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Anesthesia: Essays and Researches; 7(2); May-Aug 2013 Department of Anesthesiology and Intensive Care, Golestan University of Medical Sciences, Gorgan, 2Babol University of Medical Sciences, Babol, 3Department of Internal Medicine, Tehran University of Medical Sciences, Tehran, Iran
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Corresponding author: Dr. Ali Jabbari, Department of Anesthesiology and intensive care, 2nd Floor, Ayatollah Ruhani Hospital, University Sq, GanjAfruz Avenue, Babol City, Mazandaran Province, Iran E‑mail:
[email protected]
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Jabbari A, Tabasi S, Abbasi A, Alijanpour E. Crimean‑Congo hemorrhagic fever: Treatment and control strategy in admitted patients. Caspian J Intern Med 2012;3:443‑4. Chinikar S, Ghiasi SM, Ghalyanchi‑Langeroudi A, Goya MM, Shirzadi MR, Zeinali M, et al. An overview of Crimean Congo hemorrhagic fever in Iran. Iran J Microbiol 2009;1:7‑12. Vorou R, Pierroutsakos IN, Maltezou HC. Crimean Congo hemorrhagic fever. Curr Opin Infect Dis 2007;20:495‑500. Access this article online
REFERENCES
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1. Ergonul O. Crimean‑Congo haemorrhagic fever. Lancet Infect Dis 2006;6:203‑14. 2. Jabbari A, Besharat S, Abbasi A, Moradi A, Kalavi KH. Crimean‑Congo hemorrhagic fever: Case series from a medical center in Golestan province, northeast of Iran (2004‑2006). Indian J Med Sci 2006;60:327‑9.
Severe hypotension during general anesthesia in a patient on chronic high‑dose Tamsulosin therapy Sir, A 65‑year‑old, 70‑kg man was scheduled for cosmetic face lift surgery. Preanesthetic history and examination was insignificant except for benign prostate hypertrophy (BPH) since last 3 years, for which he was prescribed tab. Tamsulosin 0.8 mg OD and tab. Dutasteride 0.5 mg OD to be taken at night. All relevant investigations were within normal limits. Before the induction of anesthesia, the patient’s vital parameters recorded were: non‑invasive blood pressure (NIBP) of 130/70 mm Hg, heart rate (HR) of 60 bpm, with respiratory rate, temperature, and electrocardiogram (ECG) within normal limits. Premedication included inj. Midazolam 1.5 mg IV and inj. Fentanyl 120 µg IV. Additional drugs included inj. Cefuroxime 1.5 g IV, inj. Ranitidine 50 mg IV, and inj. Metoclopramide 10 mg IV. After adequate preoxygenation, general anesthesia was induced with inj. Propofol 120 mg IV and neuromuscular blockade was achieved with inj. Vecuronium 7 mg IV. Anesthesia was maintained with 1% Isoflurane in an N2O/O2 mixture and intermittent doses of inj. Vecuronium 1 mg IV were administered for muscle relaxation. The two BP readings taken at 1 min and 3 min intervals after administering the induction agent were 130/68 and 128/70 mm Hg, respectively. After laryngoscopy, the patient’s BP reading was 150/90 mm Hg and his HR was 110 bpm. Fifteen minutes into surgery, the patient’s BP decreased to 78/45 mm Hg and HR increased to 120 bpm. The rate of IV fluid administration was augmented. His HR remained at 120 bpm, and his oxygen saturation (SpO2) and end‑tidal carbon dioxide (EtCO2) were within normal limits. Inj. Mephentermine 6 mg IV bolus,
immediately administered, transiently improved the BP to 100/55 mm Hg. No ischemia‑related voltage changes were observed on the 3‑lead ECG. Furthermore, skin erythema, urticaria, facial edema, and other features of a potential anaphylaxis or anaphylactoid reaction were absent. Patient developed second episode of hypotension within minutes of the first episode, with BP decreasing to 65/35 mm Hg and HR increasing to 126 bpm. Inj. Mephentermine 6 mg IV bolus was promptly administered. Subsequently, the BP improved to 100/55 mm Hg, following which the patient was administered inj. Phenylephrine bolus of 0.5 mg IV followed by infusion of Phenylephrine at the rate of 40 μg/min. General anesthesia was now maintained with O2/N2O mixture and 0.6% Isoflurane. The total duration of surgery was 180 min and the total blood loss was 400 ml. Phenylephrine infusion was titrated throughout the surgery to maintain systolic BP above 100 mm Hg. At the end of surgery, Isoflurane was turned off and the patient’s BP increased to 158/92 mm Hg with an HR of 72 bpm. Trachea was extubated at the end of the surgery and patient’s vital parameters remained stable postoperatively. As a result of the recent surge in prescriptions of Tamsulosin for aging men with BPH, hypotension under anesthesia associated with this drug is a possibility and warrants the attention of anesthesiologist. Ligand‑binding studies report that the expression of α‑1B‑adrenergic receptor (α‑1B‑AR) concentration increases more than that of the α‑1A‑AR.[1] This suggests that the α‑1B‑AR may become more important with aging, leading to formulation of hypothesis that α‑1A/D‑AR selective antagonists such as Tamsulosin would interfere less with vascular tone and BP 285
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Anesthesia: Essays and Researches; 7(2); May-Aug 2013
regulation[2] in elderly patients with LUTS, as compared to subtype non‑selective agents.[3] However, episodes of orthostatic hypotension, palpitations, and syncope[2] are reported with use of Tamsulosin, especially with first dose and if dose is increased or an antihypertensive drug[4] or a phosphodiesterase‑5 inhibitor[5] is added to the treatment regimen. Unlike 0.4 mg OD regime of Tamsulosin, there is very less clinical data regarding safety profile of the 0.8 mg OD dose of Tamsulosin. Only one case of intraoperative hypotension attributed to interaction between Tamsulosin and Isoflurane in a patient on 0.4 mg undergoing elective left thyroid lobectomy is reported in literature.[6] The recommended dose is 0.4 or 0.8 mg OD about 30 min after the meal at the same time each day. Michel et al.[7] reported that if taken on an empty stomach, there is increased absorption which may cause a greater pharmacodynamic effect and a drop in blood pressure. Common adverse effects noted with this medication are anemia, nausea/vomiting, dysgeusia, and increase in triglyceride levels.[8] Floppy iris syndrome has been observed intraoperatively in patients on Tamsulosin treatment. Symptoms of drug overdose may include severe headache, dizziness, and fainting.[8] Removing Tamsulosin from the circulation pre‑operatively would require days of abstinence because of its long elimination half‑life of 9–15 h. It might be distressing for the patient in lieu of voiding dysfunction and can significantly decrease the quality of life.[9] In this case, the most likely explanation of hypotension, refractory to volume loading, is a decrease in the vascular tone due to the interaction of inhalational agent Isoflurane, a known vasodilator, with α‑1‑AR, facilitated by chronic use of high dose of Tamsulosin by the patient. Further evidence is compounded by the fact that hypotension was reversed with Phenylephrine infusion and there was dramatic increase in BP when Isoflurane was discontinued. The differential diagnosis, ruled out systematically based on clinical findings and normal ECG, included hypovolemia, anaphylaxis, pneumothorax, and myocardial ischemia, although the possibility of genetic sensitivity to Isoflurane still remains a confounding factor in this case. We conclude that a high index of suspicion should be maintained for persistent hypotension in a patient on 0.8 mg OD dose of Tamsulosin therapy with Isoflurane anesthesia. If hypotension does develop in these patients, we recommend the use of direct acting α‑1‑AR agonist agents, and if the
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decision to discontinue Tamsulosin is made, then the dose should be tapered gradually to avoid the side effects and BP should be monitored closely during this period.
Gaurav Chauhan, Kapil Gupta, Pavan Nayar Department of Anesthesia and Intensive Care, Safdarjang Hospital, New Delhi, India Corresponding author: Dr. Gaurav Chauhan, Department of Anesthesia and Intensive Care, Safdarjang Hospital, New Delhi, India E-mail:
[email protected]
REFERENCES 1.
Price DT, Lefkowitz RJ, Caron MG, Berkowitz D, Schwinn DA. Localization of mRNA for three distinct α1‑adrenergic subtypes in human tissues: Implications for human α‑adrenergic physiology. Mol Pharmacol 1994;45:171‑5. 2. Chung JW, Choi SH, Kim BS, Kim TH, Yoo ES, Kim CI, et al. Efficacy and Tolerability of Tamsulosin 0.4 mg in Patients with Symptomatic Benign Prostatic Hyperplasia. Korean J Urol 2011;52:479‑84. 3. Chrischilles E, Rubenstein L, Chao J, Kreder KJ, Gilden D, Shah H. Initiation of nonselective alpha1‑ antagonist therapy and occurrence of hypotension‑related adverse events among men with benign prostatic hyperplasia: A retrospective cohort study. Clin Ther 2001;23:727‑43. 4. Lowe FC. Coadministration of tamsulosin and three antihypertensive agents in patients with benign prostatic hyperplasia: Pharmacodynamic effect. Clin Ther 1997;19:730‑42. 5. Kloner RA, Jackson G, Emmick JT, Mitchell MI, Bedding A, Warner MR, et al. Interaction between the phosphodiesterase 5 inhibitor, tadalafil and 2 alpha‑blockers, doxazosin and tamsulosin in healthy normotensive men. J Urol 2004;172:1935‑40. 6. Kumar D, Khan FA. Tamsulosin‑induced severe hypotension during general anesthesia: A case report. J Med Case Rep 2010;17:4:365. 7. Michel MC, Korstanje C, Krauwinkel W. Cardiovascular Safety of tamsulosin modified release in the fasted and fed state in elderly healthy subjects. Eur Urol 2005;40(Suppl 4):9‑14. 8. Nickel JC, Sander S, Moon TD.A meta‑analysis of the vascular‑related safety profile and efficacy of α‑adrenergic blockers for symptoms related to benign prostatic hyperplasia. Int J Clin Pract 2008;62:1547‑59. 9. Jeong YB, Kwon KS, Kim SD, Kim HJ. Effect of discontinuation of 5alpha‑reductase inhibitors on prostate volume and symptoms in men with BPH: A prospective study. Urology 2009;73:802‑6.
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