Opioid-induced Rigidity Research Articles

A case of opioid-induced rigidity requiring naloxone administration at the time of anesthesia emergence

BackgroundOpioid-induced rigidity is typically observed during rapid administration of fentanyl. Herein, we present a case in which rigidity occurred after reversal of rocuronium during emergence from anesthesia.Case presentationA 73-year-old man underwent video-assisted partial lung resection. General anesthesia was induced with propofol, remimazolam, remifentanil, and rocuronium. Fentanyl was administered early during anesthesia. The surgery was completed without complications, and sugammadex sodium was administered for rocuronium reversal. The patient became agitated, but spontaneous breathing was maintained; therefore, the intratracheal tube was removed after the administration of flumazenil. The patient developed stiffness in the neck and jaw muscles along with remarkable skeletal muscle contractions. Dramatic improvement was observed immediately after administration of naloxone.ConclusionsEven as the simulated effect site concentration of fentanyl decreases during anesthesia emergence, opioid-induced rigidity may still occur. Rapid reversal of remimazolam by flumazenil might have contributed to the rigidity in this case.

Quantification of muscle tone by using shear wave velocity during an anaesthetic induction: a prospective observational study

ObjectivesThe quantitative assessment of muscle stiffness or weakness is essential for medical care. Shear wave elastography is non-invasive ultrasound method and provides quantitative information on the elasticity of soft tissue. However, the universal velocity scale for quantification has not been developed. The aim of the study is to determine the shear wave velocities of abdominal muscle during anesthetic induction and to identify methods to cancel the effects of confounders for future development in the quantitative assessment of muscle tone using the universal scale.MethodsWe enrolled 75 adult patients undergoing elective surgery with ASA-PS I – III in the period between December 2018 and March 2021. We measured and calculated the shear wave velocity (SWV) before and after opioid administration (i.e., the baseline at rest and opioid-induced rigidity condition), and after muscle relaxant administration (i.e., zero reference condition). The SWV value was adjusted for the subcutaneous fat thickness by our proposed corrections. The SWVs after the adjustment were compared among the values in baseline, rigidity, and relaxation using one-way repeated-measures ANOVA and post hoc Tukey–Kramer test. A p-value of < 0.05 was considered to be statistically significant. UMIN Clinical Trials Registry identifier UMIN000034692, registered on October 30, 2018.ResultsThe SWVs in the baseline, opioid-induced rigidity, and muscle relaxation conditions after the adjustment were 2.08 ± 0.48, 2.41 ± 0.60, and 1.79 ± 0.30 m/s, respectively (p < 0.001 at all comparisons).ConclusionThe present study suggested that the SWV as reference was 1.79 m/s and that the SWVs at rest and opioid-induced rigidity were ~ 10% and ~ 30% increase from the reference, respectively. The SWV adjusted for the subcutaneous fat thickness may be scale points for the assessment of muscle tone.

Opioid-induced Muscle Rigidity with a Delayed Manifestation Misunderstood as a Tension Pneumothorax: A case report

Opioid-induced rigidity is a potentially life-threatening complication that can occur after treatment with largedoses of opioids, but with early recognition it can be treated effectively with naloxone or with muscle relaxants.Regardinq its onset time, there have been few case reports that have described delayed manifestations ofopioid-induced rigidity. The mechanism of this complication is not well understood, In this report we describea case of incidental overdose injection of sufentanil and subsequently review the confusing clinical features thatrequire immediate diffenrentiation and the possible mechanim of this complication. (Korean J Pain 2008; 21:66-70)

Opioid-induced rigidity after intravenous fentanyl

Large doses of intravenous opioids may cause severe rigidity and prevent spontaneous or controlled ventilation. The mechanism of this effect appears to be neuraxis dopamine antagonism. Rigidity after analgesic doses of fentanyl has not been reported previously. A pregnant woman receiving haloperidol for multiple psychiatric conditions presented for evaluation of vaginal bleeding. Intravenous fentanyl was administered to facilitate vaginal examination. Severe rigidity of the extremities and truncal region occurred, which prevented spontaneous or assisted ventilation. Opioid administration may result in rigidity and respiratory embarrassment. Decreased analgesic requirements in pregnancy and concomitant butyrophenone administration may predispose to opioid-induced rigidity.

An in vivo alpha-2 assay reversal of opioid-induced muscular rigidity and neuroleptic-induced ptosis

A method is described to detect selective α-2 adrenergic agonists in vivo. Palpebral ptosis is induced in rats by the neuroleptic agent haloperidol (Hal), or by tetrabenazine (TBZ) methanesulfonate. Twenty minutes later, test compounds are injected, and ptosis is scored. In a separate test, muscular rigidity is induced by the opioid, fentanyl, and subsequently, test compounds are assessed for their ability to reverse muscular rigidity. Results indicate that only α-2 agonists reliably reverse neuroleptic-induced and TBZ-induced ptosis, as well as opioid-induced rigidity. An α-1 antagonist reversed only rigidity, whereas, α-2 antagonists and β-agonists were generally ineffective in all tests. Therefore, the ability to reverse neuroleptic and TBZ-induced ptosis along with the ability to reverse opioid-induced muscular rigidity is a characteristic unique to α-2 agonists.

Seizures during Opioid Anesthetic Induction—Are They Opioid-Induced Rigidity?

The tape recorded EEGs of 127 patients anesthetized with large doses of opioids were retrospectively analyzed for evidence of opioid-induced seizures, and in particular, correlated with movements that occurred during induction and could be clinically interpreted as seizures. Bilateral EEG leads in patients receiving fentanyl (20), sufentanil (20), or alfentanil (87) were recorded. Forty-six of these patients from all opioid groups manifested intense rigidity, as assessed both clinically and by EMGs recorded from eight muscles in 69 of the patients receiving alfentanil. This intense rigidity often resembled seizures, in that the phenomenon entailed severe stiffness of both limbs and trunk, with an explosive onset of myoclonic limb movements, and associated vertical nystagmus. Electroencephalographic observations were extensive, entailing 69 h of paper recordings played back from the tapes, at paper speeds of 30 or 60 mm/s, with detailed annotations from the voice track. These paper recordings were examined in detail independently by three of the investigators, who were unaware of the clinical phenomena that had occurred. The only observed EEG activity that could have been interpreted as epileptiform consisted of small sharp waves related to muscle activity or other artifact. The EEG never indicated seizure activity during these drug-induced movements and rigidity. Reports of opioid-induced seizures are reviewed and a set of criteria is offered to help achieve future consistency and credibility in evaluating this phenomenon. The available evidence does not support the existence of opioid-induced seizures in the clinical setting.

Reversal of opioid-induced muscular rigidity in rats: Evidence for alpha-2 adrenergic involvement

Compounds from several different pharmacological classes were tested for their ability to reverse the muscular rigidity induced by an intravenous dose of fentanyl that also caused loss of the righting reflex (LOR). Opioid antagonists reversed the entire syndrome—LOR and rigidity but, generally, rigidity could be reversed nonspecifically by doses of compounds that caused LOR by themselves (e.g., CNS depressants). Muscle relaxants and agonists of histamine, which appeared to be acting peripherally, were also effective. On the other hand, serotonergic drugs and dopamine agonists were not. However, dopaminergic antagonists with adrenolytic activity (i.e., chlorpromazine, haloperidol) reversed rigidity, whereas sulpiride did not. Moreover, rigidity reversed by neuroleptics could be restored by piperoxane, an alpha-2 adrenergic antagonist. In addition, clonidine and other alpha-2 agonists selectively reversed only rigidity following systemic or central administration at doses several orders of magnitude lower than other compounds tested. It is proposed that opioid-induced rigidity is reversed by inhibition of sympathoadrenal outflow which can be accomplished selectively, centrally, by alpha-2 agonists.

Opioid actions on motility: Possible actions on GABA-ergic and dopaminergic neurons

The role of the caudate nucleus in mediating opioid-induced rigidity was evaluated in rats by measuring the electromyographical (EMG) activity in the gastrochemius-soleus muscle. A naloxone-reversible EMG activation could be induced not only by systemic administration of morphine, but also by local administration of this drug into the head of the caudate nucleus. Injections of D-ala 2-met 5-enkephalinamide into this brain area induced a similar EMG activation. Bilateral chemolesions of the caudate nucleus with kainic acid abolished the EMG activation induced by systemic administration of morphine, but enhanced the increase in striatal DOPAC observed after systemic administration of morphine in such a manner that a rapid and a slow maximum in DOPAC increase became manifest. A synopsis of our results and those of other authors suggests that opiates induce rigidity by direct actions on neurons, the cell bodies of which are located in the caudate nucleus—probably on GABA-ergic neurons. The increase of dopamine turnover, on the other hand, is mediated via actions on different neurons.