The effectiveness of three treatments for alveolar osteitis was compared. It was found that chlorhexidine gluconate mouthwash treatment and 2.5 percent Lidocaine ointment treatment reduced the number of days a patient was symptomatic compared to the conventional eugenol-impregnated iodoform gauze treatment. With the conventional use of eugenol-impregnated iodoform gauze, the severity of the patient's symptoms were reduced more effectively than with the other two treatments, but the symptoms lasted longer.

Opioids remain at the center of most postoperative pain control therapies. The choice between full agonist opioids should be determined by the time for a given dose to produce its maximum effect (i.e,, latency to peak effect), and the duration of action. There is little to choose between different opioids administered by patient-controlled analgesia. Parenterally-administered NSAIDs (e,g., ketorolac) contribute significantly to analgesia and reduce opioid requirements. Morphine may be the opioid of choice for epidural administration. The combination of epidural opioids and local anesthetics provides synergistic analgesia and appears to provide superior analgesia with activity. Several nonopioid receptor agonists are under investigation as neuraxial analgesics.

Anesthesia-based pain services are facilitating improvements in the quality of care of surgical patients by developing and directing institution-wide perioperative analgesia programs that include interdisciplinary collaborations. However, the impact of anesthesia-based pain services has not been evaluated in a systematic fashion. This prospective multisite study (n=23 hospitals) utilized a standardized approach to evaluate the quality of pain care provided to patients who were and who were not cared for by an anesthesia-based pain service. A total of 5837 patients were evaluated using a standardized survey that consisted of a medical record review and a patient interview. The data were collected as part of the hospitals' quality improvement activities. Forty-nine percent of the patients were cared for by an anesthesia-based pain service. Patients who received pain service care reported significantly lower pain intensity scores; had lower levels of pain in the postoperative period; had a lower incidence of pruritus, sedation, and nausea; and experienced significantly less pain than expected. In addition, these patients were more likely to receive patient education about postoperative pain management; were more satisfied with their postoperative pain management; and were discharged sooner from the hospital. The findings from this study demonstrate that the care provided by anesthesia-based pain services has a significant impact on patient outcomes.

Remifentanil is an ultrashort acting mu opioid, well suited to total intravenous (i.v.) anaesthesia. Pain immediately following emergence from anaesthesia is a potential problem because of the rapid offset. This study investigated the transition from remifentanil/propofol total intravenous anaesthesia to post-operative analgesia with epidural or patient controlled analgesia morphine in 22 patients undergoing major abdominal surgery. A remifentanil post-operative infusion initiated during emergence was titrated in the recovery room for 30 min, at which time 14% of patients had a pain score of 2 and 86% had pain scores of 0 or 1 (0 = no pain; 1 = mild pain; 2 = moderate pain; 3 = severe pain), at a mean infusion rate of 0.086 microgram kg-1 min-1. A smooth transition was then made to either epidural analgesia or patient controlled analgesia with morphine; pain scores were not significantly changed during the transition. Nausea occurred in 16 of the 22 patients, but only following administration of morphine. Epidural analgesia produced significantly lower pain scores on the surgical ward compared with patient controlled analgesia.

(Fitzgibbon) Acting Assistant Professor, Department of Anesthesiology, University of Washington, Seattle.(Rapp, Terman) Assistant Professor of Anesthesiology, University of Washington, Seattle.(Butler) Associate Professor of Anesthesiology, University of Washington, Seattle.(Dolack) Assistant Professor of Cardiology, University of Washington, Seattle.(DuPen) Pain Consultation Service, Department of Anesthesia, Swedish Hospital Medical Center, Seattle.(Ready) Professor of Anesthesiology; Director of Acute Pain Services, University of Washington, Seattle.Received from the Department of Anesthesiology, University of Washington, Seattle, Washington. Submitted for publication September 14, 1995. Accepted for publication November 28, 1995.Address reprint requests to Dr. Fitzgibbon: Department of Anesthesiology, Box 356540, University of Washington, 1959 NE Pacific Street, Seattle, Washington 98195.A small percentage of patients with cancer pain suffer from refractory pain despite aggressive therapy. [1]Intra-spinal administration of opioids and local anesthetic agents may be helpful in such settings, but their use may be limited by side effects such as motor block and hemodynamic instability. [2,3]Clonidine is a centrally acting alpha2-adrenergic agonist with established analgesic effects [4,5]and has synergistic effects with spinal opioids [6,7]and spinal local anesthetics. [8,9]Epidural clonidine produces analgesia by a spinal mechanism in patients after surgery and in those with cancer pain, [10]and it appears to be an effective treatment for severe cancer pain in patients for whom other treatments are ineffective. [11].Although the risk of acute withdrawal and rebound hypertension is well recognized with sudden cessation of systemically administered clonidine, [12]no such reports exist with regard to epidurally administered clonidine. We describe a case of acute withdrawal and rebound hypertension after abrupt cessation of epidural clonidine in a patient with intractable cancer pain.A 49-yr-old man was diagnosed with metastatic adenocarcinoma of the pancreas. The patient was normotensive and did not have a history of alcohol or other drug abuse. Despite chemotherapy with 5-fluorouracil and gencitabine, increased tumor growth resulted in complaints of upper abdominal pain radiating through to the back. Pain management was further complicated by complaints of diffuse abdominal pain and intermittent constipation associated with long-standing irritable bowel syndrome. Treatment with escalating doses of sustained-release and immediate-release morphine failed to control his pain and exacerbated his constipation. A neurolytic retrocrural celiac plexus block with 40 ml of 100% anhydrous alcohol produced only minimal relief of the pain. A temporary thoracic epidural catheter was inserted at the T8-T9 interspace, and a combination of 0.125% bupivacaine and 40 micro gram/ml morphine administered at 12 ml/h resulted in adequate pain control. One week later, a subcutaneously tunneled thoracic epidural catheter was inserted. The patient's pain was successfully managed at home with this regimen for 6 weeks. Because of complaints of increasing diffuse abdominal pain and postural hypotension, the patient was readmitted for evaluation and pain control. After epidurogram confirmation of catheter placement in the epidural space, incremental increases of both the bupivacaine and morphine concentrations failed to produce adequate pain control with unacceptable lower extremity motor impairment and postural hypotension. An epidural infusion of clonidine was added in a concentration of 10 micro gram/ml and commenced at 20 micro gram/h. This resulted in satisfactory pain control, enabling a rapid reduction in bupivacaine and morphine concentrations. Pain control was deemed adequate and postural hypotension eliminated with a combination of 0.1% bupivacaine and 50 micro gram/ml morphine at 12 ml/h and 10 micro gram/ml clonidine at 3 ml/h. After 2 weeks with this regimen, we noted progressive outward migration of the tunneled catheter. We decided to replace the catheter with a long-term implantable epidural device.Because of concerns for potential infection of the new device, before inserting it, we decided to remove the tunneled catheter and administer intravenous vancomycin for 24 h. The patient was given a hydromorphone patient-controlled analgesia device with a continuous infusion for pain control. In addition, a 0.2-mg clonidine transdermal patch was applied at the time of discontinuing the epidural infusion.Two hours after discontinuation of the epidural infusions, the patient was noted to be more agitated. A further 2 h later, he became progressively diaphoretic and tremulous. Blood pressure was increased from 140/80 to 220/110 mmHg, and heart rate was 170 beats/min. During this period, the patient complained of chest tightness. An electrocardiogram showed sinus tachycardia with new left bundle branch block. Nifedipine (10 mg) was given sublingually without significant effect on blood pressure control. A presumptive diagnosis of rebound hypertension after clonidine withdrawal was made when pain control was reported by the patient to be satisfactory. Five hours after the epidural infusions were discontinued, the patient received 0.1 mg oral clonidine. The patient was transferred to the intensive care unit for observation and blood pressure control. On arrival in intensive care unit, the patient's blood pressure and heart rate were 220/100 mmHg and 160 beats/min, respectively. In addition, the patient was noted to be profoundly agitated and profusely diaphoretic. A second dose of 0.1 mg oral clonidine was administered, and agitation was treated with small, intravenous incremental doses of midazolam to a total dose of 5 mg. Over the next 4 h, the blood pressure and heart rate gradually stabilized at 140/90 mmHg and 90 beats/min. The patient was discharged from the intensive care unit 14 h later with blood pressure stabilized at 140/80 mmHg and heart rate at 95 beats/min. A repeat electrocardiogram showed resolution of the left bundle branch block, and there were no new ST segment changes. Cardiac enzymes were normal. The clonidine transdermal patch was discontinued after the long-term epidural catheter was placed, and the patient recommenced epidural infusions of bupivacaine, morphine, and clonidine. The subsequent hospital course was uneventful, and the patient was discharged home with satisfactory pain control on a continuous epidural infusion of 0.1% bupivacaine and 40 micro gram/ml morphine at 12 ml/h and 10 micro gram/ml clonidine at 3 ml/h.The management of advanced cancer pain is sometimes difficult and may be improved by epidural infusion of varying combinations of local anesthetic, opioid, and clonidine. [11]Although epidural administration of clonidine is not approved by the Food and Drug Administration for long-term use in treating cancer pain, the drug may be used on a compassionate basis in individual cases. Approval for use was sought and obtained in this case. Clinical experience to date with intraspinal clonidine is largely based on postoperative analgesia studies, although Eisenach [11]reported on its long-term use in cancer pain. This and other clinical studies [13–15]suggest that intrathecal and epidural clonidine in combination with opioids is a suitable treatment for intractable cancer pain.The major side effects reported with the use of epidural clonidine are hypotension and sedation. [11]Clonidine decreases blood pressure after epidural administration by actions in the spinal cord [16]and brainstem [17]and in the periphery. [18]alpha2-Agonists decrease blood pressure by producing a "partial sympathectomy" as a result of direct inhibitory actions on preganglionic sympathetic neurons in the spinal cord. [16]Spread of the drug to the brainstem, by either rostral circulation in cerebrospinal fluid or systemic absorption, further diminishes sympathetic nervous system activity by actions at cardiovascular centers. [19–21]Sudden discontinuation of systemically administered clonidine may precipitate a withdrawal syndrome consisting of headache, apprehension, tremors, abdominal pain, sweating, and tachycardia, [12]accompanied or followed by a rapid rise in blood pressure. [22]The mechanism of rebound hypertension appears to involve an agonist-induced downregulation of normally sympatholytic alpha2receptors with resultant hyperresponsiveness of central noradrenergic pressor pathways after abrupt cessation of alpha2-agonist treatment. [23,24].To date, there are no reports of acute withdrawal or rebound hypertension associated with discontinuation of an epidural infusion of clonidine. It is unlikely that the hypertension observed in this case was attributable to discontinuation of the bupivacaine/morphine infusion because pain was adequately controlled at the time by the use of hydromorphone patient-controlled analgesia (boluses plus background infusion). Of interest in our case, acute withdrawal and rebound hypertension were observed within 4 h of stopping the epidural clonidine infusion. This is in direct contrast to the relatively delayed onset of 18–36 h of withdrawal commonly observed with cessation of systemic administration of the drug. We speculate that abrupt withdrawal of epidural clonidine resulted in a more rapid elimination of the drug from cerebrospinal fluid than systemically administered clonidine. This more rapid and earlier decline of cerebrospinal fluid drug level at both cardiovascular brainstem centers and at spinal cord preganglionic sympathetic neurons may account for the earlier withdrawal reaction and rebound hypertension observed with epidural clonidine discontinuation.Treatment recommendations for rebound hypertension and acute withdrawal after sudden cessation of oral or parenteral clonidine therapy include aggressive treatment of severe hypertension by intravenous bolus injection of phentolamine and reinstitution of oral clonidine therapy (0.1–0.2 mg followed by 0.1 mg hourly as needed up to a maximum of 0.5 mg). Clonidine therapy subsequently may be tapered over a number of days. [12,22]Although there are no guidelines for the management of similar problems with epidural use, the onset of oral clonidine may be too slow to adequately manage the withdrawal signs and symptoms, and intravenous administration of clonidine may be preferable. In our case, after initial blood pressure control, continuous monitoring of the electrocardiogram, close observation of blood pressure in the intensive care unit, and continued treatment of hypertension with oral clonidine until epidural therapy was reinstituted, proved satisfactory.Further research is required to investigate both the time when the problems of acute withdrawal and rebound hypertension become apparent on discontinuing therapy after continuous epidural infusion of clonidine and the most appropriate method to manage these problems. This case prompts the recommendation for cautious discontinuation and tapering of the clonidine dose if clonidine has been chronically administered.

(Fitzgibbon) Acting Assistant Professor, Department of Anesthesiology.(Glosten, Wright) Assistant Professor of Anesthesiology.(Ready) Fellow, Department of Radiology.(Tu) Professor of Anesthesiology; Director of Acute Pain Services.Received from the Departments of Anesthesiology and Radiology, University of Washington, Seattle, Washington. Submitted for publication March 24, 1995. Accepted for publication July 19, 1995.Address reprint requests to Dr. Fitzgibbon: Department of Anesthesiology, Box 356540, University of Washington, 1959 NE Pacific Street, Seattle, Washington 98195.PAIN after thoracotomy is one of the most intense clinical postoperative pain experiences known. Thoracic epidural local anesthetics are administered with the aim of eliminating or reducing pain by creating a circumscribed band of dense analgesia in the dermatomal region of the thoracotomy incision. Paraplegia is a rare complication of epidural anesthesia. Data relating to problems of paraplegia associated with epidural catheterization refer to lumbar, rather than thoracic, placement. A review of more than 750,000 epidural anesthetics estimated an incidence of 1:11,000 showing sustained neurologic deficits. Kane's review found three patients with permanent paralysis or paresis in a series of 50,000 epidural anesthetics. Of 32,718 cases, Dawkins reported an incidence of transient neurologic lesions of 0.1% and permanent lesions of 0.02%.We describe a case of delayed permanent paraplegia in a patient who underwent thoracic aneurysmectomy and received thoracic epidural local anesthetic postoperatively for pain control.A 74-yr-old man developed severe chest pain radiating through to his back while playing golf. He had a 4-yr history of hypertension and, 7 months previously, had undergone a repair of an infrarenal abdominal aortic aneurysm without complications. Thoracic computerized tomography at the admitting hospital revealed a 5-cm aneurysm extending from approximately the 6th to the 10th thoracic vertebral level. After treatment with meperidine and an infusion of nitroglycerin, his blood pressure was stabilized at 120 mmHg systolic down from 180 mmHg, and he was transferred to our institution. On admission, he was free of pain, had intact peripheral pulses with no murmurs or evidence of heart failure, and had no peripheral or carotid bruits. His blood pressure was controlled with infusions of sodium nitroprusside and esmolol, and, 3 days later, he was brought to the operating room for repair of his descending thoracic aortic aneurysm. The operation was uneventful. The patient was monitored using radial and femoral arterial catheters, pulmonary artery catheter, and transesophageal echocardiography. Mean arterial blood pressure and heart rate were controlled within 20% of baseline by adjusting depth of anesthesia and infusing nitroglycerin and esmolol as appropriate. After anticoagulation with 10,000U of heparin, partial left atriofemoral bypass was established. Distal aortic pressure was maintained at 55–85 mmHg. The aorta was cross clamped between the 4th and 11th thoracic vertebral levels for a total of 31 min, and a #28 Dacron graft (Hemashield, Meadox Medical, Oakland, NJ) was inserted. It was noted that there were "minimal intercostals present in the area excised with approximately five very small branches oversewn."Postoperatively, the patient was transferred to the intensive care unit, his trachea was intubated, his lungs were ventilated, and he was hemodynamically stable. Four hours after the procedure, the trachea was extubated and the patient was noted to be moving all four extremities. Intravenous analgesia was provided with a morphine patient-controlled analgesia device. Because of problems with pain control, inability to cough, and oxygen saturation in the mid-80s in spite of supplemental oxygen, the Pain Service was consulted regarding the possible use of a thoracic epidural for postoperative analgesia. At the time of consultation (8 h after surgery), the patient was deemed neurologically intact and had normal coagulation (platelet count, prothrombin time, partial thromboplastin time, and thromboelastography values were within normal limits). The patient's systolic blood pressure varied from 100 to 110 mmHg with heart rates varying between 70 and 76 beats/min. The patient was awake, conversant, and consented to the procedure. Under sterile conditions, a paramedian approach at T6/7 interspace with an #18-G Tuohy needle was chosen. Using loss of resistance to saline technique, the epidural space was identified at 5.5 cm and the catheter was placed 3 cm into the space. No paresthesiae were elicited during placement. With negative aspiration of blood and cerebrospinal fluid (CSF), a test dose of 3 ml of lidocaine 1% with epinephrine 1:200,000 was given. No alterations in heart rate or blood pressure were detected. Five minutes after injection of the test dose, there was no evidence of motor or sensory block. Fifteen minutes after the test dose, a further 5 ml lidocaine 1% with epinephrine 1:200,000 was injected. Over the next 15 min, the patient reported a diminution in pain. A sensory block to pinprick from T4to T11was demonstrated. Systolic blood pressure and heart rate remained unchanged. Forty minutes after injection of local anesthetic, the patient reported onset of bilateral lower extremity warmth and heaviness. On examination, the patient demonstrated profound bilateral motor paresis in the lower extremities, with an upper sensory level of anesthesia to pinprick to T5bilaterally. Blood pressure and heart rate were unchanged from preblock values. We were concerned that the injection of lidocaine had been intrathecal and elected to observe the patient and to retest the catheter once the block had resolved. Ninety minutes after institution of the block, the patient became hemodynamically unstable on turning (systolic blood pressure 73 mmHg and heart rate 45 beats/min). Lower extremity paresis persisted with an unchanged upper sensory level at T5bilaterally. Because of concerns of an epidural hematoma or spinal cord ischemia, neurology and neurosurgical opinions were sought. Six hours after institution of the block, a thoracic magnetic resonance imaging (MRI) study was ordered. This study demonstrated normal thoracic cord and CSF signal characteristics on T-1 sequences. No definite explanation for persistent paresis was determined by this study, but direct cord trauma as a result of epidural placement could not be excluded. On T-2 sequences, the heterogenous signal within the CSF around the cord represents hemorrhage without evidence of cord compression (Figure 1). Location of the epidural catheter tip could not be determined because of movement artifact. Twenty-four hours after epidural placement and with the neurologic status unchanged, the MRI was repeated. This study clearly showed development of markedly abnormal high T-2 cord signal to the T10level at which normal low cord signal is maintained, and was most indicative of spinal cord ischemic change (Figure 2). There was no evidence of epidural hematoma nor direct cord trauma.Five months after the procedure, there is no sensation below the T5dermatome level, and the patient has a neurogenic bowel and bladder and has no movement in the lower extremities.The etiology of paraplegia in this case is spinal cord ischemia as demonstrated by MRI (F2-28). The cause of ischemia is interruption of spinal cord blood flow. The relative contribution of the surgical and anesthetic techniques is unknown. Possible contributory factors are considered.Ischemic damage to the spinal cord can occur after repair of a descending thoracic aneurysm. The spinal cord is supplied by one anterior spinal artery and two posterior spinal arteries. The anterior spinal artery relies on reinforcement of its blood supply by six to eight medullary arteries, the most important and largest of which is the artery of Adamkiewicz. Multiple levels of the cord do not receive feeding medullary branches, thus leaving watershed areas that are particularly susceptible to ischemic injury. The tenuous collateral anastomosis of the anterior spinal artery in the mid-thoracic region places segments of the spinal cord in jeopardy during aortic occlusion or hypotension. Damage may result from either actual surgical dissection of the artery of Adamkiewicz (because the origin is unknown) or exclusion of the origin of the artery by cross clamps (usually applied between T5and L1). Cross clamping of the proximal descending aorta interrupts the blood supply to the area supplied by the aortic segment distal to the clamp. In dogs, clamping the thoracic aorta distal to the left subclavian artery produces a 94% decrease in spinal cord blood flow. The likelihood of postoperative paraplegia rises significantly if the duration of cross clamping exceeds 30 min. .The overall incidence of paraplegia after descending and thoracoabdominal aneurysmectomy varies between 5 and 21%, with the highest incidence noted in patients with extensive thoracoabdominal disease. Crawford et al. reported neurologic deficits in a series of 198 patients undergoing descending thoracic or thoracoabdominal aneurysm repair. Postoperative deficits were defined as immediate if present at the time of recovery from anesthesia and delayed if they occurred subsequently. Fifteen patients (12 paraplegia and 3 paraparesis) had evidence of immediate deficits. Twenty patients (9 paraplegia and 11 paraparesis) had delayed deficits. These delayed deficits were first seen at times varying from 12 h to 21 days. In most cases, a precipitating cause was not identified, although some instances of delayed neurologic deficits were noted in association with complications that caused a reduction in blood flow. Delayed deficits were considered to be caused by factors that amplified subclinical ischemic states that had occurred intraoperatively (myocardial infarction or hypotension), as well as underlying atherosclerotic vascular disease. Delayed paraplegia occurring with postoperative hypotension may be seen in patients who have marginally adequate collateral circulation and who have had the artery of Adamkiewicz resected. Animal studies implicate temporary cord ischemic times of 21 min as a significant contributor to delayed-onset paraplegia occurring between 14 and 48 h after occlusion. Our patient had several risk factors for spinal cord ischemia: extensive thoracoabdominal aneurysmal disease as evidenced by two aneurysmal repairs, and an ischemic cross-clamp time of significant duration (31 min).Possible factors associated with epidural block that may contribute to a neurologic deficit include direct trauma (needle/catheter), infection, hematoma, neurotoxic reaction to injected agent, and ischemia (interruption of cord blood flow by hypotension, local anesthetic, epinephrine, spasm of spinal arteries, or a pressure effect from volume of epidural injectate). Although definite assessment of catheter tip placement could not be made because of movement artifact, direct cord trauma, abscess, and hematoma formation were excluded by MRI in this case.Magnetic resonance imaging is the imaging modality of choice to demonstrate subtle intrinsic spinal cord abnormalities. The typical MRI findings of spinal cord infarction should be assessed in the appropriate clinical setting, i.e., postthoracoabdominal aneurysm repair, because similar imaging findings may also be found with cord tumor and demyelinating disease. The evolution of hemorrhage and edema in an ischemic cord is responsible for the T-2 prolongation of signal. The markedly abnormal high T-2 cord signal, extending from the 4th to the 10th thoracic level at which normal low cord signal is maintained, is most indicative of cord ischemic changes (F2-28). Although the MRI does not indicate a possible etiology for the observed ischemic changes, the large signal abnormality accounts more for a vascular abnormality than for focal (direct cord) trauma. The extensive area of cord infarcted implicates a widespread devascularization process. Some blood was observed within the subarachnoid space at 6 h (F1-28), which persisted at 24 h, although epidural fluid collections or cord compression were not identified (F1-28and F2-28). The presence of subarachnoid blood may indicate an element of indirect trauma during catheter placement, although the frequency of this occurrence during thoracic epidural catheter placement is undefined. The possibility of blood in the subarachnoid space contributing to spinal artery spasm must be considered. Although data on the effects of blood in the thoracic subarachnoid space on spinal cord blood flow are lacking, there is ample evidence that the presence of subarachnoid blood in the basal cisterns is the cause of cerebral vasospasm after an intracranial subarachnoid hemorrhage, but only after several days have elapsed. .A direct neurotoxic effect on the spinal cord from the lidocaine used appears unlikely. Although high concentrations of lidocaine have proved to be neurotoxic in rabbits, clinically relevant concentrations do not cause neurologic damage. Local anesthetic agents and epinephrine may affect spinal cord blood flow. However, it is unknown whether local anesthetics or vasoconstrictors administered for epidural block directly or indirectly affect spinal cord blood flow in humans. Given the doses of lidocaine and epinephrine used in this case, and the conflicting reports in animal studies, it is unlikely that these agents had a direct effect on spinal cord blood flow.An epidural block may indirectly affect spinal cord blood flow as a result of changes in epidural pressure being transmitted across the dural membrane. A number of clinical reports implicate alterations in CSF dynamics and blood flow after epidural injections. Shah demonstrated that small fluid volumes injected into the lumbar epidural space produced a mean pressure increase of 14 cm H2O in pregnant women. Thomas has shown a differential pressure increase in the epidural space with different volumes injected. Pressures returned to baseline 3 min after a 2-ml injection, while pressures remained elevated after 3 min after a 6-ml injection. Similarly, Paul demonstrated a differential pressure increase with the injection of 10 and 15 ml within the lumbar epidural space. Clinical data is lacking directly correlating a reduction in spinal cord blood flow with increases in epidural pressure secondary to an increase in epidural volume. In addition, it is unknown if autoregulation of spinal cord blood flow is affected in humans during epidural anesthesia.In conclusion, in the case reported here, persistent motor block and lack of recovery from spinal or epidural block prompted aggressive evaluation. The cause of paraplegia in this case was spinal cord infarction. The factors contributing to paraplegia are unlikely to be determined with certainty. The surgical procedures (descending thoracic and abdominal aneurysm repairs) probably contributed by mechanisms of spinal cord devascularization and application of a thoracic cross clamp. The role of the epidural anesthesia in this case in contributing to paraplegia is unknown. Forty minutes after institution of what initially appeared to be a typical segmental thoracic epidural block, the patient developed a neurologic deficit that essentially has remained unchanged. Scientific evidence directly implicating the epidural anesthesia is lacking. A contributory effect to cord ischemia by the volume/pressure effect of the epidural injectate or spasm of the radicular spinal arteries by thoracic subarachnoid blood are theoretically possible. Even with careful technique, invasive hemodynamic monitoring, and early evaluation of neurologic status, our patient experienced irreversible spinal cord ischemia that resulted in permanent paraplegia. It is important to remember that, in a significant number of patients undergoing thoracic aortic aneurysm repair, paraplegia develops that may present at varying periods postoperatively. A high-risk subcategory may be identified (extensive thoracoabdominal disease or prolonged cross-clamp time) and, in such patients, the possibility of variable, unexpected onset of paraplegia should be considered when selecting a method for postoperative pain relief.

The patient with a history of current opioid consumption presenting in the acute postoperative setting presents a challenge for pain management. Standard treatment dosages and strategies are often ineffective in providing pain relief. This retrospective case-control study reviews 4 years' experience of the Acute Pain Service (APS) at our institution providing care for 202 chronic pain and opioid-consuming (CPOC) patients, 6.6% of 3058 patients undergoing urologic, gynecologic, orthopedic and general surgical procedures. Controls matched for age, gender, date and type of surgery, and postoperative pain relief modality were found for 180 (89%) of these patients. Patients were provided patient-controlled analgesia (PCA), or epidural opioid analgesia (EOA with boluses of preservative-free morphine or bupivacaine (1:16% + 2 μg/ml fentanyl (B/F)). Records were reviewed for patient demographics, diagnoses, surgical procedures, pre-operative opioid use, days-on-service, analgesic requirement, pain scores and incidence of moderate/severe side effects. Patient demographics were similar between CPOC and control groups. When considering PCA alone, mean 24-h usage in controls was 42.8 (32.0) mg morphine (MS) equivalents differing significantly from CPOC patients' use of 135.8 (68.5) mg MS equivalents (P = 0.0001). EOA and B/F case studies showed similar results. Moderate sedation was experienced by 50% of CPOC patients receiving PCA. Differences in opioid usage, side effects, pain scores, sedation and prescribed treatment with anxiolytics were shown between CPOC patients and matched controls. Treatment implications suggested by the data include: (1) PCA use by the patient with prior opioid consumption can be expected to be significantly increased beyond mere replacement; (2) pain scores will be higher in patients with prior opioid exposure; and (3) pruritic and emetic symptoms are less likely to be experienced by patients with prior opioid use.

Objective The provision of acute pain management for the chronic pain patient can pose a challenge. We sought to characterize management issues. Subjects/setting: An anonymous survey was distributed to 270 physicians and 212 nurses at University of Washington Medical Center (UWMC) in an attempt to characterize management issues. Design Caregivers were queried regarding treatment modalities, efficacy of anxiolysis, patient attributes, concern of the quantity of medication, criteria for patient evaluation, and other management issues. Results Of the respondents, 61.8% were physicians, and 38.2% were nurses. The mean duration in practice was 7.7 years. The responses from the two groups were similar. Seventy-five percent reported using different pain-evaluation techniques for chronic pain patients than those utilized for the “average” patient. Pain scores were used frequently in the average patient, whereas ability to perform activities was used more commonly in the chronic pain patient (p < 0.0001). Half of the respondents expressed concern regarding the amount of medication used and level of sedation. The same proportion found anxiolysis to be a helpful adjunct. The use of a time-contingent “pain cocktail” as an oral medication was a useful strategy for 88% of respondents. The least labor-intensive modality reported was patient-controlled analgesia (PCA) for 84.5% of respondents; intravenous opiate fusion, 5.3%; and epidural analgesia, 11.2%. Conclusions The survey describes caregiver concerns regarding this patient population, including medication use, sedation, length of hospital stay, and evaluation techniques.

Sound approaches to acute pain treatment must include appropriate assessment. There are a number of instruments that can be used at the bedside to evaluate pain and thereby gauge the success or failure of a particular treatment plan. These include subjective reports from patients, both qualitative and quantitative, as well as objective observations by the pain therapist, including the effect of therapy on important functions such as the ability to breathe deeply, cough, move in bed, or ambulate. Additional insight can be gained by asking the simple question: “Are you satisfied with the treatment of your pain?” It is important that any measurement scale be applied both before and after treatment so that the effects of treatment (success or failure) can be measured.

It is the obligation of all health care professionals to provide patients with effective relief of pain. In addition to basic humanitarian reasons, a growing number of reports are demonstrating that effective pain relief is associated with a reduced risk of certain postoperative complications, earlier mobilization, shortened hospital stay, and reduced costs. Regrettably, an examination of both older and more recent studies shows that major deficits have existed and still persist in this area of care.

This review discusses the inadequacies of postoperative pain management in the UK and recommendations to improve its quality. Advanced pain-relieving techniques are available; in this article we discuss the practical considerations of delivering these successfully to patients through the introduction of acute pain teams, and especially through extension of the nurses' role.

OBJECTIVE:The provision of acute pain management for the chronic pain patient can pose a challenge. We sought to characterize management issues.SUBJECTS/SETTING:An anonymous survey was distributed to 270 physicians and 212 nurses at University of Washington Medical Center (UWMC) in an attempt to characterize management issues.DESIGN:Caregivers were queried regarding treatment modalities, efficacy of anxiolysis, patient attributes, concern of the quantity of medication, criteria for patient evaluation, and other management issues.RESULTS:Of the respondents, 61.8% were physicians, and 38.2% were nurses. The mean duration in practice was 7.7 years. The responses from the two groups were similar. Seventy-five percent reported using different pain-evaluation techniques for chronic pain patients than those utilized for the "average" patient. Pain scores were used frequently in the average patient, whereas ability to perform activities was used more commonly in the chronic pain patient (p < 0.0001). Half of the respondents expressed concern regarding the amount of medication used and level of sedation. The same proportion found anxiolysis to be a helpful adjunct. The use of a time-contingent "pain cocktail" as an oral medication was a useful strategy for 88% of respondents. The least labor-intensive modality reported was patient-controlled analgesia (PCA) for 84.5% of respondents; intravenous opiate fusion, 5.3%; and epidural analgesia, 11.2%.CONCLUSIONS:The survey describes caregiver concerns regarding this patient population, including medication use, sedation, length of hospital stay, and evaluation techniques.

The optimal care of surgical patients includes effective control of incisional pain. Despite advances in knowledge of pathophysiology, pharmacology of analgesics, and the development of more effective techniques for postoperative pain control, many patients do not receive adequate analgesia. The reasons for inadequate treatment are many. These include deficiencies in knowledge and skills on the parts of health care providers, patients, and those responsible for the management of health care systems, including governmental agencies. It has only recently been recognized that there are wide variations from patient to patient in the amount of pain that is experienced in response to a particular insult. There are also great differences in responsiveness to particular therapeutic approaches.

BACKGROUND:Ketorolac is a nonsteroidal analgesic that may provide postoperative analgesia without opioid-related side effects. This double-blind, randomized, multicenter study evaluated the analgesic efficacy and safety of intravenous ketorolac in 207 patients during the first 24 h after major surgery.METHODS:Subjects were assigned to receive one of three analgesic regimens: a ketorolac infusion, ketorolac boluses, or placebo. All subjects had access to intravenous morphine via patient-controlled analgesia (PCA). Evaluations included PCA morphine used, pain assessment (categorical pain intensity scores and visual analogue pain scores), pain relief (categorical pain relief scores), sedation, presence of adverse events, and overall rating of regimens by study observers and patients.RESULTS:Patients in the ketorolac infusion group (but not the ketorolac bolus group) used less morphine (average 33 mg) than did the placebo group (44 mg) (P = 0.009). Significant differences favoring both ketorolac groups were seen in the pain intensity and the categorical pain relief scores at various time points during the study. At the termination of the study, compared with the placebo group, categorical pain intensity scores were lower in the ketorolac bolus group; visual analogue pain scores were lower in both ketorolac groups; and pain relief scores were higher in the ketorolac bolus group. The incidence of vomiting was significantly greater in the placebo group (27%) than in the ketorolac infusion group (12%) or bolus group (9%) (P = 0.032 and P = 0.005, respectively). The incidence of postoperative fever was 10% in the ketorolac bolus group and 25% in the placebo group (P = 0.013). Study observers noted less nursing difficulty while caring for patients in the ketorolac infusion group (P = 0.015). Study observers and patients in both ketorolac groups reported statistically significant overall drug superiority compared with placebo.CONCLUSIONS:It is concluded that intravenous boluses or infusions of ketorolac in conjunction with PCA morphine provide effective, safe analgesia after major surgery and improve on the response to PCA morphine alone.