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Year : 2015  |  Volume : 59  |  Issue : 10  |  Page : 664-669  

Reversal agents in anaesthesia and critical care

1 Department of Anaesthesiology and Critical Care, S.C.B Medical College, Cuttack, Odisha, India
2 Department of Emergency Medicine, Kempegouda Institute of Medical Sciences, Bengaluru, Karnataka, India

Date of Web Publication19-Oct-2015

Correspondence Address:
Nibedita Pani
Ashok Villa, 48, Forest Park, Bhubaneswar - 751009, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.167484

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Despite the advent of short and ultra-short acting drugs, an in-depth knowledge of the reversal agents used is a necessity for any anaesthesiologist. Reversal agents are defined as any drug used to reverse the effects of anaesthetics, narcotics or potentially toxic agents. The controversy on the routine reversal of neuromuscular blockade still exists. The advent of newer reversal agents like sugammadex have made the use of steroidal neuromuscular blockers like rocuronium feasible in rapid sequence induction situations. We made a review of the older reversal agents and those still under investigation for drugs that are regularly used in our anaesthesia practice.

Keywords: Flumazenil, naloxone, platelet factor 4, sugammadex

How to cite this article:
Pani N, Dongare PA, Mishra RK. Reversal agents in anaesthesia and critical care. Indian J Anaesth 2015;59:664-9

How to cite this URL:
Pani N, Dongare PA, Mishra RK. Reversal agents in anaesthesia and critical care. Indian J Anaesth [serial online] 2015 [cited 2021 May 12];59:664-9. Available from: https://www.ijaweb.org/text.asp?2015/59/10/664/167484

   Introduction Top

Balanced anaesthesia practice involves the use of potent sedatives, opioids, neuromuscular blocking agents (NMBA) and local anaesthetics (LA). Despite the advent of short and ultra-short acting drugs, an in-depth knowledge of the reversal agents used is a necessity for any anaesthesiologist. Reversal agents are defined as any drug used to reverse the effects of anaesthetics, narcotics or potentially toxic agents.[1] Routine reversal of neuromuscular blockade is common in many countries after surgery under general anaesthesia, in order to prevent recurarisation.[2] However, the use of reversal for opioids, LA and benzodiazepines (BZDs) is limited to overdose.

Moreover, the introduction of newer drugs such as dexmedetomidine, rocuronium and gantacurium make it important for us to update our knowledge on the newer reversal agents. Hence, we conducted literature search using the search words reversal agents, sugammadex, naloxone in Google Scholar, Medline, PubMed for the period after 2000, for research and review articles. Reversal agents, in general, fall into two categories: Receptor-specific antagonists and non-specific analeptic agents.[3] Antagonists are defined as agents which have a high affinity for a receptor and no intrinsic activity. For example anticholinesterases, naloxone, flumazenil, etc. Analeptics are defined as stimulants. For example theophylline, doxapram, caffeine, etc.

   Agents Reversing Neuromuscular Blockade Top

Routine reversal of neuromuscular blockade is more common in the United States but is not used in the European countries. However, the risk of residual neuromuscular blockade makes it necessary to reverse NMBAs.[2] NMBAs may be reversed either by increasing the concentration of acetylcholine in the synaptic junction or aid the elimination of the drug or its metabolism.[2],[4] Benzyl isoquinolinium compounds such as atracurium and cisatracurium under metabolism by Hoffmann elimination and non-specific esterases.

   Anticholinesterases Top

These drugs exert their effect primarily by inhibiting acetylcholinesterase and butyrylcholinesterase, prolonging the existence of acetylcholine at the motor end-plate.[5] In addition, anticholinesterases may have a direct agonistic effect by increasing the release of acetylcholine from presynaptic nerve terminals.[4] For neostigmine, the maximum effective dose is 60–80 µg/kg and for edrophonium, it is 1.0–1.5 mg/kg.[4] The addition of two antagonists is avoided as they are not additive and inadequate reversal can occur. It is not advisable to administer additional anticholinesterase if maximal doses of edrophonium (1.5 mg/kg), neostigmine (70 µg/kg), or pyridostigmine (350 µg/kg) fail to antagonize the residual blockade and may in turn increase the weakness.[4] They are combined with atropine or glycopyrrolate in order to neutralize the muscarinic side-effects of these drugs. The combination of glycopyrrolate to neostigmine and pyridostigmine and atropine for edrophonium is matched to their duration of action. Glycopyrrolate may be preferable to atropine in case of cardiac arrhythmias and the anticholinesterases and anticholinergics should be administered more slowly (e.g., 2–5 min) to reduce the incidence and severity of disordered rhythm. Neostigmine is the most potent and the preferred drug.[4] High-dose neostigmine or unwarranted use of neostigmine may translate to increased post-operative respiratory morbidity.[6] Recent guidelines specify the use of reversal with neostigmine based on the train of four (TOF) monitoring with the neuromuscular monitor. Neostigmine can be given for reversal in patients who were receiving drugs which augment the action of NMBAs (inhalational agents) if TOF count is 4, in patients receiving anaesthetic drugs which do not augment the blockade by NMBAs (intravenous anaesthetics) if TOF count is 2 and if TOF ratio is more than 0.9 then reversal should not be given.[7] Furthermore, the guidelines also specify that if the TOF count is <2 reversal should be delayed, if TOF count is 4 and no fade is perceived or if TOF ratio is 0.4:0.9 on qualitative neuromuscular monitoring neostigmine at a lower dose of 20 µg/kg should be considered.[7]

   Sugammadex Top

Development of this cyclodextrin is said to be the first pharmacological breakthrough in the past 60 years. It was discovered by Anton 'Ton' Bom a pharmaceutical chemist and presented in the 7th International Neuromuscular Meeting in Belfast.[8] Sugammadex (modified γ-cyclodextrin) [Figure 1] is a selective relaxant binding agent (su refers to sugar, whereas gammadex emphasizes to the structural molecule gamma-cyclodex trin). Sugammadex complexes with steroidal NMBAs in a 1:1 ratio (rocuronium > vecuronium ≫ pancuronium) by forming a guest-host complex, which helps in rapid removal of free rocuronium molecules from plasma. It completely encapsulates the molecule of steroidal NMBAs and is excreted via the kidney unchanged [Figure 2].[9] The dose of sugammadex is dependent on the dose of muscle relaxant used. The recommended doses are between 2 and 16 mg/kg body weight.[4] Studies have found the incidence of inadequate reversal with 0.5 mg/kg.[10] One case report has reported recurarisation in an obese individual with a dose of 1.74 mg/kg.[11] The use of this molecule is also very important in cardiac surgery [12] as the arrhythmogenic potential of standard neostigmine and glycopyrrolate limits their use. Sugammadex can also be used as an acute therapeutic option in the event of an allergic reaction against rocuronium.[13] Use of sugammadex makes the use of rocuronium possible in patients with neuromuscular disorders.[14] Controversy on the dose to be administered in morbidly obese patients still continues. The present recommendation is to administer sugammadex based on the actual body weight, but one study has compared the use of doses based on lean body weight, lean body weight +20% and lean body weight +40% and found the administration of lean body weight +40% to be better.[15] The disadvantage is that it cannot reverse the action of benzylisoquinolinium compounds.[4]
Figure 1: Structure of Sugammadex

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Figure 2: Sugammadex encapsulating rocuronium

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   Cysteine Top

A new class of NMBAs fumarates (gantacurium) undergo spontaneous elimination by cysteine adduction. This adduction reaction replaces chlorine and saturates the fumarate double bond. The compound formed is structurally different from gantacurium and cannot cause neuromuscular blockade.[2] Administration of cysteine will usually hasten the recovery from gantacurium induced blockade.[2],[4] Doses of 10 mg/kg have been known to reverse the effect of 8 times the ED95 of gantacurium within 1–2 min.[16]

   Other Agents Top

Four aminopyridine is a tertiary compound and a potassium channel antagonist which acts by increasing the concentration of acetylcholine. It has been used regularly in countries like Bulgaria in combination with anticholinesterases. However, its use is limited by its stimulant effect on the central nervous system (CNS).[17],[18]

Galanthamine is another tertiary compound like 4 aminopyridine whose inconsistency in reversal and stimulant effect on the CNS has unpopularised it.[17]

Suramin is an anti-trypanosomal drug used in African sleeping sickness. Its mechanism of NMBA reversal is yet unexplained. It may be due to P2 purinoceptor blockade, post-synaptic action, the release of adenosine triphosphate, etc. Its main disadvantage is its very short duration of action, but similar synthetic agents may be of use in the future.[18]

   Opioid Antagonists Top


Naloxone is chemically N-alylnor-oxymorphone and it possesses the ability to antagonise all types of opioid receptors. However, it shows high affinity for µ receptors. Naloxone shows highfirst pass metabolism. The drug is metabolised in the liver primarily by conjugation with glucuronic acid. The half-life of naloxone is about 1 h. It acts in 1–2 min when it is given intravenously (IV). Intravenous naloxone (0.4–0.8 mg) promptly antagonises all actions of morphine. In patients with respiratory depression, an increase in respiratory rate is seen within 1 or 2 min. At a dose of 10-15 mg, it also can antagonise the actions of nalorphine and pentazocine (dysphoric effects). Rebound release of catecholamines may cause hypertension, tachycardia, ventricular arrhythmias and pulmonary oedema. Primary indications are to reverse respiratory depression due to intraoperative opioid overdose (0.1–0.2 mg IV). It is used as an agent to decrease neonatal respiratory depression secondary to the intravenous or intramuscular administration of opioids to the mother. In the neonate, the initial dose is 10 µg/kg given IV, intramuscularly or subcutaneously.[19] To antagonize actions of buprenorphine naloxone, continuous infusion is required. Abrupt reversal of opioid depression with large doses of naloxone can precipitate sympathetic activity and hence nausea, vomiting, tachycardia, hypertension, tremors, sweating, seizures and cardiac arrest can occur. To prevent these, diluting the drug (0.4 mg) to 10 ml (0.04 mg/ml) and injecting 1–2 ml every 1–2 min is recommended.[5] At the end of 2014, the World Health Organization published a position paper recommending community access to naloxone in an effort to stem the tide of accidental deaths from opioids.[20]

   Other Opioid Antagonists Top

Nalmefene is effective for the reversal of opioid-induced CNS effects and may be administered orally or IV showing a dose-dependent duration of action 4–8 h following IV administration. The initial adult dose is 0.5 mg.[21] If there is an incomplete response or no response, additional doses can be given at 2–5 min interval. Nalmefene has a relatively slow onset of action, and no serious adverse reactions were noted in studies where 4 times the normal dose was given.[22] There is one case report in the literature of a healthy patient developing acute post-operative pulmonary oedema after a very low dose (75 μg) of nalmefene.[23] It is available in the oral and intravenous form. The dosage for opioid overdose is 1 ml (100 μg)/1 mg of opioid IV. For the reversal of post-operative respiratory depression, 25 μg increments are given every 2–4 min.[24] The principal advantage over naloxone is its considerably longer duration of antagonistic action. Naltrexone, primarily used for opioid detoxification is a potent, long-acting, pure opiate antagonist and effective orally. It has a longer duration of action lasting up to 72 h. It is only available in oral form and its main indication for use is during opioid withdrawal and to maintain abstinence. The recommended dose range is from 50 to 300 mg/day/oral.[24]

   Reversal Agents for Sedatives Top


Flumazenil is 1,4-imidazobenzodiazepine and has got a structural resemblance to midazolam. Flumazenil is administered IV. It is used as a reversal agent for BZDs. In addition, it is a potential reversal agent after subcutaneous, sublingual, intramuscular, submucosal, intranasal,[25] rectal and endotracheal administration. On intravenous administration, flumazenil has a half-life of about 1 h and the duration of clinical effects usually is only 30–60 min. It is eliminated via liver to inactive products and excreted renally. Therefore, re-sedation is a possibility with longer acting BZDs and may occur within 1–2 h after administration, which requires subsequent doses. It is indicated for reversal of procedural sedation, a reversal of sedation in the Intensive Care Unit, management of BZD overdose, intra-operative wake-up testing in clinical practice. For this purpose in adults 0.2 mg/dose, to a total of 3 mg, over 30 s followed by 0.3 and 0.5 mg at 1 min intervals to a maximum dose of 3 mg can be given. In children 0.01 mg/kg IV per dose, to a total of 0.05 mg/kg or 1 mg [26] is administered. A total of 1 mg flumazenil given over 1–3 min usually is sufficient to abolish the effects of therapeutic doses of BZDs such as the sedative, anxiolytic, anticonvulsant, ataxic, anaesthetic and muscle relaxant effects of BZDs. The sublingual approach would allow convenient and better treatment availability for patients with hepatic encephalopathy as well as for reversing the residual hypnotic effect after a surgical procedure.[27] Adverse effects could be dizziness, facial erythema, anxiety and headache which are often mild and disappear within several minutes. Additionally, flumazenil has been noted to precipitate seizures in epileptic patients who are on BZDs for seizure control. It should also be avoided in patients who have consumed a combination of Tricyclic anti-depressants and BZDs.[28] Recent literature on flumazenil investigate the reversal of the sedative effect of sevoflurane with its administration. Karakosta et al. have concluded that recovery from sevoflurane/remifentanil anaesthesia is faster in patients administered 0.3 mg flumazenil.[29] In another study, Liang et al. have concluded that 0.006 mg/kg of flumazenil may only partially reverse the hypnotic effect without changing the time to recovery or extubation.[30]


Use of dexmedetomidine a specific alpha 2 agonist has become common in anaesthesia practice. Use of atipamezole a specific alpha 2 antagonist to reverse the psychomotor effects of dexmedetomidine is being investigated in human volunteers way back as 1991.[31] They have been found to have sympathomimetic effects.[32] Dose range of 40:1–100:1 has been found to be effective for the rapid reversal of the effects of dexmedetomidine. 30 However, its regular use has not been approved by the Food and Drug Administration yet.

   Analeptic Agents Top

Conventionally, the use of doxapram has been reserved in patients with chronic obstructive pulmonary disease receiving oxygen therapy and because controlled ventilation and supportive therapy can manage drug-induced coma, it is not to be used for this indication.[33] Side effects could be panic attacks, palpitation, tremors, sweating and convulsions. Hence, it is relatively contraindicated in coronary artery disease and epileptic patients. In a recent study, however, doxapram has been found to hasten the recovery from dexmedetomidine – propofol - remifentanil anaesthesia in patients undergoing uvulopalatopharyngoplasty and may benefit patients with obstructive sleep apnoea.[34]

   Reversal of Anticoagulants Top

Heparin is the commonly used anticoagulant in anaesthesia practice in patients undergoing cardiac or major vessel surgery. Effect of unfractionated heparin can be reversed with protamine sulphate a component of salmon sperm. The problems are histamine release, pulmonary hypertension and allergic reactions.[35] Platelet factor 4(PF4) is a protein found in platelet alpha granules and has been found to reverse the anticoagulant effect of heparin within dose ranges of 0.5–5 mg/kg over 3 min.[36],[37] Demma et al. in a case series have commented that PF4 in a dose of 5 mg/kg reversed the effect of heparin in 10 min.[37] However, this is currently not being developed for clinical use.[38]In vitro studies have been done on heparinase 1 but, in vivo study has been done only on dogs and not on humans.[39] This study shows a promising result, but further extensive studies are required even though the in vitro and in vivo studies confirm lesser side effects in comparison to protamine. Heparin removal devices are being investigated. These involve veno-venous extracorporeal circulation with adsorption of the heparin using a polycation.[40]

   Reversal Agents in Critical Care and Toxicology Top

Naloxone and flumazenil are used in patients with opioid and BZD in the critical care setting too. Other reversal agents used in toxicology are listed in [Table 1].[41]
Table 1: Reversal agents for common drug overdoses in toxicology

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   Summary Top

The introduction of newer reversal agents such as sugammadex has revolutionised anaesthesia practice. However, much needs to be done in terms of reversal agents in critical care and toxicology.

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Conflicts of interest

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   References Top

McGraw-Hill Concise Dictionary of Modern Medicine. S.v. "Reversal Agent." Available from: http://www.medical-dictionary. Thefreedictionary.com/reversal+agent. [Last retrieved on 2015 May 04].  Back to cited text no. 1
Lien CA, Eikermann M. Neuromuscular blockers and reversal agents. In: Hemmings HC, Egan TD, editors. Pharmacology and Physiology for Anesthesia Foundations and Clinical Practice. Philadelphia: Elsevier Saunders; 2013. p. 325-48.  Back to cited text no. 2
Anderson JA. Reversal agents in sedation and anesthesia: A review. Anesth Prog 1988;35:43-7.  Back to cited text no. 3
Naquib M, Lien CA. Pharmacology of muscle relaxants and their antagonists. In: Miller RD, Eriksson LI, Fleischer LA, Weiner-Kronish JP, Young WL, editors. Miller's Anesthesia. 7th ed. Philadelphia: Churchill Livingstone Elsevier; 2010. p. 859-912.  Back to cited text no. 4
Nair VP, Hunter JM. Anticholinesterase and anticholinergic drugs. Contin Educ Anaesth Crit Care Pain 2004;4:164-8.  Back to cited text no. 5
Sasaki N, Meyer MJ, Malviya SA, Stanislaus AB, MacDonald T, Doran ME, et al. Effects of neostigmine reversal of nondepolarizing neuromuscular blocking agents on postoperative respiratory outcomes: A prospective study. Anesthesiology 2014;121:959-68.  Back to cited text no. 6
Brull SJ, Murphy GS. Residual neuromuscular block: Lessons unlearned. Part II: Methods to reduce the risk of residual weakness. Anesth Analg 2010;111:129-40.  Back to cited text no. 7
Caldwell JE. A history of neuromuscular block and its antagonism. In: Eger EI, Saidman LJ, Westhrope RN, editors. The Wondrous Story of Anesthesia. California: Springer; 2014. p. 671-91.  Back to cited text no. 8
Booij LH. Cyclodextrins and the emergence of sugammadex. Anaesthesia 2009;64 Suppl 1:31-7.  Back to cited text no. 9
Eleveld DJ, Kuizenga K, Proost JH, Wierda JM. A temporary decrease in twitch response during reversal of rocuronium-induced muscle relaxation with a small dose of sugammadex. Anesth Analg 2007;104:582-4.  Back to cited text no. 10
Le Corre F, Nejmeddine S, Fatahine C, Tayar C, Marty J, Plaud B. Recurarization after sugammadex reversal in an obese patient. Can J Anaesth 2011;58:944-7.  Back to cited text no. 11
Hemmerling TM, Zaouter C, Geldner G, Nauheimer D. Sugammadex – a short review and clinical recommendations for the cardiac anesthesiologist. Ann Card Anaesth 2010;13:206-16.  Back to cited text no. 12
[PUBMED]  Medknow Journal  
Dewachter P, Mouton-Faivre C, Emala CW. Anaphylaxis and anesthesia: Controversies and new insights. Anesthesiology 2009;111:1141-50.  Back to cited text no. 13
Gurunathan U, Duncan G. The successful use of sugammadex and uneventful recovery from general anaesthesia in a patient with myotonic dystrophy. Indian J Anaesth 2015;59:325-6.  Back to cited text no. 14
[PUBMED]  Medknow Journal  
Murphy GS, DeBoer HD, Eriksson LI, Miller RD. Reversal (Antagonism) of neuromuscular blockade. In: Miller RD, Cohen NH, Eriksson LI, Fleischer LA, Weiner-Kronish JP, Young WL, editors. Miller's Anesthesia. 8th ed. Philadelphia: Elsevier Saunders; 2015. p. 995-1027.  Back to cited text no. 15
Savarese JJ, McGilvra JD, Sunaga H, Belmont MR, Van Ornum SG, Savard PM, et al. Rapid chemical antagonism of neuromuscular blockade by L-cysteine adduction to and inactivation of the olefinic (double-bonded) isoquinolinium diester compounds gantacurium (AV430A), CW 002, and CW 011. Anesthesiology 2010;113:58-73.  Back to cited text no. 16
Mirakhur RK, Donati F. Neuromuscular blocking agents and their antagonists. In: Healy TE, Knight PR, editors. Wylie and Churchill-Davidson's a Practice of Anesthesia. London: Arnold; 2003. p. 583-98.  Back to cited text no. 17
Henning RH, Nelemans A, Houwertjes M, Agoston S. Reversal by suramin of neuromuscular block produced by pancuronium in the anaesthetized rat. Br J Pharmacol 1993;108:717-20.  Back to cited text no. 18
American Academy of Pediatrics Committee on Drugs: Naloxone dosage and route of administration for infants and children: Addendum to emergency drug doses for infants and children. Pediatrics 1990;86:484-5.  Back to cited text no. 19
WHO. Community Management of Opioid Overdose. Geneva: WHO; 2014. p. 88.  Back to cited text no. 20
Gal TJ, DiFazio CA. Prolonged antagonism of opioid action with intravenous nalmefene in man. Anesthesiology 1986;64:175-80.  Back to cited text no. 21
Dixon R, Howes J, Gentile J, Hsu HB, Hsiao J, Garg D, et al. Nalmefene: Intravenous safety and kinetics of a new opioid antagonist. Clin Pharmacol Ther 1986;39:49-53.  Back to cited text no. 22
Henderson CA, Reynolds JE. Acute pulmonary edema in a young male after intravenous nalmefene. Anesth Analg 1997;84:218-9.  Back to cited text no. 23
Choi YS, Billings JA. Opioid antagonists: A review of their role in palliative care, focusing on use in opioid-related constipation. J Pain Symptom Manage 2002;24:71-90.  Back to cited text no. 24
Scheepers LD, Montgomery CJ, Kinaham AM, Dunn GS, Bourne RA, McCormack JP. Plasma concentration of flumazenil following intranasal administration in children. Can J Anaesth 2000;47:120-1.  Back to cited text no. 25
Sugarman JM, Paul RI. Flumazenil: A review. Pediatr Emerg Care 1994;10:37-43.  Back to cited text no. 26
Saadi T, Kramskay R, Zilberman Peled B, Katz N, Peled N, Baruch Y. Pharmacokinetics and safety of sublingual flumazenil (CRLS035) in healthy adults (potential therapy for hepatic encephalopathy). J Pharmacogenomics Pharmacoproteomics 2014;5:4.  Back to cited text no. 27
Quan D. Benzodiazepines. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, editors. Tintinalli's Emergency Medicine. 7th ed. China: McGraw Hill Medical; 2011. p. 1216-9.  Back to cited text no. 28
Karakosta A, Andreotti B, Chapsa C, Pouliou A, Anastasiou E. Flumazenil expedites recovery from sevoflurane/remifentanil anaesthesia when administered to healthy unpremedicated patients. Eur J Anaesthesiol 2010;27:955-9.  Back to cited text no. 29
Liang P, Zhou C, Li KY, Guo LJ, Liu B, Liu J. Effect of flumazenil on sevoflurane requirements for minimum alveolar anesthetic concentration-awake and recovery status. Int J Clin Exp Med 2014;7:673-9.  Back to cited text no. 30
Karhuvaara S, Kallio A, Salonen M, Tuominen J, Scheinin M. Rapid reversal of alpha 2-adrenoceptor agonist effects by atipamezole in human volunteers. Br J Clin Pharmacol 1991;31:160-5.  Back to cited text no. 31
Aho M, Erkola O, Kallio A, Scheinin H, Korttila K. Comparison of dexmedetomidine and midazolam sedation and antagonism of dexmedetomidine with atipamezole. J Clin Anesth 1993;5:194-203.  Back to cited text no. 32
Stoelting RK, Hillier SC. Central nervous system stimulants and muscle relaxants. Pharmacology and Physiology in Anesthetic Practice. 4th ed., Ch. 31. Philadelphia: Lippincott Williams and Wilkins; 2006. p. 591-8.  Back to cited text no. 33
Wang HL, Tang SH, Wang XQ, Gong WH, Liu XM, Lei WF. Doxapram hastens the recovery following total intravenous anesthesia with dexmedetomidine, propofol and remifentanil. Exp Ther Med 2015;9:1518-1522.  Back to cited text no. 34
Stoelting RK, Hillier SC. Anticoagulants. Pharmacology and Physiology in Anesthetic Practice. 4th ed., Ch. 27. Philadelphia: Lippincott Williams and Wilkins; 2006. p. 505-20.  Back to cited text no. 35
Dehmer GJ, Fisher M, Tate DA, Teo S, Bonnem EM. Reversal of heparin anticoagulation by recombinant platelet factor 4 in humans. Circulation 1995;91:2188-94.  Back to cited text no. 36
Demma L, Levy JH. A case series of recombinant platelet factor 4 for heparin reversal after cardiopulmonary bypass. Anesth Analg 2012;115:1273-8.  Back to cited text no. 37
Mixon TA, Dehmer GJ. Recombinant platelet factor 4 for heparin neutralization. Semin Thromb Hemost 2004;30:369-77.  Back to cited text no. 38
Michelsen LG, Kikura M, Levy JH, Lee MK, Lee KC, Zimmermann JJ, et al. Heparinase I (neutralase) reversal of systemic anticoagulation. Anesthesiology 1996;85:339-46.  Back to cited text no. 39
Zwischenberger JB, Tao W, Deyo DJ, Vertrees RA, Alpard SK, Shulman G. Safety and efficacy of a heparin removal device: A prospective randomized preclinical outcomes study. Ann Thorac Surg 2001;71:270-7.  Back to cited text no. 40
Hack JB, Hoffman RS. General management of poisoned patients. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, editors. Tintinalli's Emergency Medicine. 7th ed. China: McGraw Hill Medical; 2011. p. 1189-90.  Back to cited text no. 41


  [Figure 1], [Figure 2]

  [Table 1]

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