SummaryA fully automatic instrument for the determination of electrophoretic mobility of colloidal particles was applied to human platelets. A significant increase in platelet electrophoretic mobility was observed one day after a laparotomy. This suggests that a selective consumption of platelets with smaller surface negative charge may occur during postoperative hemostatic plug formation or under surgical stress. In addition, the difference in electrophoretic mobility observed between males and females suggests an effect of estrogen on platelets.
8533 Background: Lidocaine, a local anesthetic, is often used as an anti-arrhythmic and as an analgesic of best support care (BSC) for patients with neuropathic pain. However, little is known about the effect of low-dose lidocaine on the abdominal pain of terminally-ill patients with peritoneal carcinomatosis. Aim: To evaluate whether visceral pain is controlled and activities of daily life (ADL) are improved during continuous lidocaine infusion. Methods: 28 terminally ill patients with peritoneal carcinomatosis due to the gastrointestinal (26) and gynecologic (2) cancers were studied. Despite aggressive pain management with opiates, non-steroidal anti-inflammatory drugs and other adjuvants, debilitating pain persisted. After a test dose of 2mg/kg intravenously, lidocaine was administered at low-doses (0.4 and/or 0.8mg/kg-h) through a vein and continued for more than 24 hours. Pain was quantitated on a faces rating scale from the level 0 (no pain) to 5 (severe pain); doses of opiates, amounts of oral intake, side effects, and ADL were measured before and after lidocaine. Results: Age (mean±SE) was 62±2, and percentage of males was 54%. Patients were not hypercalcemia but were slightly malnutrished (albumin 2.9±0.1g/dl) and anemic (hemoglobin 10.3±0.4g/dl). The duration of lidocaine administration in hospital was 18±3days. Abdominal symptoms improved within 1.2±0.1days after beginning lidocaine, and pain scale decreased from 2.7±0.2 to 0.6±0.2; p<0.001. In 68% of patients, the pain level became zero. Blood concentration of lidocaine at 0.8mg/kg-h was 3.0±0.4μg/ml 1 week later. 68% of patients needed no increase in opiate dosage during lidocaine administration. Waist size did not decrease, however, oral intake increased (p=0.002) during lidocaine administration. No obvious side effects, such as perioral numbness, were seen except for emotional lability noted in 4 patients. 43% patients were able to be discharged for continued end-of-life comfort care with home parenteral nutrition and continuation of lidocaine administration. Conclusions: We suggest that continuous, low-dose intravenous lidocaine is BSC and is a very effective approach for analgesia and improvement of ADL in patients with peritoneal carcinomatosis. No significant financial relationships to disclose.
9031 Background: Our team reported at the 42nd ASCO meeting that continuous, low-dose intravenous (IV) lidocaine is an effective method for pain relief in terminal patients with peritoneal carcinomatosis. Our aim was to explore the mechanism by which abdominal pain of terminally-ill patients with peritoneal carcinomatosis was improved by continuous IV lidocaine. Methods: 48 patients with peritoneal carcinomatosis due to GI (46) and GYN (2) malignancies were administered lidocaine at low-doses (0.4 and/or 0.8mg/kg- h) for >24 hours, because opiates, NSAIDs, and other adjuvants were ineffective in relieving their abdominal pain. Pain (faces rating scale; 0-no pain, 5-worst pain), oral intake, side effects, and activities of daily life were quantified. Two days after beginning lidocaine, ascites was sampled to measure ascitic concentration of lidocaine, tumor markers and cytology. Results: Mean age (±SE) was 60±2. The volume of ascites was estimated to be 2,700±400ml by the ultrasound 5 points methodology. Abdominal symptoms improved in 1.5±0.2days after beginning lidocaine, and the pain scale decreased from 1.9±0.2 to 0.5±0.1; p<0.001; 75% of patients had improvement in pain of whom 78% had complete relief of pain. Oral intake increased from 18% to 49% of baseline (p<0.001), and 67% in those with improvement in pain had an increased volume of oral intake. There were no obvious differences in response to 0.4 and 0.8 mg/kg-h in patients receiving both doses. Serum concentrations of lidocaine at 0.4 and 0.8 mg/kg-h were 1.7±0.2 and 3.2±0.2 μg/ml, respectively; lidocaine concentrations in the ascites were 1.2±0.2 and 2.1±0.2 μg/ml. No patient complained of pain at the time of peritoneal puncture. Side effects included bradycardia of <60 beats per minutes (3 patients). The duration of lidocaine administration was 23±3 days; 43% of patients were able to be discharged home for end-of-life care, with parenteral nutrition and continuation of lidocaine administration or oral mexiletine (300–450 mg/day) for adjuvant analgesia. Conclusions: Lidocaine diffuses into ascites and almost equilibrates with serum concentrations acting as a peritoneal anesthesia which, as a result, controls abdominal pain in patients with peritoneal carcinomatosis. No significant financial relationships to disclose.
Fourteen VE deficient rats (VEDR) and 12VE supplemented rats (VESR) were injected with sodium arachidonate 3mg/kg into the central vein in 30 sec. VEDR developed acute respiratory distress and 11 out of 14 VEDR (79%) died shortly after the injection. All of these rats demonstrated obstruction of capillaries, arterioles and small pulmonary arteries by platelet aggregates.On the other hand, VESR developed much attenuated respiratory insufficiency and only 2 out of 12 (17%) died. In 25 pairs of VEDR and VESR citrated blood was examined for platelet functions and determination of MDA formation.The aorta was quickly removed and lipid peroxides content (MDA) and PGI2 production were measured.VEDR demonstrated increases in platelet count and aggregability as compared with VESR. Platelet 14C-serotonin release and ATP content were not different between VEDR and VESR. ADP content was decreased in VEDR. Lipid peroxides (MDA) in platelets, plasma and the aorta were significantly increased in VEDR. PGI2-like activity released from the aorta was not different between the two. The pronounced respiratory distress, high mortality rate and pulmonary embolism with platelet aggregates in VEDR might be attributed to the increase in platelet number and aggregability which is probably due to an increase in platelet prostaglandin metabolism.
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