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Biomedical subjects

Jørgen B Dahl

Publications and source records attributed to Jørgen B Dahl.

13 recordsLinked to original sources
PubMed2006

[Why is surgery risky?].

Major surgical procedures are still beset with morbidity and hospitalisation. This short survey discusses different pathogenic factors that may contribute to morbidity, with an emphasis on surgical stress responses, pain relief and all-over perioperative care in accordance with the principles of fast-track surgery. It is emphasized that further advances require a multi-disciplinary approach with a focus on process organization and where sufficient quantity is available to secure anaesthesiological, surgical and nursing care expertise.

Clinical Competence↗
PubMed2006

[Treatment of postoperative pain--a status report].

Substantial progress has been made in our understanding of acute pain mechanisms, and our insight into postoperative convalescence and rehabilitation has increased dramatically. There is a lack of evidence for pre-emptive analgesia, whereas studies of antihyperalgesic drugs and multimodal analgesic regimens are promising. The use of opioids should be restricted, and it may be rational to develop procedure-specific pain treatment guidelines. There is a need for increased collaboration and integration of acute pain treatment and multimodal postoperative rehabilitation efforts.

Analgesia↗
PubMed2004

Pre-emptive analgesia.

Transmission of pain signals evoked by tissue damage leads to sensitization of the peripheral and central pain pathways. Pre-emptive analgesia is a treatment that is initiated before the surgical procedure in order to reduce this sensitization. Owing to this 'protective' effect on the nociceptive system, pre-emptive analgesia has the potential to be more effective than a similar analgesic treatment initiated after surgery. Theoretically, immediate postoperative pain may be reduced and the development of chronic pain may be prevented. Although some clinical studies have demonstrated significant effects on acute postoperative pain, no major clinical benefits of pre-emptive analgesia have been documented. The only way to prevent sensitization of the nociceptive system might be to block completely any pain signal originating from the surgical wound from the time of incision until final wound healing. Other pharmacological interventions, including 'antihyperalgesic' drugs such as NMDA-receptor antagonists and gabapentin, may interfere with the induction and maintenance of sensitization. Future studies will investigate the analgesic effect of prolonged multimodal combinations of different classes of 'traditional' analgesics and 'antihyperalgesics' on postoperative pain.

Analgesia↗
PubMed2003

Anaesthesia, surgery, and challenges in postoperative recovery.

Surgical injury can be followed by pain, nausea, vomiting and ileus, stress-induced catabolism, impaired pulmonary function, increased cardiac demands, and risk of thromboembolism. These problems can lead to complications, need for treatment in hospital, postoperative fatigue, and delayed convalescence. Development of safe and short-acting anaesthetics, improved pain relief by early intervention with multimodal analgesia, and stress reduction by regional anaesthetic techniques, beta-blockade, or glucocorticoids have provided important possibilities for enhanced recovery. When these techniques are combined with a change in perioperative care a pronounced enhancement of recovery and decrease in hospital stay can be achieved, even in major operations. The anaesthetist has an important role in facilitating early postoperative recovery by provision of minimally-invasive anaesthesia and pain relief, and by collaborating with surgeons, surgical nurses, and physiotherapists to reduce risk and pain.

Anesthesia↗
PubMed2003

A randomized study of the effect of oral lamotrigine and hydromorphone on pain and hyperalgesia following heat/capsaicin sensitization.

In this randomized double-blind placebo-controlled study, the analgesic effect of oral lamotrigine (400 mg) on cutaneous sensitization induced with the heat/capsaicin sensitization model was compared with the effect of oral hydromorphone (8 mg) in healthy volunteers. In a separate session, intravenous remifentanil (0.10 microg.kg(-1).min(-1)) and placebo were administered. This session was used as an additional reference comparator. Outcome measures were the areas of secondary hyperalgesia to brush and von Frey hair stimulation and the painfulness of noxious thermal stimulation in nonsensitized skin. Compared with placebo, both intravenous remifentanil and oral hydromorphone significantly suppressed secondary hyperalgesia and acute thermal nociception. Oral lamotrigine did not reduce secondary hyperalgesia or acute thermal nociception but produced side effects of severity comparable with that of oral hydromorphone. Although lamotrigine is efficacious in the management of some types of chronic neuropathic pain, the lack of effect of this agent on human experimental pain suggests that its analgesic effects depend on nerve injury-associated abnormalities, which cannot be simulated in healthy human volunteers.

Adult↗
PubMed2003

The heat/capsaicin sensitization model: a methodologic study.

The heat/capsaicin sensitization model induces cutaneous sensitization by using a combination of heat and topical capsaicin. It has been suggested that the stability and duration of the cutaneous sensitization are due to a synergistic effect between heat and capsaicin. The aim of this study was to evaluate a possible synergistic effect between heat and capsaicin in inducing cutaneous sensitization. Twenty healthy male volunteers completed this random order, 4-session study. Three different stimulation combinations were used to induce cutaneous sensitization: day A, heat and capsaicin; day B, heat alone; day C, capsaicin alone. Combination A was repeated on day D to determine between day reproducibility. Rekindling was performed 3 times at 40-minute intervals to maintain stable areas of secondary hyperalgesia. Brief thermal sensitization (45 degrees C for 3 minutes) was induced at each session. Within and between day reproducibility was calculated. There was no difference between the size of areas of secondary hyperalgesia after stimulation with heat/capsaicin compared to heat and capsaicin stimulation alone. The within day reproducibility was better with heat/capsaicin than with either stimulation alone. There was no synergistic or additive effect between heat and capsaicin in inducing cutaneous sensitization. Rekindling seems to be the important factor in maintaining stable and long-lasting cutaneous sensitization.

Adolescent↗
PubMed2003

Nonsteroidal antiinflammatory drugs and the risk of operative site bleeding after tonsillectomy: a quantitative systematic review.

UNLABELLED: The use of nonsteroidal antiinflammatory drugs (NSAIDs) for analgesia after tonsillectomy is controversial because NSAIDS, through platelet inhibition, may increase the risk of perioperative bleeding. We systematically searched for randomized, controlled trials that reported on the incidence of perioperative bleeding attributable to the use of NSAIDs in patients undergoing tonsillectomy. As secondary outcome measures, we analyzed the quality of pain relief and the incidence of postoperative nausea and vomiting. Twenty-five studies with data from 970 patients receiving a NSAID and 883 receiving a non-NSAID treatment or a placebo were analyzed. Data were combined using a fixed-effect model. Of four bleeding end points (intraoperative blood loss, postoperative bleeding, hospital admission, and reoperation because of bleeding), only reoperation happened significantly more often with NSAIDs: Peto-odds ratio, 2.33 (95% confidence interval [CI], 1.12-4.83) and number-needed-to-treat, 60 (95% CI, 34-277). Compared with opioids, NSAIDs were equianalgesic, and the risk of emesis was significantly decreased (relative risk, 0.73; 95% CI, 0.63-0.85; numbers-needed-to-treat, 9; 95% CI, 5-19). IMPLICATIONS: The evidence for nonsteroidal antiinflammatory drugs to increase the risk of bleeding after tonsillectomy is equivocal, and the risk-benefit ratio is not straightforward. There is some evidence for an increased likelihood of reoperation because of bleeding. The agenda must be one of further research rather than of clinical recommendations.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Gabapentin suppresses cutaneous hyperalgesia following heat-capsaicin sensitization.

BACKGROUND: The anticonvulsant gabapentin, proven effective for neuropathic pain in two large, placebo-controlled clinical trials, is widely used for treatment of chronic pain. Preclinical studies have demonstrated analgesic and antiallodynic effects in models involving neuronal sensitization and nerve injury, without affecting acute pain transmission. The aim of the present study was to link data from animal models and clinical trials for chronic pain by investigating the effect of gabapentin on acute nociception and experimentally induced cutaneous hyperalgesia in healthy volunteers. METHODS: The human experimental hyperalgesia model, the heat-capsaicin sensitization model, was induced in 25 healthy male volunteers. Subjects received oral gabapentin (1,200 mg) or placebo after heat-capsaicin sensitization was established on the forearm. The primary outcome measures were the sizes of the areas of secondary hyperalgesia to von Frey hair and brush stimulation on the forearm. Secondary outcome measures were as follows: (1) size of secondary hyperalgesia area in response to brief thermal sensitization procedure on the thigh; (2) heat pain detection thresholds in normal and sensitized skin; and (3) painfulness of 1 min of 45 degrees C stimulation in normal skin. RESULTS: Oral gabapentin profoundly suppressed established cutaneous sensitization on the forearm and prevented development of cutaneous sensitization on the thigh. Thermal nociception in normal skin was unchanged. Side effects were modest. CONCLUSION: The results link preclinical findings with results from clinical trials of neuropathic pain. The results further suggest that gabapentin may prove effective in acute pain disorders involving neuronal sensitization, such as postoperative pain and acute herpetic pain, and could prove effective in prevention of chronic pain.

Acetates↗
PubMed2002

A randomized study of the effects of single-dose gabapentin versus placebo on postoperative pain and morphine consumption after mastectomy.

BACKGROUND: The anticonvulsant gabapentin has proven effective for neuropathic pain in three large placebo-controlled clinical trials. Experimental and clinical studies have demonstrated antihyperalgesic effects in models involving central neuronal sensitization. It has been suggested that central neuronal sensitization may play an important role in postoperative pain. The aim of the study was to investigate the effect of gabapentin on morphine consumption and postoperative pain in patients undergoing radical mastectomy. METHODS: In a randomized, double-blind, placebo-controlled study, 70 patients received a single dose of oral gabapentin (1,200 mg) or placebo 1 h before surgery. Patients received patient-controlled analgesia with morphine at doses of 2.5 mg with a lock-out time of 10 min for 4 h postoperatively. Pain was assessed on a visual analog scale at rest and during movement, and side effects were assessed on a four-point verbal scale 2 and 4 h postoperatively. RESULTS: Thirty-one patients in the gabapentin group and 34 patients in the placebo group completed the study. Gabapentin reduced total morphine consumption from a median of 29 (interquartile range, 21-33) to 15 (10-19) mg (P< 0.0001). Pain during movement was reduced from 41 (31-59) to 22 (10-38) mm at 2 h postoperatively (P < 0.0001) and from 31 (12-40) to 9 (3-34) mm at 4 h postoperatively (P = 0.018). No significant differences between groups were observed with regard to pain at rest or side effects. CONCLUSION: A single dose of 1,200 mg oral gabapentin resulted in a substantial reduction in postoperative morphine consumption and movement-related pain after radical mastectomy, without significant side effects. These promising results should be validated in other acute pain models involving central neuronal sensitization.

Acetates↗
PubMed2002

Mechanisms of postoperative pain: clinical indications for a contribution of central neuronal sensitization.

BACKGROUND: The relative importance of different nociceptive mechanisms for the intensity, duration, and character of postoperative pain is not well established. It has been suggested that sensitization of dorsal horn neurones may contribute to pain in the postoperative period. We hypothesized that wound hyperalgesia in postoperative patients and experimentally heat-induced secondary hyperalgesia share a common mechanism, sensitization of central neurones, and consequently, that the short-acting opioid remifentanil would have comparable effects on hyperalgesia in both conditions. METHODS: In a randomized, controlled, double-blind trial, we assessed mechanical hyperalgesia in skin bordering the surgical wound, and an area of experimentally heat-induced secondary hyperalgesia on the thigh, in 12 patients who underwent abdominal hysterectomy within 5 days prior to the investigation. Observations were made before and during a drug challenge with remifentanil, which has been demonstrated to reduce the area of heat-induced secondary hyperalgesia in volunteers. RESULTS: The area of skin with surgically-induced mechanical hyperalgesia, the area of heat-induced secondary hyperalgesia, and pain during cough, were significantly reduced during remifentanil infusion compared with placebo (P = 0.008, P = 0.006, and P = 0.002, respectively). The relative reduction (% of baseline) of the area of skin with surgically-induced hyperalgesia and heat-induced secondary hyperalgesia during infusion of remifentanil was significantly associated (R2 = 0.72, P = 0.001). CONCLUSIONS: Although remifentanil is not a highly targeted "antihyperalgesic," these results support the hypothesis that both wound hyperalgesia in postoperative patients and experimentally heat-induced secondary hyperalgesia may share common mechanisms, and that central neuronal sensitization may contribute to some aspects of postoperative pain. Antihyperalgesic drugs should be further developed and evaluated in clinical trials of postoperative pain.

Adult↗
PubMed1994

Quantitative sensory examination of epidural anaesthesia and analgesia in man: effects of pre- and post-traumatic morphine on hyperalgesia.

The objectives of the study were: (1) comparison of hypoalgesic effects of pre- and post-traumatic epidural morphine (EM) on primary and secondary hyperalgesia, and (2) comparison of EM hypoalgesia in normal and injured skin. Burn injuries (25 x 50 mm rectangular thermode, 47 degrees C, 7 min) were produced on the calves of healthy volunteers, at 2 different days at least 1 week apart. In randomized order, the subjects received 4 mg of EM administered via the L2-L3 intervertebral space on one day and no treatment on the other day. One calf was injured 30 min prior to and the other calf 2.5 h after administration of morphine. Hence, the calf injured prior to morphine administration was a model of postinjury treatment, and the calf injured after morphine administration, a model of pretraumatic treatment. The timing of injuries was identical on the morphine treatment and control days. The injuries induced decrease in heat pain detection and tolerance thresholds within the area of injury (area of primary hyperalgesia) as well as reduction of areas of allodynia for brush and pinprick surrounding the injury (area of secondary hyperalgesia). Both pre- and post-traumatic administration of EM increased heat pain detection and tolerance thresholds, and decreased by approximately 50% the areas of secondary hyperalgesia 2.5 h postinjury. The effects of morphine were naloxone (NAL)-reversible (0.1 mg/kg, i.v.). There was no significant difference between pre- and post-traumatic administration of morphine on the effect of either primary or secondary hyperalgesia. EM increased the heat pain detection threshold more within the injury than at a corresponding non-injured site. There was no significant difference in the effect of morphine on heat pain tolerance in injured and non-injured skin. Following NAL, the areas of secondary hyperalgesia expanded beyond control size. It is suggested that the major effect of EM on secondary hyperalgesia is inhibition of C fibre-mediated activity which maintains the altered response properties of central neurons responsible for secondary hyperalgesia. Possible mechanisms of action of NAL in enhancement of hyperalgesia are discussed.

Adult↗
PubMed1993

The effect of pre- versus postinjury infiltration with lidocaine on thermal and mechanical hyperalgesia after heat injury to the skin.

The aim of the study was to evaluate the effects of pre- and postinjury infiltration with lidocaine on alterations in mechanical and thermal sensitivity after heat injury to the skin. In the first part of the study, burn injuries (15 x 25 mm rectangular thermode, 50 degrees C, 7 min) were produced twice in each subject on the medial side of the left and right calves at least 24 h apart in 8 healthy, unmedicated male volunteers, in order to investigate the effects of the injury on sensitivity in untreated skin. In the second part of the study, burn injuries (15 x 25 mm rectangular thermode, 50 degrees C, 6 min) were produced twice in each subject on the medial side of the left and right calves at least 24 h apart (n = 10). This was preceded by subcutaneous (s.c.) infiltration with 5-6 ml of 1% plain lidocaine (pre-injury block) on one day, and the same block was performed 35 min after injury (postinjury block) on the other day. Warm detection thresholds (WDT) and heat pain detection thresholds (HPDT) were determined within and outside the injury before and at regular intervals after injury. Areas of hyperalgesia to pinprick and brush were determined at regular intervals after injury. In the first part of the study, it was observed that both WDT and HPDT were decreased within but not outside the injury, and areas of hyperalgesia to pinprick and brush were found in- and outside the injury in all subjects. These findings were relatively constant throughout the study period and reproducible between the 2 days of examination. In the second part of the study, it was observed that pre-injury infiltration with lidocaine reduced hyperalgesia to pinprick and brush outside the injury more effectively than postinjury block, but only for the first 70 min after injury, while no significant difference was observed 100-190 min after injury. Likewise, there was no difference in thermal thresholds inside the injury between pre- and postinjury treatment at the end of the study period. It is concluded, that a shortlasting 'preemptive' infiltration with lidocaine may postpone but not prevent the occurrence of hyperalgesia outside a thermal injury.

Adult↗