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PubMed2004

Use of narcotic analgesics in the emergency department treatment of migraine headache.

OBJECTIVE: Treatment of acute migraine headache with narcotics is potentially ineffective and may lead to abuse. The authors examined the treatment practice variation across five linked EDs in one Canadian center, focusing on the use of narcotic analgesics and factors associated with their use. METHODS: Five hundred acute migraine headache patient charts were randomly selected from five Canadian EDs. Charts underwent a structured review to determine medication use. Data were analyzed, comparing those who received narcotics as first-line treatment with those who did not, using chi(2) and t-tests and logistic regression. RESULTS: The majority of patients (59.6%) received narcotics as first-line treatment. Numerous factors were associated with first-line narcotic treatment. Having taken antiheadache medications prior to ED presentation (odds ratio [OR]: 2.63; 95% CI: 1.53, 4.51) and hospital of presentation being other than Hospital A (e.g., Hospital D, OR: 6.32; 95% CI: 2.76, 14.46) increased the odds of receiving first-line narcotics. Having received a more urgent triage score (OR: 0.4; 95% CI: 0.24, 0.65) or having a longer duration of headache (OR: 0.994; 95% CI: 0.99, 0.99) decreased the odds of receiving first-line narcotics. CONCLUSIONS: Acute migraine management in these EDs does not meet current consensus guidelines. Factors associated with narcotic use are predictable, and a concerted effort to replace narcotics with more evidence-based first-line treatments is needed.

Adult↗
PubMed1980

Comparative cardiac contractile actions of six narcotic analgesics: morphine, meperidine, pentazocine, fentanyl, methadone and l-alpha-acetylmethadol (LAAM).

Cardiac muscle contractile responses to six narcotic analgesics (morphine, meperidine, pentazocine, fentanyl, methadone and l-alpha-acetylmethadol), at concentrations from 10(-8) to 10(-4) M, both in the presence and absence of the narcotic antagonist, naloxone, were studied in the isolated, isometric cat right ventricular papillary muscle preparation. Measurements of maximum developed tension (T), maximum rate of tension development (dT/dt) and time to peak tension indicated that no major changes in contractile function occurred with any narcotic at concentrations of 10(-8) to 10(-6) M except for small but significant (P < .05) increases in all three parameters at 10(-6) M fentanyl, and small but significant increases in dT/dt at 10(-8) to 10(-6) M meperidine. At 10(-5) M narcotic, dT/dt was significantly elevated in meperidine-treated muscles (+7%), but significantly reduced in muscles exposed to pentazocine (-8%) or l-alpha-acetylmethadol (-11%). For all six narcotics, the 10(-4) M drug concentration resulted in depression of contractile function that was often associated with nonresponsiveness to electrical stimulation. Pretreatment of muscles with naloxone (10(-4) M) did not prevent this reduction of contractile performance except at the highest concentration (10(-4) M) of meperidine. Following removal of drug, contractile performance improved to varying degrees (recovery to 72-97% of control T), except in l-alpha-acetylmethadol-treated muscles, in which there was no recovery of T. Isoproterenol (0.8 X 10(-7) M) elicited a positive inotropic response whether administered in the presence of 10(-4) M narcotic or following narcotic removal. We conclude that narcotic analgesics in high concentrations exert a direct myocardial depressant effect which is not prevented by naloxone and therefore is not mediated by interaction with opiate receptors. Rather, several effects, including myocardial depression, its reversibility by both drug removal and isoproterenol and decreased muscle excitability are consistent with the hypothesis that narcotic analgesics in high concentrations exert nonspecific, local anesthetic effect on the myocardium.

Analgesics, Opioid↗
PubMed1980

[Narcotic analgesics and endorphins and the release of pituitary hormones (author's transl)].

This report concerns a review of the neuroendocrine effects of narcotic analgesics and endorphins. Acute administration of narcotic analgesics to rats increases the blood levels of ACTH, GH and prolactin, and decreases levels of LH and TSH, however, there is no general consensus regarding changes in serum FSH, ADH and oxytocin as induced by narcotics in rats. In humans, the narcotic analgesic increases in serum prolactin, decreases in serum LH and has no effect on the release of other known pituitary hormones. Endorphins mimic morphine regarding hormonal effects. Effects of naloxone on the basal levels of prolactin, LH or GH were inverse to the effects seen with narcotics and endorphins, therefore endorphins may play a role in regulating the basal levels of these hormones. Narcotics analgesics depress the increased blood levels of prolactin, gonadotropins or TSH elicited by specific measures. While chronic administration of morphine results in tolerance to the stimulant effect of ACTH, and possibly of prolactin secretion, tolerance does not develop to the stimulant effect on GH secretion. The analgesic potency of narcotic analgesics correlates with their suppressive effect on the pituitary-gonadal system and the potency with which endorphins bind to the opiate receptors correlates with their prolactin releasing activity. It is assumed that narcotic analgesics and endorphins exert their hormonal effects by altering the release of neurotransmitters in the CNS. Thus, a release of hypothalamic releasing hormones is involved rather than a direct action on the pituitary. The central neurotransmitter systems involved in the hormonal effects of narcotics are now being intensively investigated by various groups of workers.

Adrenocorticotropic Hormone↗
PubMed1977

Naloxone antagonizes narcotic self blockade of emesis in the cat.

Morphine, levorphanol, fentanyl and methadone given by intracerebroventricular (i.c.v.) injection blocked the vomiting response to a standard emetic test dose of apomorphine subsequently injected i.c.v. Of these narcotics, only morphine initially evoked vomiting. Systemic pretreatment with naloxone (5 mg/kg i.p. or i.v.) uniformly abolished the antiemetic activity of all the represented narcotic agents, moreover, naloxone thus administered was followed consistently by emetic responses to those narcotics which separately failed to evoke vomiting. When naloxone was injected i.c.v. in addition to being given systemically, both antiemetic and emetic activities of the narcotic agents were essentially abolished, whereas apomorphine continued to evoke vomiting. In the presence of systemic naloxone, given to counteract self-blockade of vomiting, the narcotics were shown to induce vomiting through excitation of the medullary emetic chemoreceptor trigger zone and emetic receptor tolerance as well as cross-tolerance developed acutely. The present differentiation by naloxone of the emetic and antiemetic properties of narcotic agents placed in the cerebrospinal fluid indicates that the opposing narcotic actions are exercised at different sites in the brain and that the narcotic receptor specificity of the chemoreceptor trigger zone does not encompass the emetic action of apomorphine.

Animals↗
PubMed1998

Variation among neonatal intensive care units in narcotic administration.

OBJECTIVES: To compare rates of narcotic administration for medically treated neonates in different neonatal intensive care units (NICUs) and to compare treated and untreated neonates to assess whether narcotics provided advantages or disadvantages for short-term outcomes, such as cardiovascular stability (ie, blood pressure and heart rate), hyperbilirubinemia, duration of respiratory support, growth, and the incidence of intraventricular hemorrhage. STUDY DESIGN: The medical charts of neonates weighing less than 1500 g, admitted to 6 NICUs (A-F), were abstracted. Neonates who had a chest tube or who had undergone surgery were excluded from the study, leaving the records of 1171 neonates. We modeled outcomes by linear or logistic regression, controlling for birth weight (<750, 750-999, and 1000-1499 g) and illness severity (low, 0-9; medium, 10-19; high, > or =20) using the Score for Neonatal Acute Physiology (SNAP), and adjusted for NICU. RESULTS: Narcotic use varied by birth weight (<750 g, 21%; 750-999 g, 13%; and 1000-1499 g, 8%), illness severity (low, 9%; medium, 19%; and high, 37%), day (1, 11%; 3, 6%; and 14, 2%), and NICU. We restricted analyses to the 1018 neonates who received mechanical ventilation on day 1. Logistic regression, adjusting for birth weight and SNAP, confirmed a 28.6-fold variation in narcotic administration (odds ratios, 4.1-28.6 vs NICU A). Several short-term outcomes also were associated with narcotic use, including more than 33 g of fluid retention on day 3 and a higher direct bilirubin level (6.8 micromol/L higher [0.4 mg/dL higher], P = .03). There were no differences in weight gain at 14 and 28 days or mechanical ventilatory support on days 14 and 28. Narcotic use was not associated with differences in worst blood pressure or heart rate or with increased length of hospital stay. CONCLUSIONS: Our study found a 28.6-fold variation among NICUs in narcotic administration in very low-birth-weight neonates. We were unable to detect any major advantages or disadvantages of narcotic use. We did not assess iatrogenic abstinence syndrome or long-term outcomes. These results indicate the need for randomized trials to rationalize these widely differing practices.

Birth Weight↗
PubMed1978

Narcotic tolerance and operant behavior.

Narcotic tolerance was measured as a shift to the right in dose-effect relations on operant behavior following repeated administration of drug. Tolerance has been observed with operant responding in both pigeons and rhesus monkeys. The amount of tolerance observed with food-reinforced responding is related both to the amount of morphine administered and to the nature of the drug-induced change in operant responding. Pharmacological specificity of the narcotic tolerance has been confirmed by equivalent loss of sensitivity to other narcotics without concomitant changes in sensitivity to nonnarcotic stereoisomers. Tolerant birds do not show disturbed operant behavior when narcotic administration is terminated abruptly. Tolerance has been induced by narcotic self-injection and its effects measured on rates and patterns of food- and narcotic-reinforced responding. Tolerance does not necessarily confer changes in narcotic-reinforced responding. Moreover, narcotic-reinforced responding may be initiated and maintained for periods of over one month without conferring tolerance.

Animals↗
PubMed1989

Prenatal narcotic exposure: perinatal and developmental effects.

Infants prenatally exposed to narcotics become passively addicted in-utero and may undergo neonatal abstinence at birth. Methadone maintenance in conjunction with intensive prenatal care for pregnant narcotic dependent women can reduce the incidence of intrauterine death, neonatal death, prematurity and its concomitant problems. However, methadone exposed infants have consistently been found to have smaller birthweights and head circumference than non-drug exposed infants. Although neonatal abstinence can be treated successfully with pharmacotherapy, the effects of in-utero narcotic exposure in the developing central nervous system are not fully understood. Infants exposed to narcotics in-utero have been found to have slit-like ventricles with smaller lateral ventricle and intracranial hemidiameter measurements during the first month of life. The incidence of strabismus is also greater in infants exposed to narcotics in-utero than the general population, but this appears to be related to lower birth weight, rather than a direct consequence of narcotic exposure. There does not appear to be developmental sequelae associated with prenatal narcotic exposure. After abstinence has abated, infants function well within the normal range of development during the first two years of life, although developmental scores may be lower than non-drug exposed comparisons groups. There are a myriad of confounding medical, pharmacological and environmental variables within this population and the relative importance of prenatal narcotic exposure in a continuum of risk factors needs to be more clearly delineated before the etiology of perinatal and developmental effects can be determined.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Analgesia with oral narcotics and added ibuprofen in cancer patients.

A scheduled regimen of oral narcotic analgesics was compared with a regimen of oral narcotic analgesics plus ibuprofen for analgesic efficacy in patients with cancer. Ten patients with metastatic cancer were randomly assigned to receive either ibuprofen 400 mg or a look-alike placebo four times daily in addition to each patient's existing regimen of scheduled oral narcotics. A two-period changeover study design was used. The 24-hour narcotic intake equated to injectable morphine was computed for each patient at baseline and during the nine study days. A visual analogue scale was used to evaluate pain relief, nausea, mood depression, daytime drowsiness and nighttime sleeplessness. The analgesic efficacy of the narcotic-ibuprofen combination was significantly greater than the analgesic efficacy of the narcotic-placebo combination. Eight patients demonstrated a positive treatment effect with added ibuprofen; the overall improvement in analgesia averaged 39.1% in these patients. There was no significant increase from baseline in the incidence of nausea, mood depression, daytime drowsiness or nighttime sleeplessness. At the doses used in this study, a treatment regimen of oral narcotic analgesics plus ibuprofen was more effective than oral narcotics alone in relieving pain associated with cancer.

Administration, Oral↗
PubMed1982

Classification of narcotics on the basis of their reinforcing, discriminative, and antagonist effects in rhesus monkeys.

Drug discrimination and drug reinforcement procedures were used to classify a variety of narcotic agonists, mixed agonist-antagonists, and antagonists in the rhesus monkey. A five-way classification was formed. Morphine-like agonists were compounds that shared the capacities to reinforce responding, to produce discriminative stimulus effects similar to those of morphine, and to suppress withdrawal in morphine-dependent rhesus monkeys. Morphine-like mixed agonists-antagonists were differentiated from pure agonists primarily by their capacity to elicit abstinence signs in morphine-dependent monkeys. A third class of narcotic agonists had ethylketazocine as a prototype. These compounds shared a distinctive set of interoceptive stimuli, failed to maintain significant responding relative to morphine-like agonists, and neither suppressed nor elicited withdrawal in morphine-dependent rhesus monkeys. The ethylketazocine-like mixed agonist-antagonists were similar to the ethylketazocine-like agonists, except that they shared the capacity to precipitate a morphine withdrawal syndrome. Narcotic antagonists (e.g., naltrexone) did not share interoceptive effects with either morphine or ethylketazocine, but were able to block the discriminative effects of both types of agonists. Furthermore, narcotic antagonists induced narcotic abstinence in morphine-dependent rhesus monkeys. The present classification scheme may be useful in identifying the properties of new narcotics, for clarifying relationships between narcotics and other pharmacological classes, and in comparing classifications based on other effects of narcotics.

Animals↗
PubMed1977

Narcotics and the hypothalamic-pituitary-gonadal axix: acute effects on luteinizing hormone, testosterone and androgen-dependent systems.

The effects of narcotics on several aspects of the hypothalamic-pituitary-gonadal axis were examined in the male rat. Our results indicate that a large number of narcotics acutely depress serum luteinizing hormone levels and that these reduced gonadotropin levels lead to a subsequent fall (1-2 hours later) in serum testosterone levels. The luteinizing hormone-depleting effect of the narcotics appears to represent a specific narcotic action since the (-)-isomers of the narcotics were much more effective than the ()-isomers, naloxone antagonized their effects and tolerance rapidly developed. Further, our studies indicate that the impairment of the functional and structural integrity of the secondary sex organs produced by chronic narcotic administration is not due to a direct effect of these drugs since they have no effect on the uptake of subcellular distribution of testosterone in the secondary sex organs or on the androgen-dependent accumulation of myo-inositol. Consequently, it appears that the testosterone depletion produced by the narcotics is solely responsible for their adverse effect on the secondary sex organs. The results of these studies suggest that the effects of the narcotics on the hypothalamic-pituitary-gonadal axis are confined to either the hypthalamus or the pituitary gland.

Androgens↗
PubMed2002

Gender differences in narcotic-induced emesis in the ED.

Narcotic analgesia is commonly given in the emergency department. Narcotic-induced nausea and vomiting is thought to be a common occurrence, but the gender incidence and associations are not well defined. The aim of this study was to document the sex-related complication of nausea and vomiting after opiate administration for pain relief in the ED. The study hypothesis was that men and women have the same rate of narcotic-induced emesis in the ED. A prospective, convenience study of the use of narcotic analgesic on patients in an innercity Level I Trauma Center was undertaken. Information concerning the reason for narcotics, complications, number of doses, and route of administration were studied. The emergency physicians were allowed clinical judgment to treat the patients with any narcotic agent in any dose increment. The data were entered into an SPSS program (Chicago, IL). Analysis between groups (men v women) was then conducted by an independent t test. We compared the 2 groups across 6 categories: cause of injury, presenting pain scale, first drug given, first dose given, first route of drug, and requires an anti-emetic. A Bonferroni procedure was used to correct for the higher probability of significant findings when multiple tests were performed. All findings that are significant are after Bonferroni. The study was Institutional Review Board (IRB) approved. A total of 325 consenting patients were studied from October 1996 to April 1998. The patients consisted of 174 men and 151 women, with an average of 35.8 years of age. The race of the patients was 70% African American and 20% Hispanic. Of the total of 325 patients, 20.3% (74) required an anti-emetic because of nausea and/or vomiting. A significant difference occurred in causes of pain for women (t = 2.79, P <.007). The causes of pain for women were general pain, fracture, abdominal, back pain, and other as compared with men with gun shot wounds, general, fracture, low back, and flank. Women showed no significant difference with regard to presenting pain scale (t =.122, P <.903), first drug given (t = 1.643, P <.101), and first dose given (t =.708, P <.408). The majority of patients received morphine (55.4%), followed by meperidine (24.3%), and hydrocodone (13.5%). The most frequent route of administration was intravenous (IV, 45.2%), intramuscular (IM, 35.7%), with oral being the least frequent route (19.1%). There was a difference for women with first route given (t = 2.543, P <.01) and requires anti-emetic (t = 3.06, P <.002). The majority of women received IM (58.6%) versus IV (37.7%), whereas the majority of men (62.3%) received IV versus IM (41.4%). A significant number of patients became nauseated and/or vomited from Emergency Department-administered narcotics. The nausea and vomiting was associated with female sex and the cause of pain. A comparative study of other pain medications versus narcotics for incidence of induced nausea and emesis would be useful.

Adolescent↗
PubMed1980

Effect of prior narcotic addiction on response to treatment of alcoholism.

We studied the effect of prior narcotic addiction on response to treatment of alcoholism. Patients in the Elmhurst Alcoholism Treatment Program are offered medical care, counseling, disulfiram, and close affiliation with Alcoholics Anonymous. We compared 85 alcoholics who had a history of narcotic use with a control group of 85 alcoholics matched for age, sex, and race who had never used narcotics. Among controls, 30 (35%) became abstinent from alcohol for at least half the time that they were known to us. Of the former narcotic users, only 8 (9%) became abstinent for at least half the time they were known to us. Former narcotic users did poorly in alcoholism treatment, whether or not they had ever been treated with methadone maintenance. Alcohol use, often heavy, began before heroin use in at least half the narcotic group. We conclude that a history of narcotic use reduces markedly the chance of success in conventional alcoholism treatment, and that alcoholism and narcotic addiction develop independently.

Adolescent↗
PubMed1976

Blockade of the specific lethal effects of narcotic analgesics in the mouse.

The capacity of the narcotic antagonists naloxone and nalorphine and the benzodiazepine derivatives diazepam and oxazepam to increase the LD50s of the narcotic analgesics morphine and methadone administered at convulsant doses was eveluated in the mouse. Naloxone produced a dose-related increase in the LD50s of both morphine and methadone. Iiazepam and oxazepam were also effective in increasing the LD50s of the narcotics; this effect was additive with that of naloxone. However, the maximal increase in the LD50s of the narcotics produced by pretreatment with naloxone alone was not increased further by the combined pretreatment of naloxone and a benzodiazepine. The anticonvulsant trimethadione did not elevate the LD50s of methadone, nor did it potentiate the effects of naloxone. These results suggest that the benzodiazepines may reduce the lethality of narcotic analgesics administered at high doses by a mechanism other than by an anticonvulsant effect alone. Therefore, the present results support the conclusion that the capacity to increase the convulsant LD50 of the narcotic analgesics is a general property of the narcotic antagonists.

Animals↗
PubMed1989

Non-cardiogenic pulmonary edema after narcotic treatment for cancer pain.

During recent years, better awareness of the problem of cancer pain has resulted in the use of increased doses of narcotics. We report the cases of 3 patients who presented non-cardiogenic pulmonary edema while receiving large doses of narcotics for cancer pain. In all cases, pulmonary edema occurred after patients required large increases in the dose of narcotic over a short period of time for rapidly progressing pain. Although pulmonary edema has been described after overdose of narcotics, it had not been previously reported during the course of treatment for cancer pain. Its mechanism appears to be increased capillary permeability because of immunoglobulin and complement deposition of the lung, or due to neurogenic increase in permeability by the effect of narcotics on the brain-stem. We conclude that narcotic-induced pulmonary edema should be suspected in patients who require massive increases in the dose of narcotics. The use of adjuvant pharmacologic and non-pharmacologic analgesic treatments in order to minimize the need for dose increase, as well as the prevention of precipitating factors such as over hydration, corticosteroids or excessive oxygen therapy, should be contemplated in this population.

Aged↗
PubMed2002

Opposing effects of narcotic gases and pressure on the striatal dopamine release in rats.

Nitrogen-oxygen breathing mixtures, for pressures higher than 0.5 MPa, decrease the release of dopamine in the rat striatum, due to the narcotic potency of nitrogen. In contrast, high pressures of helium-oxygen breathing mixtures of more than 1-2 MPa induce an increase of the striatal dopamine release and an enhancement of motor activity, referred to as the high pressure nervous syndrome (HPNS), and attributed to the effect of pressure per se. It has been demonstrated that the effect of pressure could be antagonized by narcotic gas in a ternary mixture, but most of the narcotic gas studies measuring DA release were executed below the threshold for pressure effect. To examine the effect of narcotic gases at pressure on the rat striatal dopamine release, we have used two gases, with different narcotic potency, at sublethargic pressure, nitrogen at 3 MPa and argon at 2 MPa. In addition, to dissociate the effect of the pressure, we have used nitrous oxide at 0.1 MPa to induce narcosis at very low pressure, and helium at 8 MPa to study the effect of pressure per se. In all the narcotic conditions we have recorded a decrease of the striatal dopamine release. In contrast, helium pressure induced an increase of DA release. For the pressures used, the results suggest that the decrease of dopamine release was independent of such an effect of the pressure. However, for the same narcotic gas, the measurements of the extracellular DA performed in the striatum seem to reflect an opposing effect of pressure, since the decrease in DA release is lower with increasing pressure.

Animals↗
PubMed2001

Chronic narcotic use in inflammatory bowel disease patients: prevalence and clinical characteristics.

BACKGROUND: Narcotic addiction can be a significant problem in inflammatory bowel disease (IBD). However, there are few published reports about this problem. METHODS: All patients prescribed narcotics chronically in the absence of demonstrable organic pathology were identified on the computerized Brisbane IBD Research Group database (n=332 patients with informative data as of 1 January 1999). Individual case records were reviewed with regard to clinical, psychiatric and social characteristics of these patients, and the prevalence of psychiatric disorders were compared with a control group of IBD patients. RESULTS: Eleven patients were identified. Nine had complete datasets, eight with Crohn's disease (CD), of which six had previous stricturing ileal disease, and one patient had ulcerative colitis, making a prevalence of 2.7% of IBD patients and 5.1% of CD patients. A 67% prevalence of a psychiatric disorder in narcotic users was significantly greater than the 8% prevalence in the control group of IBD patients (odds ratio 22, 95% CI 3.24-177). CONCLUSIONS: A significant proportion of IBD patients without demonstrable organic pathology were chronic narcotic users. Psychiatric disorders are common in this subgroup, as with chronic functional abdominal pain syndromes. It is suggested that inappropriate narcotic use in IBD patients can be reduced by appreciating that narcotics are a temporary therapy only for IBD patients, and awareness of pre-existing social and psychiatric disorders, which not only impact on clinical presentation of pain, but also help define the subgroup of patients who are at risk of narcotic misuse.

Adolescent↗
PubMed1999

A postpartum self-medication program: effect on narcotic use.

Our objective was to determine the impact of a self-medication program on postpartum narcotic use. We retrospectively studied narcotic use in patients who underwent vaginal delivery before and after implementation of a self-medication program in April 1997. Narcotic use was compared between patients who delivered in January 1997 (n = 263) and those who delivered in January 1998 (n = 254). Oral narcotic use was also analyzed with respect to type of vaginal delivery (spontaneous vs. operative), extent of episiotomy or laceration, and use of epidural analgesia during labor. Narcotic use was significantly reduced (p < 0.001) in postpartum patients who participated in the self-medication program. The reduction was consistent despite the type of vaginal delivery or use of epidural analgesia during labor. A more extensive episiotomy or laceration at delivery (fourth-degree episiotomy or vaginal sulcus tear) was associated with an increase in narcotic use, although there was still a statistically significant decrease in use in patients in the self-medication program. A significant reduction in postpartum narcotic use may be achieved through implementation of a self-medication program. As a result, substantial benefits are potentially gained by both the patients and the nursing staff.

Administration, Oral↗
PubMed1998

Nontreatment and aggressive narcotic therapy among hospitalized pancreatic cancer patients.

OBJECTIVES: Strong feelings about patient autonomy as expressed in living wills, polls, and legislative referenda have been challenging the medical establishment to increase nontreatment, defined as foregoing a life-prolonging treatment, and even to provide treatments having life-shortening potential to selected patients. Because there are little data about the actual practice of these procedures, including aggressive narcotic therapy as defined herein, we studied the terminal management of 417 pancreatic cancer patients. DESIGN AND PARTICIPANTS: The medical records of 417 residents of King County, Washington, who died of pancreatic cancer in the time periods 1959-1962, 1969-1972, and 1985-1990, were reviewed to study the frequency of, and risk factors for, end-of-life nontreatment decisions and aggressive narcotic therapy decisions, defined here as the decision to administer treatment doses of narcotics or major sedatives to already comatose patients within 4 hours of death. RESULTS: Antibiotics were not provided to 71% of the 70 febrile patients (two readings >38.33-38.83 degrees C or one reading of 38.88 degrees C), intravenous fluid was not provided to 43% of 294 dehydrated patients (oral intake <500 mL/24 hours), transfusions were not provided to 39% of 57 severely anemic patients (hematocrit <20%), and laparotomy was not performed for 86% of 36 patients with abdominal emergencies (obstruction, bleeding, dehiscence). Also, 46% of the 118 patients who were comatose for at least 24 hours before death received aggressive narcotic therapy, as defined above. A total of 335 of the 417 patients had documentation of at least one of the above life-threatening conditions or were comatose for at least 24 hours before death, and 289 (86%) of these patients experienced nontreatment of one or more of these conditions or received aggressive narcotic therapy. Nontreatment decisions for febrile, dehydrated, or anemic patients tended to be more frequent if the patient was comatose (P=.004, .010, and .065, respectively), if there was a nontreatment statement in the medical record (P=.009, .035, and .001, respectively), or if the patient was described as terminal (P=.262, .029, and .002, respectively). Aggressive narcotic therapy in comatose patients was more common among patients who had regular visitors (P=.002), who had pre-coma pain (P=.006), who had nontreatment statements in their charts (P=.031), whose in-charge physician was an oncologist (P < .001), who were treated in a community nonprofit hospital compared with a Catholic hospital (P=.007), or who were treated in recent years (P=.011). CONCLUSION: Both nontreatment and aggressive narcotic therapy forms of medical management have been occurring commonly in terminal pancreatic cancer patients in King County, Washington, during the past 3 decades, the latter with greater frequency in recent years.

Adult↗