Rate of administration of intravenous ondansetron

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as sinus bradycardia, atrial fibrillation, prolongation of QTc interval and fatal ventricular tachycardia have been reported following administration of ondansetron.
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myocardial infarction and pulmonary embolism were kept in mind. Finally, investigations and inquiry to staff nurse helped us to conclude this serious condition was due to inj. ranitidine given in the recovery room. The skin and intra-dermal tests confirmed the diagnosis. Ranitidine may induce immunoglobulin-mediated anaphylaxis but also non-immunological mechanisms may be involved in hypersensitivity reaction. Recording in anaesthesia notes and preserving records for further reference is necessary. Educating the patients and their relatives about anaphylaxis to a drug is very important. Documenting the allergy or sensitivity to specific drugs by use of electronic medical records can prevent such hypersensitivity to the same drug and these records become ubiquitous.[5] Clinicians should be aware of possible life-threatening adverse reactions and must be cautious while administrating H2R antagonist to prevent anaphylactic reaction. Varsha H Vyas, Shubha N Mohite, Sonal S Khatavkar, Sheetal R Jagtap Department of Anaesthesiology, Dr. D.Y. Patil Medical College, Hospital and Research Centre, Nerul, Navi Mumbai, India Address for correspondence: Dr. Sonal Khatavkar, B-303, Tirupati Complex, Plot-3, Sector-44, Nerul (W), Navi Mumbai - 400 706, India. E-mail: [email protected]

Rate of administration of intravenous ondansetron Sir, Ondansetron, a selective 5- HT3 receptor antagonist, is a popular drug for prevention and treatment of postoperative nausea and vomiting (PONV) because of its efficacy, safety and lack of drug interactions. Although rare, cardiovascular adverse effects such as sinus bradycardia, atrial fibrillation, prolongation of QTc interval and fatal ventricular tachycardia have been reported following administration of ondansetron.[1-4] A case of severe bradycardia with respiratory arrest and loss of consciousness has been described.[5] Most of the case reports regarding serious adverse effects, including that reported in Indian Journal of Anaesthesia by Sahu et al.,[4] do not describe the rate at which ondansetron had been administered to the patient. It is not uncommon for residents to administer ondansetron as a bolus perioperatively. Not many clinicians are aware that ondansetron 4 to 8 mg iv should be administered over 2 to 5 min [6] and certainly not as a bolus or in less than 30 s. Perhaps slow administration of ondansetron as recommended over 2-5 min would decrease the incidence of potentially life-threatening adverse effects associated with ondansetron. Smita Prakash, Meenu Aggarwal

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Frampton JE, McTavish D. Ranatidine. A pharmcoeconomic evaluation of its use in acid related disorders. Pharmcoeconomics 1994;6;57-89. Demirkan K, Bozkurt B, Karakya G, Kalyonuc AF. Anaphylactic reaction to drugs commonly used for gastrointestinal system disease. J Investig Allergol Clin Immunol 2006;16:203-9. Powell JA, Maycock EJ. Anaphylactoid reaction to ranitidine in an obstetric patient. Anaesth Intensive Care 1993;21;702-3. Rethnam U, Yesupalan RS. Anaphylactic reaction associated with ranitidine in a patient with acute pancreatitis; A case report. J Med Case Reports 2007;1:75. Classens DC, Pestotnik SL, Evans RS, Burke JP. Computerised surveillance of adverse drug events in hospital JAMA 1991;266:2847-51. Access this article online Quick Response Code:

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DOI: 10.4103/0019-5049.84826

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Department of Anaesthesia and Intensive Care, Vardhman Mahavir Medical College and Safdarjang Hospital, New Delhi, India Address for correspondence: Dr. Smita Prakash, C 17 HUDCO Place, New Delhi − 110 049, India. E-mail: [email protected]

REFERENCES 1.

Moazzam MS, Nasreen F, Bano S, Amir SH. Symptomatic sinus bradycardia: A rare adverse effect of intravenous ondansetron. Saudi J Anaesth 2011;5:96- 7. 2. Kasinath NS, Malak O, Tetzlaff J. Atrial fibrillation after ondansetron for the prevention and treatment of nausea and vomiting: A case report. Can J Anesth 2003;50: 229- 31. 3. Chandrakala R, Vijayashankara CN, Kumar K, Sarala N. Ondansetron induced ventricular tachycardia. Indian J Pharmacol 2008;40:186- 7. 4. Sahu S, Karna ST, Agarwal A, Ambesh SP, Srivastava A. Ondansetron causing near fatal catastrophe in a renal transplant recipient. Indian J Anaesth 2011;55:81- 2. 5. Afonso N, Dang A, Namshikar V, Kamat S, Rataboli PV. Intravenous ondansetron causing severe bradycardia: Two cases. Ann of Card Anaesth 2009;12: 172- 3. Indian Journal of Anaesthesia | Vol. 55| Issue 4 | Jul-Aug 2011

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Stoelting RK, Hillier SC, editors. Pharmacology and physiology in anesthetic practice 4th ed. Philadelphia (PA): Lippincott Williams and Wilkins; 2006. p. 444- 55. Access this article online Quick Response Code:

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DOI: 10.4103/0019-5049.84827

Lignocaine toxicity after anterior nasal packing Sir, A 26 year old male with acute epistaxis was planned for anterior nasal packing under local anaesthesia. He was weighing 50 kg with no past significant medical and surgical illness. Anterior nasal packing was done with Lignocaine soaked pack (5 ml of 4% Lignocaine). About 1 minute after application of the pack, the patient developed perioral numbness, restlessness and ultimately generalized tonicclonic seizures. Immediately, he was diagnosed as Lignocaine toxicity and resuscitation was started with Oxygen via face mask and Midazolam 3 mg was given intravenously. The seizure subsided after Midazolam injection and the patient remained haemodynamically stable. Laboratory tests were normal except for mild metabolic acidosis. Electroencephalography and a computerized tomography scan revealed no abnormalities. No neurological sequelae were noted. Lignocaine is used widely for pain relief as a local anaesthetic and in nasal packing. Local use of Lignocaine can have severe toxic effects on the cardiovascular and neurological systems. Most of these have been seen in young children who were given doses higher than recommended for local use. [1] Lignocaine is mostly (70%) eliminated through liver. Animals with experimentally produced hepatic damage are much more susceptible to the toxic actions of Lignocaine [2] and the chances of toxic reactions are maximum when there is both, hepatic and renal impairment. [3] However, in this patient, both the liver and kidney functions were normal. Indian Journal of Anaesthesia | Vol. 55| Issue 4 | Jul-Aug 2011

The recommended single parental adult dose of Lignocaine is 4.5 mg/kg. In this patient 5 ml of 4% Lignocaine (200 mg) was used, that is within the safe maximum level. Toxicity depends largely on the balance between the rate of absorption and the rate of metabolism.[1] In this way, the absorption of Lignocaine from the nasal mucosa may be higher due to absence of hepatic first pass effect. In addition, the absorption may be more rapid because of the rich vascular supply in the nasal mucosa despite incomplete and variable absorption in this route.[4] Addition of vasoconstrictors decreases systemic absorption and higher doses can be used safely. In this case, the close temporal relationship, the lack of previous or subsequent seizures strongly suggests that Lignocaine was responsible for the seizure in this patient. So, we concluded that for anterior nasal packing with local anaesthetics in patients of actively bleeding epistaxis, the risk of potential toxicity of Lignocaine should be kept in mind, and it should be done under close monitoring, and if such complications do arise, prompt diagnosis and intervention can save patients. Mridu Paban Nath, Rumi Baruah, Dipika Choudhury, Anulekha Chakrabarty Department of Anaesthesiology and Critical Care, Gauhati Medical College & Hospital, Guwahati, Assam, India Address for correspondence: Dr. Mridu Paban Nath, Department of Anaesthesiology and Critical Care, Gauhati Medical College & Hospital, Guwahati - 781 032, Assam, India. E-mail: [email protected]

REFERENCES 1. 2.

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Hess PD, Walson PD. Seizures secondary to oral viscous lidocaine. Ann Emerg Med 1988;17:725-7. Mofenson HC, Caraccio TR, Miller H, Greensher J. Lidocaine toxicity from topical mucosal application. Clin Pediatr (Phila) 1983;22:190-2. Sundaram MB. Seizures after intraurethral instillation of lidocaine. CMAJ 1987;137:219-20. Scavone JM, Greenblatt DJ, Fraser DG. The bioavailability of intranasal lignocaine. Br J Clin Pharmacol 1989;28:722-4. Access this article online Quick Response Code:

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DOI: 10.4103/0019-5049.84828

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