| | Risk Factors for Opioid-Induced Excessive Respiratory DepressionReceived 7 January 2010; received in revised form 24 January 2010; accepted 1 February 2010. published online 26 July 2010.
Corrected Proof Abstract Opioid use has increased significantly over the past ten years and so has the incidence of reportable adverse events, such as respiratory depression and/or arrest. It is important for nurses to understand and know how to assess patients for risk factors for respiratory depression secondary to opioid therapy. This paper presents the pharmacodynamics of opioids, the risk factors for excessive respiratory depression, recommendations for identifying patients at high risk, and interventions to prevent adverse effects. After reading this paper, nurses will have the knowledge to provide safe administration of opioid medications for the management of acute pain. According to the Adverse Event Reporting System (AERS) used by the Food and Drug Administration (FDA) to track adverse effects as reported by health care professionals, oxycodone and fentanyl were the two most frequently reported drugs associated with death and serious nonfatal outcomes from 1998 to 2005 (Moore, Cohen, & Furberg, 2007). In the hospital setting, despite nurses' vigilance, adverse events associated with the opioid class of medications continue to occur (Eckstrand et al., 2009). The most common etiology of the events is excessive sedation resulting in respiratory depression that is life threatening. The present article reviews the risk factors for postoperative pulmonary complications, the mechanism of respiratory depression from opioids, and the known risk factors for adverse events related to the use of opioid medications in the inpatient setting. Risk Factors for Postoperative Pulmonary Complications  Predictors of pulmonary complications during the post operative period can be divided into five categories: 1) individual characteristics; 2) general state of health; 3) presence of certain diseases; 4) type of anesthesia; and 5) type of surgical procedure (Gross et al., 2006, Smetana et al., 2006, Tsai et al., 2003, Wolters et al., 1996) (Tables 1 and 2). Recognizing the patient at risk allows for more intense monitoring and the appropriate management before the adverse event occurs.  | Individual Characteristics | | | Age >70 years | | | General state of health: | | |  Albumin level >30 g/L | | | Blood urea nitrogen level >30 mg/dL | | | Dependent functional status | | | Presence of Certain Diseases | | | ASA classification >2 (Table 2) | | | Chronic obstructive pulmonary disease | | | Congestive heart failure | | | Type of Anesthesia | | | General | | | Prolonged surgery | | | Emergent surgery | | | Type of Surgical Procedure | | | Abdominal aortic aneurysm repair | | | Thoracic surgery | | | Neurosurgery | | | Upper abdominal surgery | | | Peripheral vascular surgery | | | Neck surgery | | | Vascular surgery | | | | |
| Class I | Normal healthy | | | Class II | Patient with mild systemic disease | | | Class III | Patient with severe systemic disease | | | Class IV | Patient with severe systemic disease that is a threat to life | | | Class V | Morbid patient who is not expected to survive without the operation | | | Class VI | A declared brain-dead patient whose organs are being removed for donor purposes | | | | |
Case Study #1. T.S. is a 70-year-old woman, 140 pounds, 5′6″, retired postal worker who underwent an emergent appendectomy under general anesthesia with an endotracheal tube. Preoperative vital signs include blood pressure 160/78 mmHg, pulse 72/min, respirations 12/min, temperature 99.2°F. Preoperative blood work: Hct 38%, albumin 25 g/L, blood urea nitrogen (BUN) 38 mg/dL, creatinine 1.4 mg/dL. Past medical history was significant only for smoking 1 pack per day for past 42 years. The surgery went well without complications, and she recovered uneventfully in the postoperative care unit. Just before transfer to the floor, she had received hydromorphone 2 mg IV for pain. She was transfered to the general surgical floor at 2 p.m. and was found to be easily arousable, appropriately oriented, and responsive to vocal commands. She reported a pain intensity of 3/10 at rest and 6/10 with positioning. Once admitted to the surgical floor, she was started on morphine PCA with a basal rate of 2 mg/h and as-needed dosing intervals of 1 mg/10 min. At the 3 p.m. assessment, her sedation scale (Table 3) score was 3 (frequently drowsy, drifts to sleep during conversation) and pain level was reported as 6/10. The nurse encouraged her to push the PCA button as needed for pain control. At 3:30 p.m. she was found to be unresponsive. | S = sleep, easy to arouse | | | Acceptable; no action necessary; may increase opioid dose if needed | | | 1 = awake and alert | | | Acceptable; no action necessary; may increase opioid dose if needed | | | 2 = slightly drowsy, easily aroused | | | Acceptable; no action necessary; may increase opioid dose if needed | | | 3 = frequently drowsy, arousable, drifts off to sleep during conversation | | | Unacceptable; monitor respiratory status and sedation level closely until sedation level is stable at <3 and respiratory status is satisfactory; decrease opioid dose 25%-50%†or notify primary‡or anesthesia provider for orders; consider administering a nonsedating opioid-sparing nonopioid, such as acetaminophen or a nonsteroidal antiinflammatory drug, if not contraindicated; ask patient to take deep breaths every 15-30 minutes. | | | 4 = somnolent, minimal or no response to verbal and physical stimulation | | | Unacceptable; stop opioid; consider administering naloxone§; call Rapid Response Team (code blue); stay with patient, stimulate, and support respiration as indicated by patient status; notify primary‡or anesthesia provider; monitor respiratory status and sedation level closely until sedation level is stable at <3 and respiratory status is satisfactory. | | | | |
| ∗ Appropriate action is given in italics at each level of sedation. †Opioid analgesic orders or a hospital protocol should include the expectation that a nurse will decrease the opioid dose if a patient is excessively sedated. ‡For example, the physician, nurse practitioner, advanced practice nurse, or physician assistant responsible for the pain management prescription. §For adults experiencing respiratory depression, mix 0.4 mg naloxone and 10 mL normal saline in syringe and administer this dilute solution very slowly (0.5 mL over 2 minutes) while observing the patient's response (titrate to effect). If sedation and respiratory depression occurs during administration of transdermal fentanyl, remove the patch; if naloxone is necessary, treatment will be needed for a prolonged period, and the typical approach involves a naloxone infusion (see text). Patient must be monitored closely for ≥24 hours after discontinuation of the transdermal fentanyl. Hospital protocols should include the expectation that a nurse will administer naloxone to any patient suspected of having life-threatening opioid-induced sedation and respiratory depression. |
Opioids To produce the analgesic effect, the opioid attaches to opioid receptors, where it modulates pain by inhibiting and/or opening voltage-gated calcium and/or potassium channels. The decrease in neuronal excitability within pathways and nuclei that are related to nociception translates into diminished pain sensation (Bessler et al., 2006, Gupta and Weber, 2006, Gutstein and Akil, 2005, Teichtahl et al., 2005, Walker et al., 2007). Although all opioids are associated with pain control, the opioids that bind primarily to the mu receptors have the strongest analgesic effect and the greatest potential for central nervous system depression. Opioids that exert their main effect on the mu receptor depress respiration by various mechanisms. They blunt the chemoreceptive response to carbon dioxide and oxygen, prolong exhalation time, and suppress the depth of respiration. In addition, they increase upper airway resistance by decreasing pharyngeal tone (Cox, 1991, Dahan and Teppema, 2003, Fukuda, 2000, Lalley, 2003, Leino et al., 1999, Schumacher et al., 2004). The mechanisms of developing respiratory depression from opioid use are self-potentiating in that hypoventilation impairs gas exchange, resulting in increased carbon dioxide (hypercapnia) and decreased oxygen (hypoxia) and pH (respiratory acidosis). In turn, suppression of the chemoreceptor responses to increased carbon dioxide levels blunt the normally protective central response which would increase breathing efforts. This “vicious cycle” may result in profoundly low oxygen (hypoxemia) and/or respiratory arrest. Although it is thought that patients previously exposed to opioids are “tolerant” to the respiratory depressive effects of opioids, there is evidence that when exposed to either a different opioid medication or increased doses of the same opioid, a degree of respiratory depression occurs (Ladd et al., 2005, Mercadante and Bruera, 2006, Nielsen et al., 2007). Knowing that opioids are associated with respiratory depression isn't enough to prevent adverse effects. Because nurses are likely to have many patients to assess, it is important to know when patients are at their highest risk for respiratory depression. There are two main factors, peak effect of opioid and state of consciousness. Opioid medications are distinguished by their formulations (e.g., intravenous, dermal, oral, short-acting, continuous-release). The specific drug and its formulation, as well as the drugs taken with it, are responsible for time to peak absorption (point of highest risk of adverse effect) and duration of action. Opioid medications that are formulated to be absorbed more quickly have increased risk of causing respiration-related adverse events, owing to unpredictable peak effect site concentration and/or changes in potency. For example, 1 mg hydromorphone given intravenously with midazolam (a benzodiazepine) is expected to have a higher potential of causing respiratory depression compared with administering 7.5 mg hydromorphone orally (Thomson Healthcare, 2007). Furthermore, not all patients metabolize opioid medications the same. Seven to ten percent of caucasians are poor metabolizers of all opioid medications (Mikus, Somogyi, Bochner, & Chen, 1991). Patients who are genetically deficient of a specific isoenzyme (cytochrome P450 isomer or 3A4 or 2DC isoenzyme) will poorly metabolize drugs that require the deficient isoenzyme for their metabolism. Clinically, this means that some patients will be hyperresponsive to certain opioids and have normal sensitivities to others. Also, coadministration of an interacting drug can either increase opioid metabolism (by inducing the isoenzyme metabolizing a given opioid) or decrease opioid metabolism (by inhibiting the isoenzyme metabolizing a given opioid). If one discontinues a drug that was inducing the isoenzyme, there is the potential to precipitate respiratory depression, because the amount of opioid will begin to accumulate as metabolic clearance of the opioid begins to fall back to normal. The converse is also true. Case Study #1 Resolution. In the first case study T.S. was an elderly female who presented in a compromised situation requiring emergent surgery under general anesthesia. Her preoperative blood work revealed mild liver and renal compromise that would affect metabolism and excretion of the anesthetic and analgesic agents. Knowing this, the nurse could have reported her concerns to the surgeon, advocating for PCA without a basal rate along with the use of opioid sparing medications and complementary therapies (e.g., ice, heat, relaxation, music). Remembering that this patient's BUN was 38 mg/dL (slightly increased) and albumin was 25 g/L (low) opioid sparing medications should be used cautiously. With this patient's need for opioid medications, a heightened level of care with the use of oximetry and increased frequency of assessments will be necessary. Case Study #2. B.J., a 250-lb 5′8″ engineer is a 54-year-old man (body mass index [BMI] 38 kg/m2) admitted for same day surgery to repair an inguinal hernia. He denies any medical problems or regular medication use, nor does he have any social vices. His blood pressure is 142/82 mm Hg, pulse 72/min, respiration 10/min, temperature 98.6°F, oxygen saturation 97%. His uneventful procedure was performed under general anesthesia. In the postoperative care unit (PACU), he initially receives morphine 4 mg IV for pain. A short time later, the PACU nurse notices that B.J.’s oxygen saturations are dropping into the low 70s and he is having 15–20-second periods of apnea. The anesthesiologist is called to evaluate and B.J. ends up reintubated. [What happened and how could this have been prevented?] Sleep/Deep Sedation, the Point of Greatest Respiratory Vulnerability Respiration is initiated and maintained by voluntary and involuntary stimuli. The involuntary stimulus initiates in the respiratory centers of the central nervous system and is regulated by chemoreceptors in the carotid and aortic bodies that respond to changing levels of oxygen and carbon dioxide within the vascular system (Fink, 1961, Hudgel et al., 1984). The ability of the central respiratory center to maintain oxygen and carbon dioxide levels depends on adequate airway patency and function of the muscles involved with the mechanical movement of the chest. Other factors that influence respiration are metabolic activity, age, gender, BMI, and state of consciousness (Wagner & West, 2005). During sleep/deep sedation, voluntary stimuli for respiration are absent. In addition, the involuntary control mechanisms are challenged by increased upper airway resistance, motor and neuronal hypotonia, and diminished chemoreceptor responses to oxygen and carbon dioxide levels (Hudgel & Devadatta, 1984). Knowledge of the physiology of respiratory depression can be applied to prevent adverse events. Preventing adverse events begins with assessing for risk factors. Assessing patients for a history of respiratory complications after a surgical procedure or assessing patients breathing during a similar situation (sleep) will assist the nurse in discovering patients at risk (Nitu, Medregoniu, Olteanu, Olteanu, & Maceseanu, 2008). First, background information on respiratory depression during sleep (sleep disordered breathing) will be discussed. Second, understanding the pathophysiology of sleep disordered breathing will help in the detection of patients at risk. Sleep-Disordered Breathing Sleep-disordered breathing is an encompassing term that includes obstructive sleep apnea (OSA), central sleep apnea (CSA), and upper airway resistance syndrome (snoring). Sleep disorders are formally diagnosed using a sleep study (polysomnography), but there are screening assessments and questions that are highly predictive of the disorders (Table 4). | 1. Do you wake up frequently during the night? | | | 2. Do you fall asleep easily during the day? | | | 3. Do you snore? | | | 4. Has your bed partner witnessed pauses in your breathing during the night? | | | 5. Do you wake up gasping for breath during the night? | | | | |
Obstructive sleep apnea syndrome is characterized by recurrent absence of breath for periods of ≥10 seconds owing to collapse of the lower posterior pharynx during sleep, along with daytime somnolence, and is more prevalent in men than in women. Prevalence of OSA is estimated to range between 7% and 14% in men and between 2% and 7% in nonelderly women (Young & Peppard, 2005). Upper airway resistance syndrome is the term used to describe a lesser form of OSA, in which only partial airway collapse occurs and may be manifested by snoring. The most effective treatment for OSA is continuous positive airway pressure. Signs associated with OSA are witnessed apneic events during sleep and excessive daytime sleepiness (Flemons et al., 1994, Guilleminault and Bassiri, 2005, Young et al., 2002). Some patients have vulnerability for sleep-disordered breathing based on their individual characteristics, including an overbite (micro- or retrognathia; Fig. 1), enlarged tongue, narrowed or an occluded oropharyngeal lumen (Mallampati scale class 3 or 4; Fig. 2), large neck circumference, and/or central obesity. These characteristics may contribute to impaired respiratory function in a variety of ways, including altered upper airway resistance (increased), reduced ventilatory mechanical capacity, and diminished residual lung volume. Central sleep apnea (CSA) disorder is the repeated absence of breath for periods of ≥10 seconds owing to the temporary loss of ventilatory stimulus to breathe (American Academy of Sleep Medicine, 1999, White, 2005). On observation, the person experiencing central sleep apnea will have decreased respiratory rate and depth as well as an irregular breathing pattern. Whereas OSA results from an obstructed airway, CSA results from failure of the system that initiates breathing efforts. CSA, a less common sleep disorder, can be found in isolation or associated with obstructive sleep apnea. Because hypoxia that occurs as the result of OSA can produce CSA events, risk factors for OSA are also risk factors for CSA. Additional risk factors for the development of CSA include: age >65 years; medical conditions that affect the cardiovascular and respiratory systems; and medications that depress the central nervous system (Ancoli-Israel et al., 1994, Hiestand et al., 2006, Strassburg et al., 2008, Szollosi et al., 2008) (Table 5). Treatment for CSA is focused on the presumed cause, such as treating the cardiac or respiratory disease, lowering or discontinuing the medication, or in some cases applying continuous or bilevel positive airway pressure (Bingold et al., 2007, Ferreyra et al., 2008, Javaheri, 2006, Meng, 2008, Renault et al., 2008, Squadrone et al., 2005, Zarbock et al., 2009). | Age >65 years | | | History of cerebral vascular disease | | | Presence of cardiac disease | | | Presence of respiratory disease | | | Nocturnal oxygen desaturations | | | Frequent awakenings during the night | | | | |
Case Study #2 Resolution. On admission to the preoperative unit, the nurse assessed B.J. for risks of excessive respiratory depression secondary to opioids by assessing his BMI (38 kg/m2), Mallampati airway class (class 4), asked him and his wife if he snored and/or had pauses in his breathing during sleep (yes to both), and checked his admission lab work to make sure his BUN was <30 mg/dL and his albumin was >30 g/L (both normal). The nurse determined that he was at risk, and she discussed the risks with the anesthesiologist. Together they developed a plan to support his airway until fully awake, then once extubated, to place him in a sitting position and monitor his respiratory status using oximetry as well as continuous bedside observation by the nurse. Morphine 2 mg IV and ketorolac 30 mg IV was administered before transfer to the PACU. B.J. recovered safely and comfortably and was able to go home that evening. He was started on ibuprofen 600 mg three times/day as needed for pain, and if ibuprofen didn't relieve ≥50% of his pain he would take hydrocodone 5/500 1 tablet three times/day as needed. The nurse instructed him to avoid the narcotic medications during times of naps or nighttime sleep owing to his increased risk of respiratory depression while asleep. The patient was also instructed on his risk factors for sleep-disordered breathing and encouraged to see his primary care provider for a referral to a sleep specialist. Although formal diagnosis of OSA or CSA requires a polysomnographic procedure, there is some evidence that subjective screening for sleep apnea is correlated with polysomnography findings (Netzer, Stoohs, Netzer, Clark, & Strohl, 1999). Some patients with sleep-disordered breathing may go undiagnosed, because they do not present with excessive daytime sleepiness and/or do not have a bed partner to witness the apneic events. For this reason, it is important for all health care providers to be aware of the individual characteristics that put patients at risk (Table 6). | Instruct the patient to bring their continuous or bilevel positive airway pressure (CPAP/biPAP) equipment to the facility for use when sedated or asleep. | | | If the patient's equipment is not available, provide the appropriate airway support (e.g., CPAP, biPAP, oral device) and/or position patient sitting upright until fully able to maintain his or her own airway. | | | Increase frequency of nursing assessments, and use a valid and reliable sedation scale that was developed for purpose of monitoring to prevent excessive sedation. | | | Use opioid-sparing medications and therapies. | | | Educate all patients on the potential added risk of opioid-induced respiratory sedation due to their sleep-disordered breathing. | | | | |
Case study #3. J. G. is a 70-year-old woman, 5′5″ and 140 pounds (BMI 23.3 kg/m2), admitted to the hospital for severe pain from compression fractures of the L2 and L3 spine. She has a history of chronic thoracic back pain from severe osteoporosis and thoracic compression fractures. Her medications include alendronate, calcium with vitamin D, fluoxetine, gabapentin, and oxycodone extended release. Admission vital signs: blood pressure 150/82 mm Hg, pulse 78/min, respiration 12/min, temperature 97.8°F, oxygen saturation 97% on room air. At home, J.G. has been taking a stable dose of oxycodone extended release 80 mg every 12 hours over the past year for localized thoracic back pain. Her pain has significantly increased and now she is having pain radiating into her hips and thighs. The hospitalist decides to change her opioid medication to methadone 10 mg three times/day. On day 2 of the methadone, J.G. was complaining of increased and severe pain; the hospitalist increased the methadone to 20 mg three times/day starting immediately. That day, her vital signs were stable while awake, but during that night, the nurse noted breathing to be 8/min and paradoxical, with an oxygen saturation of 92%. She applied oxygen via nasal cannula at 2 L/min per orders. On day 3 at 7 a.m., J.G. was found to be somnolent and appearing a bit gray, with respiration 4/min. The house staff was called stat,and naloxone was administered. J.G. became more alert but her pain was severe. Respiratory Depression in the Setting of Chronic Opioid Exposure In the setting of long-term opioid use, e.g., methadone maintenance therapy for addiction or chronic pain management, the relationship between opioids and respiratory depression is less understood. In general, it is thought that for most patients the respiratory depressive effect of opioids dissipates over the first few days of exposure. Yet there is some evidence that patients who have been receiving long-term opioid therapy continue to exhibit signs of respiratory depression, specifically sleep-disordered breathing (Teichtahl et al., 2005; D. Wang & Teichtahl, 2007; D. Wang et al., 2008; J. Wang et al., 2006, Webster et al., 2008). Additionally, when these patients are exposed to increased doses or a different opioid, they remain at risk of further respiratory compromise (Athanasos et al., 2006, Stoermer et al., 2003). Case Study #3 Resolution. J.G.’s nurse was not familiar with methadone. Before she administered J.G.’s first dose, the nurse read about methadone in the medication reference materials on the unit. The nurse found out that methadone has a long half-life that could result in accumulation of the drug and should be used cautiously in the elderly. Additionally, she noted that methadone and fluoxetine compete for isoenyzmes and could predispose her to increased risk of adverse effects. She also remembered that previous patients had exhibited significant sedation from the use of gabapentin. The nurse then looked up J.G.’s admission lab work and found that her BUN was 45 mg/dL (high) and her albumin was 37 g/L (normal). Realizing that J.G. could be at risk of opioid-induced respiratory depression, she initiated the use of a sedation scale and increased the frequency of assessment to every 2 hours for the next 3 days. At change of shift, the nurse reported the patient's condition as high risk for opioid-induced respiratory depression. With the increased frequency of assessments and communication of the patient's risk, the nurses recognized J.G.’s decline in level of consciousness as increasing sedation that always precedes opioid-induced respiratory depression. They were able to alert the prescribing provider to decrease the opioid dose, therefore avoiding the excessive respiratory sedation and need for naloxone. If naloxone were to be administered in this opioid-tolerant patient, the goal would be to gently reverse the sedation effects and not the pain-relieving effects. Clinical experience and case reports support the American Pain Society statement that patients who are opioid tolerant can be sensitive to the reversal effects of naloxone (Manfredi, Ribeiro, Chandler, & Payne, 1996). As one other consideration for this case, according to American Pain Society guidelines, if the patient is tolerating her current opioid, the dose should be increased before switching to a different opioid medication (American Pain Society, 2002). Opioid therapy remains a primary avenue to control pain and can be safely prescribed with the appropriate safety mechanisms put in place. 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School of Nursing, University of Rochester, Rochester, New York  Address correspondence to Carla R. Jungquist, RN-C, PhD, Research Fellow, School of Nursing, University of Rochester, 601 Elmwood Avenue, Box HWH, Rochester, NY 14642.
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