patients presenting to hospital (18 per 100 000) or at necropsy (376 per 100 000). Our studies show that these patterns are likely to be related to the diminished (and frequently absent) sensation of acid infusion in the oesophagus in patients with Barrett’s oesophagus.9 Perhaps symptomatic treatment of reflux oesophagitis turns down the flame but does not put out the fire. Department of Surgery, University of Sydney, Royal North Shore Hospital, Sydney NSW 2065, Australia

transfusion requirements despite scrupulous surgical technique.5,6 Pharmacological control of blood loss after surgery failed, apart from aprotinin, but the safety of this drug in routine coronary surgery has not been proven.7 Furthermore, the cost of one unit of blood is about 40.00, whereas that of the autotransfusion system is about the same as that of a standard drainage system. Risk of infection on the basis of our study and that of others8 is slight. Cardiothoracic Unit,


study of the quality and duration of survival following resection, endoscopic intubation and surgical intubation in oesophageal carcinoma. Br J Surg 1982; 69: 585-88. 2. Hesketh PJ, Clapp RW, Doos WG, Spechler SJ. The increasing frequency of adenocarcinoma of the oesophagus. Cancer 1989; 64: 526-30. 3. Alpern D, Buell C, Olson J. Increasing percentage of adenocarcinoma in primary carcinoma of the esophagus. Am J Gastroenterol 1989; 84: 574. 4. Watson A. Pathologic changes affecting survival in esophageal cancer. In: Delarue NC, Wilkins EW, Wong J, eds. International trends in general thoracic surgery. St Louis. Mosby, 1988: 90-97. 5. Attwood SEA, DeMeester TR, Brenner CG, Barlow AP, Hinder RA. Alkaline gastroesophageal reflux: implications in the development of complications in Barrett’s columnar-lined lower oesophagus. Surgery 1989; 4: 764-70. 6. Flook D, Stoddard CJ. Gastrooesophageal reflux and oesophagitis before and after vagotomy for duodenal ulcer. Br J Surg 1985; 72: 804-07. 7. Saltzman M, Barwick K, McCallum RW. Progression of cimetidine-treated reflux oesophagitis to a Barrett’s stricture. Dig Dis Sci 1982; 27: 181-86. 8. Cameron AJ, Zinmeister AR, Ballard DJ, Carney JA. A population based study of Barrett’s oesophagus: comparison of clinically diagnosed prevalence versus autopsy determined prevalence. Gastroenterology 1988; 94: A57. 9. Ball CS, Watson A. Acid sensitivity in reflux oesophagitis with or without complications. Gut 1988; 29: 729. 1. Watson A. A

Groby Road Hospital, Leicester LE3 9QE, UK

An improved technique for autotransfusion of shed mediastinal blood. Ann Thorac Surg 1985; 40: 519-20. 2. Joyce MH, McGrath LB. A method for the reinfusion of shed mediastinal blood in cardiac surgery. J Cardiac Surg 1990; 4: 315-17. 3. Sethi KG, Copeland JG, Goldman S, Montz T, Zadina K, Henderson WG. Implications of postoperative administration of aspirin in patients undergoing coronary artery bypass grafting J Am Coll Cardiol 1990; 15: 15-20. 4. Taggart DP, Siddiqui A, Wheatley DJ. Low-dose preoperative aspirin therapy, postoperative blood loss, and transfusion requirements. Ann Thorac Surg 1990; 50: 924-28. 5. Cosgrove DM, Lytle BW, Loop FD, Baillet R, Gill CC. Does bilateral internal mammary grafting increase surgical nsk? J Thorac Cardiovasc Surg 1988; 95: 850-56. 6. Kouchoukos NT, Waremg TH, Murphy SF, Pelate C, Marshall WG Jr. Risk of bilateral internal mammary artery bypass grafting. Ann Thorac Surg 1990, 49: 210-19. 7. Blauhut B, Gross CH, Necek S, Doran JE, Spath P, Lundsgaard-Hansen P. Effects of high dose aprotinin on blood loss, platelet function, fibrinolysis, complement, and renal function after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1991; 101: 958-67. 8. Fox MA. Mediastinal autotransfusion. Perfusion 1990; 5 (suppl): 21-23. 1.

Cosgrove DM, Meserko JJ.

Iron in

Autotransfusion in open heart surgery SiR,—In your Aug 17 editorial you raise doubts about the value of autotransfusion of blood shed from the mediastinum after open heart surgery. Although we agree that successful cardiac surgery is dependent on blood and blood products, effort should be made to reduce this dependence, thus allowing many patients to benefit from this form of treatment. In a prospective randomised trial done at this hospital, 80 patients undergoing routine coronary artery surgery were assigned to receive autotransfusion (n = 40) or to be controls (40). In the autotransfusion group blood was collected in the hard-shell reservoir that had been used during the surgical procedure. We regard the Sorensen system as obsolete.1,2 Autotransfusion was started after at least 200 ml of blood was collected in the cardiotomy reservoir, and continued for 12 h or until no more than 50 ml of blood was left. Packed cell volume (PCV) drained from the mediastinal blood was 17-7 (SD 6-6) gjdl, diminishing to 15-4 (13-8) g/dl 4 h later. Initial platelet count in the drained blood was 61-4 (27-9) x 103/ml, increasing to 100-7 (63-1) x 103/ml 4 h later. The two groups did not differ with respect to age, sex, number of grafts, use of arterial conduits, and length of bypass time, and the mean postoperative blood loss was similar (889-9 [556] ml in the autotransfusion group and 820-0 [602-9] ml in the controls) in the first 24 h after operation. 9 units of bank blood were transfused in 4 patients in the autotransfusion group and 108 in 33 controls (Student’s t-test, p < 0-001). Bank blood was transfused only if haemoglobin (Hb) was less than 8-5 g/dl. Hb on discharge was 11 -27 (1 -43) g/dl in the autotransfusion group and 11 35 (1-89) g/dl in the controls. Blood cultures were done on the mediastinal aspirates, blood from the cardiotomy reservoir, and on the patients’ blood (from two veins) immediately and 3, 6, 12, and 24 h postoperatively. One cardiotomy reservoir culture obtained 6 h after operation was positive for Escherichia coli. No signs of systemic or sternal wound infection were seen. 1129 open heart procedures were done in this hospital in 1990, and a substantial number of these patients received autotransfusion. An average of 0-9 blood units per patient was used in coronary surgery. 15 % of operations were done on the first hospital admission as urgent or emergency. Most patients were receiving aspirin until the day of operation. There is little doubt that aspirin increases postoperative blood loss.3,4 Similarly, the use of bilateral internal thoracic artery for coronary grafting results in increased


neuroleptic malignant syndrome

SIR,-Dr Rosebush and Dr Mazurek (July 20, p 149) write that "serum iron may be a useful biochemical marker for neuroleptic malignant syndrome (NMS), and a helpful adjunct in the diagnosis of the disorder". Although we find their comments on the role of serum iron in the pathophysiology of NMS interesting, we have reservations as to its usefulness as a biochemical marker. Physiological serum iron concentrations are variable and, as Rosebush and Mazurek state, a reduction in serum iron is found during the acute phase response, which can be caused by any form of tissue injury, even the common cold. Rosebush and Steward comment that "one of the more difficult problems in the differential diagnosis of neuroleptic malignant syndrome is presented by the patient who develops infection while taking neuroleptics". For an investigation to be recommended as being useful in the diagnosis of a condition, one must show that the test distinguishes one diagnosis from others with which it is likely to be confused clinically; this cannot be said of serum iron in NMS. We do not believe that the data presented are adequate to enable the authors to recommend serum iron as a biochemical marker of NMS until they address both the specificity and sensitivity of this test.

Department of Clinical Chemistry, Royal Infirmary, Edinburgh EH3 9YW, UK


1. Cavill

I, Jacobs A, Worwood M. Diagnostic methods for iron status. Ann Clin Biochem 1986; 23: 168-71.

2. Rosebush P, Stewart T. A prospective analysis of 24 episodes of syndrome. Am J Psychiatry 1989; 146: 717-25.

neuroleptic malignant

%*This letter has been shown to Dr Rosebush and Dr Mazurek, reply follows.-ED. L. SiR,—We agree with Dr Turner and Dr Reddy that hypoferraemia is not specific for neuroleptic malignant syndrome (NMS). Indeed, we adduced this fact as evidence for our suggestion that NMS might represent a manifestation of the acute-phase whose

reaction. This is not to say, however, that a finding of hypoferraemia may not be a helpful adjunct for the diagnosis of the disorder. NMS is, by definition, a syndrome-ie, a collection of clinical characteristics-that seem to indicate a common underlying pathophysiology. In NMS, none of the generally accepted clinical

Autotransfusion in open heart surgery.

820 patients presenting to hospital (18 per 100 000) or at necropsy (376 per 100 000). Our studies show that these patterns are likely to be related...
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