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10/15/15
1
UND Nurse Anesthesia Student Presenta6ons
2015 Fall Educa6onal Mee6ng North Dakota Associa6on of Nurse Anesthe6sts
Bismarck, ND
Anesthe6c Management & Considera6ons of the Pediatric
Pa6ent with an Atrial Septal Defect
Luke Schumacher, SRNA
Introduc6on • Congenital Heart Disease – 40,000 children diagnosed with CHD yearly, 10% of that number have an Atrial Septal Defect (ASD)
– Most common ASD is known as a Secundum ASD • Pathophysiology of ASD – LeS-‐to-‐right shunt is most common – Symptoms vary due to size, site and direc6on of the shunt flow
– Symptoms can be undetected due to acyano6c characteris6cs
McEwan, 2013
DiNardo et al., 2011
Geva et al., 2014
hZp://posterng.netkey.at/esr/viewing/index.php?module=viewing_ poster&task=viewsec6on&pi=112981&6=352292&searchkey=
Case Informa6on • Surgical Procedure: Nasal adenoidectomy and bilateral ear
exam • Male, 17 months • 11.5kg • NKDA • ASA 1 • PMH: ASD (diagnosed 2 days aSer birth), resolved
pneumonia, pulmonary hemorrhage, persistent pulmonary hypertension of the newborn (PPHN), respiratory distress, sepsis, feeding difficul6es
• Imagining: Day 2 Echo showing moderate secundum ASD, Day 6 Echo showing a small-‐moderate secundum ASD (~3mm)
Case Informa6on
• PSH: None • Medica6ons: Tylenol PRN • Pre-‐op labs: none • Pre-‐op vital signs: – BP: 88/42 – HR: 110 – RR: 26 – T: 36.7 – SaO2: 100
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Case Informa6on
• Airway evalua6on: – Mallampa6 I – Neck: Full ROM – Den66on: intact, none missing or loose
• Per6nent review of systems: – No report of SOB, orthopnea, or “blue spells” at the 6me of surgery
– S1S2, RRR, absent for murmurs
Anesthe6c Course
• Technique: GETA – Mask Induc6on: Sevoflurane 8% and Oxygen 8L/min • IV start-‐ 24 ga.
– LR at 42ml/hr (case total: 100ml) – Fentanyl 15 mcg IV – Ondansetron 1mg IV – Dexamethasone 2 mg IV
• 4.5 cuffed ETT inserted with Mac 2 x 1 aZempt – Maintenance: • Sevoflurane 2.4%, oxygen 1.5 L/min, and air 1.5 L/min
Anesthe6c Course
• Emergence – Deep extuba6on with sevoflurane 2.4% and oxygen 8L/min
– Transferred to PACU with blow by oxygen 6L/min – PACU: unevennul x 1 hour then discharged home
Discussion
• Determinates of flow direc6on between atrium: – Size of the ASD – SVR – PVR – Ventricular Compliance – Flow ul;mately determined by the right and le> atrial pressure gradient
– Anesthesia can have a great effect on SVR and PVR
Discussion
• Recommend IV induc6on for a symptoma6c ASD
• Mask induc6on may lead to: – hypoven6la6on → hypoxemia → increased pulmonary pressure → increased shunt
DiNardo et al., 2011
Discussion
• Induc6on agents: – Goal: to maintain hemodynamic stability – Propofol and Thiopental: May cause myocardial depression and vasodila6on
– Opioids in conjunc6on with pancuronium – Ketamine (1mg/kg – 2 mg/kg): Minimal change in PVR – Etomidate: Short-‐ac6ng, minimal effect on BP, HR, and CO
– Key Point: Decreased SVR and/or an increased PVR will lead to increased right-‐to-‐leS shunt flow
DiNardo et al., 2011
DiNardo et al., 2011
McEwan, 2013
DiNardo et al., 2011
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Discussion
• Maintenance: – Fentanyl or sufentanil, sevoflurane or benzodiazepine • Cau6on: synergis6c effects may reduce SVR
• Inhaled anesthe6cs: – Sevoflurane: ideal agent: minimal myocardial effect, minimal hypotension and minimal bradycardia
– Nitrous oxide: Avoid, due to expansion of air emboli
DiNardo et al., 2011
DiNardo et al., 2011
McEwan, 2013
Discussion
Avoidance of Nitrous Oxide • Nitrous oxide is 34 6mes more soluble than nitrogen
• Expansion of nitrogen increases size of air emboli
• Avoidance of air entry through IV – Me6culous set up of IV tubing, syringes, and the use of an air trapping filter
Discussion
Air Embolism • ASDs allow for a direct communica6on from venous circula6on to systemic circula6on
• Vapor lock created by air embolism – Restricts blood flow past the emboli • Leading to mul6ple outcomes
– Dependent on specific loca6on
Discussion Air Embolism Cont’d • Loca6on and size of air bubble determine signs and symptoms – Coronary arteries:
• Chest pain, hypotension, dysrhythmias, myocardial depression, ventricular failure, cardiac arrest, AV block, ST eleva6on, mill wheel murmur
– Cerebral arteries: • Abrupt headache, confusion, motor weakness, disorienta6on, hemiparesis, convulsions, LOC, coma, abnormal RR, asymmetrical pupil response
– Pulmonary arteries: • apnea, hypoxia, SOB, tachypnea, decreased ETCO2, decreased O2 satura6on, hypercarbia, acidosis
Webber et al., 2012
Discussion
Air Embolism Cont’d • Treatments: Dependent on loca6on and degree of
symptoms – Hemodynamic support: inotropes, coronary vasodilators, balloon
pump, CPR – Direct aspira6on (right side up, head down) through central catheter
(mul6-‐orifice) under fluoroscopy – Hyperbaric oxygen treatment for cerebral embolism
Kumar et al., 2014
LeDez & Zbitnew, 2005
Discussion
Air Embolism Cont’d • Preven6on of air embolism is the best prac6ce!
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Discussion Acyano;c Shunt • LeS-‐to-‐Right Flow – Typically resembles conges6ve heart failure, tachypnea and dyspnea, jugular vein disten6on, pulmonary conges6on, hepatomegaly, poor exercise intolerance
– Signs/Symptoms: usually absent unless a shunt flow is significant
Stayer, 2010 Kaye et al., 2012
Discussion
Acyano;c Shunt Management • Overall: minimize shunt flow and maintain adequate oxygena6on
• Avoid condi6ons that increase L-‐R shunt: – Low hematocrit, increased SVR, decreased PVR, hyperven6la6on,
hypothermia, and inhaled isoflurane Macksey, 2009
Kaye et al., 2012
Discussion
Cyano;c Shunt Management • Right-‐to-‐LeS – Blood bypasses lungs and unoxygenated blood is delivered to systemic circula6on
– Cyano6c presenta6on and a lack of CHF symptoms – Avoid condi6ons that increase shunt:
• decreased SVR, increased PVR, hypoxia, hypercarbia, acidosis, possible NO and ketamine
– Avoid air entrance at all costs!
Macksey, 2009
Discussion
What about An;bio;cs?? • DiNardo et al. (2011), “prophylaxis against infec6ve endocardi6s is not recommended for pa6ents with an ASD unless a concomitant valvular abnormality (mitral valve prolapse or mitral valve cleS) is present” (p. 612).
Recommenda6ons
• Aim for anesthesia: – Develop a plan that is personalized to the child’s current ASD and hemodynamics
– Limit changes in exis6ng shunt flow and provide hemodynamic stability
– Prevent any entrance of air into IV lines
– Avoid Nitrous oxide
Conclusion
Anesthesia providers must have a comprehensive understanding of ASD pathophysiology and anesthesia considera6ons to ensure safe and effec6ve care of the pa6ent with an ASD.
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References • Barash, P.G., Cullen, B.F., Stoel6ng, R.K., Cahalan, M.K., Chris6ne Stock, M. Clinical Anesthesia. 6th
ed. Philadelphia, PA: LippincoZ Williams & Wilkins; 2009. • Cladis, F.P., Davis, P.J., Motoyama, E.K. Smith’s Anesthesia for Infants and Children. 8th ed. In J.
DiNardo, A. Shukla & F. McGowen Jr (Eds.), Anesthesia for Congenital Heart Surgery (pp. 605-‐673). Philadelphia, PA: Mosby, Inc.; 2011.
• Cohen, G.A., Karamlou, T. (2015) Atrial Septal Defects. UCSF Department of Surgery. Retrieved from hZp://www.surgery.ucsf.edu/condi6ons-‐-‐procedures/atrial-‐septal-‐defect.aspx
• Djer, M.M., Ramadhina, N.N., Idris, N.S., Wilson, D., Alwi, I., Yamin, M., Wijaya, I.P. (2013). Transcatheter closure of atrial septal defects in adolescents and adults: technique and difficul6es. The Indonesian Journal of Internal Medicine, 45(3), 180-‐186.
• Farquhar, M., Fitzgerald, D.A. (2010). Pulmonary hypertension in chronic neonatal lung disease. Paediatric Respiratory Reviews, 11, 149-‐153.
• Ferri, F.F. (2015). Ferri’s Clinical Advisor. Atrial Septal Defect. Retrieved from hZp://www.clinicalkey.com
• Geva, T., Mar6ns, J.D., Wald, R.M. (2014) Atrial Septal Defects. Lancet, 383, 1921-‐1932. • Griza, G.G. (1999). Cyano6c congenital heart disease with increased pulmonary blood flow.
Pediatric Cardiology, 46(2), 405-‐425. • Kaye, A.D., Stout, T.B., Pandos, I.W., Schwartz, B.G., Baluch, A.R., Fox, C.J., Liu, H. (2012). LeS-‐to-‐
right cardiac shunt: periopera6ve anesthe6c considera6ons. M.E.J Anesthesia, 21(6), 793-‐806.
References • Kumar, D., Gadhinglajkar, S.V., Moorthy, K., Bhandari, D. (2014). Paradoxical air embolism to leS anterior
descending artery during induc6on of anesthesia in a pa6ent with an atrial septal defect. InternaPonal Anesthesia Research Society, 2(6), 66-‐69.
• LeDez, K.M., Zbitnew, G. (2005). Hyperbaric treatment of cerebral air embolism in an infant with cyano6c congenital heart disease. Canadian Journal of Anesthesia, 52(4), 403-‐408
• Macksey, L.F. (2009). Pediatric AnesthePc and Emergency Drug Guide. Sudbury, MA: Jones and BartleZ Publishers. • McEwan, A. (2013). A Prac6ce of Anesthesia for Infants and Children. Anesthesia for Children Undergoing Heart
Surgery, 5, 327-‐353.e6. • Nagelhout, J.J., Plaus, K.L. (2014). Nurse Anesthesia (5th ed.) St. Louis, MO: Saunders Elsevier. • Porta, N.F., Steinhorn, R.H. (2012). Pulmonary vasodilator therapy in the NICU: inhaled nitric oxide, sildenafil, and
other pulmonary vasodila6ng agents. Clin Perinatol, 39, 149-‐164. • Somura, J., Nakagawa, M., Ukiami, M., Sagawa, H., Furukawa, O., Hoshino, S., Fujino, H., Takeuchi, Y. (2015).
Rela6onship between electrocardiographic signs and shunt volume in atrial septal defect. Pediatrics InternaPonal. doi: 10.1111/ped.12569.
• Stayer, S. (2010). Anesthesia for the PaPent with Congenital Heart Disease Undergoing Non-‐cardiac Surgery. SPA Refresher Course; April, 2010.
• Tobis, J., Shenoda, M. (2012). Percutaneous Treatment of Patent Foramen Ovale and Atrial Septal Defects. Journal of the American College of Cardiology, 60 (18), 1722-‐1732.
• Vasquez, A.F., Lasala, J.M. (2013). Atrial septal defect closure. Cardiol Clin, 31, 385-‐400. • Webber, S., Andrzejowski, J., Fancis, G. (2002). Gas embolism in anaesthesia. BriPsh Journal of Anaesthesia, 2(2),
53-‐57.
Thank You Are There Any Ques6ons?
Vasopressin to Treat Refractory Hypotension for Pa6ents taking RAAS
Antagonists
Robert Walz, SRNA
Introduc6on
• The pathophysiologic cardiovascular condi6on that is most commonly encountered in pa6ents who require surgery is hypertension (Nagelhout & Plaus, 2014)
– 60 million Americans have a diagnosis of hypertension. (Thoma, 2013)
– The risk for developing severe hypotension following the induc6on of anesthesia increases in pa6ents that are taking RAAS antagonists.
(Nabbi, Woehlck & Riess, 2013)
Introduc6on • Vasopressin
– Vasopressin is an endogenous stress hormone also known as arginine vasopressin or ADH
– It is secreted from the posterior pituitary gland in response to decreased MAP, decreased plasma volume, and increased plasma osmolality. (Thoma, 2013)
– Elimina6on half-‐life of 6 minutes – Potent vasoconstrictor that work on the V1 receptor – In circumstances when hypotension does not respond appropriately to
common vasopressor and fluid administra6on, vasopressin or terlipressin becomes an effec6ve alterna6ve. (TroZer, 2012)
– The use of low dose vasopressin can be used to restore vasomotor tone in pa6ents that are resistant to catecholamines, preserving renal blood flow and urine output. (Mitra, Roy, Sengupta, 2011)
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Case Informa6on
• Procedure: Tympanomastoidectomy with mastoid oblitera6on, canalplasty, and car6lage graS placement
• Age: 72 year old • Weight: 57 kg • Gender: Female • ASA: 3
Pre-‐opera6ve Evalua6on • Past Medical Hx: Stage 3 CKD, orthosta6c hypotension,
migraines, Vit B12 anemia, pep6c ulcer disease, osteoporosis, HTN, abdominal aor6c aneurysm, renal cell CA, hyperlipidemia
• Surgical Hx: lap chole, laparotomy, appendectomy, extrac6on of teeth, hernia repair, ureteral stent, abdominal hysterectomy, triple A repair
• Meds: Imitrex, Elavil, Vit B12, Prolia, Penarin, Losartan-‐hydrochlorothiazide, Aspirin, Mul6-‐vitamin, Fish oil
• Pre-‐op VS: HR 98, BP 142/93, Resp 16, SpO2 95%, Temp 97.5 degrees F
• Labs: Hgb 11.7, Hct 36.7, Plt 212, Glucose 93, Na 143, K 4.1, BUN 25, Creat 1.6
Anesthe6c Course • Technique: GETA, 7.0 cm ETT, Mac 3 blade • Drugs: – Versed 1 mg – Fentanyl 100 mcg – Propofol 150 mg – Rocuronium 30 mg – Sevoflurane 1.4% – Neo 800 mcg – Ephedrine 40 mg – Vasopressin 3 units – Zofran 4 mg – Decadron 5 mg
Intraopera6ve Issues • Hypotension – ASer induc6on the blood pressure dropped into the 50’s/30’s with a heart rate at 78 bpm. – A 500 ml fluid bolus was started – Neosynephrine boluses of 100 mcg was given. – Ephedrine 10 mg boluses were also given with the pressure remaining in the 70’s/40’s.
– A total of 800 mcg of Neo and 40 mg of Ephedrine were given.
– Vasopressin 1 unit boluses were given for a total of 3 units.
PACU
• Pt extubated at end of case once all criteria for extuba6on was met
• Pt transferred to PACU on simple mask with 02 at 6 Lpm
• VSS in PACU • Pt discharged home later that evening
Discussion
• Three ways to maintain blood pressure – Sympathe6c nervous system – RASS system – Vasopressenergic system
• Pa6ents taking RAAS inhibitors, who undergo anesthesia, are blocking two of the main ways to control blood pressure, leaving only vasopressin to maintain blood pressure. (Nagelhout & Plaus, 2014)
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Discussion • Medica6ons that can lead to hypotension – Histamine Release (e.g. morphine, atracurium) – Vasodila6on by relaxing of arterial smooth muscle (e.g. vola6le inhala6onal agents, spinal anesthe6cs, induc6on agents, narco6cs)
• Consequences of not trea6ng Hypotension – Cerebral ischemia/stroke – Myocardial ischemia or infarc6on – Renal ischemia – Bowel ischemia – Spinal cord damage
Discussion • Ace Inhibitors
– Ace inhibitors can be dis6nguished by a medica6on name ending with “pril”.
– ACEIs work by preven6ng the conversion of angiotensin I to angiotensin II, which results in a reduc6on of arterial resistance, increased vascular capacitance, increased cardiac output, and stroke work. (Shear & Greenberg, 2012)
• ARBs – ARBs are similar to ace inhibitors but the mechanism of ac6on is slightly different as they are a compe66ve blocker of type I angiotensin II (AT1) receptors. (Nagelhout & Plaus, 2014)
– ARBs can oSen be dis6nguished as medica6ons that end with “sartan”.
Discussion
• Common ACEI’s – Lisinopril – Enalapril – Captopril – Fosinopril – Quinapril
• Common ARBs – Losartan – Valsartan – Azilsartan – Eprosartan
Discussion • Vasodilatory shock – Results from excessive vasodila6on and the relaxa6on of blood vessels
– Results in hypotension • Vasopressin to treat vasodilatory shock – Exogenously administered vasopressin restores vascular tone, increases responsiveness to infused catecholamines and raises blood pressure. (Neto et al., 2012)
– The successful treatment of intraopera6ve hypotension in the se|ng of RAAS blockade includes adequate intravascular volume reple6on, as well as the use of AVP agonists (terlipressin, vasopressin) and adrenergic agonists. (Auron et al., 2011)
Discussion
• Vasopressin Treatment – A 0.5-‐1.0 unit bolus of vasopressin may be given followed by an infusion dose of 0.03 units/min for vasopressin or 1-‐2 mcg/kg/hr for terlipressin as needed. (Nagelhout & Plaus, 2014)
– Correc6ng severe hypotension can generally be achieved using low dose (1-‐3 U/h) vasopressin while also avoiding excessive splanchnic and hepa6c vasoconstric6on. (John, Yeh, Boyd & Greilich, 2010)
Discussion • Vasopressin Treatment – A systema6c review and meta-‐analysis of nine randomized controlled trials done by Neto et al., showed that the combina6on of vasopressin with norepinephrine in vasodilatory shock was safe, is associated with a reduc6on in pa6ent mortality, and facilitates weaning of catecholamines. (Neto et al., 2012)
– According to Shear and Greenberg (2012): At least 5 clinical trials have demonstrated that pa6ents on chronic ACEI/ARB undergoing general anesthesia respond to exogenous vasopressin deriva6ves with an increase in blood pressure and fewer hypotensive episodes. Typically, a 0.5-‐1 unit bolus of AVP is administered to achieve a rise in mean arterial pressure (p. 2).
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Discussion • Vasoplegic syndrome during heart surgery
– Severe hypotension refractory to catecholamine therapy most commonly seen during cardiac surgery, although it can occur during any anesthe6c. (Shear & Greenberg, 2012)
– ASer coming off pump, these pa6ents oSen become resistant to phenylephrine and respond much beZer to norepinephrine (16-‐32 mcg) or vasopressin (1-‐2 units). (Nagelhout & Plaus, 2014)
– Omar, Zedan & Nugent (2015) found that the use of low dose vasopressin (<0.04 U/min) can be beneficial in these pa6ents because they have low circula6ng levels of endogenous vasopressin (p. 84).
– A study conducted by Morales found that the prophylac6c use of a vasopressin infusion (0.03 U/min) ini6ated before CPB in pa6ents receiving ACE inhibitors for >2 weeks required lower peak norepinephrine doses, a shorter 6me on catecholamines, had fewer hypotensive episodes, a shorter intuba6on 6me, and a shorter ICU stay. (Hasija et al., 2010)
Discussion
• Complica6ons of Vasopressin – Gastrointes6nal ischemia – Decreased cardiac output – Myocardial ischemia or infarc6on (cardiac arrest) • Decreased myocardial oxygen • Increased oxgen demand
– Skin or digit necrosis – Decreased organ perfusion
Recommenda6ons
• Start with IV fluid boluses • Give Ephedrine and Neosynephrine first • If BP unresponsive to standard treatments give Vasopressin 0.5-‐1 Unit IV bolus – Mix 20 units (1ml) in 19 ml NS
Conclusion • The risk for anesthesia induced arterial hypotension is increased in pa6ents chronically treated with angiotensin conver6ng enzyme inhibitors and angiotensin II receptor blockers. (Lange, Van Aken, Westphal & Morelli, 2008)
– Trea6ng hypotension aSer the induc6on of general anesthesia in pa6ents taking RAAS antagonists can be difficult.
– Studies have shown that the administra6on of vasopressin may be effec6ve in reversing periopera6ve refractory hypotension in pa6ents whose sympathe6c system and RAS is blunted by general anesthesia. (Lange, Van Aken, Westphal & Morelli, 2008)
References • Auron, M., Harte, B., Kumar, A., & Michota, F. (2011). Renin-‐angiotensin system antagonists in the
periopera6ve se|ng: Clinical consequences and recommenda6ons for prac6ce. Postgraduate Medical Journal, 87(1029), 472-‐481. doi:10.1136/pgmj.2010.112987 [doi]
• Barak, M. A., Yoav, L., & Abu el-‐Naaj, I. (0326). Hypotensive anesthesia versus normotensive anesthesia during major maxillofacial surgery: A review of the literature Retrieved from 2015 database.
• Bijker, J. B., van Klei, W., Kappen, T. H., van Wolfswinkel, L., Moons, K., & Kalkman, C. J. (2007). Incidence of intraopera6ve hypotension as a func6on of the chosen defini6on: Literature defini6ons applied to a retrospec6ve cohort using automated data collec6on. Anesthesiology, 107(2), 213-‐220. Retrieved from hZp://ezproxy.undmedlibrary.org/login?url=hZp://search.ebscohost.com.ezproxy.undmedlibrary.org/login.aspx?direct=true&AuthType=ip,url,uid,cookie&db=c8h&AN=2009640492&site=ehost-‐live
• Bijker, J. B., van Klei, W., Vergouwe, Y., Eleveld, D. J., van Wolfswinkel, L., Moons, K. G., et al. (2009). Intraopera6ve hypotension and 1-‐year mortality aSer noncardiac surgery. Anesthesiology, 111(6), 1217-‐1226. doi:10.1097/ALN.0b013e3181c14930
• Guidelines 2000 for cardiopulmonary resuscita6on and emergency cardiovascular care. part 6: Advanced cardiovascular life support: Sec6on 6: Pharmacology II: Agents to op6mize cardiac output and blood pressure. the american heart associa6on in collabora6on with the interna6onal liaison commiZee on resuscita6on(0919). Retrieved from 2000 Aug 22 database.
• Hall, JE. Nervous regula6on of circula6on, and rapid control of arterial pressure. In: Hall JE, ed. Guyton and Hall Textbook of Medical Physiology. Philadelphia: Saunders; 2011: 204
References • Hasija, S., Makhija, N., Choudhury, M., Hote, M., Chauhan, S., & Kiran, U. (2010). Prophylac6c vasopressin in
pa6ents receiving the angiotensin-‐conver6ng enzyme inhibitor ramipril undergoing coronary artery bypass graS surgery. Journal of Cardiothoracic and Vascular Anesthesia, 24(2), 230-‐238. doi:10.1053/j.jvca.2009.08.001 [doi]
• John, A., Yeh, C., Boyd, J., & Greilich, P. E. (2010). Treatment of refractory hypotension with low-‐dose vasopressin in a pa6ent receiving clozapine. Journal of Cardiothoracic and Vascular Anesthesia, 24(3), 467-‐468. doi:10.1053/j.jvca.2009.09.005 [doi]
• Lange, M., Van Aken, H., Westphal, M., & Morelli, A. (2008). Role of vasopressinergic V1 receptor agonists in the treatment of periopera6ve catecholamine-‐refractory arterial hypotension. Best Prac6ce & Research.Clinical Anaesthesiology, 22(2), 369-‐381.
• Lonjaret, L., Lairez, O., Minville, V., & Geeraerts, T. (2014). Op6mal periopera6ve management of arterial blood pressure. Integrated Blood Pressure Control, 7, 49–59. doi:10.2147/IBPC.S45292
• Mase|, P., Murphy, S. F., & Kouchoukos, N. T. (2002). Vasopressin therapy for vasoplegic syndrome following cardiopulmonary bypass. Journal of Cardiac Surgery, 17(6), 485-‐489. Retrieved from hZp://ezproxy.undmedlibrary.org/login?url=hZp://search.ebscohost.com.ezproxy.undmedlibrary.org/login.aspx?direct=true&AuthType=ip,url,uid,cookie&db=c8h&AN=2004038132&site=ehost-‐live
• Mitra, J. K., Roy, J. F., & Sengupta, S. (1110). Vasopressin: Its current role in anesthe6c prac6ce [Cardiopulmonary resuscita6on; hemorrhagic shock; opera6ng room; sep6c shock; vasopressin EDAT-‐ 2011/08/05 06:00 MHDA-‐ 2011/08/05 06:01 CRDT-‐ 2011/08/05 06:00 AID -‐ 10.4103/0972-‐5229.83006 [doi] AID -‐ IJCCM-‐15-‐71 [pii] PST -‐ ppublish] Retrieved from 2011 Apr database.
• Nabbi, R., Woehlck, H. J., & Riess, M. L. (2013). Refractory hypotension during general anesthesia despite preopera6ve discon6nua6on of an angiotensin receptor blocker. F1000research, 2, 12-‐12.v1. eCollec6on 2013. doi:10.12688/f1000research.2-‐12.v1 [doi]
• Nagelhout, JJ, & Plaus, KL. Nurse Anesthesia. 5th ed. St. Louis, Missouri: Saunders Elsevier; 2014. • Omar, S., Zedan, A. F., & Nugent, K. (0227). Cardiac vasoplegia syndrome: Pathophysiology, risk factors and
treatment Retrieved from 2015 Jan database.
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References • Papadopoulos, G., Sintou, E., Siminelakis, S., Koletsis, E., Baikoussis, N. G., & Apostolakis, E. (2010). Periopera6ve
infusion of low-‐ dose of vasopressin for preven6on and management of vasodilatory vasoplegic syndrome in pa6ents undergoing coronary artery bypass graSing-‐A double-‐blind randomized study. Journal of Cardiothoracic Surgery, 5, 17-‐8090-‐5-‐17. doi:10.1186/1749-‐8090-‐5-‐17 [doi]
• Serpa Neto, A., Nassar, A. P., Cardoso, S. O., ManeZa, J. A., Pereira, V. G., Esposito, D. C., et al. (2012). Vasopressin and terlipressin in adult vasodilatory shock: A systema6c review and meta-‐analysis of nine randomized controlled trials. Cri6cal Care (London, England), 16(4), R154. doi:10.1186/cc11469 [doi]
• Shear, T., Greenberg, S. (2012). Vasoplegic syndrome and renin-‐angiotensin system antagonists. APSF NewsleZer; 27. Retrieved from hZp://www.apsf.org/newsleZers/html/2012/spring/12vasoplegic.htm
• Thoma, A. (2013). Pathophysiology and management of angiotensin-‐ conver6ng enzyme inhibitor-‐associated refractory hypotension during the periopera6ve period. AANA Journal, 81(2), 133-‐140. Retrieved from hZp://ezproxy.undmedlibrary.org/login?url=hZp://search.ebscohost.com.ezproxy.undmedlibrary.org/login.aspx?direct=true&AuthType=ip,url,uid,cookie&db=c8h&AN=2012070334&site=ehost-‐live
• TroZer, J. (2012). Catecholamine-‐resistant hypotension following induc6on for spinal explora6on. AANA Journal, 80(1), 55-‐60. Retrieved from hZp://ezproxy.undmedlibrary.org/login?url=hZp://search.ebscohost.com.ezproxy.undmedlibrary.org/login.aspx?direct=true&AuthType=ip,url,uid,cookie&db=c8h&AN=2011485358&site=ehost-‐live
• Turner, D. W., AZridge, R. L., & Hughes, D. W. (0719). Vasopressin associated with an increase in return of spontaneous circula6on in acido6c cardiopulmonary arrest pa6ents [acidosis; cardiac arrest; epinephrine; return of spontaneous circula6on; vasopressin EDAT-‐ 2014/05/30 06:00 MHDA-‐ 2014/05/30 06:00 CRDT-‐ 2014/05/30 06:00 PHST-‐ 2014/05/28 [aheadofprint] AID -‐ 1060028014537037 [pii] AID -‐ 10.1177/1060028014537037 [doi] PST -‐ aheadofprint] Retrieved from 2014 May 28 database.
• Yavuz, S. F., Toktas, F. F., Surer, S. F., & Eris, C. (0314). eComment. poten6al therapeu6c agents in vasoplegic syndrome aSer cardiac surgery Retrieved from 2013 Sep database.
Thank You Are There Any Ques6ons?
Oxytocin Administra6on following Cesarean Delivery
Amanda Lundgren, SRNA
Introduc6on • Oxytocin is used in the majority of hospital deliveries in the United States – Rou6nely the first-‐line agent for preven6on of PPH aSer cesarean delivery
– Uterotonic agents have been shown to decrease the incidence of PPH by up to 40% (Munn et al., 2001)
• Dosing and method of administra6on varies greatly among anesthesia and obstetric providers.
Introduc6on Cont’d • In 2007, oxytocin was added to the Ins6tute of Safe Medica6on Prac6ce’s list of “High Alert Medica6ons”
– Medica6ons that “bear a heightened risk of causing significant pa6ent harm when they are used in error” (ISMP, 2009)
– “the inability of technological safeguards, […] to consistently prevent pa6ent harm” (Clark, Simpson, Knox, & Garite, 2009)
– “remains the drug most commonly associated with preventable adverse events during childbirth” (Clark et al., 2009)
– “the drug implicated in nearly half of all paid obstetric li6ga6on claims” (Tsen & Balki, 2010)
Introduc6on Cont’d
• No evidence-‐based guidelines on the administra6on of oxytocin following cesarean delivery have been established. – Most texts suggest ‘20-‐40 units IV, Ptrate to uterine tone’
What does the current evidence suggest is the
appropriate dose and method of administra4on of oxytocin following cesarean delivery?
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Case Informa6on
• 26 year old, G2P1 • Elec6ve cesarean d/t
previous cesarean delivery 2° failure to progress.
• 79 kg, 157 cm • 39 week gesta6on • ASA II
• Medical Hx: unremarkable • Surgical Hx: previous
cesarean • NKA • Pre-‐op VS: WNL: • Labs: WNL • Airway: mallampa6 I,
adequate TM & HM
Anesthe6c Course
• 500mL LR infused prior to OR • SAB w/ 1.4 mL 0.75% bupivacaine and 20 mcg Fentanyl
• Addi6onal 500 mL LR infused throughout SAB procedure
• T4 level of anesthesia iden6fied à LUD • VSS remained stable on 2L O2 per NC
Anesthe6c Course • Within 6 min of incision, 2.9 kg male delivered w/o complica6on, APGAR 8, 9
• Following delivery of placenta, 10 IU oxytocin IV push administered, followed by 20 IU in remaining 600 mL LR.
Intraopera6ve Issues
• Within 1-‐2 min of oxytocin 10 IU bolus, pt reported nausea and was anxious – BP 82/46, HR 110
• Phenylephrine 100 mcg and ondansetron 4 mg given IV
• Oxytocin infusion slowed • Symptoms and VS improved within several minutes
Recovery
• Surgeon reported sa6sfactory uterine tone • EBL ~ 800 mL • Uncomplicated closure • Mild nausea • VSS on RA • Total 1400 mL LR and 200 mL LR w/ oxytocin
Post Partum Hemorrhage
• Leading cause of maternal mortality – Accounts for 30% of maternal deaths (Weeks, 2014)
• PPH increased by over 26% between 1994-‐2006 (Callaghan, Kuklina, & Berg, 2010)
• Cesarean deliveries have increased drama6cally over last several decades: significant risk factor for PPH (Murphy, MacGregor, Munishankar, & MacLeod, 2009)
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Discussion: Oxytocin
• Mechanism of ac6on: – Binds to G-‐protein on uterine myocyte surface à increases release of calcium from the SR
– Leads to ac6va6on of myosin light chain kinase to increase uterine contrac6on
– ALSO, systemically, oxytocin ini6ates release of nitric oxide from endothelium of vascular smooth muscle • Vasodila6on, ↓ SVR, ↑ venous capacitance • Vasoconstric6on of splanchnic and coronary arteries, release of atrial & brain natriure6c pep6de
(Dryer, Butwick, & Carvalho, 2011)
Discussion Cont’d • Hemodynamic effects of oxytocin: – Dose & pa6ent dependent – Range from transient to fatal – Include:
• Hypotension (↓ SVR) • Compensatory tachycardia • Increased CO (↑ HR & SV) • Coronary vasoconstric6on à ST segment changes
• Excerpt from Why Mothers Die 1997-‐1999: two case studies describe maternal cardiac arrest immediately aSer oxytocin 10 unit bolus dose (Thomas & Cooper, 2002)
Discussion Cont’d • Hemodynamic studies: – 10 IU bolus in non-‐pregnant, non-‐anesthe6zed women found tachycardia, ↓ MAP, ST changes (Svanstrom et al. 2008)
– Hemodynamics may be similar in trend, but oxytocin induced changes are significantly greater than delivery alone (CO, SVR, HR, SV) (Archer et al., 2008)
– Comparing 5 or 10 IU bolus doses – 10 IU doses were sta6s6cally significantly more likely to cause ST depression (Johsson et al., 2009) • Prevent hypotension à likely prevent ST changes
Discussion: Bolus
Carvalho et al. (2004) • Found ED90 to be 0.35 IU
– 40 healthy, term, elec6ve/non-‐laboring
– Concluded no more than 1 IU bolus needed
Balki et al. (2006) • Aim to find ED 90 in labor
arrest cesarean • Found ED90 to be 2.99 u
Kiran et al. (2013) • 90 primip, healthy, elec6ve
cesarean deliveries – Concluded 0.5-‐2 units bolus
doses result in adequate uterine tone
Butwick et al. (2010) • Aimed to find ED90 * • 0, 0.5, 1, 2, or 5 unit bolus • Concluded 0.5-‐3 unit bolus
results in adequate UT
Discussion: Bolus
Sartain et al. (2008)
• 2 unit vs 5 unit followed by dilute infusion 10 u/hr
• Phenylephrine infusion to maintain BP
• No difference b/w groups re: EBL, uterine tone, addi6onal uterotonics – 5 IU group ↑ hypotension
Langesaeter et al. (2009)
• Parturients w/ cardiac disease • Study began with 5 unit bolus
doses • adjusted dose throughout study
from 5 IU bolus to 0.5 IU (as low as 0.1u)
• Concluded ultra low doses, repeated frequently resulted in less hemodynamic changes, yet achieved adequate UT
Discussion: Bolus vs. Infusion • Mechanism of bolus and infusion are thought to differ:
“A bolus causes constric6on of the venous sinuses, leading to placental separa6on and placental bed haemostasis, whereas an infusion maintains uterine contrac6lity” (Sheehan et al., 2011)
• However, Kovacheva, Soens, & Tsen (2015) concluded that low dose bolus (3 unit with placebo infusion) required less total oxytocin than infusion group (placebo bolus with 30 IU infusion), – Similar hemodyamic effects – Infusion group received double the rescue bolus amount to achieve same UT
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Discussion: Infusion
George et al. (2010) • 40 healthy, non-‐laboring
cesarean deliveries • Diluted in 500mL NS infused
over 1 hr • Found ED90: 0.29 IU/min
(approx. 17 IU/hr)
Murphy et al. (2009) • Compared 5 IU bolus and
placebo infusion vs 5 u bolus and 30 IU dilute infusion
• Concluded ↓ incidence of PPH and ↓ prolonged admission rates in group with infusion
Discussion: Infusion
Sheehan et al. (2011)
• Compared 5 unit bolus and 40 IU infusion vs 5 unit bolus and placebo infusion
• Concluded bolus + infusion
reduced need for addi6onal uterotonic agents – did not decrease incidence of PPH. – Also noted adverse effects did
not increase with infusion – *infusion rate less than ED90
found by George et al. (2010)
• 143 with at least 1 risk factor for PPH.
• Compared 5 IU bolus and 40 IU in 500mL NS vs placebo bolus and 40 IU in 500mL NS
• Concluded 5 IU bolus dose may not be necessary: – provided immediate UT, but
dissipated aSer 5 min – did not significantly affect end results of EBL or addi6onal uterotonic agents
King et al. (2010)
Recommenda6ons
• 10 IU bolus doses of oxytocin are not appropriate, regardless of PPH risk factors – Even 5 IU bolus becoming less acceptable
• Ini6al bolus dose considera6ons: – Healthy (low/no risk for PPH), non-‐laboring, elec6ve CD: 0.5-‐3 IU over 15-‐30 seconds
– Health, non-‐laboring, primpara, elec6ve CD: 0.5-‐2 IU over 15-‐30 seconds
– Laboring/failure to progress CD: 3 IU over 15-‐30 seconds
Recommenda6ons Cont’d
• Rule of 3’s: (Tsen & Balki, 2010) – 3 IU bolus over 15-‐30 seconds • Assess uterine tone a`er 3 minutes
– 3 IU bolus rescue dose #1 if needed (over 15-‐30 seconds) • Assess uterine tone a`er 3 minutes
– 3 IU bolus rescue dose #2 if needed (over 15-‐30 seconds) • Asses uterine tone a`er 3 minutes
– Consider another uterotonic agent if uterine tone not sa6sfactory/concern for PPH
Recommenda6ons Cont’d
• High risk for PPH: – Rule of 3’s plus dilute infusion – If higher doses requested, consider vasopressor preemp6vely
• High cardiovascular risk: – Ultra-‐low dose: 0.5 IU slow bolus, repeat as necessary
– Consider vasopressor preemp6vely
Conclusion • Oxytocin dose-‐dependent side effects may be transient to fatal, important to consider especially in cardiac complicated and hypovolemic parturients.
• Anesthesia prac66oners must consider appropriate dosing of oxytocin according to pa6ent history and presenta6on and understand preven6on/treatment of adverse effects.
• Need for addi6onal research and evidence supported recommenda6ons
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References • Archer, T. L., Knape, K., Liles, D., Wheeler, A. S., and Carter, B. (2008). The hemodynamics of oxytocin and
other vasoac6ve agents during neuraxial anesthesia for cesarean delivery: findings in six cases. InternaPonal Journal of Obstetric Anesthesia, 17(3). doi: 10.1016/j.ijoa.2008.03.003
• Balki, M., Ronayne, M., Davies, S., Fallah, S., Kingdom, J., Windrim, R. Carvalho, J. (2006). Minimum oxytocin dose requirement aSer cesarean delivery for labor arrest. American College of Obstetricians and Gynecologists, 107(1). doi: 10.1097/01.AOG.0000191529.52596.c0
• Balki, M., Erik-‐Soussi, M., Kingdom, J., Carvalho, J. (2013). Oxytocin pretreatment aZenuates oxytocin-‐induced contrac6ons in human myometrium in vitro. Anesthesiology, 119(3). doi: 10.1097/ALN.0b013e318297d347
• Bateman, B., Berman, M., Riley, L., Leffert, L. (2010). The epidemiology of post-‐partum hemorrhage in a large, na6onwide sample of deliveries. Anesthesia & Analgesia, 110(5). doi: 10.1213/ANE.0b013c3181d74898
• BhaZacharya, S., Ghosh, S., Ray, D., Mallik, S., Laha, A. (2013). Oxytocin administra6on during cesarean delivery: Randomized controlled trial to compare intravenous bolus with intravenous infusion regimen. Journal of Anaesthesiology Clinical Pharmacology, 29(1). doi: 10.4103/0970-‐9185.105790
• Butwick, A., Coleman, L., Cohen, S., Riley, E., Carvalho, B. (2010). Minimum effec6ve bolus dose of oxytocin during elec6ve caesarean delivery. BriPsh Journal of Anaesthesia, 104(3). doi: 10.1093/bja/aeq004
• Callaghan, W., Kuklina, E,, Berg, C. (2010). Trends in postpartum hemorrhage: United States, 1994-‐2006. American Journal of Obstetrics and Gynecology, 202(4). doi: 10.1016/j.ajog.2010.01.011
• Carvalho, J., Balki, M., Kingdom, J., Windrim, R. (2004) Oxytocin requirements at elec6ve cesarean delivery: A dose-‐finding study. American College of Obstetricians and Gynecologists, 104(5). doi: 10.1097/01.AOG.0000142709.04450.bd
• Clark, S., Simpson, K., Knox, E., & Garite, T. (2009). Oxytocin: new perspec6ves on an old drug. American Journal of Obstetrics & Gynecology, 35(e2). doi: 10.1016/j.ajog.2008.06.010
• Devikarani, D. and Harsoor, S. (2010). Are we using right dose of oxytocin? Indian Journal of Anaesthesia, 54(5). doi: 10.4103/0019-‐5049.71020
References • Dyer, R., Reed, A., van Dyk, D., Arcache, M., Hodges, O., Lombard, C.,… James, M. (2009). Hemodynamic
effects of ephedrine, phenylephrine, and the coadministra6on of phenylephrine with oxytocin during spinal anesthesia for elec6ve cesarean delivery. Anesthesiology, 111(4). doi: 10.1097/ALN.0b013e3181b437e0
• Dyer, R., Butwick, A., Carvalho, B. (2011). Oxytocin for labour and caesarean delivery: Implica6ons for the anesthesiologist. Current Opinion in Anesthesiology, 24(3). doi: 10.1097/ACO.0b013e328345331c
• Fortner, C. L., Manley, Jr., E. S., & Woodbury, R. A. (1969). Effects of synthe6c oxytocin with and without preserva6ves upon coronary blood flow in the dog. Journal of Pharmacology and Experimental TherapeuPcs, 165(2). Pg. 258-‐266. Retrieved from hZp://jpet.aspetjournals.org.ezproxy.undmedlibrary.org/content/165/2/258.long
• Gabbe, S., Niebyl, J., Simpson, J., Landon, M., Galan, H., Jauniaux, E., & Driscoll, D. (2012). Obstetrics: Normal and Problem Pregnancies (6th ed.). Philadelphia: Elsevier Saunders.
• George, R., McKeen, D., Chaplin, A., McLeod, L. (2010). Up-‐down determina6on of the ED90 of oxytocin infusions for the preven6on of postpartum uterine atony in parturients undergoing cesarean delivery. Canadian Journal of Anesthesia, 57(6). doi: 10.1007/s12630-‐010-‐9297-‐1
• Gongorduk, K., Ascoglu, O., Celkkol, O., Olgac, Y., Ark, C. (2010). Use of addi6onal oxytocin to reduce blood loss at elec6ve caesarean sec6on: a randomised control trial. Australian and New Zealand Journal of Obstetrics and Gynaecology, 50(1). doi: 10.1111/j.1479-‐828X.2009.01106.x
• Ins6tute for Safe Medica6on Prac6ces. (2014). ISMP list of high-‐alert medica6ons in acute care se|ngs. [online publica6on]. Retrieved from hZps://www.ismp.org/tools/ins6tu6onalhighAlert.asp
References • Jonsson, M., Hanson, U., Liedell, C., & Norden-‐Lindeberg, S. (2009). ST depression at caesarean sec6on and
the rela6on to oxytocin dose. A randomized controlled trial. BriPsh Journal of Gynecology, 117(1). doi: 10.1111/j.1471-‐0528.2009.02356.x
• King, K., Douglas, Unger, Wong, King (2010). Five unit bolus oxytocin at cesarean delivery in woman at risk of atony: A randomized, double blind, controlled trial. InternaPonal Anesthesia Research Society, 111(6). doi: 10.1213/ANE.0b013e3181f8930a
• Kiran, S., Anand, A., Singh, T., and Gupta, N. (2013). To es6mate the minimum effec6ve dose of oxytocin required to produce adequate uterine tone in women undergoing elec6ve caesarean delivery. EgypPan Journal of Anaesthesia, 29(2). doi: 10.1016/j.egja.2012.10.001
• Kovacheva, V., Soens, M., and Tsen, L. (2015). A randomized, double-‐blinded trial of a “Rule of Threes” algorithm versus con6nuous infusion of oxytocin during elec6ve cesarean delivery. Anesthesiology, 123. Advance online publica6on. doi: 10.1097/ALN.0000000000000682
• Langesaeter, E., Rosseland, L. A., and Stubhaug, A. (2009). Haemodynamic effects of repeated doses of oxytocin during caesarean delivery in healthy parturients. BriPsh Journal of Anaesthesia, 103(2). doi: 10.1093/bja/aep137
• Mockler, J., Murphy, D., & Wallace, E. (2010). An Australian and New Zealand survey of prac6ce of the use of oxytocin at elec6ve caesarean sec6on. Australian and New Zealand Journal of Obstetrics and Gynaecology, 50(1). doi: 10.1111/j.1479-‐828X.2009.01108.x
• Munn, M., Own, J., Vincent, R., Wakefield, M., Chestnut, D., & Hauth, J. (2001). Comparison of two oxytocin regimens to prevent uterine atony at cesarean delivery: A randomized controlled trial. Obstetrics and Gynecology, 98(3). 386-‐390.
References • Murphy, D., MacGregor, H., Munishankar, B., McLeod, G. (2009). A randomized controlled trial of oxytocin 5IU and placebo
infusion versus oxytocin 5 IU and 30 IU infusion for the control of blood loss at elec6ve caesarean sec6on – Pilot study. European Journal of Obstetrics & Gynecology and ReproducPve Biology, 142(1). doi: 10.1016/j.ejogrb.2008.09.004
• NOVARTIS Pharmaceu6cals. (2009). Syntocinon. [online pamphlet]. Approved by Therapeu6c Goods Administra6on. Retrieved from hZp://www.novar6s.com.au/pi_pdf/syt.pdf
• Phaneuf, S., Rodriguez Linares, B., TambyRaja, R., MacKenzie, I., & Bernal, A. (2000). Loss of myometrial oxytocin receptors during oxytocin-‐induced and oxytocin-‐augmented labour. Journal of ReproducPon and FerPlity, 120(1). doi: 10.1530/jrf.0.1200091
• Sartain, J., Barry, J., Howat, P., McCormack, D., Bryant, M. (2008). Intravenous oxytocin bolus of 2 units is superior to 5 units during elec6ve caesarean sec6on. BriPsh Journal of Anaesthesia. 101(6). doi: 10.1093/bja/aen273
• Sheehan, S., Montgomery, A., Carey, M., McAuliffe, F., Eogan, M., Gleeson, R.,… Murphy, D. (2011). Oxytocin bolus versus oxytocin bolus and infusion for control of blood loss at elec6ve caesarean sec6on: double blind, placebo controlled, randomised trial. BriPsh Medical Journal, 343(1). doi: 10.1136/bmj.d4661
• Stephens, L., & Bruessel, T. (2012). Systema6c review of oxytocin dosing at caesarean sec6on. Anesthesia and Intensive Care, 40(2). 247-‐252.
• Svanstrom, M., Biber, B., Hanes, M., Johansson, G., Naslund, U., & Balfors, E. (2008). Signs of myocardial ischaemia aSer injec6on of oxytocin: A randomized double-‐blind comparison of oxytocin and methylergometrine during caesarean sec6on. BriPsh Journal of Anaesthesia, 100(5). doi: 10.1093/bja/aen071
• Thomas, T. A. and Cooper, G. M. (2002). Maternal deaths from anaesthesia. An extract from Why Mothers Die 1997-‐1999, the confiden6al enquiries into maternal deaths in the United Kingdom. BriPsh Journal of Anaesthesia, 89(3). 499-‐508.
• Thomas, J., Koh, S., Cooper, G. (2007) Haemodynamic effects of oxytocin given as i.v. bolus or infusion on women undergoing caesarean sec6on. BriPsh Journal of Anesthesia, 98(1). doi:10.1093/bja/ael302
• Tsen, L., & Balki, M. (2010). Oxytocin protocols during cesarean delivery: Time to acknowledge the risk/benefit ra6o? InternaPonal Journal of Obstetric Anesthesia, 19(3). doi: 10.1016/j.ijoa.2010.05.001
• Wedisinghe, L., Macleod, M., & Murphy, D. (2007). Use of oxytocin to prevent haemorrhage at caesarean sec6on – a survey of prac6ce in the United Kingdom. European Journal of Obstetrics and Gynecology and ReproducPve Biology, 128(1). doi: 10.1016/j.ejogrb.2007.04.007
• Weeks, A. (2015). The preven6on and treatment of postpartum haemorrhage: what do we know, and where do we go to next? BriPsh Journal of Gynecology, 122(2). doi:10.1111/1471-‐0528.13098
Thank You Are There Any Ques6ons?
Postopera6ve Nausea and Vomi6ng Preven6on For a Pa6ent Undergoing
Thyroidectomy
David Ames, SRNA
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Introduc6on
• Prevalence of Postopera6ve Nausea and Vomi6ng (Apfel et al. 1999): – General Anesthesia PONV development • 20-‐30% of all pa6ents • 50-‐80% with previous history of PONV
Pathophysiology
• Located in medulla oblongata and brainstem region (Pierre and Whelan, 2013): – Chemoreceptor Trigger Zone (CRTZ) • Caudal end 4th Ventricle
– Nucleus Tractus Solitaries • Lower pons area in the area postrema
• Blood Brain Barrier not as developed in this region (Pierre and Whelan, 2013) – Direct s6mula6on
Pathophysiology
• Gastrointes4nal tract – Enterochromaffin cells – Direct Vagus nerve s6mula6on – Serotonin (5HT3) Receptors
• CRTZ communicates with NTS via – Dopamine 2 (D2) Receptors
• Ves4bular System – Histamine 1 (H1) Receptors – And acetylcholine (Ach)
Receptors
• Cerebral Cortex – Communicates with NTS via mul6ple complex pathways
• Vagal tract – Neurokinin 1 (NK1) Receptor • Located within NTS • Substance P can also bind to NK1 Receptor
Nausea and Vomi6ng is s6mulated through receptors (Pierre and Whelan, 2013):
Case Informa6on
• Surgical Procedure: Comple6on of Thyroidectomy
• Age: 22 years old • Weight: 63 kg • Gender: Female • ASA: 1
Preopera6ve Evalua6on • Past Medical Hx
– Anxiety – Depression – Thyroid Cancer – PONV
• Previous hemithyroidectomy
• Surgical Hx – Hemithyroidectomy
• Medica;ons – Docusate Sodium – Oxycodone/acetaminophen – Excedrin – Levonorqestrel – Ondansetron
• Pre-‐op VS – HR: 65 – BP: 125/63 – RR: 16 – Temp: 98.2 – SaO2: 98%
• Labs – Hbg: 12.6 – Hct: 37.3 – Plt: 201
• Airway Evalua;on – Mallampa6: 2 – Neck: Full ROM – Den66on: Intact
Preopera6ve Evalua6on
• Preopera;ve – Transdermal Scopolamine Patch 1.5 mg • Applied upon arrival to Pre-‐op holding room
– LR IVF – Midazolam 2mg IV • anxioly6c
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Anesthe6c Course • Induc;on
– Fentanyl 100 mcg IV – Pre-‐oxygenated – Propofol 150 mg – Rocuronium 5 mg
• Priming dose – Rocuronium 35 mg
• ASer successful ven6la6on – Intubated with 7.0 ETT without issues
• A>er Induc;on – TIVA to maintain general anesthesia • Propofol gZ
– Titrated to keep BIS between 40-‐60
– Acetaminophen IV 1000 mg
– Dexamethasone 10 mg IV – Cefazolin 2 g IV
• Ondansetron 4 mg IV – Given towards end of surgical procedure
Intraopera6ve Issues
• No issues intraopera6vely – Hemodynamically stable through out case – Surgical case lasted approx. 60 min – Neuromuscular blockade reversed with • Glycopyorrlate 0.4 mg IV • Neos6gmine 3 mg
• No issues with emergence
PACU/Postopera6ve
• No issues in PACU – Only received Fentanyl IV twice for post op pain
• Pa6ent discharged later during the day – No signs or symptoms of PONV
Discussion • Predica;ve Scoring System – Study done by Apfel, Koivuranta, Greim, and Roewer (1999) • Large two center study evaluated risk factors for PONV • Included 2722 pa6ents • Risk factors were ploZed on receiver opera6ng chart curve and area under the curve (AUC-‐ROC) – Done to help eliminate bias – Created a probability chart
• Results Found Strongest Predictors – Female gender – History of PONV or Mo6on Sickness – Smoking Status – Postopera6ve Opioid Usage
Discussion
• Serotonin Antagonist – Moon, Joo, Kim, and Lee (2012) • Female pa6ents undergoing thyroidectomy • Evaluated efficacy of ondansetron vs. palonosetron
– Double Blind Randomized Clinical Control Trial
– Metaxari et al. (2011) Double-‐Blind RCT Evalua6on of Three Serotonin Antagonists • Pa6ents undergoing thyroidectomy • Evaluated at one hour, 6-‐12 hours, 18 hours, and 24 hours postopera6vely
Discussion
• Serotonin Antagonist Cont’d – Ondansetron at the beginning vs. end of case – Cruz, Por6lla, and Vela (2008)
• Evaluated efficacy of ondansetron for PONV preven6on postopera6vely at – 0-‐2 hours – 2-‐24 hours
• Double-‐Blind RCT – Ondansetron given at beginning of case – Ondansetron given within 30 min of end of the case
• All pa6ents received dexamethasone 4 mg IV at start of the case
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Discussion
• Dexamethasone – Feroci et al. (2011) RCT Double-‐blind study thyroidectomy pa6ents evaluated effects of dexamethasone for PONV, Pain, Vocal Cord Func6on
– Noted blood sugar increase 8 hours postopera6vely • Nazar, Lacassie, Lopez, and Munoz, (2009) RCT evaluated BS eleva6on with dexamethasone administra6on – Found BS eleva6on peak at 8-‐10 hours post administra6on
Discussion
• Dexamethasone Cont’d – Doksrod et al., (2012) Prospec6ve randomized double blind clinical trial hemithyroidectomy pa6ents • Dexamethasone for PONV reduc6on and postopera6ve pain relief – Found reduc6on in PONV – Found no benefit for pain relief
Discussion • An;cholinergic and Neurokinin 1 Antagonist – Gan et al., 2009 evaluated efficacy of TDS
• RCT for high risk PONV development • Found TDS most effec6ve when applied at least 2 hours before induc6on
• TDS combined in mul6modal treatment highly effec6ve at PONV preven6on
– Green et al. (2012) evaluated aprepitant alone vs aprepitant with transdermal scopolamine patch (TDS) in RCT-‐double blind trial • No difference with TDS when combined with aprepitant
– Aprepitant is Neurokinin 1 antagonist
Discussion
• An;histamines – Forrester, Benfield, Matern, Kelly, and Pellegrini (2007) performed a double-‐blind, randomized control study that involved 77 pa6ents that evaluated the effec6veness of meclizine combined with ondansetron with pa6ents that had four to five risk factors for PONV.
– Gan et al. (2014) • Diphenhydramine it is a safe and effec6ve medica6on when combined in a mul6modal approach, for high-‐risk pa6ents, for PONV preven6on.
Discussion
• Dopamine 2 antagonists – Apfel et al. (2009), evaluated droperidol’s an6eme6c effect in a double-‐blind, randomized clinical trial done via mul6center study.
– Ebneshahidi, Akbari, and Mohseni (2013) found that haloperidol helped to reduce the incidence of delayed PONV from a double-‐blind, randomized clinical trial with 98 pa6ents. • Improved efficacy when combined with dexamethasone
Discussion • Modifying risk factors – Park and Cho (2011) performed a randomized clinical control trial that evaluated TIVA versus an inhala6on agent in the preven6on of PONV. • PONV was significantly reduced in the TIVA group more than the sevoflurane group
• IV Fluid Rehydra;on – Yavuz et al. (2014), evaluated the effects PONV reduc6on of IVF hydra6on in a randomized clinical trial for pa6ents undergoing laparoscopic cholecystectomies.
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Discussion • Limi;ng Opioids – Singla et al. (2015) performed a randomized clinical double-‐blind trial on total hip arthroplasty pa6ents that supports the use of IV acetaminophen can decrease the amount of opioids needed for postopera6ve pa6ents
– Cai, Lin, Yu, and Lin (2012) evaluated the efficacy of performing a bilateral cervical plexus block in pa6ents undergoing a thyroidectomy.
– Tufanogullari et al. (2008) performed randomized clinical control trial that assessed the efficacy of different dexmedetomidine dosages versus a placebo. • Evaluated amount of opioids used
Discussion Cont’d
• Post Discharge Nausea and Vomi;ng – Apfel et al. (2012) conducted a study, with 12 different centers, to evaluate poten6al risk factors for PDNV
– Risk factors found were female gender, age less than 50 years old, history of PONV, opioid use in the PACU, and nausea and vomi6ng in the PACU.
– Dexamethasone had a significant reduc6on in PDNV when u6lized with a mul6modal approach
Recommenda6ons
• Mul6modal approach works best – Nausea and Vomi6ng is mul6factorial
• Tailor preven6on to pa6ent specific situa6ons • Limit risk factors as able • Use longer ac6ng an6eme6cs for those with limited access to healthcare
• Beneficial for future research to focus on: – Most Efficacious Dosages – Adjunc6ve Medica6on and Treatments
Conclusion
• Reduc6on of risk factors and mul6modal treatment plan does work at 6mes
• At least one-‐third of all general anesthesia pa6ents will develop PONV
• Mul6modal treatment recommended for moderate to high risk pa6ents – Adjust plan to pa6ent wish or situa6on
References • Apfel, C. C., Koivuranta, M., Greim, C., & Roewer, N. (1999). A Simplified Risk Score for Predic6ng Postopera6ve Nausea and
Vomi6ng: Conclusions from Cross-‐valida6ons between Two Centers. Anesthesiology. doi:10.1097/00000542-‐199909000-‐00022
• Apfel, C. C., Cakmakkaya, O. S., Frings, G., Kranke, P., Malhotra, A., Stader, A., . . . Kolodzie, K. (2009). Droperidol has comparable clinical efficacy against both nausea and vomi6ng. BriPsh Journal of Anaesthesia, 103(3), 359-‐363. doi:10.1093/bja/aep177 [doi]
• Apfel, C. C., Philip, B. K., Cakmakkaya, O. S., Shilling, A., Shi, Y. Y., Leslie, J. B., . . . Kovac, A. (2012). Who is at risk for postdischarge nausea and vomi6ng aSer ambulatory surgery? Anesthesiology, 117(3), 475-‐486. doi:10.1097/ALN.0b013e318267ef31 [doi]
• Cai, H. D., Lin, C. Z., Yu, C. X., & Lin, X. Z. (2012). Bilateral superficial cervical plexus block reduces postopera6ve nausea and vomi6ng and early postopera6ve pain aSer thyroidectomy. The Journal of InternaPonal Medical Research, 40(4), 1390-‐1398.
• Cruz, N. I., Por6lla, P., & Vela, R. E. (2008). Timing of ondansetron administra6on to prevent postopera6ve nausea and vomi6ng. Puerto Rico Health Sciences Journal, 27(1), 43-‐47.
• Doksrod, S., Sagen, O., Nostdahl, T., & Raeder, J. (2012). Dexamethasone does not reduce pain or analgesic consump6on aSer thyroid surgery; a prospec6ve, randomized trial. Acta Anaesthesiologica Scandinavica, 56(4), 513-‐519.
• Ebneshahidi, A., Akbari, M., & Mohseni, M. (2013). Intraopera6ve haloperidol does not improve quality of recovery and postopera6ve analgesia. Advanced Biomedical Research, 2, 85-‐9175.122501. eCollec6on 2013. doi:10.4103/2277-‐9175.122501 [doi]
• Feroci, F., ReZori, M., Borrelli, A., Lenzi, E., OZaviano, A., & Sca6zzi, M. (2011). Dexamethasone prophylaxis before thyroidectomy to reduce postopera6ve nausea, pain, and vocal dysfunc6on: A randomized clinical controlled trial. Head & Neck, 33(6), 840-‐846. doi:10.1002/hed.21543 [doi]
• Forrester, C. M., Benfield, D. A.,Jr, Matern, C. E., Kelly, J. A., & Pellegrini, J. E. (2007). Meclizine in combina6on with ondansetron for preven6on of postopera6ve nausea and vomi6ng in a high-‐risk popula6on. AANA Journal, 75(1), 27-‐33.
References • Gan, T. J., Sinha, A. C., Kovac, A. L., Jones, R. K., Cohen, S. A., Ba|kha, J. P., . . . Glass, P. S. (2009). A randomized, double-‐blind, mul6center
trial comparing transdermal scopolamine plus ondansetron to ondansetron alone for the preven6on of postopera6ve nausea and vomi6ng in the outpa6ent se|ng. Anesthesia and Analgesia, 108(5), 1498-‐1504. doi:10.1213/ane.0b013e31819e431f [doi]
• Gan, T. J., Diemunsch, P., Habib, A. S., Kovac, A., Kranke, P., Meyer, T. A., … Tramer, M. R. Society for Ambulatory Anesthesia. (2014). Consensus guidelines for the management of postopera6ve nausea and vomi6ng. Anesthesia and Analgesia, 118(1), 85-‐113. doi:10.1213/ANE.0000000000000002
• Green, M. S., Green, P., Malayaman, S. N., Hepler, M., Neubert, L. J., & Horrow, J. C. (2012). Randomized, double-‐blind comparison of oral aprepitant alone compared with aprepitant and transdermal scopolamine for preven6on of postopera6ve nausea and vomi6ng. BriPsh Journal of Anaesthesia, 109(5), 716-‐722. doi:10.1093/bja/aes233 [doi]
• Moon, Y. E., Joo, J., Kim, J. E., & Lee, Y. (2012). An6-‐eme6c effect of ondansetron and palonosetron in thyroidectomy: A prospec6ve, randomized, double-‐blind study. BriPsh Journal of Anaesthesia, 108(3), 417-‐422. doi:10.1093/bja/aer423 [doi]
• Metaxari, M., Papaioannou, A., Petrou, A., Chatzimichali, A., Pharmakalidou, E., & Askitopoulou, H. (2011). An6eme6c prophylaxis in thyroid surgery: A randomized, double-‐blind comparison of three 5-‐HT3 agents. Journal of Anesthesia, 25(3), 356-‐362. doi:10.1007/s00540-‐011-‐1119-‐2 [doi]
• Nazar, C. E., Lacassie, H. J., Lopez, R. A., & Munoz, H. R. (2009). Dexamethasone for postopera6ve nausea and vomi6ng prophylaxis: Effect on glycaemia in obese pa6ents with impaired glucose tolerance. European Journal of Anaesthesiology, 26(4), 318-‐321. doi:10.1097/EJA.0b013e328319c09b [doi]
• Tufanogullari, B., White, P. F., Peixoto, M. P., Kianpour, D., Lacour, T., Griffin, J., . . . Provost, D. A. (2008). Dexmedetomidine infusion during laparoscopic bariatric surgery: The effect on recovery outcome variables. Anesthesia and Analgesia, 106(6), 1741-‐1748. doi:10.1213/ane.0b013e318172c47c [doi]
• Pierre, S., & Whelan, R. (2013). Nausea and vomi6ng aSer surgery. Coun6ng Educa6on Anesthesia Cri6cal Care and Pain. 13(1): 28-‐32. • Park, S. K., & Cho, E. J. (2011). A randomized controlled trial of two different interven6ons for the preven6on of postopera6ve nausea and
vomi6ng: Total intravenous anaesthesia using propofol and remifentanil versus prophylac6c palonosetron with inhala6onal anaesthesia using sevoflurane-‐nitrous oxide. The Journal of InternaPonal Medical Research, 39(5), 1808-‐1815.
• Yavuz, M. S., Kazanci, D., Turan, S., Aydinli, B., Selcuk, G., Ozgok, A., & Cosar, A. (2014). Inves6ga6on of the effects of preopera6ve hydra6on on the postopera6ve nausea and vomi6ng. BioMed Research InternaPonal, 2014, 302747. doi:10.1155/2014/302747 [doi]
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Thank You Are There Any Ques6ons?
Pre-‐oxygena6on and Posi6oning of Obese Pa6ents
Brandon Vesel, SRNA
Introduc6on • Obesity is an epidemic that con6nues to rise around the
world. • 300 million people worldwide are considered obese. The
World Health Organiza6on (WHO) predicts by the year 2025 the number of severely overweight people to double.
• Pa6ent safety can be enhanced when anesthesia
providers develop anesthesia care plans that take into account the specific needs of pa6ents with obesity.
Introduc6on Cont’d Obesity and Risk Factors in Anesthesia • Pa6ents with a body mass index (BMI) of 30 or more are considered obese.
• Risk Factors during Intuba6on – Thicker neck – Diminished Func6onal Reserve Capacity – Sleep Apnea – Airway obstruc6on – Limited mouth opening – Diminished range of neck mo6on – Increased metabolic rate – Lower alveolar concentra6on of oxygen
Introduc6on Cont’d
Pre-‐oxygena;on and Posi;oning of Obese Pa;ents • An obese pa6ent being pre-‐oxygenated for three
minutes in the 25 degree head up positon will give the anesthesia professional more 6me to intubate before the onset of cri6cal hypoxia, providing a safer anesthe6c to the obese pa6ent.
Case Informa6on • Emergent Laparoscopic
Cholecystectomy • 34 year old • 125 kg • BMI 38 • Female • Mallampa6 III airway • ASA 2 • Pre-‐op VS: – HR 96, BP 154/66, Oxygen satura6on 97%
• Past Medical history – GERD – Asthma – HTN – Obstruc6ve Sleep Apnea – Current smoker – Obesity
• Surgical history – Appendectomy – Right Knee Replacement (Pa6ent reported severe nausea and vomi6ng post-‐op)
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Anesthe6c Management • Preopera;ve: – Midazolam not administered, due to severe obstruc6ve sleep apnea
• Intraopera;ve: – Standard monitors applied – Vital signs obtained: BP 150/62, HR 92, 96% – Induc6on: Propofol 200 mg, Succinylcholine 200 mg – RSI, due to NPO status uncertain, obese and history of GERD
– Intubated with 7.0 ETT aSer 3 aZempts • Placement confirmed with bilateral breath sounds and posi6ve ETCO2
Anesthe6c Management
• Intraopera;ve Cont’d: – Ven6lator -‐ volume mode
• TV 600, rate 14, 50% FiO2 – End 6dal Sevoflurane maintained at 1.6% -‐ 2.2% – End 6dal CO2, 30-‐35 during maintenance phase – BIS 39-‐43 – An6eme6c's given
• Zofran 4 mg IV • Decadron 10 mg IV
– MAP kept above 65mmHg throughout case
Anesthe6c Management
Intraopera;ve Issues: • During direct laryngoscopy with a MAC 3 blade, oxygen
satura6on rapidly dropped from 97% to 86% within the first 5 seconds.
• The second DL aZempt with a Miller 2 blade did not provide a view of the cords, with oxygen satura6on dropping to 66%.
• The third DL aZempt with Glidescope provided successful intuba6on, with pa6ent manually ven6lated to 100%.
Anesthe6c Management
• Emergence: – Glycopyrrolate 1 mg IV and Neos6gmine 5 mg IV given for paraly6c reversal
– Ven6lator SIMV mode when RR dropped – Throat suc6oned – Sevoflurane discon6nued – Pa6ent breathing on her own and following commands
– Pa6ent extubated without incident
PACU
• Postopera;ve: – Pa6ent was transported to PACU on 2L nasal cannula
Discussion
• The review of literature looked at answering this ques6on: – Does pre-‐oxygena6ng a pa6ent, for three minutes in a 25 degree head up posi6on extend the amount of 6me for the anesthesia prac66oner to safely secure the airway, before hypoxia occurs.
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Discussion Pre-‐oxygena;on • Delivering 100% oxygen through a 6ghtly sealed mask,
replaces nitrogen in the lungs with oxygen. This is called de-‐nitrogena6on.
• This build up of oxygen in the lungs provides an increased amount of 6me to intubate before the pa6ent becomes hypoxic.
• Recommended Techniques for Pre-‐oxygena6on: – Three minute Tidal volume Breathing (TVB) – Eight deep breaths in 60 seconds
Discussion Pre-‐oxygena;on Cont’d • Indicator of the completeness of pre-‐oxygena6on – End 6dal oxygen frac6on (FEO2)
• Having an FEO2 greater than 90% is the most accurate end point of preoxygena6on (Tanoubi et al., 2009)
• The research showed that by applying 100% oxygen over an open airway and allowing it to passively flow into the lungs built up FRC (Sirian and Wills, 2009). – Important for obese pa6ents with GERD who need an RSI. – Decreased build up of air in the stomach
Discussion
Pre-‐oxygena;on Cont’d • Pre-‐oxygena6on becomes more important if pa6ent exhibits traits that could lead to a difficult mask ven6la6on – BMI greater than 35 – Age greater than 55 years – Limited jaw protrusion – Lack of teeth – Beard – Mallampa6 class 3 or 4
Discussion
Posi;oning • Plays a key role in prolonging 6me to safely manage the airway before desatura6on occurs.
• The studies show that an obese pa6ent in a head up posi6on has less weight compressing their lungs, improving Func6onal Residual Capacity (FRC) (Dixon et al., 2005)
Discussion
Posi;oning Cont’d • Types of Posi6ons – Ramped
• Placing blankets under the upper body
– 25 degree reverse Trendelenburg • Adjus6ng the en6re bed where the upper body is higher then the lower body
– Near-‐si|ng • Moving the bed to a beach chair posi6on
Discussion
Posi;oning Cont’d • Posi6oning the pa6ent allowing downward displacement of the adipose 6ssue will – Reduced intra-‐abdominal pressure – Reduced risk of reflux – Reduced risk of aspira6on – Increase FRC build up
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Discussion
Pre-‐oxygena;on and Posi;oning • Pre-‐oxygena6on and posi6oning used together on an obese pa6ent, have the greatest impact on extending the amount of 6me for an anesthesia provider to safely secure the airway before hypoxia occurs.
Discussion
Pre-‐oxygena;on and Posi;oning Cont’d • Dixon et al. (2005) determined that pa6ents with BMI’s >40 who were pre-‐oxygenated in the 25 degree head up posi6on for three minutes had: – Pre-‐induc6on oxygen tension of 442 compared to 360 in the supine posi6on.
– Time to desatura6on of 92% • Head up posi6on 201 seconds • Supine posi6on 86 seconds
Discussion
Pre-‐oxygena;on and Posi;oning Cont’d • AltermaZ (2005) looked at the correla6on of pre-‐oxygena6on
and body posi6oning in the si|ng vs supine posi6on of 40 pa6ents with BMI’s > 35. – Divided into two groups of 20
• Pre-‐oxygenated with 8 deep breaths in one minute • Oxygen flow rate 10 liters • RSI performed • Breathing circuit disconnected
– Time measured for oxygen satura6on allowed to drop to 90%
– Si|ng group • Time to desatura6on of 90% was 214 seconds
– Supine group • Time to desatura6on of 90% 162 seconds
Conclusion • Analyzing this case, the pa6ent exhibited difficult airway traits: – Limited jaw protrusion – Mallampa6 class 3 – Short neck
• Pre-‐oxygena6ng at a 25 degree head-‐up posi6on would have maximized this pa6ent’s oxygen stores providing the anesthesia team more 6me to safely intubate, without a decrease in oxygen satura6on.
Conclusion Cont’d
• It is recommended that anesthesia care providers pre-‐oxygenate pa6ents, with a BMI over 30, for three minutes in a 25 degree head raised posi6on.
• This will allow more 6me to intubate before the onset of cri6cal hypoxia, greatly enhancing the safety of the anesthe6c for the obese pa6ent.
References • AltermaZ, F., Munoz, H., Delfino, A., Cor6nez, L. (2005). Pre-‐oxygena6on in the obese pa6ent: Effects of posi6on on tolerance to apnea. BriPsh Journal of Anesthesia, 95(5), 706-‐709.
• Dixon, B., Dixon, J., Carden, J., Burn, A., Schachter, L.,Playfair, J., Laurie, C., O’Brien, (2005). Pre-‐oxygena6on is more effec6ve in the 25 degree head-‐up posi6on than in the supine posi6on in severely obese pa6ents: A randomized control study. Anesthesiology, 102(6), 1110-‐1115. • Gaszynski, T. (2010). Pre-‐oxygena6on in morbidly obese pa6ents. Anestezjol IntensTer, 42(3), 133-‐136. • Nagelhout, J.J. & Plaus, K.L. (2013). Nurse Anesthesia (5th ed.). St. Louis, MO: Elsevier Sanders. • Sirian, R., Wills, J. (2009). Physiology of apnea and the benefits of preoxygena6on. Con6nuing educa6on in anaesthesia. CriPcal Care & Pain, 9(4), 105-‐108.
• Tanoubi, I., Pierre, D., Francois D. (2009). Op6mizing preoxygena6on in adults. Can J Anesth, 56, 449-‐466.
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Thank You Are There Any Ques6ons?
Intravenous Acetaminophen to Decrease Narco6c Usage
Nathan Palm, SRNA
Introduc6on • General anesthesia can produce undesirable condi6ons that may lead to adverse outcomes.
• Narco6cs are oSen used to blunt the sympathe6c response for intuba6on and are frequently re-‐dosed throughout the case in response to increased heart rate and blood pressure.
• Intravenous (IV) acetaminophen has shown promising results in providing non-‐narco6c adjunc6ve analgesia in the periopera6ve and postopera6ve pa6ent.
Significance • Increased use of narco6cs may cause adverse effects such as:
– Respiratory distress – Airway obstruc6on – Hypoxia – Confusion – Postopera6ve nausea and vomi6ng – Decreased pa6ent sa6sfac6on
• Under the Affordable Care Act, pa6ent sa6sfac6on will become increasingly important for reimbursement rates.
• U6liza6on of mul6modal pain management by administra6on of non-‐narco6c analgesics may decrease overall narco6c use and their undesirable effects.
• Decreased narco6c usage may provide cost savings along with improved pa6ent outcomes.
Case Informa6on • 32 year-‐old female
• 98 kg
• Diagnosis: cholelithiasis
• Surgery: laparoscopic cholecystectomy under general anesthesia
• PMH: – Obesity – Type II DM – Asthma – Hypertension – Depression – Anxiety – GERD (well controlled)
Anesthe6c Course • RSI due to GERD
– Lidocaine 50 mg IV – Fentanyl 50 mcg IV – Propofol 180 mg IV – Succinylcholine 200 mg IV
• Anesthesia maintained with Desflurane – Addi6onal 50 mcg fentanyl IV throughout case – Acetaminophen 1000 mg IV
• Extubated awake • A postopera6ve visit was done in same day surgery unit
approximately 1.5 hours later. – No recall, PONV, or pain
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Discussion
• Many research studies have shown that the use of acetaminophen IV has been shown to significantly decrease the use of narco6cs and their nega6ve side effects in the postopera6ve period.
• Tradi6onal algorithms of pain management involve use of opioids, such as fentanyl, as first line therapy for pain control in the periopera6ve and immediate postopera6ve period.
Discussion
• Overzealous use of narco6cs can cause adverse effects that may increase length of stay, cost, and morbidity and mortality which decrease pa6ent sa6sfac6on. – Conversely, poorly controlled pain also decreases pa6ent sa6sfac6on.
– Joint Commission on Accredita6on of Health Care Organiza6ons have suggested that decreased pa6ent sa6sfac6on can be correlated with higher opioid usage.
Discussion • It is thought that the analgesic and an6pyre6c ac6vity of acetaminophen act in a dose dependent manner with acetaminophen IV, leading to greater central penetra6on and higher levels in the cerebrospinal fluid.
• The exact mechanism of ac6on is not completely understood. – It is thought to act centrally by inhibi6ng cyclooxygenases, effec6ng serotonin and decreasing prostaglandin levels.
Discussion Oral Acetaminophen • Oral acetaminophen cannot be absorbed in the stomach leading to challenges in reliable dosing in the surgical pa6ent.
• Delayed gastric emptying may lead to unreliable absorp6on of oral acetaminophen in pa6ents whose condi6on predisposes delayed gastric emptying, such as:
• Diabetes Mellitus • Cardiac surgery • Laparoscopic cholecystectomies • Gynecological surgeries
Discussion
IV vs. PO Acetaminophen • Addi6onally, opioids, oSen given during and aSer surgery, are known to slow gastric emptying leading to poten6ally unreliable dosing and pain control of oral analgesic medica6ons in the intraopera6ve and immediate postopera6ve periods.
• A study by Schuitmaker et al. (1999) observed that a 2000 mg dose of PO acetaminophen did not achieve a plasma level that would produce adequate pain relief in the postopera6ve period.
Discussion IV vs. PO Acetaminophen Cont’d • Acetaminophen is known to express its effects centrally.
– It must cross the blood brain barrier to achieve the desired results. • In an IRB-‐approved, inves6gator-‐ini6ated single site, open-‐label study by Singla et
al. (2012), the concentra6on of acetaminophen was measured in the plasma and cerebrospinal fluid (CSF) to compare the pharmacokine6cs of oral, rectal, and IV acetaminophen. – The doses of acetaminophen for this study were 1000 mg IV over 15 minutes, 1000 mg
PO, or 1300 mg rectally.
• The IV plasma levels had a 76% higher C-‐max than oral dosing and 256% higher C-‐max than rectal dosing.
• The plasma half-‐life was slightly longer with IV administra6on but was not sta6s6cally significant.
• CSF levels were also higher with the IV route than the other routes.
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Discussion IV vs. PO Acetaminophen Cont’d • A study by Bannwarth, et al. (1992) indicated that the effect of acetaminophen is correlated to the CSF level.
• Singla et al. also found a correla6on between acetaminophen’s effec6veness on pain and it’s concentra6on in the CSF (2012).
• “Passive diffusion of acetaminophen into the CNS is highly dependent on a concentra6on gradient with the C-‐max being of primary importance” (Singla et al., 2012, p. 524).
Discussion IV vs. PO Acetaminophen Cont’d • Singla et al. (2012) cited that higher plasma levels of
acetaminophen are correlated to beZer analgesia in the postopera6ve period as acetaminophen crosses the blood brain barrier through passive diffusion rather than an ac6ve transport mechanism.
• Apfel et al. (2013) concluded that the main advantage of IV administra6on over oral administra6on of acetaminophen is that: – “One g of IV acetaminophen is associated with about twice the plasma
and effect site concentra6ons as 1 g of its oral or rectal applica6ons, resul6ng in greater central nervous system penetra6on which corroborates the superior analgesic efficacy seen with IV compared to oral acetaminophen in the surgical se|ng” (p. 677).
Discussion Pediatrics • Children are at increased risk for adverse respiratory events from opioids.
• One of the most common surgeries in children is a tonsillectomy, oSen due to either tonsilli6s or obstruc6ve sleep apnea.
• “The high prevalence of sleep-‐disordered breathing (80%) in children undergoing tonsillectomy is a major concern limi6ng the safe upper dose range of intraopera6ve opioids” (Subramanyam et al., 2014, p. 471).
• Pa6ents with OSA, who most likely have desatura6on with the apneic episodes, are more sensi6ve to opioids than those who have not been exposed to repeated desatura6on. – This is most likely due to an altera6on in mu receptors and leads to analgesia
and anesthesia that occurs at lower blood levels (Cote, 2015).
Discussion Pediatrics Cont’d • Mul6modal analgesia is recommended as evidenced based prac6ce
for treatment of postopera6ve pain in the pediatric pa6ent popula6on (Lonnqvist & Morton, 2005).
• Including acetaminophen IV in the intraopera6ve and postopera6ve analgesic plan may decrease opioid requirements in the pediatric pa6ent (Wong, 2013).
• Pediatric pa6ents have varying sensi6vity to opioids which may result in unexpected apnea in the postopera6ve period.
• Decreased opioid consump6on may reduce the risk of adverse respiratory events, increase pa6ent sa6sfac6on and early mobility, and decrease the length of hospital stay.
Discussion
Reduc;on of PONV • Opioids and inhaled anesthe6cs are known triggers for PONV which affects about 30% of pa6ents who receive general anesthesia (Norred, 2003).
• Gan et al. (2013) found that preven6on of PONV is more important to pa6ents than postopera6ve pain control.
• It is difficult to completely eliminate opioids from an anesthe6c plan. – However, a reduc6on of opioid use has been shown to decrease the incidence of PONV by approximately 30% (Marret, et al., 2005).
Discussion
Reduc;on of PONV Cont’d • A meta-‐analysis by Apfel et al. (2013) examined 30 research ar6cles
with 2364 pa6ents and found that giving acetaminophen IV prophylac6cally, before the onset of pain, had the greatest reduc6on of PONV.
• The results were further analyzed by sources of funding for the study. In the inves6gator-‐ini6ated trials there was decreased PONV versus in the industry sponsored trial there was no reduc6on in PONV. – It was discovered upon further review that in the industry sponsored trials
acetaminophen IV was only used as a rescue analgesic, aSer the onset of pain, and not given prophylac6cally whereas in the inves6gator-‐ini6ated trials it was given prophylac6cally, before the onset of pain.
• The data Apfel et al. (2013) collected “suggest that IV acetaminophen reduces PONV at least as well as established an6eme6cs” (p. 684).
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Discussion
Reduc;on of PONV Cont’d • Acetaminophen may have a direct ac6ng an6eme6c effect. Apfel et al. (2013) found the following: Acetaminophen is metabolized in the brain into A M404, a metabolite that is able to inhibit the reuptake of anandamide, a known cannabinoid CB1 and CB2 receptor agonist. It has been shown that decreased anandamide levels are associated with an increased rate of nausea and vomi6ng in humans. Therefore, it is possible that acetaminophen simply has a direct effect on PONV by increasing anandamide levels. (p. 685)
Discussion
Reduc;on of PONV Cont’d • Whether the reason for decreased PONV is due to
decreased opioid usage or a direct ac6ng effect of acetaminophen, there is consistent evidence to support that the incidence of PONV is decreased when acetaminophen IV is used prophylac6cally
• Preven6on of PONV is very important to pa6ents and subsequently pa6ent sa6sfac6on may be lower in incidences where PONV occurs.
• Use of prophylac6c acetaminophen IV may increase pa6ent sa6sfac6on by decreasing the incidence of PONV.
Discussion
IV Acetaminophen in the Bariatric Popula;on • Adverse outcomes due to respiratory complica6ons,
PONV, and increased PACU 6me occur more frequently in the obese popula6on.
• Due to increased adipose 6ssue the airway is narrower and obstruc6ve sleep apnea may be present.
• Addi6onally, obese pa6ents may have a higher sensi6vity to opioids and hypercapnia. This may put this pa6ent popula6on at an increased risk for adverse outcomes with increased opioid use.
Discussion IV Acetaminophen in the Bariatric Popula;on Cont’d • Gonzalez et al. (2014) performed a retrospec6ve study of 92 pa6ents
in 2014 to determine if acetaminophen IV decreased opioid requirements in the obese pa6ent undergoing bariatric surgery.
• 38 pa6ents in the study received acetaminophen IV and 50 pa6ents did not.
• No sta6s6cally significant differences were noted in age, BMI, gender, ASA score, periopera6ve complica6ons, surgical 6me, or number or procedures per surgeon.
• Pa6ents in the acetaminophen IV group received an average of 99.5 mg of opioid and the pa6ents who did not receive acetaminophen IV received an average of 164.6 mg of opioids, a difference of 39.5% less opioids.
Discussion
Cost Effec;veness • Acetaminophen IV, while more expensive than oral acetaminophen, has been shown to be an appropriate choice in many pa6ents that may lead to overall cost savings due to decreased opioid consump6on and shorter PACU 6me (Subramanyam et al., 2014).
• Use of oral medica6ons in the immediate preopera6ve, periopera6ve, and postopera6ve se|ngs has shown to have unreliable rates of absorp6on.
Discussion Cost Effec;veness Cont’d • A review by Subramanyam et al. (2014) of the cost-‐effec6veness of
acetaminophen IV for pediatric tonsillectomy found that administra6on of acetaminophen IV was associated with a decrease in overall cost.
• The decreased cost was aZributed to decreased incidence of adverse outcomes such as respiratory depression and PONV leading to decreased PACU 6me.
• Subramanyam et al. (2014) determined that a combina6on of acetaminophen IV and opioids decreased costs and was more effec6ve than opioids alone. – “Although the medica6on cost of the combina6on strategy were higher, the
overall costs were less than the compe6ng strategy due to reduced adverse effects and reduced 6me spent in PACU” (Subramanyam et al., 2014, p. 467).
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Recommenda6ons • Due to the high cost per dose, some organiza6ons and providers
may be reluctant to use acetaminophen IV instead applying opioid only analgesia.
• However, a reduc6on in PACU 6me and adverse events, including decreased incidence of PONV and respiratory depression from overuse of opioids, may provide more cost-‐effec6ve care and beZer overall outcomes.
• More studies should be done examining the effec6veness and reliability of cost-‐reduc6on with this route versus oral acetaminophen to determine if the increased cost for this route is actually more effec6ve than oral or rectal administra6on.
Conclusion • Acetaminophen IV has been shown to be a safe, effec6ve analgesic which provides excellent pain relief in combina6on with opioids.
• Mul6ple studies have demonstrated that acetaminophen IV decreases opioid consump6on in mul6ple types of surgical pa6ent popula6ons.
• Opioids have many undesirable side effects which may lead to adverse outcomes and increased costs; decreasing the overall use of opioids may reduce the incidence of these adverse effects.
Conclusion
• While oral acetaminophen remains an op6on for administra6on, delayed gastric emptying from fas6ng or opioid induced ileus may decrease the reliability and effec6veness of this route.
• Evidenced-‐based prac6ce algorithms, such as including mul6-‐modal analgesia, will become increasingly important as healthcare reimbursement is further driven by outcomes and pa6ent sa6sfac6on.
References • Apfel, C. C., Turan, A., Souza, K., Pergolizzi, J., & Hornuss, C. (2013). Intravenous
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