Evaluation of Different Doses of Fentanyl in Controlling Agitation in Acute Opioid Withdrawal Syndrome Induced by Naltrexone Misuse

Document Type : Original Article (s)

Authors

1 Associate Professor, Department of Forensic Medicine and Poisoning, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

2 Student of Medicine, Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background: Opioid addiction is one of the problems in all human societies including our country (Iran). It causes several kinds of disability in individual performance. Inappropriate use of naltrexone drug addicts causes acute opioid withdrawal syndrome. Agitation is the prominent sign of this syndrome. The aim of this study was to elucidate the efficacious and safe dose of fentanyl in controlling agitation.Methods: In a clinical trial study, 45 eligible opioid addicted patients were evaluated. They were divided into 3 groups with different doses of fentanyl (50, 75, 100 µg). Each patient's agitation score was then measured by Richmond Agitation Sedation Scale (RASS). The values were compared between the 3 groups.Findings: The mean age of participants was 30.5 ± 7.3 years. There were no significant differences between the 3 groups in terms of the last opioid use, naltrexone consumption, and vital signs on arrival. RASS scores in all 3 groups were significantly reduced (P < 0.05) 9 hours after initiation of treatment. The changes RASS scores of the 3 groups had significant differences (P < 0.001). Patients receiving 100 µg fentanyl suffered severe drowsiness. All patients were discharged with no adverse effects. Conclusion: Bolus and maintenance doses of fentanyl have no significant effects on patients' vital signs. On the other hand, dose of 100 µg caused excessive sedation for patients. Therefore, fentanyl would be recommended at a dose of 75 or 50 µg to control agitation in acute opioid withdrawal syndrome following naltrexone misuse.

Keywords

References

  1. Schievink WI. Intracranial aneurysms. N Engl J Med 1997; 336(1): 1758-9.
  2. Mayberg MR, Okada T, Bark DH. Morphologic changes in cerebral arteries after subarachnoid hemorrhage. Neurosurg Clin N Am 1990; 1(2): 417-32.
  3. Wickman G, Lan C, Vollrath B. Functional roles of the rho/rho kinase pathway and protein kinase C in the regulation of cerebrovascular constriction mediated by hemoglobin: relevance to subarachnoid hemorrhage and vasospasm. Circ Res 2003; 92(7): 809-16.
  4. Torbey MT, Hauser TK, Bhardwaj A, Williams MA, Ulatowski JA, Mirski MA, et al. Effect of age on cerebral blood flow velocity and incidence of vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2001; 32(9): 2005-11.
  5. Conway JE, Tamargo RJ. Cocaine use is an independent risk factor for cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2001; 32(10): 2338-43.
  6. Qureshi AI, Suri MF, Yahia AM, Suarez JI, Guterman LR, Hopkins LN, et al. Risk factors for subarachnoid hemorrhage. Neurosurgery 2001; 49(3): 607-12.
  7. Dalbasti T, Karabiyikoglu M, Ozdamar N, Oktar N, Cagli S. Efficacy of controlled-release papaverine pellets in preventing symptomatic cerebral vasospasm. J Neurosurg 2001; 95(1): 44-50.
  8. Smith WS, Dowd CF, Johnston SC, Ko NU, DeArmond SJ, Dillon WP, et al. Neurotoxicity of intra-arterial papaverine preserved with chlorobutanol used for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2004; 35(11): 2518-22.
  9. Ausman JI, Slavin KV, Charbel FT. Commentary to the article "Pupillary changes after intracisternal injection of papaverine" by M. Pritz. Surg Neurol 1994; 41(4): 283.
  10. Bala I, Ghai B, Kumar A, Pratap M. Bilateral pupillary dilatation after intracisternal papaverine application. Anesth Analg 2006; 102(3): 965.
  11. Lang EW, Neugebauer M, Ng K, Fung V, Clouston P, Dorsch NW. Facial nerve palsy after intracisternal papaverine application during aneurysm surgery--case report. Neurol Med Chir (Tokyo) 2002; 42(12): 565-7.
  12. Pritz MB. Pupillary changes after intracisternal injection of papaverine. Surg Neurol 1994; 41(4): 281-2.
  13. Rath GP, Mukta, Prabhakar H, Dash HH, Suri A. Haemodynamic changes after intracisternal papaverine instillation during intracranial aneurysmal surgery. Br J Anaesth 2006; 97(6): 848-50.
  14. Chia RY, Hughes RS, Morgan MK. Magnesium: a useful adjunct in the prevention of cerebral vasospasm following aneurysmal subarachnoid haemorrhage. J Clin Neurosci 2002; 9(3): 279-81.
  15. Dehdashti AR, Mermillod B, Rufenacht DA, Reverdin A, de TN. Does treatment modality of intracranial ruptured aneurysms influence the incidence of cerebral vasospasm and clinical outcome? Cerebrovasc Dis 2004; 17(1): 53-60.
  16. Roos YB, de Haan RJ, Beenen LF, Groen RJ, Albrecht KW, Vermeulen M. Complications and outcome in patients with aneurysmal subarachnoid haemorrhage: a prospective hospital based cohort study in the Netherlands. J Neurol Neurosurg Psychiatry 2000; 68(3): 337-41.
  17. Liu JK, Tenner MS, Gottfried ON, Stevens EA, Rosenow JM, Madan N, et al. Efficacy of multiple intraarterial papaverine infusions for improvement in cerebral circulation time in patients with recurrent cerebral vasospasm. J Neurosurg 2004; 100(3): 414-21.
Journal of Isfahan Medical School
Volume 29, Issue 156 - Serial Number 156
July and August 2011
Pages 1484-1492

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History

  • Receive Date: 29 August 2011
  • Revise Date: 01 November 2024
  • Accept Date: 06 April 2022

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