121

Furthermore, in a continuing study in which platelets stored for 3-4 days are often given according to the restrictive transfusion guidelines we reported, we have seen no increase in the frequency of haemorrhagic complications (unpublished). Finally, we are not aware of any studies showing that pooled random-donor platelets are inferior to random single-donor products (apart from a higher alloimmunisation rate; see ref7 in our original report). We feel that the proposed transfusion guidelines are also valid for pooled random-donor platelets and for platelets stored appropriately for up to

72 hours.

Department of Internal Medicine, University Hospital of Zurich, CH-8091 Zurich, Switzerland

J. GMÜR A. SCHAFFNER

SIR,-Professor Gmur and colleagues provide the scientific basis for what many physicians treating patients with acute leukaemia are actually practising, since the 20 x 109/1 platelet count threshold is neither practical nor medically justified. In addition to the guidelines they propose, we suggest that the use of the antifibrinolytic drug tranexamic acid can further reduce platelet transfusions without conferring greater bleeding risks.l In 131 cycles of marrow ablative chemotherapy in 54 patients with acute leukaemia, tranexamic acid 4 x 1 g was given during days when platelets counts were less than 20 x 109/1. The mean number of platelet transfusions given per therapy course was 3-4, and platelet transfusions were withheld in 71 % of the days that the patient was at risk. These data are very similar to those reported by Gmur and colleagues; however, we encountered fewer major non-lethal bleeding episodes (6/131, 4-6%) or lethal bleeding (1/131, 0-7%). The

use

of tranexamic acid

was

safe and without any untoward

side-effects. We are conducting a randomised controlled trial to test these preliminary observations. Department of Haematology, Chaim Sheba Medical Centre and Sackler School of Medicine, Tel-Aviv University, Israel

ISAAC BEN-BASSAT BRACHA RAMOT

1. Ben-Bassat I, Douer D, Ramot B Tranexamic acid therapy m acute myeloid leukemia: possible reduction of platelet transfusions. Eur J Haematol 1990; 45: 86-89.

D-dimer as therapeutic and diagnostic aid in pulmonary embolism SIR,-Fewer patients with pulmonary embolism (PE) are seen in than in the USA. However, many patients dying from unknown causes may be misdiagnosed. Bounameaux and colleagesl,2 reported that measurement of D-dimer in plasma is diagnostic of PE in non-diagnostic ventilation-perfusion lung scanning. We report a case of PE diagnosed angiographically, in which measurement of D-dimer was useful therapeutically as well

Japan

as

saphenous veins was done. D-dimer gradually fell from 13 to 0.2 the following five weeks. She is now well and maintenance receiving anticoagulation therapy with warfarin. PE is difficult to diagnose and treat, especially when thrombotic events, such as deep-vein thrombosis, are not identified. Varicose veins in the legs are unlikely to be a cause of PE. In our patient the return to normal of plasma D-dimer after stripping of varicose veins in the legs confirms that the cause of PE was these veins.

ng/ml during

diagnostically.

58-year-old woman was admitted because of exertional dyspnoea. Arterial POz was 57 mm Hg, PCOz was 34 mm Hg, and ventilation-perfusion lung scanning revealed multiple defects. Puhnonary arterial pressure was 55/14 mm Hg, and pulmonary angiography disclosed multiple filling defects in the right pulmonary artery and branches of the left pulmonary artery. Although she had varicose veins of the left leg, no deep-vein thrombi were detected. No malignant tumours were found. The prothromin time was 11 ’6 s; activated-partial thromboplastin time was 25 s; fibrinogen was 496 mg/dl; fibrinogen degradation product was 4-9 fig/mi. D-dimer was 5-9 jig/mi, assayed with a latex-agglutinin assay kit (’LPIA-100’, Dia-iatron, Japan). Antithrombin-III activity was 97%, !x2-plasminogen activator inhibitor 113%, protein C 106%, and protein S 11-4 Ilg/ml. Urokinase 68 000 U/kg and heparin 850 U/kg were given for 72 h. Pulmonary arterial pressure fell to 37/12 mm Hg, arterial POz rose to 91 mm Hg, and a second pulmonary angiogram showed no defects. D-dimer, however, persisted above 0-5 fig/mi after thrombolysis. Three days later, she had exertional dyspnoea and arterial POz fell to 68 mm Hg despite proper anticoagulation with warfarin instead of heparin. A third pulmonary angiogram showed a new filling defect in the branches of the right pulmonary artery. Alteplase (rt-PA) 08 mg/kg was given, and stripping of the A

2nd Department of Internal Medicine, School of Medicine, Kanazawa University, Takara-machi 13-1, Kanazawa 920, Japan

HIDEKAZU INO MASAMI SHIMIZU NORIHIKO SUGIHARA KUNIYOSHI SHIMIZU HIROYUKI YOSHIO KATSUSHI MISAWA RYOYU TAKEDA

H, Slosman D, de Moerloose P, Reber G. Diagnostic value of plasma D-dimer in suspected pulmonary embolism. Lancet 1988; ii: 628-29. 2. Bounameaux HK, Cirafici P, de Moerloose P, et al. Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism. Lancet 1991, 337: 196-200. 1. Bounameaux

Haemoperitoneum induced by fine-needle aspiration of liver in patients with disseminated intravascular coagulation SiR,—Haemopentoneum is a rare but potentially fatal complication of fine-needle aspiration (FNA) of the liver.1-3 In published cases the patient concerned has always had malignant disease or haemangioma of the liver but the mechanism for the haemoperitoneum has not been commented on. We report here on two patients with metastatic malignant disease in whom a non-guided FNA was done in the presence of normal prothrombin (PT) and partial thromboplastin (PTT) time. Massive haemoperitoneum developed with laboratory evidence of disseminated intravascular coagulation (DIC). Case 1 (69, F; symptomless gallstones and non-insulindependent diabetes; admitted in April, 1987, with acute cholecystitis). 8 days later her liver was enlarged. Total bilirubinalanine aminotransferase, aspartate aminotransferase, PT, and PTT were normal, the platelet count was 123 000/jl, and alkaline phosphatase was high (2840 U/1). An ultrasound scan pointed to a space-occupying lesion in the gallbladder. On day 12 (platelet count 80 000/nl, PT and PTT normal) the patient had haematemesis. On day 16 (platelets 40 000/1, PT 9-6 s [normal 9-10-7), and PTT 28-5 s [28-36]) direct FNA of the liver was done with a short 23G needle. Cytological examination revealed inflammatory aspirate, liver cells, and columnar epithelial cells, some atypical. 3 h later, the patient’s abdomen became distended and tender with rapid onset of hypovolaemic shock. A massive haemoperitoneum was diagnosed. Tests on blood taken just before FNA revealed a fibrinogen of 304 mg/dl (200-400), a thrombin time of 27-5 s (14-16 s), and a level ofD-dimers above 8000 ng/ml, indicating DIC. After transfusions the patient improved clinically but on day 17 there was persistent laboratory evidence of DIC (platelets 27 000/jj.l, fibrinogen 147 mg/dl, D-dimers above 8000 ng/ml, PTT 78-4 s). On day 20 an exploratory operation disclosed 2 litres of noncoagulated blood in the peritoneal cavity, diffuse peritoneal petechiae, pancreatic cancer with lymph node involvement, and a tumour mass in the gallbladder. After surgery, cardiorespiratory failure developed and the patient died. Case 2 (73, M; admitted in June, 1990, with constipation and rectal bleeding, diagnosed as poorly differentiated adenocarcinoma of sigmoid). 3 months after surgery he was admitted with septicaemia and investigations revealed metastases to retroperitoneum and liver. A few days later (platelet count, PT, PTT all normal) a non-guided FNA of the liver revealed adenocarcinoma. 3 hours after this procedure his abdomen became distended and tender and he went into hypovolaemic shock. Massive haemoperitoneum was diagnosed. Thrombin time (TT) and D-dimers proved to have been abnormal at 27-2 s (control 20) and 4 ng/ml, indicating chronic DIC. Computed tomography revealed a large amount of free intraperitoneal bleeding in

122

Moraison’s pouch, paracolic gutters, and pelvis. The patient died 2 weeks later. Necropsy was not permitted. Most complications of FNA are avoidable.4 However, we have seen a patient with metastatic carcinoma of the pancreas in whom an ultrasonographically guided FNA of a liver metastasis (platelet count, PT, and PTT being normal) resulted in a fatal intraabdominal haemorrhage.5 Necropsy revealed evidence of DIC and this DIC may have contributed to the fatal bleeding. We suggested that in patients with migratory deep-vein thrombosis (as in that case) FNA should be done only after DIC has been excluded. The two cases reported here support that policy and extend it. Metastatic malignant disease has been associated with chronic DIC in which the clinical findings often differ significantly from those of acute DIC.6 Occasionally, however, patients with chronic DIC secondary to malignant disease have laboratory abnormalities with no clinical evidence of thrombosis or haemorrhage.6 Patients with chronic DIC may have normal PT and PTT values yet be at risk of overt bleeding after FNA. The haemoperitoneum that followed FNA in these two cases may have been induced by incipient chronic DIC. Testing TT and measuring fibrin/fibrinogen degradation products to exclude DIC would increase the cost of FNA but that would be justified if haemoperitoneum is avoided. We suggest that FNA of the liver should not be done in patients suspected of having malignant disease until DIC has been excluded. Departments of Internal Medicine C and B, Rambam Medical Centre and Faculty of Medicine, Technion-Israel Institute of 31096 Haifa, Israel

Technology,

YEOUDA EDOUTE JONATHAN KAPLAN SHLOMO A. BEN-HAIM YAACOV BARUCH

F, Civardi G, Cavanna L, et al Complications of ultrasonically guided fine-needle abdominal biopsy: results of a multicentre Italian study and review of the literature: the cooperative Italian Study Group. Scand J Gastroenterol 1989; 24:

1. Foman

949-55. 2. Bret PM, Labadie carcinoma:

M, Bretagnolle M, Paliard P, Fond A, Valette PJ. Hepatocellular diagnosis by percutaneous fine needle biopsy Gastrointest Radiol 1988;

13: 253-55. 3. Hertzanu Y, Peiser JL, Zirkin HL. Massive bleeding after fine needle aspiration of liver angiosarcoma Gastrointest Radiol 1990; 15: 43-46. 4. Malberger E, Edoute Y, Nagler A. Rare complications after transabdominal fine needle aspiration. Am J Gastroenterol 1984; 79: 458-60. 5 Edoute Y, Ben-Haim SA, Brenner B, Malberger E. Fatal hemoperitoneum following fine needle aspiration of a liver metastasis. Am J Gastroenterol (in press) 6. Bick RL. Disseminated intravascular coagulation and related syndromes: a clinical review. Semin Thromb Hemost 1988; 14: 299-38. 7. Brozovic M. Acquired disorders of blood coagulation. In: Bloom AL, Thomas DP, eds. Haematostasis and thrombosis Edinburgh. Churchill Livingstone, 1981. 415-22.

Gestational age and obstetric performance SIR,-Mr Saunders and Dr Paterson (Nov 9,

p 1190) report a of risk in the frequency of obstetric complications associated with spontaneous labour, which was low at 37 weeks’ gestation and which rose progressively with each successive week of pregnancy in primagravidae. Such a finding is, however, dependent on the management of pregnancy and will therefore not be universal. To illustrate this point, data for 174 310 singleton live-births to primigravidae in Scotland between 1980 and 1987 were examined; data were obtained routinely for 98% of pregnancies (Scottish Morbidity Record: Maternityl). Two outcomes were investigated--early neonatal deaths (of which there were sufficient for meaningful analysis) and caesarean section, the risk that Saunders and Paterson found to increase progressively from 37 weeks’ gestation for primigravidae who had spontaneous or induced labour. The effects of gestation, mode of onset of labour, and year of delivery on the data were estimated by logistic regression analysis (table). The comparison group consisted of women who had spontaneous labour at 40 weeks. For both outcomes, whether labour was spontaneous or induced, the risk decreases from 37 to 40 or 41 weeks and rises subsequently. These broadly U-shaped distributions retain their form over analvsis for earlier years: the odds of first-week death for all categories are multiplied by I - 15 for every year before 1987; those for caesarean section remain constant in women whose labour was spontaneous but should be multiplied by 0-95 per year before 1987 for women who had induced labour. The observation that caesarean section rates have remained at

gradient

ADJUSTED ODDS RATIOS* FOR EARLY NEONATAL DEATH AND CAESAREAN SECTION FOR SINGLETON TERM BIRTHS TO PRIMAGRAVIDAE IN SCOTLAND

*For most recent year available from 1987 and before then

(1987)

12-7% in the spontaneous labour group should

not pass without in view of previously reported increases in the Scottish rate.2The fact that the proportion of women for whom this mode of delivery was used has increased from 12-7% in 1980 to 14-0% in 1987 is due entirely to an increase in such deliveries among women in whom labour was induced (from 12-6% to 16-5%), despite a decline in the proportion of induced pregnancies from 32-0% to 23-6%. Caesarean section rates for spontaneous and induced labours diverge as 42 weeks’ gestation is approached, in contrast to Saunders and Paterson’s fmdings. The management of pregnancies in Scotland varies between hospitals, at least in respect of caesarean section.3 Because such variations exist, generalisations should be viewed with caution. Operative intervention and outcomes vary with gestational age, even between 37 and 42 weeks; where the optimum delivery date lies within this period will probably depend on variations in regional comment

practice. Public Health Research Unit, University of Glasgow, Glasgow G12 8RZ, UK

A. H. LEYLAND

Chalmers I, Mcllwaine GM Perinatal audit and surveillance. London. Royal College of Obstetricians and Gynaecologists, 1980: 39-51. 2 Leyland AH. Trends in caesarean section. Lancet 1991; 337: 1481-82. 3 Leyland AH, Pntchard CW, McLoone P, Boddy FA. Measures of performance in Scottish maternity hospitals. Br Med J 1991; 303: 389-93. I Cole SK. Scottish maternity and neonatal records. In:

SiR,—Mr Saunders and Dr Paterson’s report puts into

perspective the information that has emerged over the past few years. Although the fact that the risks increase as gestation advances is important, the worry is that this information would be misinterpreted and result in preference for induction. The central issue is whether intervention (eg, induction of labour) would alter outcome. The North-West Thames data show clearly that it would not. The real danger that confronts a woman who has had induction of labour is the increased risk of caesarean section. We calculate from their published graph that the relative risk of caesarean section at 42 weeks is about 1.6 (induction versus spontaneous onset of labour). It strikes us that this still carries substantial morbidity. That some women (who have longer pregnancies than do others) are unlucky has to be accepted, but we, as obstetricians, should not compound their misfortune by meddling with their labour until we know more precisely who needs the intervention. Division of Obstetrics and St Thomas’s Hospital, London SE1 7EH, UK

Gynaecology,

OLIVER CHAPPATTE EBOO VERSI

SIR,-Mr Saunders and Dr Paterson are to be congratulated on their review of obstetric data for the North-West Thames region, but they leave out important information about the total numbers of births in each subset of their data, presenting the complication rate as a percentage for each week of gestation. This approach makes interpretation of their data with respect to improvement of management very difficult. For instance, their results suggest that a primigravida undelivered by 42 weeks of pregnancy will have a higher chance of an obstetric complication than if she had delivered at 41 weeks; if,

Haemoperitoneum induced by fine-needle aspiration of liver in patients with disseminated intravascular coagulation.

121 Furthermore, in a continuing study in which platelets stored for 3-4 days are often given according to the restrictive transfusion guidelines we...
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