456 PREVENTION OF POSTOPERATIVE DEEP VEIN THROMBOSIS
SIR,-We were impressed by Dr Colditz and colleagues’ meta-analysis of randomised clinical trials on the rate of deep vein thrombosis (DVT) after general surgery (July 19, p 143). However, we
have
a
few
comments:
(1) Pooling the results of different studies may provide very useful information, but which results should be pooled? In the placebocontrolled studies referred to as refs 17, 18, 20, 28, 38, 39, and 42, the incidence of DVT in the placebo group was very low (ranging from 2%in ref 38 to 140in ref 28, which suggests that (very) low risk patients were enrolled in these trials. (2) Refs 56 and 52 in table vi and vii, respectively, should be switched around. (3) The authors did not consider the intermittent pneumatic compression arm of the three-arm study ref 50. In this group of 76 patients, 5 had postoperative DVT. The inclusion of this result would have reduced the very wide confidence interval (61 to 29 l"n) that the authors obtained for this kind of prevention. (4) Colditz et al suggest that the most effective means of prevention would consist of intermittent pneumatic compression combined with gradient compression stockings. They admit that this conclusion is based on very few studies. We would like to point out that none of these three studies [refs 53, 56 (and not 52), 57], which had a total of 137 patients, was placebo-controlled, and none of them was considered by the American College of Chest Physicians and the National Heart, Lung and Blood Institute National Conference on Antithrombotic Therapy in its recent, careful evaluation of the different ways of preventing postoperative DVT.1 Further, large, controlled studies are needed to establish the effectiveness of mechanical prevention.
Levels of plasma ANP in patients with
severe
Bars represent means ± SD. The hatched *p < 0-05, **p < 0-01 (compared with control).
thermal injury.
area
is the normal range.
patients with severe burn injuries may result from volaemic disturbance during resuscitation, a post-burn hypertensive crisis3,4 (ANP levels being increased in hypertensive patients5,6), or the increase -in pulmonary resistance observed in burn-injured patients.’ Clinical Research Unit, Army Burn Centre,
MONIQUE BRAQUET
Clamart
HERVÉ CARSIN JEAN GUILBAUD
Research Laboratories, Institut Henri Beaufour, 91940 Les Ulis, France
ETIENNE CHABRIER ISABELLE VIOSSAT PIERRE BRAQUET
Unit
of Angiology, Department of Medicine, University Hospital, CH-1211 Geneva 4, Switzerland 1.
H. BOUNAMEAUX B. KRAHENBUHL
Hyers TM, Hull RD, Weg JG. Antithrombotic therapy for venous thromboembolic disease. Chest
1986; 89: S26-S35.
PLASMA ATRIAL NATRIURETIC PEPTIDE IN SEVERE THERMAL INJURY
SIR,-Atrial natriuretic peptide(s) (ANP) play a part in the regulation of volume homoeostasis and, possibly, in the patho-
physiology of water and electrolyte disorders.1 Patients with serious burn injuries risk huge body fluid losses which are compensated for by perfusion of, say, Ringer’s lactate solution. Blood volume and the renin and aldosterone system are greatly disturbed.2 We have measured circulating levels of ANP in patients with severe bums. 8 males and 4 females (mean age 45 years) with severe flame injury (mean total burn surface area [TBSA] 4500) were studied. Standard treatment was given. Compensation of the initial body fluid loss was based on Ringer’s lactate and human serum albumin at doses, derived from the Percy formula, of 2 ml Ringer’s per kg body weight per 0 TBSA during the first 8 hours and 0-5 ml Ringer’sjkgj 00plus 0,5 ml albuminjkgj duringthenext 16 hours, modified according to the clinical response. Fresh frozen plasma was added as required on day 2. 7 patients had severe inhalation injuries and respiratory tract damage requiring controlled ventilation. 5 of the 12 patients died during the first 3 weeks. 15 volunteers (mean age 31 years; 9 males, 6 females) were used as controls. Venous blood was collected into plastic tubes with 2°o edetic acid. Plasma was separated by centrifugation and stored at - 20°C. ANP was extracted by ’Sep-Pak’ C-18 column and eluted with acetonitrile with a recovery of 60+4"u. The radioimmunoassay used a specific antibody directed against human a-ANP (Amersham kit 1871), and synthetic human x-ANP (Novabiochem) was used for the standard curves. In the patients with burns ANP levels were very high on days 1, 5, and 10 (see figure) though individual values varied. The increase in plasma ANP that we found in almost all these
Laragh JH. Atrial natriuretic hormone, the renin-aldosterone axis, and blood pressure-electrolyte homeostasis. N Engl J Med 1985; 313: 1330--40. 2. Griffiths RW, Millar JG, Albano J, Shakespeare PG. Observations on the activity of the renin-angiotensin-aldosterone (RAA) system after low volume colloid resuscitation for burn injury. Ann R Coll Surg Engl 1983; 65: 212-15. 3. Brizio-Molteni L, Moltem A, Cloutier LC, Rainey S. Incidence of post bum hypertensive crisis in patients adnutted to two bum centers and a community hospital in the United States. Scand 3’ Plast Reconst Surg 1979; 13: 21-28. 4. Falkner B, Roven S, De Clement FA, Bendlm A. Hypertension in children with burns. y Trauma 1978; 18: 213-17. 5. Sugawara A, Nakao K, Sakamoto M, Morit N, Yamada T, Itoh H, Shiono S, Imura H. Plasma concentration of atrial natriuretic polypeptide in essential hypertension. 1.
Lancet 1985; ti: 1426-27.
Sagnella GA, Markandu ND, Shore AC, MacGregor GA Raised circulating levels of atrial natriuretic peptides in essential hypertension. Lancet 1986; i: 179-81 7. Hartter E, Weissel M, Stummwoll HK, Woloszczuk W, Punzengruber C, Ludvik B. Atrial natriuretic peptide concentrations in blood from right atrium in patient with severe right heart failure. Lancet 1985; ii: 93-94.
6.
RELATION BETWEEN 131I THERAPY FOR THYROTOXICOSIS AND DEVELOPMENT OF THYROID CARCINOMA
SIR,-Professor Hennemann and his group have done an extremely useful survey of the place of radioiodine in the treatment of thyrotoxicosis (June 14, p 1369). However, their statement that "no
relationship was found between 1311I treatment for thyrotoxicosis and subsequent development of thyroid carcinoma", based partly on the largest study1 in this area, may give a false sense of security to those using 1311 therapeutically. Dobyns and colleagues’ detailed and complex paper on nearly 35 000 patients is open to differing interpretations. There were 8 deaths from thyroid cancer among their "post-occurring" group-those presenting than 1 year after the start of treatment. Of these, 7 occurred among 22 505 patients whose treatment included 1311, followed up for an average of 8 years, while 1 occurred among 10 940 patients treated by surgery without 1311, followed up for an average of 12; years. These figures differ from those given in the paper’s summary, where deaths occurring within a year of therapy are combined with those subsequently, and patients treated with surgery followed by 131are included in the surgical treatment group but not the radioiodide group. Most of the deaths were due to anaplastic malignancy; there were 6 anaplastic tumours, all had been treated
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