Biomedical subjects
Publications and source records attributed to C Lund.
Jacobsen's theory of affects and psychotic depression can be of benefit to the management of patients, even when recourse to physical therapies is required. Awareness of such psychodynamic issues would improve staff training, morale, and practice; rotation schemes for junior staff may have serious effects through the abandonment of patients and established therapeutic relationships.
Intensive research during recent years concerning treatment of postoperative pain has demonstrated that the majority of operation patients can be rendered free from pain but that this is far from being the case in clinical practice. This article reviews the physiological mechanisms of acute pain and the methods available for treatment of pain related to acute physiology of pain. Postoperative treatment of pain should be aggressive with the object of preventing pain and normalizing the vital functions with the object of reducing the perioperative morbidity and mortality. A series of recommendations are given for treatment of pain after surgical intervention.
We have studied the effect of surgical injury on cutaneous sensitivity and somatosensory evoked potentials (SSEP) to dermatomal electrical stimulation in 10 patients undergoing hysterectomy. Forty-eight hours after surgery, sensory threshold increased from 2.2 (SEM 0.3) mA to 4.4 (1.1) mA (P less than 0.01) and SSEP amplitudes in P1, N1, P2 and the peak-to-peak amplitudes decreased (P less than 0.05). Latency was prolonged only in the N3 component (P less than 0.05). No changes were seen in threshold and SSEP in a control group studied over the same interval. The results suggest that surgical injury activates antinociceptive modulatory systems.
A middle-aged man with only slight symptoms of disease of short duration died suddenly. On autopsy he was found to have not only disseminated visceral giant cell vasculitis with involvement of large and medium-sized arteries and veins, but also sarcoid granulomas in many organs, especially in enlarged mediastinal lymph nodes as well as in several vessel walls. Death was caused by myocardial infarction due to granulomatous vasculitis. This combination of diseases has not previously been described, and the question is whether it represents giant cell arteritis and sarcoidosis, separately, or whether it is a manifestation of a broad spectrum of the same disease.
Twenty-two patients undergoing upper abdominal surgery were entered into a randomized, double-blind study to receive extradural (T7-T8) 0.5% bupivacaine 9 ml followed by 25 mg h-1 with or without additional extradural morphine (bolus 4 mg plus 0.5 mg h-1), for 16 h after operation. Addition of morphine was associated with total alleviation of pain, and a stable level of sensory analgesia, but not with changes in blood glucose and cortisol concentrations or postoperative impairment of lung function (PEFR, FEV1, FVC). Two patients were withdrawn because of hypotension or respiratory depression.
We have examined the effects of extradural clonidine 150 micrograms or morphine 4 mg on postoperative pain, stress responses, cardiopulmonary function and motor and sensory block in a double-blind, randomized study in 20 patients undergoing hysterectomy with general anaesthesia. Observations were made for 6 h after each patient's first request for analgesia. Clonidine provided greater pain relief than morphine only for the first 2 h of observation (P less than 0.001). Plasma cortisol concentrations decreased to a greater extent (P less than 0.05) with morphine, while plasma glucose concentration increased by a similar extent in both groups. After clonidine, mean arterial pressure decreased from 100 (SEM 3) mm Hg to 70 (3) mm Hg (P less than 0.05), but there was no change after morphine. There were no significant changes in heart rate, pulmonary function (FEV1), motor function or sensory analgesia to touch, temperature and pinprick in both groups. Additional systemic opioids were required by five and six patients in the clonidine and morphine groups, respectively.
Twelve horses suffering from navicular bone disease were examined in a prospective, controlled histomorphometric study for six months. The objective was to compare the histology of navicular bones from untreated animals to those treated with the egg-bar shoeing technique. These data were compared to similar sections from three normal animals. The current investigation provided quantitative support to previous findings concerning clinical improvement. Detailed histology, changes in bone morphometry and pathophysiological reactions are discussed.
The effect of lumbar epidural clonidine 150 micrograms on early (less than 0.5 s) somatosensory evoked potentials (SEP) to electrical stimulation of the L1 and S1 dermatomes was examined in twelve cancer patients. Epidural clonidine led to a minor but significant decrease in amplitude of two components (N1 and N3) following S1 stimulation while SEP latency was prolonged only in the P1 and P3 components (P less than 0.05). In all patients the pain score decreased, mean score at rest from 4.9 +/- 0.5 to 0.6 +/- 0.2 and during mobilization from 7.4 +/- 0.6 to 1.3 +/- 0.5 (P less than 0.01). Mean systolic and diastolic blood pressures decreased from 118 +/- 4/72 +/- 5 mmHg to 99 +/- 5/60 +/- 3 mmHg (P less than 0.01), respectively. It is concluded that epidural clonidine has a minor effect on the early SEPs to electrical dermatomal stimulation. Additionally, a pronounced effect on cancer pain was seen.
Twenty-four otherwise healthy patients scheduled for elective major abdominal surgery received general anaesthesia plus lumbar extradural analgesia. A loading dose of 0.5% plain bupivacaine was given to produce sensory analgesia (pin prick) from T4 to S5 and followed by a continuous infusion of 0.5% plain bupivacaine 8 ml h-1. Pain, scored on a 5-point scale, and sensory analgesia were assessed hourly for 16 h after skin incision. If sensory analgesia decreased by more than 5 segments from its preoperative level, or if the pain score reached 2 (moderate pain), the patients were removed from the study, and pain was treated otherwise. Only three patients maintained their initial levels of sensory analgesia and a pain score of less than 2. In the remaining patients sensory analgesia decreased at least 5 segments or pain score reached 2 between 4 and 16 h after skin incision. We found a weak correlation between increasing age and the duration of sensory analgesia (r = 0.46, P less than 0.05), but no significant correlations between duration of sensory analgesia and sex, weight, height, body surface area, serum albumin concentration, duration or site of operation.
The purpose of this study was to investigate whether regression of sensory analgesia during constant epidural bupivacaine infusion was different in postoperative patients with acute pain than in patients with chronic nonsurgical pain. Sensory levels of analgesia (to pinprick) and pain (on a five-point scale) were assessed hourly for 16 hours during continuous epidural infusion of 0.5% plain bupivacaine (8 ml/hr) in 12 patients with chronic nonsurgical pain and in 30 patients after major abdominal surgery performed under combined bupivacaine and halothane--N2O general anesthesia. No opiates were given. If sensory analgesia decreased more than five segments from the initial level or if the pain score reached 2 (moderate pain), the patient was removed from the study. Initial levels of sensory analgesia after loading doses of 21.8 +/- 0.5 and 19.3 +/- 0.8 ml bupivacaine 0.5% were similar (T3.8 +/- 0.3 and T3.8 +/- 0.5) in the surgical and chronic pain patients, respectively (mean +/- SEM). Of the surgical patients, only 4 of the 30 (13%) maintained the initial level of sensory analgesia, and a pain score below 2 throughout the study compared with 7 of the 12 patients with chronic pain (58%) (P less than 0.01). Mean duration of sensory blockade was significantly longer (P less than 0.005) in the patients with chronic pain than in surgical patients (13.1 +/- 1.2 and 8.5 +/- 0.7 hours, respectively). Thus, surgical injury hastens regression of sensory analgesia during continuous epidural bupivacaine infusion. The underlying mechanism remains to be determined.
The effect of the extradural (L2-3) administration of morphine 6 mg on early (less than 0.5 s) somatosensory evoked cortical potentials (SEP) to electrical stimulation of the L1- and S1-dermatomes was examined in eight patients. Extradural morphine did not influence SEP amplitude. SEP latency did not change, except for a minor increase in the latencies of the onset and the P2 components following S1 stimulation.
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The effect of spinal anesthesia with 3.6 +/- 0.1 ml (mean +/- SEM) of 0.5% bupivacaine on early (less than 150 msec) somatosensory evoked potentials (SEPs) with electrical stimulation of the L1 and S1 dermatomes was examined in 12 patients. The mean level of sensory analgesia (pinprick) was T8,9 +/- 1.0 (+/- SEM) and the mean degree of motor blockade was 1.3 +/- 0.1 (Bromage scale). Intrathecal bupivacaine significantly (P less than 0.05) decreased the amplitude of all SEP components after stimulation of the L1 dermatome and most components during stimulation of the S1 dermatome. Intrathecal bupivacaine also increased the latency of SEPs (P less than 0.05) of both dermatomes. The L1 SEP disappeared in 7 and the S1 SEPs in 5 of the 12 patients during neural blockade. In three patients the SEPs disappeared at both locations. Sensory thresholds increased significantly during blockade. We found no correlation between decrease of amplitude and degree of motor blockade or level of sensory analgesia. Thus, intrathecal plain bupivacaine has a strong depressant effect on the neural afferent transmission as assessed by SEPs. However, despite clinically effective blockade as assessed by pinprick and motor blockade nerve potentials after nociceptive stimulation within the area of sensory block were often able to pass to the cerebral cortex.
The effect of epidural bupivacaine (9 ml 0.5%) analgesia on early (less than 500 msec) somatosensory evoked potentials (SEPs) with electrical stimulation of the T-10 and L-1 dermatomes was examined in eight patients. Cortical amplitudes decreased only insignificantly after stimulation of both dermatomes, despite the presence of sensory analgesia (pin prick) from T-3.5 +/- 0.4 to L-2.9 +/- 0.4 (mean +/- SEM). Latency of the SEP components remained unchanged and sensory threshold increased only insignificantly during blockade. We conclude that thoracic epidural analgesia with conventional doses of bupivacaine provides only a limited blockade of fast conducting afferent nerve fibers.
The effect of lumbar epidural analgesia with plain bupivacaine, 0.5%, on early (less than 0.5 sec) somatosensory evoked potentials (SEP) to electrical stimulation of the T-10, L-1, and S-1 dermatomes and the posterior tibial nerve was examined in eight patients. A decrease of the cortical amplitude and an increase in latency were seen, most pronounced at the L-1 level, but with only minor effect on the S-1 dermatome. No correlation was found between segmental level of analgesia and decrease in amplitude of the evoked potentials. Thus despite clinically adequate surgical anesthesia, the neural pathways as assessed by SEP were incompletely blocked except at the L1 dermatome near the epidural injection site.
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The effect of epidural analgesia with plain bupivacaine 0.5% on somatosensory evoked potentials (SEP) to electrical stimulation of the posterior tibial nerve was examined in six patients. Epidural analgesia significantly increased onset time and latencies of the early components in SEP, while the amplitudes decreased. These results suggest that SEP may be valuable in the objective evaluation of possible differential neural effects of local anaesthetic agents following epidural or intrathecal administration.
In a retrospective study of long term survival in patients with small cell carcinoma of the lung who had been treated purely by surgery, 1820 patients with lung cancer seen during the 15 years 1962-77 were reviewed and reclassified histologically and according to the TNM system. Of these patients, 924 had had resections and 284 exploratory thoracotomies. Cancer chemotherapy was not used in this period and radiotherapy was given only occasionally as palliative treatment. Seventy seven of the patients having pulmonary resections had small cell carcinoma (8.4%), and there were six survivors among the 71 with T1-2, N0-1, M0 tumours. The five and 10 year survival rates were both 12%. The histological specimens from these six patients with a small cell carcinoma who survived more than 10 years were re-evaluated and confirmed as small cell by an independent group of pathologists. It seems justified to conclude that a selected group of patients with small cell carcinoma should be treated by surgery alone without adjuvant chemotherapy, which might reduce the long term survival.