Loss Of Analgesia Research Articles

Combination spinal analgesic chemotherapy: a systematic review.

Combination spinal analgesic chemotherapy: a systematic review.

A Simple System to Prevent Epidural Catheter Hub Disconnections

To the Editor: Epidural catheter hub disconnections in the postoperative setting are a frustrating problem for the busy anesthesiologist, who must quickly proceed to the patient's bedside to examine and reconnect. Such disconnections may result in the introduction of contamination, possibly leading to an epidural abscess [1]. Disconnections may also result in loss of analgesia with subsequent patient dissatisfaction and in the waste of anesthesiologists' time, possibly at the cost of delaying care to other patients. Possible causes of disconnections include loose or improper connection, patient movement, excessive tension, and erroneous disconnection by health-care personnel. For the past 2 yr, we have been utilizing a simple and inexpensive improvement that appears to have totally eliminated all epidural catheter hub disconnections and their resultant problems (Figure 1). The epidural catheter is inserted, then securely taped up along the patient's back to the shoulder. The external tip of the epidural catheter is firmly secured to the hub, which is tightly connected to a 30-cm arterial line extension tubing at its male Luer-Lok end. The female Luer-Lok end of this extension tubing is securely connected to either the distal end of a continuous epidural infusion line or capped if no continuous infusion is utilized.Figure 1: Depiction of the simple system to prevent epidural catheter hub disconnections.At the patient's shoulder, the loose epidural catheter, hub, and beginning of the arterial line extension are coiled, placed onto a sterile gauze, and covered with a tightly applied, 15 x 20 cm, waterproof, transparent, self-adherent dressing. This dressing permits visualization of the connection, minimizes the number of health-care personnel manipulating the hub connection site, decreases the probability of introduction of contaminants and extraneous fluids into the hub, and provides a safeguard against unplanned disconnections during patient movement. The sterile gauze between the skin and the protruding hub provides a cushion of comfort for the patient. The cost of the arterial line extension plus the dressing approximates $3.00. This arrangement represents a significant improvement due to protection of the hub against contamination, tension, and manipulation by health-care personnel and the patient. Securing this weak link permits the patient to move in bed and ambulate with minimum risk of disconnection. Finally, the arterial catheter Luer-Lok facilitates both intermittent epidural boluses and continuous infusion line changes without pulling on the hub. David Breznick, MD Sheryl Artmann, MD Gordon A. Irving, MD Department of Anesthesiology; University of Texas-Houston Medical School; Houston, Texas 77030

Endocrine and hemodynamic effects of antagonism of fentanyl-induced respiratory depression by nalbuphine.

Endocrine and hemodynamic changes associated with the antagonism of fentanyl by nalbuphine have not been reported. Therefore, the authors studied ten patients after anesthetic induction with thiopental, fentanyl, tracheal intubation aided by succinylcholine and maintenance with diazepam, pancuronium, N2O, and further doses of fentanyl. Eight of the patients underwent cholecystectomy, one had a hysterectomy, and another had an abdominoplasty. After reversal of neuromuscular block at the conclusion of surgery, normal ventilation was restored by 0.22 +/- 0.02 mg/kg intravenous nalbuphine (mean +/- SEM). Plasma levels of free norepinephrine, histamine, and cortisol did not increase after antagonism of the fentanyl-induced respiratory depression, but plasma concentration of epinephrine increased significantly but without significant hemodynamic changes. Minute ventilation was 1.5 +/- 0.4 L/min before and 11 +/- 1, 10 +/- 1, 11 +/- 1, and 10 +/- 1 L/min at 15, 30, 45, and 60 min after antagonism; corresponding PaCO2 levels were 56 +/- 2, 44 +/- 1, 49 +/- 7, 49 +/- 1, 42 +/- 1 mm Hg. The mean analogue pain score remained below 1.5. We conclude that nalbuphine effectively antagonizes fentanyl-induced respiratory depression without adverse endocrine and circulatory changes or loss of analgesia.

Analgesic properties of a systemically-administered synthetic dipeptide of 5-hydroxytryptophan

Synthetic peptides of 5-hydroxytryptophan (5-HTP), including N-acetyl-5-HTP-5-HTP amide (5-HTP-ACETYL-DP), specifically inhibit the binding of serotonin to serotonin binding protein. 5-HTP-ACETYL-DP also produces a long-lasting, opiate-sensitive analgesia following central, but not systemic administration. The present study evaluated an apolar derivative of 5-HTP dipeptide, N-hexanoyl-5-HTP-5-HTP amide (5-HTP-HEX-DP), for its analgesic properties in rats following systemic administration. 5-HTP-HEX-DP (5–50 mg/kg) significantly increased jump thresholds in a dose-dependent manner with peak analgesia occurring at 2.5 hr after injection, and lasting up to 5 hr. In the tail-flick assay, 5-HTP-HEX-DP (20 mg/kg) produced a significant antinociceptive effect at 1 hr post-injection using both high and low intensity levels of radiant heat. While 5-HTP-HEX-DP and morphine each elicited analgesia following acute administration, chronic (14 days) incremental dosing with 5-HTP-HEX-DP or morphine resulted in persistent analgesia in 5-HTP-HEX-DP-treated animals, and a loss of analgesia in morphine-treated rats. Thus, significant tolerance to morphine, but not 5-HTP-HEX-DP analgesia developed using this protocol. Hence, 5-HTP-HEX-DP is a systemically-active analgesic which fails to develop tolerance when administered daily over 14 days.

Reversal by Naluphine of Respiratory Depression Caused by Fentanyl

In 60 ASA class I or II patients given intravenous fentanyl for elective operations in doses large enough to produce postoperative respiratory depression, the intravenous administration of 20 mg nalbuphine resulted in prompt reversal of respiratory depression without loss of analgesia.

The peripheral narcotic antagonist N-allyl levallorphan-bromide (CM 32191) selectively prevents morphine antipropulsive action and buprenorphine in-vivo binding in the rat intestine.

The assumed low ability of the quaternary narcotic antagonist N-allyl levallorphan-bromide (CM 32191) to cross the blood-brain barrier and its selectivity in relieving the peripherally-elicited antipropulsive action of morphine while preserving analgesia has been tested. To ascertain the extent of penetration of CM 32191 into the cns, its relative potency in preventing the in-vivo binding of high specific activity [3H]buprenorphine in the rat cns and small intestine was compared. Pretreatment was with CM 32191 at 16, 30 or 60 mg kg-1 s.c., 20, 60 or 120 min before buprenorphine, the concentrations of which in cerebrum and spinal cord were comparable with control values, but were consistently reduced in the intestine (longitudinal muscle with attached myenteric plexus). Pretreatment with naloxone (20 min, 0.5 or 1 mg kg-1 s.c.) lowered buprenorphine binding in intestine and cns. Neither narcotic antagonist produced significant changes in buprenorphine plasma concentrations. The peripheral selectivity of CM 32191, methyl naloxone and naloxone was examined by investigating in the same rats nociception in the hot plate (central opiate-sensitive mechanism) and the transit of a charcoal meal along the small intestine (local opiate-sensitive mechanism). Both effects were inhibited by morphine (5 mg kg-1 i.v.). Naloxone (10 min pretreatment, 0.5 or 1 mg kg-1 s.c.) did not selectively antagonize intestinal action of the morphine since the relief of charcoal transit inhibition was consistently associated with complete loss of analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

EFFECT OF LEVALLORPHAN TARTRATE ON LEVORPHANOL TARTRATE ANALGESIA IN POSTOPERATIVE PATIENTS

After major thoracic surgery it is important to provide efficient analgesia without the hazard of respiratory despression. In 1952 Fromherz and Pellmont1suggested, on the basis of animal experiments, that there may exist a ratio at which the respiratory depression induced by levorphan tartrate (Levo-Dromoran Tartrate)* could be counteracted by levallorphan tartrate (Lorfan Tartrate)† without significant loss of analgesia. Support for this theory was provided by Gross and Hamilton.2In normal human volunteers they found that on simultaneous administration less levallorphan tartrate was required to prevent respiratory depression than was necessary to affect the analgesia produced by levorphan tartrate. Cullen and Santos3reported favorably on a combination of 10 parts of levorphan tartrate and 1 part of levallorphan tartrate in patients with chronic pain. The present study represents an attempt to evaluate this combination in patients after major thoracic surgery. The aim of the study was to