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NEUROMUSCULAR BLOCKADE REVERSAL PRACTICE

NEUROMUSCULAR BLOCKADE REVERSAL PRACTICE. Julia lienesch & carrie mcmahon Gonzaga university PROVIDENCE SACRED HEART MEDICAL CENTER MARCH 20, 2014. STATEMENT OF THE PROBLEM. Residual neuromuscular blockade and its management are well-established topics in current literature

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NEUROMUSCULAR BLOCKADE REVERSAL PRACTICE

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  1. NEUROMUSCULAR BLOCKADE REVERSAL PRACTICE Julia lienesch& carriemcmahon Gonzaga university PROVIDENCE SACRED HEART MEDICAL CENTER MARCH 20, 2014

  2. STATEMENT OF THE PROBLEM • Residual neuromuscular blockade and its management are well-established topics in current literature • The incidence of residual blockade has not significantly declined even with the introduction of intermediate acting paralytics • From 2000-2008, 15 studies revealed 20-65% of postoperative incidence TOFR <0.9 • Associated with hypoxia, weakness, aspiration, impairment of the hypoxic ventilatorydrive, and respiratory failure

  3. RESIDUAL BLOCKADE DEFINITION • Residual blockade definition • TOFR of < 0.9 • Clinical signs and symptoms of muscle weakness in the postoperative period • Evolution of TOFR standard for extubation • 0.70.8currently 0.9 • Increased respiratory events, pharyngeal dysfunction, and aspiration risk with TOFR <0.9 (Eriksson et al, 1997)

  4. PURPOSE STATEMENT “The purpose of this study was to assess, through survey, current practices among CRNAs in states from various regions regarding the use of reversal agents after pharmacologic neuromuscular blockade.”

  5. RESEARCH QUESTIONS To what degree are reversal agents being given by CRNAs after the administration of neuromuscular blocking agents? What are the benefits and risks of neuromuscular blockade reversal? What factors influence CRNAs’ management of neuromuscular blockade reversal? How is the dose of reversal agent determined?

  6. REVIEW OF LITERATUREMONITORING • Acceleromyography monitoring gold standard • Tactile fade lost at TOFR 0.3-0.4 • 5-second head lift possible at TOFR of <0.6 • Pharyngeal tissue and upper esophageal sphincter dysfunction at TOFR 0.6-0.9  aspiration risk • Murphy et al. (2008) • Compared acceleromyography to conventional tactile TOF • TOFR ≤0.9 in PACU: 4.5% acceleromyographyvs 30% conventional, P <0.0001 • TOFR <0.7 in PACU: 0% acceleromyographyvs 13.3% conventional, P<0.001 • Acceleromyography had less respiratory events in PACU

  7. REVIEW OF LITERATUREMONITORING (Plaud et al, 2010)

  8. REVIEW OF LITERATUREMONITORING • Ulnar nerve superior site for planning emergence: • Less likelihood of direct muscle stimulation • Increased margin of safety as slower recovery vs diaphragm • 5-fold increased risk of residual block when monitoring at eye • Placement • Electrode placement 2-6cm apart

  9. REVIEW OF LITERATURETIMING • Debaene, Plaud, Dilly, & Donati (2003) • Single dose of intermediate acting paralytic to 526 patients • No reversal and > two hours post-administration • 16% TOFR of <0.7 and 45% TOFR <0.9 in PACU • Fuchs-Buder et al. (2010) • Addressed neostigmine dose for shallow levels of paralysis • Normal doses of neostigmine can produce paradoxical weakness at shallow residual paralysis (Caldwell, 1995) • Groups with TOFR 0.4 and 0.6 given neostigmine 0.01, 0.02, 0.03 mg/kg, or none • Reversal at TOFR 0.4-0.6 with neostigmine 0.02 mg/kg produced successful reversal within 10 minutes

  10. REVIEW OF LITERATURETIMING • Kim et al. (2004) • Administered neostigmine 0.07 mg/kg to surgical patients at a TOF of 1,2,3,4 • Median times from neostigmine reversal administration until a TOFR of 0.9 • TOF count 1 – 28.6minutes • TOF count 2 – 22.6 minutes • TOF count 3 – 15.6 minutes • TOF count 4 – 9.7 minutes • Authors recommend a TOF count of 4 for adequate reversal from rocuroniumwithin 15 minutes • Thilen et al. (2012) • Every 10 minutes since paralytic dose = 10% less residual block

  11. REVIEW OF LITERATURENEOSTIGMINE DOSING TOF 4/4 with minimal fade: 0.015-0.025 mg/kg TOF 2-3/4: 0.04-0.05 mg/kg Dosing >0.07 mg/kg unlikely to achieve additional effect (Kopman & Eikermann, 2009) Avoiding blanket full reversal of light paralysis will minimize paradoxical weakness effect, risk for cholinergic crisis, and side effects Most effective reversal when given >15-20 minutes prior to extubation(Brull & Murphy, 2010)

  12. REVIEW OF LITERATUREPONV SIDE EFFECT • King et al. (1988) said Yes to PONV • 38 orthopedic patients: Neostigmine 2.5mg/Atropine 1.2mg, 68% PONV compared with 32% at 24hr postop, (P<0.01) • Joshi et al. (1999) said No difference • 100 ambulatory surgery, Neostigmine 2.5mg/Robinul 0.5mg, (P<0.05) • Hovorka et al. (1997) said No difference • DB*, 162 hysterectomy cases. Neostigmine 2mg/Robinul 0.4mg (P<0.05) • Cheng et al. (2005) said No difference • Lit review, 933 patients, compared Neostigmine 2.5 vs 1.5mg doses and Robinul vs Atropine (P=0.08) • Lovstad et al. (2001) said Yes to nausea • DB, 90 lap-gyn cases, Mivacurium, Neostigmine 0.05mg/kg + Robinul 0.01mg/kg. (P=0.03). First 6hrs, 30% vs 11% nausea. No difference in vomiting. *(DB=double blind)

  13. METHODOLOGY • Qualitative study • Online survey utilizing SurveyMonkey • Survey distributed via state CRNA organizations • Participants • 289 CRNA survey participants • Participating states: WA, AZ, NC, MD

  14. FINDINGSREVERSAL AND TIME

  15. FINDINGSREVERSAL AND TIME

  16. FINDINGSREVERSAL AND TIME

  17. FINDINGSREVERSAL AND TIME

  18. FINDINGSTOP 3 FACTORS

  19. FINDINGSPATIENT FACTORS

  20. FINDINGSSIDE EFFECTS

  21. FINDINGSMONITORING

  22. RECOMMENDATIONS • Time from last paralytic dose is not an adequate determinant of residual blockade • Monitoring of blockade should be standard practice • Acceleromyography superior as tactile fade lost at TOFR of 0.4 • Not all patients need a full reversal dose • Risk for paradoxical weakness and increased side effects • Majority can benefit from a partial reversal dose • Increased PONV is inconclusive and appears to be dose-dependent • Faster recovery after reversal with increasing TOF count • Allow 15-20 minutes after reversal for maximal effect

  23. REFERENCES Brull, S.J., & Murphy, G.S. (2010). Residual neuromuscular block: lessons unlearned. Part II: methods to reduce the risk of residual weakness. Anesthesia and Analgesia, 111(1), 129-140. Cheng, C., Sessler, D. I., & Apfel, C. C. (2005). Does neostigmine administration produce a clinically important increase in postoperative nausea and vomiting? Anesthesia & Analgesia, 101, 1349-55. Debaene, B., Plaud, B., Dilly, M., & Donati, F. (2003). Residual paralysis in the PACU after a single intubating dose of nondepolarizing muscle relaxant with an intermediate duration of action. Anesthesiology, 98(5), 1042-1048. Retrieved from http://journals.lww.com/anesthesiology/Fulltext/2003/05000/Residual_Paralysis_in_the_PACU_after_a_Single.4.aspx Eriksson, L. I., Sundman, E., Olsson, R., Nilsson, L., Witt, H., Ekberg, O., & Kuylenstierna, R. (1997). Functional assessment of the pharynx at rest and during swallowing in partially paralyzed humans: Simultaneous videomanometry and mechanomyography of awake human volunteers. Anesthesiology, 87(5), 1035-1043. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9366453 Fuchs-Buder, T., Meistelman, C., Alla, F., Grandjean, A., Wuthrich, Y., & Donati, F. (2010). Antagonism of low degrees of Atracurium-induced neuromuscular blockade. Anesthesiology, 112(1), 34-40.

  24. REFERENCES • Hovorka, J., Korttila, K., Nelskyla, K., Soikkeli, A., Sarvela, J., Paatero, H., ... Yli-Hankala, A. (1997). Reversal of neuromuscular blockade with neostigmine has no effect on the incidence or severity of postoperative nausea and vomiting. Anesthesia & Analgesia, 85, 1359-61. • Joshi, G. P., Garg, S. A., Hailey, A., & Yu, S. Y. (1999). The effects of antagonizing residual neuromuscular blockade by neostigmine and glycopyrrolate on nausea and vomiting after ambulatory surgery. Anesthesia & Analgesia, 89, 628-31. • Kim, K., Cheong, M., Lee, H., Lee, J. (2004) Tactile assessment for the reversibility of rocuronium induced neuromuscular blockade during propofol or sevoflurane anesthesia. Anesthesia Analgesia, 99, 1080-1085. • King, M. T., Milazkiewicz, R., Carli, F., & Deacock, A. R. (1988). Influence of neostigmine on postoperative vomiting. British Journal of Anaesthesia, 61, 403-6. • Kopman, A.F., & Eikermann, M. (2009). Antagonism of non-depolarising neuromuscular block: current practice. Anaesthesia, 64, 22-30.

  25. REFERENCES • Lovstad, R. Z., Thagaard, K. S., Berner, N. S., & Raeder, J. C. (2001). Neostigmine 5mcg/kg with glycopyrrolate increases postoperative nausea in women after laparoscopic gynaecological surgery. ActaAnaesthesiologica, 45, 495-500. • Murphy, G. S., Szokol, J. W., Marymont, J. H., Greenberg, S. B., Avram, M. J., Vender, J. S., & Nisman, M. (2008). Intraoperative Acceleromyographic Monitoring Reduces the Risk of Residual Neuromuscular Blockade and Adverse Respiratory Events in the Postanesthesia Care Unit. Anesthesiology, 109, 389-398. • Plaud, B., Debane, B., Donati, F., Marty, J. (2010) Residual paralysis after emergence from anesthesia. Anesthesiology, 112(4), 1013-1022. • Thilen, S. R., Hansen, B. E., Ramaiah, R., Kent, C. D., Treggiari, M. M., & Bhananker, S. M. (2012). Intraoperative neuromuscular monitoring site and residual paralysis. Anesthesiology, 117, 964-972.

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