Takotsubo cardiomyopathy post-adrenaline infiltration—in nasal surgery

Sathya. T. V, Mohana Rangam*

Department of Anaesthesiology, Kauvery Hospital, Radial Road, Chennai

Abstract

Adrenaline causes cardiovascular crisis when enters systemic circulation. Here we discuss about a young female patient with no prior cardiovascular compromise developing cardiovascular side effects following administration of local anesthetic with diluted adrenaline during nasal surgery. Here we emphasize the need to anticipate and manage any cardiovascular side effects of topical or submucosal adrenaline

Introduction

Adrenaline is commonly used in nasal surgeries to decrease bleeding in the surgical site. If this drug gets absorbed in systemic circulation it can cause sympathomimetic effects like hypertension, arrhythmia, pulmonary edema and cardiac arrest(ref2). In this case report we discuss about a patient developing ventricular tachycardia following adrenaline infiltration and its intraoperative and postoperative events

Case Presentation

A 26-year-old female, weighing about 56kg, was admitted in our hospital for procedure of septorhinoplasty for external nasal deformity. She had a history of RTA 15months back involving face for which she had undergone cartilage and facial nerve repair followed by ORIF of bilateral maxilla under GA. She had no comorditities or any previous cardiac compromise. She was assessed under ASA I.

Patient was shifted to operation theatre(OT) then standard monitors placed and ringer lactate started. General anesthesia was induced with IV fentanyl 100mcg, IV propofol 110mg, IV vecuronium 6mg and intubated with 7mm cuffed PVC ETT and connected to closed circuit under PCV-VG mode with FiO2 60%. Maintanence of anesthesia was done with oxygen, air and desflurane and fentanyl 40mcg. Rib graft was obtained from right 9th rib. Then local infiltration in nasal area was done with 4ml of 0.5% ropivacaine with 1:2,00,000 dilution of adrenaline. Within few seconds patient developed ventricular bigeminy followed by Ventricular tachycardia (VT) upto heart rate of 150bpm. Immediately 60mg IV lidocaine was administered, and within 30 sec VT was reverted. Then surgery was resumed.

During intraoperative period, patient developed hypotension which was not responding to ephedrine or phenylephrine, so noradrenaline was initiated and titrated based on BP. IV dex amethasone, IV paracetamol and diclofenac suppository were given. At the end of procedure of 2 hours, noradrenaline was weaned off and after adequate respiratory efforts and motor function, patient was extubated with IV sugammadex 200mg.

Patient was shifted to ICU for observation and evaluation. She had episodes of hypotension requiring noradrenaline. Troponin I was elevated postoperatively and her Echo showed RWMA, hypokinesia of basal and mid anteroseptum of LV and LVEF of 50%(reduced from preop EF64%). Holter monitor placed for 48hrs and NTproBNP taken which was elevated and started on Tablet Cardivas 3.125mg BD. Patient was shifted to ward after 2 days and then discharged.

Discussion

Generally, diluted adrenaline is applied along with local anaesthetic locally for three purposes – a) adrenaline causes local vasoconstriction providing better visibility of surgical field; b) Slower LA absorption enables prolonged action; c) Slower adrenaline absorption reduces its systemic side effects. But this can cause sympathomimetic effects if absorbed systemically. These effects are very common during nasal infiltration due to high vascularity of nasal mucosa. There are many studies showing rise in plasma concentration of adrenaline following infiltration.

We need to know the systemic effects of adrenaline to understand and manage them. Its vasoconstrictor effects cause systemic hypertension, increase in left ventricular afterload, decrease in left ventricular compliance and decrease in cardiac output resulting in left heart failure [1]. In those patients treated with beta blockers, decrease in myocardial contractility and inability to increase heart rate further compromises cardiopulmonary function.

Adrenaline further affects potassium levels, initially it causes transient increase in potassium mediated by alpha receptors through activation of hepatic calcium dependant K+ channels followed by decrease due to beta2 receptors mediated influx of potassium into liver and skeletal muscle through Na+ K+ ATPase pump. Due to severe hypokalemia, it can cause ventricular tachyarrythmia due to prolonged ventricular repolarisation, slowed conduction and abnormal pacemaker activity [3,4].

Use of volatile agents like sevoflurane, desflurane, isoflurane, nitrous oxide can depress myocardial contractility and also potentiate arrythmogenic effects of adrenaline through synergistic interaction between alpha and beta receptors and also slow the automaticity of SA node andmyocardial conduction causing arrhythmias [5].

Stress or Takotsubo cardiomyopathy or Broken heart syndrome [6,7] is a clinical syndrome characterized by acute transient reversible apical ventricular dysfunction without obstructive coronary disease. It can be triggered by emotional or physical stress or exogenous adrenaline. There will be new ST segment elevation or T wave inversion, mild elevation of cardiac troponin and dyskinesia of left ventricular mid segments. When we are suspecting this, it is better to do echo cardiogram and coronary angiogram to rule out ACS.

Conclusion

Therefore, anticipating and being equipped to manage potential cardiovascular events during adrenaline infiltration is crucial. Additionally, the use of beta-blockers and volatile agents should be approached with caution, as they can further compromise cardiovascular stability.

References

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