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  1. This can happen….
  2. First Case Reports
  3. What they recommended…1920’s
  4. Pathogenesis and Etiology
  5. Calcium in normal VS MH muscle
  6. Calcium
  7. Triggers for MH
  8. Convincing Stats
  9. Ambulatory Surgery Center (ASC) Key Actions…
  10. Communication is KEY
  11. Bibliography
  12. Bibliography
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This can happen…. Use media converter to get a you tube video into a PPT 3 First Case Reports 4 What they recommended…1920’s Dr. Jones wrote a letter to the “sister of the house”Dear Miss….” in view of what occurred in the case of mother and brother….Family member should never have chloroform for an operation, but rather any operation should be with either gas and oxygen or ether by open method preceded by morphine gr 1/6 and atropine gr 1/20 ….and the risks should be practically negligible….Yours truly” #1 reference same as abovePicture from: 5 Pathogenesis and Etiology Syndrome genetically transmitted-heterogenic (more than one gene) Mutation in Ryanodine receptor–abnormal Ca releaseIncreased Ca release greater than Ca removalHypermetabolic state-no compensatory mechanismsDepletes ATP and glycogen storesAccelerated metabolism no muscle relaxationincreased O2 consumption excess CO2 production The increased rate of CO2 and respiratory acidosis leads to release of catecholamines which in turn cause vasoconstriction and tachycardia. The peripheral vasoconstriction leads to a powerful and overwhelming hyperthermic syndrome and rapid deterioration in overall cellular metabolism and eventual death of cells and demise of patient. #2 10 Calcium in normal VS MH muscle Induction of MH caused by abnormalities in the Ca release of the SR.LEFT is Normal function of Ca: remember that muscle contraction, glycolysis and mitochondrial function are regulated by cytoplasmic Ca. In the normal relaxation/contraction cycle (left) Ca is pumped into the ST by Ca ATPase to initiate relaxation, stored in the lumen in association with calsequestrin and released thru a Ca release channel to initiate contraction. Glycolytic and metabolism proceed only rapidly enough to maintaine the energy balance of the cell. The Ca release can be regulated by Ca itself, ATP, Mg and calmodulin and even when stimulated has a short open time.RIGHT: The abnormal malignant hyperthermia Ca release channel is sensitive to lower concentrations of stimulator for opening, releases Ca at enhanced rates, and does NOT close rapidly. The abnormal channel floods the cell with Ca and overpowers the Ca pump that ordinarily lowers cytoplasmic Ca. Sustained muscle contraciton account the rigidity and sustained glycoytic and metabolism . This causes a build up of lactic acid, Co2 and heat with enhanced O2 consumption and ultimate depletion of energy stores. This leads to systemic manifestations and ultimately cell death. Reference: #4 Malignant Hyperthermia by David MacLennan and Michael S Phillips. Science, vol 256 may 8 1992, p. 789-794 11 Calcium 12 Triggers for MH SuccinylcholineAnesthetic GasesHalothaneIsofluraneEnfluraneSevofluraneDesfluraneMethoxyfluraneCyclopropaneOthers arepotassium salts, curare and phenothiazines Clinical Anesthesia, Barash #3. pg 598-621Succs pic: pic: 13 Convincing Stats Mortality: Hospital vs. Ambulatory Settings January 2006-May 2008 MHAUS MH Hotline503 calls from hospitals28 determined MH-2 deaths - (7% mortality) 44 calls from ambulatory settings13 determined MH-3 deaths-(21% mortality) Fulminant MH episode occurring outside of the hospital setting is more likely to lead to a bad outcome 30 Ambulatory Surgery Center (ASC)Key Actions… Recognition of suspected MHD/C of trigger agentsInitiation of treatmentInitiation of emergent MH transfer planTransfer considerations/capabilitiesImplementation of transfer decisionNotification of receiving health care facility-communication 32 Communication is KEY Patient DataEnd Tidal CO2 declining or normalHeart rate stable or decreasing-no dysrhythmiasIV Dantrolene-point of administrationTemperature decliningGeneralized muscle tone statusDirect Personal CommunicationASC anesthesia care provider and Critical care, primary or ER physician 34 Bibliography Allen, G. L. (1998). Sensitivity and Specificity of the Caffeine-halothane contracture test. Anesthesiology , 88 (3), 579-88.ASC. (2011). Retrieved June/July 2011, Ambulatory Surgery Center Association. http://ascassociation.orgChristian, A. E. (1989). Is there a relationship between masseteric muscle spasm and malignant hyperpyrexia? Bristish Journal of Anesthesia , 62, 540-44.Denborough, M. (1998). Malignant Hyperthermia. The Lancet , 352, 1131-36.Deufel, T. G. (1992). Evidence for Genetic Heterogeneity of Malignant Hyperthermia Susceptibility. American Journal of Human Genetics , 50, 1151-61.Ellis, F. H. (1990). Clinical Presentation of suspected malignant hyperthermia during anesthesia in 402 probands. Anaesthesia , 45, 838-41.Fletcher, J. R. (1999). Comparison of European and North American Malignant Hyperthermia Diagnostic Protocol Outcomes for Use in Genetic Studies. Anesthesiology , 90 (3), 654-61.Glahn, K. E. (2010). Recognizing and managing a malignant hyperthermia crisis: guideline from the European Malignant Hyperthermia group. British Journal of Anaesthesia , 105 (4), 417-410.Gronert, G. A. Clinical Management of Malignant Hyperthermia.Hall, S. (2001). General Pediatric Emergencies Malignant Hyperthermia Syndrome. Anesthesiology Clinics of North America , 19 (2), 367-82.Harrison, G. I. (1992). Malignant Hyperthermia. Anaesthesia , 47, 54-56.Hartung, E. K. (1996). Malignant hyperthermia (MH) diagnostics: a comparison between the halothane-caffeine-and the ryanodine-contracture-test results in MH susceptible, normal and control muscle. ACTA Anaesthesiologica Scandinavica , 40, 437-44.Hommertzheim, R. S. (2006). Malignant Hyperthermia: the perioperative nurse's role. AORN Journal , 83 (1), 149-164.Hopkins, P. H. (1994). Diagnosing malignant hyperthermia susceptibility. Anaesthesia , 49, 373-75.Hopkins, P. (2000). Malignant Hyperthermia: advances in clinical management and diagnosis. British Journal of Anaesthesia , 85, 118-28. 36 Bibliography Isaacs, H. B. (1993). False-negative results with muscle caffeine halothane contracture testing for malignant hyperthermia. Anesthesiology , 79 (1), 5-9.Jurkat-Rott, K. M.-H. (2000). Genetics and Pathogenesis of Malignant Hyperthermia. Muscle and Nerve , 23, 4-17.Larach, M. L. (1994). A Clinical Grading Scale to Predict Malignant Hyperthermia Susceptibility. Anesthesiology , 80 (4), 771-79.Larach, M. R. (1997). Prediction of Malignant Hyperthermia Susceptibility by Clinical Signs. Anesthesiology , 66 (4), 547-50.Malignant Hyperthermia: An OR Emergency. (2000). Plastic Surgical Nursing , 20 (4), 222-26.Martin, S. V. (2000). Malignant Hyperthermia: A case study. Seminars in Perioperative Nursing , 9 (1), 27-36.MHAUS. (2011). Retrieved January 2011, from Malignant Hyperthermia Association of the United States: www.MHAUS.orgNelson, T. L. (1996). Dantrolene Sodium can Increase or Attenuate Activity of Skeletal Muscle Ryanodine Receptor Calcium Release Channel. Anesthesiology , 84 (6), 1368-79.Ording, H. G. (1997). 4-chloro-m-cresol test-a possible supplementary test for diagnosis of malignant hyperthermia susceptibility. ACTA Anaesthesiologica Scandinavica , 41, 967-72.Schick, L. Malignant Hyperthermia.Should We Use Muscle Biopsy to Diagnose Malignant Hyperthermia Susceptability? (1993). Anesthesiology , 79 (1), 1-4.Stanton, C. (2010, September). Transferring patients with malignant hyperthermia. Retrieved from www.aorn.orgStolworthy, C. H. (1998). Malignant Hyperthermia: A Potentially Fatal Complication of Anesthesia. Seminars in Perioperative Nursing , 7 (1), 58-66.Tegazzin, V. S. (1996). Chlorocresol, an Additive to Commercial Succinylcholine, Induces Contracture of Human Malignant Hyperthermia-susceptible Muscles Via Activation of the Ryanodine Receptor Ca+ Channel. Anesthesiology , 84 (6), 1380-85.  37