries or acute burns because of hyper(?)kalemia (Ragnar, et al, you are welcome to correct me). He wouldn't necessarily be intubated if the injury is low enough. Recall that C3-4-5 keep the diaphragm alive. I think he was C6.> > Medical cardiac arrest, traumatic cardiac arrest and acute spinal cord injuries are three VERY different animals...I wouldn't get too excited over a few saves. > > RRD> > > > > Date: Fri, 14 Sep 2007 13:05:50 -0700> From: fpcems at yahoo.com> To: trauma-list at trauma.org> Subject: RE: NFL player recoverey> > I was watching national news last nite, and I guess the hypothermia was started bycool IV therapy was started in the ambulance. Whatever happened after that, couldnt say. I would assume that this patient would be intubated....I have a couple of questions about that. Would Succs be indicated or no, b/c of the side effect of maliginant hypothermia? > > I believe a field trial of induced hypothermia post cardiac arrest is happening or is going to happen with Boston EMS. There is an article about a saved patient and this therapy on boston.com. > > dave> > > Roy Danks <roydanks at hotmail.com> wrote:> I echo your comments. Sounds great, but as I read the USA Today article, I cringed....however did the team physician get the goods to start the therapy in the ambulance? How is this covered by the > > > > Nuremberg Code - Declaration of Helsinki> > It sounds good. He may walk again...they're doing it at a big research facility. But it certainly makes one wonder what would be the response if the player's outcome hadn't been so (apparently) favorable.> > We work hard to get protocols through IRBs, things like this could potentially set us back.> > > > > > > From: KMATTOX at aol.com> Date: Thu, 13 Sep 2007 22:10:00 -0400> To: trauma-list at trauma.org> Subject: Re: NFL player recoverey> > We each have and will be asked to treat future patients with similar > protocols. We MUST be sure that any such treatment be via an IRB approved tightly > controled protocol. I have searched and searched for OUTCOME data to > support both the continuing use of steroids or this new HYPOTHERMIA treatment, > or even early decompression in acute spinal cord injury. By outcome, I am > talking about a favorable FUNCTIONAL outcome, not the hocus pocus non > functional tiny change reports from the several methylprednisolone studies. > > Because we are going to be innundated with questions, does anyone know the > exact protocol used in Miami and in this patient. Was there a lamenectomy. > Was there local hypothermia, what drugs were used. Were steroids used. > What has been the exact functional improvement and in how many patients?> > Even some of the> hypothermia in cardiac and stroke patients is marginal. > We are all being asked to buy cooling cradles and blankets for regional EMS > mandated protocols, with very very marginal , but marketing, information. ONE > MUST NOT equate the studies in MI and stroke to cervical spinal cord injury. > > > k> > > > ************************************** See what's new at http://www.aol.com> --> trauma-list : TRAUMA.ORG> To change your settings or unsubscribe visit:> http://www.trauma.org/index.php?/community/> _________________________________________________________________> More photos; more messages; more whatever – Get MORE with Windows Live™ Hotmail®. NOW with 5GB storage.> http://imagine-windowslive.com/hotmail/?locale=en-us&ocid=TXT_TAGHM_migration_HM_mini_5G_0907--> trauma-list : TRAUMA.ORG> To change your settings or unsubscribe visit:> http://www.trauma.org/index.php?/community/> > > > ---------------------------------> Be a better Heartthrob. Get better relationship answers from someone who knows.> Yahoo! Answers - Check it out. > --> trauma-list : TRAUMA.ORG> To change your settings or unsubscribe visit:> http://www.trauma.org/index.php?/community/> _________________________________________________________________> Can you find the hidden words?  Take a break and play Seekadoo!> http://club.live.com/seekadoo.aspx?icid=seek_wlmailtextlink--> trauma-list : TRAUMA.ORG> To change your settings or unsubscribe visit:> http://www.trauma.org/index.php?/community/


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