Butorphanol Disease Interactions

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic E. coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

Opioid agonists are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

Opiate partial agonists may increase systemic and pulmonary arterial pressure and systemic vascular resistance, particularly when given by intravenous administration. Data are available for pentazocine and butorphanol. Therapy with opiate partial agonists should be administered cautiously and only if the benefit justifies the risk in patients with acute myocardial infarction (especially if accompanied by hypertension or left ventricular failure) or coronary insufficiency.

Opiate partial agonists have the potential to cause dependence and abuse, particularly in patients with a history of drug abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use, and abrupt cessation or a significant reduction in dosage may precipitate withdrawal symptoms. Because of their opiate antagonistic effect, withdrawal symptoms may also occur if opiate partial agonists are administered to patients with an opiate dependence or in whom substantial amounts of narcotics have recently been administered. Therapy with opiate partial agonists is not recommended in patients who are physically dependent on narcotics. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate partial agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

The hypoventilation associated with administration of opiate partial agonists can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opiate partial agonists are given to patients head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opiate partial agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

Opiate partial agonists may produce respiratory depression by decreasing respiratory drive and increasing airway resistance. A "ceiling effect" has been noted for these agents, and increasing doses do not produce proportional or further respiratory depression. However, the duration of effect is prolonged. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate partial agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS or respiratory depression; acute alcohol intoxication; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate partial agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral routes are used. Naloxone may be administered to reverse clinically significant respiratory depression. However, in the case of buprenorphine, naloxone may not be effective due to buprenorphine's slow rate of dissociation from mu receptors.

Butorphanol may increase blood pressure and rarely causes severe hypertension. Therapy with butorphanol should be administered cautiously in hypertensive patients, particularly when given before surgery or anesthesia.

Butorphanol may rarely induce vasodilation and hypotension with syncope during the first hour following intranasal administration, particularly in patients with a history of similar reactions to opioid analgesic agents. Therapy with butorphanol should be administered cautiously in patients with circulatory shock, hypovolemia, or a predisposition to hypotension.

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the biliary tract, which can lead to spasm and elevated biliary tract pressure, especially in the sphincter of Oddi. Biliary effects appear to be the most pronounced with morphine, although they do not always occur with therapeutic doses. Therapy with opioids should be administered cautiously in patients with biliary or gallbladder disease.

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Narcotic (opioid) analgesic agents may exacerbate seizures in patients with seizure disorders and, at higher dosages, have been reported to induce seizures in patients without previous history of seizures. The proconvulsant activity may be the greatest with meperidine, the active metabolite of which is thought to be responsible. Therapy with opioids should be administered cautiously in patients with or predisposed to seizures.

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in elderly patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.