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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Laparoscopic cholecystectomy is a relatively new surgical procedure, enjoying ever-increasing popularity and presenting new anesthetic challenges. The advantages of shorter hospital stay and more rapid return to normal activities are combined with less pain associated with the small limited incisions and less postoperative ileus compared with the traditional open cholecystectomy. Complications are mostly due to traumatic injuries sustained during blind trocar insertion, and physiologic changes associated with patient positioning and pneumoperitoneum creation. The choice of anesthetic technique for laparoscopic cholecystectomy is limited most frequently to general anesthesia. Controlled ventilation avoids hypercarbia, and an anesthetic technique incorporating antiemetics and nonsteroidal antiinflammatory agents has reduced postoperative nausea and vomiting. The use of nitrous oxide and narcotics during laparoscopic cholecystectomy is controversial. Laparoscopic cholecystectomy is a major advance in the management of patients with symptomatic gallbladder disease. However, in the present era of cost containment, older and sicker patients may present for this procedure on the day of surgery without adequate preoperative evaluation. Anesthesiologists thus should be prepared to recommend conversion to an open procedure if hemodynamic, oxygenation, or ventilation difficulties occur during the procedure.
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PMID:Laparoscopic cholecystectomy: anesthetic implications. 831 5

A total of 52 patients with myocardial infarction have been examined. The patients have been subjected to HBO procedures. 40-62 min sessions with a working pressure of 0.3-1.1 atm were performed. The optimal pressure during the first days is 0.3 atm with a gradual increase to 0.7 atm. It is important to prepare the patient before the session with the end in view to achieve hemodynamic normalization and pain relief and to ensure a possibility of coronarolytic intake during the session. By session 4-5 hypercapnia and hypoxia, hyperventilation syndrome were eliminated, hemodynamic and respiratory parameters normalized, and immunity recovered. Only in one case a session had to be interrupted because of pulmonary edema recurrence. In 7 patients usual complications which were easily relieved have been observed. HBO shortened the patients' stay in an intensive care unit by 1.6 days and decreased lethality by 9.5%.
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PMID:[Hyperbaric oxygenation in myocardial infarct]. 808 Jan 31

In a double-blind, randomized study, we have compared the effects of i.v. ketoprofen 200 mg followed by 12.5 mg h-1 over 13 h, with those of extradural morphine 4 mg in 32 patients after hip and knee arthroplasty. A visual analogue scale was used to score pain before analgesic administration (first complaint after operation), 1 h after and every 2 h subsequently. Pain reduction 1 h after the start of analgesia was mean 44% (SEM 17%) in the extradural morphine group and 54% (9%) in the ketoprofen group (ns). There were no significant differences between groups in pain scores, pain reduction and additional analgesia requirement (i.v. paracetamol). Naloxone 5 micrograms kg-1 h-1 was required for hypercapnia exceeding 6.0 kPa in three patients in the extradural morphine group (vs none in the ketoprofen group; ns). There were no differences between groups in side effects, except for urinary retention, which was more frequent in the extradural morphine group (P < 0.05). As there were few differences between i.v. ketoprofen and extradural morphine, we conclude that ketoprofen may be an efficient alternative to extradural morphine after hip and knee arthroplasty.
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PMID:Ketoprofen for pain after hip and knee arthroplasty. 815 35

This paper reviews cardiac dysrhythmias occurring in the perioperative period. Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of dysrhythmias remains the most important use of this technology today. While the description of dysrhythmias dates back to the early 1900's, the first large series was reported in 1936. Early descriptions of the kinds seen and the predisposing factors have changed little in the past 50 years. Several factors tend to emerge when one evaluates perioperative dysrhythmias. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculocardiac reflex, stimulation of the central nervous system the presence of pre-existing heart disease, and the use of intracardiac devices. In the evaluation of cardiac dysrhythmias several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery which may explain the dysrhythmia. In addition, one needs to evaluate the heart rate, the regularity, the number of P waves per QRS, and the configurations of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. The two major abnormalities of sinus rhythm are sinus bradycardia and the sinus tachycardia. Sinus bradycardia can be due to hypoxia, vagal stimulation, drug effects, a high sympathetic block or an acute myocardial infarction. Sinus tachycardia can be due pain, light anesthesia, hypovolemia, sepsis, hypoxia, hypercapnia and drug effects. The major atrial dysrhythmias are paroxysmal atrial tachycardia, atrial fibrillation and atrial flutter. Each require treatment if perfusion is impaired or if the heart rate is persistently elevated. The new agents esmolol and adenosine are particularly useful in managing atrial dysrhythmias. The major ventricular dysrhythmias are ventricular premature contractions, ventricular tachycardia and ventricular fibrillation. The later two demand emergency management with DC cardioversion when perfusion is impaired. The major abnormality of conduction is complete heart block which usually requires emergency treatment in the perioperative period. Prompt evaluation and management of perioperative dysrhythmias reduce anesthetic morbidity and mortality.
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PMID:Management of perioperative dysrhythmias. 828 46

The present study compared epidural tramadol with epidural morphine for postoperative analgesia in 20 patients undergoing major abdominal surgery. Intraoperatively, the patients were anaesthetized by a balanced technique of general anaesthesia combined with lumbar epidural lidocaine. In ten of the patients 100 mg tramadol diluted in 10 ml normal saline was also injected epidurally, while 4 mg epidural morphine was used in the other ten patients. In all patients, the visual analogue pain score, PaO2, PaCO2 and respiratory rate were monitored every hour for the first 24 hr postoperatively. In both the tramadol and morphine groups, the mean hourly pain scores ranged from 0.2 +/- 0.6 to 1.4 +/- 2.5 throughout the period of observations. However, the mean PaO2 was decreased postoperatively in the epidural morphine group, while no change was observed in the epidural tramadol group. The maximal decrease of PaO2 in the epidural morphine group was observed at the tenth hour postoperatively, when it decreased to 72.8 +/- 10.3 mmHg. This was not associated with any increase in PaCO2 or a decrease of respiratory rate, suggesting that hypoxaemia rather than hypercarbia or decreased respiratory rate may be an earlier indicator of respiratory rate, suggesting that hypoxaemia rather than hypercarbia or decreased respiratory rate may be an earlier indicator of respiratory depression in patients breathing room air without oxygen supplementation. The absence of clinically relevant respiratory depression following epidural tramadol compared with epidural morphine may be attributed to the different mechanisms of their analgesic action. The results suggest that epidural tramadol can be used to provide prolonged postoperative analgesia without serious side effects.
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PMID:A comparison of epidural tramadol and epidural morphine for postoperative analgesia. 848 89

We investigated analgesia and the adverse effects of epidural sufentanil infusion in a double-blind randomized study of 37 patients undergoing thoracic surgery. Sufentanil 1 microgram/mL was administered at a thoracic (Ts, n = 12) or lumbar level (Ls, n = 11), or combined with bupivacaine 1 mg/mL at a thoracic level (Tsb, n = 14). Postoperatively, the epidural infusion rate was titrated (4-20 mL/h) according to the visual analog pain scale when assessed during function (VAS-F) or the occurrence of side effects. When epidural analgesia failed, nonsteroidal antiinflammatory drugs (NSAIDs) were given. VAS-F was lowest in the Tsb group (Tsb < Ts = Ls) despite its having both the lowest rate of epidural infusion (Tsb < Ts < Ls) and need of additional NSAIDs (Tsb < Ts = Ls). Sedation (Tsb < Ts < Ls) and hypercapnia (Tsb = Ts < Ls) occurred most frequently in the Ls group. Vital capacity (VC) was reduced in all groups by 43%-58% (Ls > Ts) and had recovered only partially at 24 h after discontinuation of the epidural infusion. The slopes of the ventilatory response (minute ventilation [VE], inspiratory flow, and mouth occlusion pressure at 0.1 s [P0.1]) to 7% CO2 decreased during treatment in Ls, Ts, and Tsb groups at the most by 73%, 55%, and 52% (not significant [NS] between groups), 59%, 45%, and 38% (NS between groups), and 81%, 43%, and 18% (Ls > Tsb), respectively. Twenty-four hours after discontinuation of the epidural infusion, there was a complete recovery of the VE, inspiratory flow, and P0.1 response to CO2 in the Tsb group only. The study shows that, after thoracotomy, epidural sufentanil analgesia is optimal when tailored to the site of nociceptive input and combined with bupivacaine.
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PMID:The analgesic efficacy and adverse effects of continuous epidural sufentanil and bupivacaine infusion after thoracotomy. 869 25

The respiratory and analgesic effects of i.v. meperidine, tramadol and their correlation with plasma concentrations of meperidine, tramadol and O-demethyltramadol were determined. Forty-eight patients after total hip or knee replacement were randomly distributed into 3 groups (n = 16 each). At the time of analgesia request, they received in a double-blind manner, i.v. single doses of 100 mg meperidine, 100 mg tramadol, or saline. Thirty minutes after treatment, patients who requested additional analgesia were rescued with 75 mg diclofenac and morphine as required. Patients were evaluated at the time of analgesia request and at set intervals during 4 h. Meperidine induced sedation (p < 0.05), respiratory depression (tidal volume, p < 0.047; respiratory rate, p < 0.004; % O2 Sat, p < 0.036), and hypercapnia (PaCO2, p < 0.002). Incidence of nausea and vomiting was higher with tramadol (p < 0.02). For the first 30 min, meperidine produced lower pain intensity scores than tramadol or saline (p < 0.05). At this time, 14/16 patients on saline, 8/16 on meperidine and 11/16 on tramadol were rescued. Onset for meperidine analgesia was 10 min and > 30 min for tramadol. Both opioids produced similar degree of analgesia in patients who were not rescued. A negative correlation (r = -0.99) between analgesia and tramadol concentrations and a poor positive correlation (r = +0.54) with O-demethyltramadol (a metabolite of tramadol) was observed. Pain intensity differences correlated negatively with meperidine plasma concentrations during the first 30 min (r = -0.97) and positively thereafter (r = +0.92). In the present study, meperidine and tramadol produced comparable analgesia, with a different time course profile, but meperidine induced sedation and respiratory depression while tramadol did not.
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PMID:Respiratory and analgesic effects of meperidine and tramadol in patients undergoing orthopedic surgery. 873 73

Reversal of opioid-related respiratory depression is often accompanied by an "acute abstinence like syndrome" with hypertension, tachycardia, and pain. This overshoot was used to investigate the extent at which opioids of high potency but different structure are involved in naloxone-induced abstinence. In 10 awake and trained mongrel dogs two highly mu-selective compounds, alfentanil and fentanyl, were given in cumulative doses and at different occasions (30-60-120-240 micrograms/kg, and 6-12-24-48 micrograms/kg, respectively). Subsequently, a high dose of naloxone (100 micrograms/kg) was given at 5 min intervals while arterial blood gases, blood pressure, heart rate and the somatosensory evoked potential (SEP) were measured continuously. Following a wash-out period, the 19-isoamyl derivative of etorphine (M-140; 10,000 times more potent than normorphine and a 4.5 fold potency of ethylketocyclazocine in a bioessay preparation) was also given in increasing doses (0.2-0.4-0.8-3.2 micrograms/kg). Again, naloxone was given (100 micrograms/kg) at 5 min interval, while cardiovascular parameters, blood gases and SEPs were measured continuously. All three opioids induced a dose-related respiratory depression with hypercarbia and hypoxia, a dose-related bradycardia, and a modest hypotension. This was accompanied by a dose-related depression of the amplitude of the SEP, reflecting the degree of blockade of nociceptive afferents. Naloxone was sufficient to reverse respiratory impairment after fentanyl, alfentanil and M-140. However, in contrast to fentanyl and alfentanil, there was no cardiovascular or evoked potential overshoot following naloxone reversal of M-140. After alfentanil naloxone increased blood pressure, heart rate and amplitude of the SEP by 7%, 41% and 38%, respectively. After fentanyl this increase in blood pressure, heart rate and amplitude of the SEP was 17%, 43% and 96%, respectively. The study indicates that the more potent the opiate mu ligands are the more is naloxone liable to induce a hyperexcitatory state of the cardiovascular system and an increase of nociceptive stimuli to pain modulating centres. After M-140 reversal of mu-related respiratory depression by naloxone was possible. However, no precipitation on an acute abstinence-like syndrome affecting antinociception or inducing cardiovascular overshoot was observed. This may stem from an intense binding and slow dissociation of the ligand from the receptor site or may be due to high binding affinity to both the mu and the kappa receptor site. Opioids which interact with various receptor sites may be of clinical interest for substitution therapy in opioid dependent addicts.
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PMID:Studies on the abstinence-like overshoot following reversal of the potent 19-isoamyl derivative of etorphine with naloxone. A comparison with the opioids fentanyl and alfentanil. 903 35

The management of patients with acute ischaemic stroke, which was once accompanied by a sense of futility, has shifted to emergency intervention, as a result of clinical trials demonstrating the efficacy of acutely administered therapies in reducing mortality and morbidity. The current approach to stroke thus emphasises early recognition, rapid transport to hospital, speedy evaluation and urgent treatment. In the emergency room, treatment decisions are largely influenced by the neurological status of patients, although their respiratory, cardiovascular and metabolic status are also considered. Initially, efforts are aimed at reducing hypoxia and hypercarbia, controlling symptoms such as pain or vomiting, and reducing the morbidity and mortality associated with stroke. Most patients with stroke require hospitalisation; in-hospital care continues to focus on preventing and controlling subacute and chronic complications, but also includes planning for rehabilitation and care after discharge, and treatment to prevent recurrent stroke. Administration of newer treatment interventions, such as thrombolytic therapy, requires the availability of teams of stroke specialists; furthermore, the management of stroke patients in a dedicated unit has been shown to reduce death and disability and to shorten the hospital stay. While therapies aimed at reducing the neurological consequences of stroke are the keystone of current and future care, the control of acute, subacute, or chronic medical and neurological complications, prevention of recurrent stroke, and rehabilitation to maximise recovery from stroke remain crucial components of patient management.
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PMID:Management of patients with acute ischaemic stroke. 936 Aug 53

We audited and analysed the adverse effects and safety of postoperative pain management on 2509 consecutive patients under care of the Acute Pain Service at a tertiary referral teaching hospital over a 32-month period. Our standard respiratory monitoring consisted of continuous pulse oximetry, hourly respiratory rate counting, sedation scoring and intermittent arterial blood gas sampling. This protocol was reliable and detected six episodes of bradypnoea, 13 of hypercapnia and 23 of oxygen desaturation occurring in 39 patients (1.8% of all spontaneously breathing patients). Two patients required naloxone injection and none had long-term sequelae. Hypotension due to epidural bupivacaine 0.0625% and fentanyl 3.3 micrograms.ml-1 infusion occurred in four patients (1.2%), all with a sensory block higher than T5. They readily responded to fluid infusion and ephedrine (two patients). Postoperative nausea or vomiting occurred in 723 (28.8%) and 380 (15.1%) patients, respectively. Odds ratio analysis showed that the risk factors for postoperative nausea and vomiting were: female gender, gynaecological operations, nongeriatric patients and systemic analgesia. Postoperative nausea and vomiting decreased analgesic efficacy by discouraging the use of patient-controlled analgesia and was regarded as equally distressing as pain. Other side-effects included: pruritus in 182 patients; dizziness in 333 and lower limb weakness in 73 (21.2% of patients receiving epidural local anaesthetics). It is concluded that a standard monitoring and management protocol, an experienced nursing team and reliable Acute Pain Service coverage is mandatory for the safe use of modern analgesic techniques.
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PMID:An audit of the safety of an acute pain service. 940 64


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