Graduated compression stockings can reduce the incidence of deep vein thrombosis by 60 per cent1, by providing a decreasing compression gradient from the ankle towards the thigh. There is both theoretical and clinical evidence that compression of the thigh as well as the calf does not give extra benefit2,3. Although regarded as safe, improperly used stockings are not without risk. Problems are usually due to areas of localized high pressure, especially under ‘rucked up’ constricting bands of stocking. This is particularly so in the presence of ischaemia; manufacturers state that ischaemia is a contraindication to stocking use. Cases of arterial thrombosis have been reported4, as well as more frequent skin necrosis, when stockings have been used in the presence of reduced arterial blood supply5.
Summary
A double‐blind, randomised, placebo‐controlled study was performed to assess the antiemetic efficacy of ondansetron in women receiving morphine from a patient‐controlled analgesia system after total abdominal hysterectomy. Sixty‐six ASA grade 1 or 2 patients scheduled for total abdominal hysterectomy were randomly allocated into one of two groups. All patients received a standardised anaesthetic and postoperative patient‐controlled analgesia regimen. Group 1 received ondansetron 4 mg at induction of anaesthesia, repeated 8 h later. Group 2 received saline as a placebo at the same times. Pain scores, nausea scores, episodes of vomiting, use of rescue antiemetics and recollection of nausea and vomiting were not different between the groups. Only 15% of patients who received ondansetron and 30% of patients who received the placebo recorded no nausea or vomiting in the first 24 h. We conclude that ondansetron, in the dose studied, does not reduce nausea and vomiting in women receiving morphine from a patient‐controlled analgesia system after total abdominal hysterectomy.
Summary
We describe a patient with unexpected spina bifida who underwent spinal anaesthesia for trans‐urethral resection of prostate and developed serious neurological signs. An unexpected spinal tumour was removed two weeks later. This report demonstrates that not all neurological problems associated with spinal anaesthesia should be blamed on the technique.
anaphylactoid reactions to a polypeptidal plasma substitute by H, plus H,-receptor antagonists; synopsis of three randomised controlled trials. Klinische Wochenschrift 1982; 60: .
Epidural analgesia and hypotensionDrs Shorten and Furness (Anaesthesia 1990; 45: 169) described severe hypotension caused by bladder distension in a 72-year-old diabetic man with autonomic dysfunction. The patient had had a crossover femoropopliteal graft inserted under spinal anaesthesia. A recent experience suggests this problem may not be confined to elderly diabetics.A 28-year-old primiparous patient in labour requested an epidural for pain relief. Her circulation was preloaded with 500 ml compound sodium lactate solution, and an epidural catheter was inserted in the L2-3 interspace. A test dose of 3 ml 0.5% bupivacaine was followed by 10 ml of 0.25% bupivacaine 10 minutes later, which produced complete analgesia. A second 50 ml bag of compound sodium lactate solution was started, to run over 6 hours and an infusion of syntocinon was also commenced. Twenty minutes after the epidural was inserted an infusion of 0.25% bupivacaine was started at a rate of 5 ml/hour. Her arterial blood pressure was monitored every 5 minutes for the first half hour and quarter hourly after that. One and a quarter hours after the epidural was inserted her blood pressure was found to have decreased from 100/60 mmHg to 75/50 mmHg. She was lying on her left side, the epidural block was at the level of TI, bilaterally with minimal motor blockade, and it was still providing complete analgesia. She was given a further 500ml of compound sodium lactate solution and a total of 30 mg of ephedrine in 6-mg increments, which increased her blood pressure to 95/50 mmHg.Further examination revealed her to have a distended bladder; a catheter was inserted and 1100 ml of urine was drained. Following this her arterial pressure increased to 115/60 mmHg. She remained stable over the next 4 hours until her blood pressure was again found to be decreasing, initially to 90/60 mmHg, then to 80/60 mmHg. Again she was on her side with a block to T,o. A urinary catheter was inserted and 600ml urine drained. Her blood pressure increased to 105/60 mmHg without any other treatment. A live baby boy was delivered 2.5 hours later. The rapid resolution of the hypotension on both occasions following drainage of the bladder implicates bladder distension as a major contributory factor. The degree of hypotension and its resistance to treatment was not in keeping with the level of the epidural blockade. In conclusion, drawing on this experience and the experience of Shorten et al., bladder distension can cause significant hypotension in patients undergoing both spinal and epidural anaesthesia, and this easily remediable cause should be borne in mind particularly when the degree of hypotension is not in keeping with the level of the block.
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