The Effects of Residual Pain on Oxygenation and Breathing Pattern During Morphine Analgesia

Combes, X.; Cerf, Charles; Bouleau, D.; Duvaldestin, P.; Dhonneur, Gilles

doi:10.1097/00000539-200001000-00033

Cited by 12 publications

(8 citation statements)

References 15 publications

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“…Indeed, several studies and case reports indicated an important role of pain in the maintenance of breathing. Combes et al [9] demonstrated in patients treated postoperative pain by i.v. morphine that complete pain resolution by supplemental peripheral nerve block worsened respiratory depression.…”

Section: Discussionmentioning

confidence: 98%

Postoperative Apnea Induced by Fentanyl and Other Multiple Respiratory-Modulating Factors

Matsuda¹,

Sato²

2014

OJAnes

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Purpose: Opioids are concerned as a major cause of postoperative respiratory depression. In the immediate postoperative period, however, other factors can produce instability of breathing such as pain, agitation, and residual effects of anesthetics. Such factors might be overlooked masked by the fear for opioid-induced respiratory depression. We report a case who presented apnea immediately after emergence from anesthesia that we considered was produced by an interaction among such factors accompanied with fentanyl-induced respiratory depression. Clinical Features: A 31-year-old woman underwent ovarian cystectomy under general anesthesia with continuous infusions of propofol and remifentanil, and bolus doses of fentanyl. Transversus abdominis plane blocks with ropivacaine were given upon completion of surgery. She complained of severe wound pain and was agitated at the emergence from anesthesia. Fentanyl 50 µg was administered intravenously. In several minutes, she developed apnea, unconsciousness, and difficulty of mechanical ventilation via a face mask. The estimated effect site concentration at the onset of the episode (2.9 ng•ml −1 ) was approximately the same (3.0 ng•ml −1 ) as after 30 min when she regained consciousness and spontaneous breathing. It indicated that not only direct inhibition of the respiratory center by fentanyl but also other stimulatory and inhibitory factors contributed to respiratory arrest. Conclusion: In the immediate postoperative period, transient factors, such as pain, mental instability and anesthetic residues, which are indirectly-related with breathing, can interact each other and with opioids. The interaction would induce apnea through mechanisms combined among direct inhibition of the respiratory center, and modulation of chemical and cortical controls of breathing.

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Section: Discussionmentioning

confidence: 98%

Postoperative Apnea Induced by Fentanyl and Other Multiple Respiratory-Modulating Factors

Matsuda¹,

Sato²

2014

OJAnes

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“…22 Of 1616 monitoring hours in 103 patients, 342 episodes of desaturation with pulseoximetry monitoring were noted, and 710 notification pages were generated 36% of the time for clinically relevant desaturation. 23 Nursing response time was 52.1 seconds (confidence interval, 46.4-57.7 seconds), which was longer at night (63.8 seconds [confidence interval, 51.2-76.35 seconds]; P = .035). This delay in response to alarms at night was unrelated to unit staffing patterns.…”

Section: Naloxone Usementioning

confidence: 94%

Avoiding Adverse Events Secondary to Opioid-Induced Respiratory Depression

Jungquist

Correll

Fleisher

et al. 2016

JONA: The Journal of Nursing Administration

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“…Patients who received morphine patient-controlled analgesia (PCA) after knee surgery, and whose pain was then completely abolished by a nerve block, subsequently manifested an increased incidence of oxygen desaturation an d obstructed airwa y events. 16 Borgbjerg et al 17 examined the effects of experimental pain stimulation on the ventilatory response to carbon dioxide-and morphine-induced (0,2 mg/kg IV) respiratory depression in 10 healthy volunteers. Experimental pain stimulated respiration and abolished morphine-induced respiratory depression.…”

Section: Infl Uence Of Painmentioning

confidence: 99%

“…1 The purpose of this paper is to re-examine the known features of morphine-induced respiratory depression and to revise its characteristics in the light of newer pharmacokinetic-pharmacodynamic (PKPD) research. This will be done by means of a case presentation and applied PKPD modelling of a patient who died after a 2010; 16(2) S Afr J Anaesthesiol Analg tonsillectomy, and around whom the discussion will revolve.…”

Section: Introductionmentioning

confidence: 99%

Safety of pain control with morphine: new (and old) aspects of morphine pharmacokinetics and pharmacodynamics

Coetzee

2010

Southern African Journal of Anaesthesia and Analgesia

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Background: A 26-year-old, 59 kg female was administered morphine 10 mg during tonsillectomy, and 5 mg in the recovery room. She died 5 hours after the operation. Hypoxic cerebral injury, arising from morphine side-effects, was pronounced the cause of death, in spite of morphine being undetectable in blood. Recent pharmacokinetic-pharmacodynamic modelling indicates that, after a single intravenous dose, maximum respiratory depression occurs after 1 hour and 40 minutes and persists for hours. Furthermore, respiratory depression is accompanied by airway obstruction, sleep potentiates respiratory depression and airway obstruction, pain stimulates breathing and antagonises respiratory depression, pain relief unmasks respiratory depression, and a slow breathing rate is uncommon. Methods: Pharmacokinetic-pharmacodynamic simulations were used to estimate the time course of morphine effect-site concentrations in an "average" 59 kg female, and to calculate the degree of resulting respiratory depression. Results: Morphine effect-site concentrations approached dangerous levels for respiratory depression and persisted for hours, while plasma concentrations were undectectably low. Discussion: Court testimony indicates that additional factors contributed to the patient's demise. Respiratory depression was potentiated by pain relief following quinsy tonsillectomy, and by falling asleep. The airway was obstructed, as witnessed both by nurses and a fellow patient. In addition, nursing staff failed to recognise that snoring can indicate a dangerously obstructed airway. Conclusions: Dangerous respiratory depression often goes unrecognised in surgical wards. Strategies for improved safety include education of nursing and other staff regarding the following aspects of respiratory depression: (i) recognition of delayed and prolonged respiratory depression; (ii) noisy breathing indicates obstructed breathing; (iii) respiratory rate is an unreliable monitor of respiratory depression; (iv) training in airway management should be compulsory; (v) sleeping patients should be administered oxygen, and pulse oximetry monitoring should be done (especially at night); (vi) more local anaesthesia should be administered for postoperative pain; (vii) combination analgesic therapy (NSAIDs, paracetamol, ketamine, dexmedetomidine, gabapentin) should be utilised to reduce morphine requirements; (viii) high risk patients (e.g. elderly, obese, sleep-apnoea syndrome) should be identi ed; (ix) sedation scores should be recorded to detect obtunded patients. Morphine plasma concentrations do not re ect pharmacological activity.

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The Effects of Residual Pain on Oxygenation and Breathing Pattern During Morphine Analgesia

Abstract: Pain relief with regional analgesia in patients previously treated with opioids increases the incidence of abnormal respiratory events associated with oxygen desaturation.

Cited by 12 publications

References 15 publications

Postoperative Apnea Induced by Fentanyl and Other Multiple Respiratory-Modulating Factors

Postoperative Apnea Induced by Fentanyl and Other Multiple Respiratory-Modulating Factors

Avoiding Adverse Events Secondary to Opioid-Induced Respiratory Depression

Safety of pain control with morphine: new (and old) aspects of morphine pharmacokinetics and pharmacodynamics

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