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From the Department of Anaesthesia and Intensive Care, Prince of Wales Hospital and Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, PRC.
Address correspondence to: Dr. Anthony Ho, Phone: 852-2632-2735; Fax: 852-2637-2422; E-mail: hoamh{at}hotmail.com
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Abstract |
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Clinical features: A 60 yr old man for femoral-popliteal artery bypass grafting developed right upper quadrant abdominal pain after preoperative morphine and scopolamine. He had a previous cholecystectomy. His pain was relieved with naloxone.
Conclusion: Choledochal sphincter spasm should be part of a differential diagnosis in right upper quadrant pain after sedative doses of morphine, especially if there is a previous cholecystectomy.
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Case report |
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The patient received 10 mg morphine, 0.4 mg scopolomine, im, one hour before surgery. Forty minutes later, he complained of sharp right upper quadrant pain with radiation to the back below the right scapula, and slight nausea. It was similar to his gallbladder attacks many years ago. On examination, the patient was restless. Vital signs were unchanged and abdominal examination revealed no abnormalities and did not exacerbate his pain. Blood taken at that time was reported later to contain normal levels of liver and cardiac enzymes, alkaline phosphatase, and bilirubin. His ECG and Chest X-ray revealed no acute problems. A test dose of 0.05 mg naloxone iv resulted in slight but definite improvement of his pain. A further dose of 0.1 mg naloxone resulted in further improvement. Complete relief was achieved after a total of 0.4 mg over 10 min. About 15 min later,the pain recurred, and he required small aliquots of naloxone to a total of 0.4 mg before the pain subsided. By this time, the diagnosis of probable CS spasm had been made and the patient was taken to the operating room where an epidural anesthetic was planned. Another 15 min after the last dose of naloxone, his pain recurred and was finally controlled with an additional dose of 0.1 mg naloxone. A lumbar epidural catheter was inserted uneventfully and 3 ml lidocaine 2% with epinephrine 1/200,000 and 11 ml bupivacaine 0.5% were used to produce surgical anesthesia.
Postoperatively he was maintained for 48 hr with an infusion of bupivacaine 0.2% at 7-10 ml•hr–1 for pain control. He did not suffer any further right upper quadrant pain during the rest of his hospital stay. Serial postoperative ECGs revealed no changes. He recovered from his surgery with no complication.
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Discussion |
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The apparent predisposition to CS spasm of patients with previous cholecystectomy after preoperative opioid sedation has important anesthetic implications, and deserves an explanation.
Asymptomatic gallstones are common, but when CS dysfunction leads to biliary symptoms, management often includes cholecystectomy. In other words, CS spasm-susceptible people may more likely to have had a cholecystectomy than non-susceptible people.
It is also possible that the absence of a gallbladder exacerbates CS spasm-induced common bile duct hypertension. The biliary system is highly innervated with pain fibres.4 The pain of CS spasm is not necessarily from the spasm itself but is due to the resultant common bile duct distention.1 Mengay et al.5 found, in cholecystectomized dogs, that the absence of a normally distensible gallbladder resulted in much higher biliary pressure than in intact dogs when opioid-induced CS spasm occurs.
Another mechanism of increased CS spasm in post-cholecystectomized patients may be disruption of nerve fibres (that inhibit CS spasm) that pass between the gallbladder and the CS via the cystic duct.6,7
Opioids are used more frequently after than before surgery. Yet, CS spasm is rare in the immediate postoperative period. One explanation is the development of tachyphylaxis to the spasmogenic effects of opioids in the biliary system,8,9 and the resulting spasm is relatively transient. In addition, while analgesia is proportional to opioid dosage, the maximum opioid-induced pain of CS spasm is reached once the CS closes and biliary ductal pressure plateaus. With the large doses of opioids used intraoperatively and for postoperative analgesia, the pain from CS spasm-induced ductal hypertension, if it occurs, is easily masked by the opioids and by the discomfort caused by the operation. The small preoperative sedative dose of opioids, on the other hand, is enough to induce CS spasm but inadequate to mask the resulting pain. Since preoperative sedation, especially with opioids, is uncommon nowadays, this problem is likely to occur very infrequently.
Although anti-cholinergics should relieve CS spasm, the concomitant administration of scopolomine did not completely prevent the spasm. Nalbuphine, an opioid with µ-receptor antagonistic properties, may be a useful alternative to naloxone.10 Other drugs that can potentially relieve CS spasm include glucagon, calcium channel blockers, aminophylline, and nitrates.
In summary, choledochal sphincter spasm may be more likely to occur in patients with previous cholecystectomy, and may accompany smaller doses of morphine or other opioids, and may not be relieved with the concomitant use of scopolamine. The pain appears highly responsive to naloxone, which normally aggravates most other pain. When used with caution, therefore, naloxone can serve both diagnostic and therapeutic purposes. An increased awareness of CS spasm can at times avoid unnecessary work up and case postponement. Opioids are not the drugs of choice for most situations requiring preoperative sedation, especially in patients with previous cholecystectomy.
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Acknowledgments |
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Accepted for publication September 6, 1999.
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2
Radnay PA, Duncalf D, Novakovic N, Lesser ML. Common bile duct pressure changes after fentanyl, morphine, meperidine, butorphanol, and naloxone. Anesth Analg 1984; 63: 441–4.
3 Bird KJ. Narcotic-induced choleduchoduodenal sphincter spasm reversed by naloxone. Anaesthesia 1986; 41: 1120–3.[Medline]
4 Britton J, Bickerstaff KI, Savage A. Benign diseases of the biliary tract. In: Morris PJ, Malt RA (Eds.). Oxford Textbook of Surgery. New York: Oxford University Press, 1994: 1209–39.
5 Menguy RB, Hallenbeck GA, Bollman JL, Grindlay JH. Pancreatic and biliary intraductal pressures. Surg Forum 1955; 6: 359–63.
6 Rolny P, Funch-Jensen P, Kruse A, Thommesen P. Effect of cholecystectomy on the relationship between hydrostatic common bile duct pressure and sphincter of Oddi motility. Endoscopy 1991; 23: 111–3.[Medline]
7 Grace PA, Pitt HA. Cholecystectomy alters the hormonal response of the sphincter of Oddi. Surgery 1987; 102: 186–94.[Medline]
8
Crema A, Benzi G, Frigo GM, Berte F. The response of the terminal bile duct to morphine and morphine-like drugs. J Pharmacol Exp Ther 1965; 149: 373–8.
9 Greenstein AJ, Kaynan A, Singer A, Dreiling DA. A comparative study of pentazocine and meperidine on the biliary passage pressure. Am J Gastroenterol 1972; 58: 417–27.[Medline]
10 Humphreys HK, Fleming NW. Opioid-induced spasm of the sphincter of Oddi apparently reversed by nalbuphine. Anesth Analg 1992; 74: 308–10.[Medline]
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