No abstract

No abstract

The variety of possible presentations of myocardial infarction is well known, but chest pain is perhaps the most constant of symptoms. Evidence has linked duration of pain with size of infarct,' and Mitchell suggested that analgesic requirements should be used as an early guide to whether infarction has taken place.' I carried out a study to evaluate the diagnostic potential of analgesic requirements. Patients, methods, and resultsAltogether, 217 consecutive admissions to the coronary care unit were considered for study. Reasons for exclusion (97 patients) included rapid death, muscular trauma, and chest pain apparently not due to myocardial ischaemia. Analgesia was given as intravenous diamorphine, usually after a trial of glyceryl trinitrate 0-5-1-0 mg sublingually.Infarction was assumed (80 patients) if the criteria of Rowley and Hampton for definite or probable myocardial infarction were fulfilled.3 The remaining patients were assumed not to have had myocardial infarction, and 40 were included in the study. Infarct size was estimated by plasma creatine kinase activity (highest of four estimations in three days), hydroxybutyrate dehydrogenase activity (highest of three estimations), and the number of electrocardiographic territories (inferior, anterior, lateral, posterior, or The time after admission of the final injection was the most useful variable: only one (250°,,) of the group without myocardial infarction required analgesia after two hours compared with half of the group with infarction. Values in patients with equivocal electrocardiographic changes and in the one or two territory groups were 5-7, 7-6, and 13-3 hours respectively; the correlation with creatine kinase activity was r= 0 40 (p < 0 001). CommentThe results of this study were consistent with a relation between severity of myocardial infarction and amount of analgesia required in the first hospital day. One fifth of the patients with myocardial infarction, however, did not need any analgesia at all, and one patient without myocardial infarction required 20 mg diamnorphine. Moreover, there seems little clinical advantage in attempting to guess the size of myocardial infarction after only 24 hours. In the early decision of whether infarction has taken place analgesic requirements may be of greater value. This study suggests that if a second injection of analgesia is required in the first 24 hours the chances of myocardial infarction being excluded lengthen to one in eight and myocardial infarction is four times more likely. If three or more injections are needed myocardial infarction is 10 times more likely. If a second injection is required more than three hours after admission exclusion of myocardial infarction becomes a 40 to one chance and infarction is 20 times more likely. Thus if this three hour rule was applied it would indicate infarction with a specificity of 97 5%, and a similar predictive value. A negative result is less reliable, the sensitivity being 50%/ These results confirm that analgesic requirement can be related to the s...

One hundred hospital in-patients treated for pulmonary embolism (PE) and/or deep vein thrombosis (DVT) were randomly allocated to receive 3 or 6 weeks' anticoagulation with heparin and warfarin. At one year recurrence rates were 12% in the 6 week group and 10% in those treated for 3 weeks. No patient died as a result of recurrence. Our study suggests that 3 weeks' anticoagulation therapy, using intravenous heparin for the first 5 days and warfarin from the third day, is adequate for patients without persisting risk factors.

1 In 55 patients in whom warfarin control had been satisfactory for at least 4 months, warfarin dose, plasma warfarin concentration and plasma clearance were measured. 2 The mean dose to maintain the BCR (INR) between 2.3 and 3.3 was 5.1 + 2 mg dayt1 (range 1.5-10 mg). Plasma warfarin concentrations and warfarin clearance were lognormally distributed with 95% confidence limits between 0.8 and 2.4 mg 17' and 2.5 and 8.71 day-1 respectively. These confidence limits were used to construct algorithms which correctly predicted the cause of abnormal warfarin sensitivity in two patients and resistance in two further patients. 3 These algorithms should help to identify the cause of abnormal warfarin responsiveness in the clinical setting.

No abstract

191 pyrexia. This abated over 48 hours of treatment, which included tobramycin, and repeat endoscopic retrograde cholangiography showed a biliary tree free of stones. She made an uneventful recovery, and subsequently eight consecutive stool samples over a period of three months showed clearance of the salmonella. CommentThis patient was a chronic carrier of S eastbourne despite a cholecystectomy 18 years previously. This appeared to be resistant to appropriate antibiotics until a common bile duct stone was removed. Salmonella carriage was probably perpetuated by biliary stasis analogous to that caused by a stone filled gall bladder.

SummaryReversal of the anticoagulant effect of warfarin in patients with no active haemorrhage can be achieved by administration of intravenous vitamin K1. Currently recommended doses of intravenous vitamin K1, for this purpose often result in subsequent difficulties in anticoagulation. We observed the response to low dose intravenous vitamin K1 in patients requiring reversal of anticoagulant therapy. Ten consecutive patients received L mg and 2l further patients received 0.5 mg of intravenous vitamin K1. In 50% of the patients who received 1 mg of vitamin K1 the INR (International Normalised Ratio) fell below 2 at 24 h whereas in patients who received 0.5 mg the INR fell below 5.5 in all subjects after 24 h and in none did it fall below 2.0. No patient had any thrombotic or haemorrhagic complications and no difficulty was encountered in re-establishing anticoagulant control after 24 h. We recommend 0.5 mg of vitamin K1 as an effective and convenient method of predictable and fine control of oral anticoagulant therapy.