Ascitic fluid protein concentration

Of the 26, seven had protein excretion in of 2 g per 24 h (four had protein excretion greater than 3 g per 24 h). The table shows results of renal biopsy in our patients with renal artery stenosis, and reasons for failure to biopsy. Of the 26 patients diagnosed with renovascular disease, 16 had serum creatinine greater than 300 mol/L at diagnosis, eight required renal replacement therapy, and 16 died. Despite the small numbers, we suggest that older patients (>50 years) with focal segmental glomerulosclerosis have a similar disease to that seen in younger patients, rather than the aggressive course observed in patients with renovascular disease. Reasons for a difference between our group of patients and those reported from the Massachusetts General Hospital are not clear; there seems no obvious difference in renal biopsy policy, and only one patient from Thadhani’s group was from the black community, in which an increased frequency of focal segmental glomerulosclerosis has been observed.4 Thus we are unable to support Thadhani’s claim of an association between focal segmental

angiography). excess

glomerulosclerosis and renovascular disease. *Kevin

McLaughlin, Keith Simpson,

Renal Unit,

1

2 3

4

J Michael Boulton-Jones Glasgow Royal Infirmary, Glasgow G4 0SF, UK

Thadhani R, Pascual M, Nickeleit V, Tolkoff-Rubin N, Colvin R. Preliminary description of focal segmental glomerulosclerosis in patients with renovascular disease. Lancet 1996; 347: 231-33. D’Agati V. The many masks of focal segmental glomerulosclerosis. Kidney Int 1994; 46: 1223-41. Haas M, Spargo BH, Coventry S. Increasing incidence of focalsegmental glomerulosclerosis among adult nephropathies: a 20-year renal biopsy study. Am J Kidney Dis 1995; 26: 740-50. Bakir AA, Bazilinski NG, Rhee HL, Ainis H, Dunea G. Focal segmental glomerulosclerosis: a common entity in nephrotic black adults. Arch Intern Med 1989; 149: 1802-04.

Cavernous

haemangioma of the liver

Figure: Computed tomograph haemangioma

of liver

showing portal

cavernous

Despite this report, we believe that pregnancy should be discouraged in patients with cavernous haemangioma as the increased metabolic demands of pregnancy may compromise the unaffected part of the liver. Vomiting may elevate subdiaphragmatic pressure with ensuing rupture of the tumour.3,4 Furthermore, development of the placento-fetal circulation may provoke or aggravate maternal portal hypertension leading to rupture of oesophageal varices.

and

pregnancy

*Mariano Malaguarnera, Giuseppe Ettore, Franca Nocera, Paolo Scollo, Giovanni Pistone

majority of cavernous haemangiomas of the liver are symptom-free, although some present with signs or symptoms of abdominal mass, infarction, rupture with thrombocytopenia, or hypofibrinogenaemia. To our knowledge, no reports of this tumour have been described during pregnancy. A 37-year-old woman came to our observation at 22 weeks’ gestation because of a severe episode of haematemesis and melena caused by rupture of oesophageal varices. A portal cavernous haemangioma (figure) had been diagnosed when the patient was 5 years old after severe haematemesis and melena. The patient had undergone splenectomy at the age of 5 years, omentocavopexy’ 3 years later, and left renal mesenteric artery anastomosis at the age

*Department of Internal Medicine and Geriatrics, University of Catania, 95126 Catania, Italy; and Department of Gynaecology and Obstetrics, Cannizzaro Hospital, Catania

of 15. Anaemia due to haematemesis and melena had twice necessitated interruption of pregnancy (at week 13 and week 16 of gestation). Our patient had severe anaemia and platelet deficiency. Her liver function indices were normal. Abdominal ultrasound at weeks 23 and 32 of gestation revealed adequate fetal biometry for gestational age. Morphology of the other organs was normal. The patient was treated with blood transfusions and sclerosis or oesophageal varices. Her advanced stage of gestation and desire for a child were taken into consideration; the patient was informed of the risks involved in proceeding with the pregnancy. She decided to go ahead with the pregnancy under strict clinical and laboratory control. She gave birth to a live girl (APGAR score 10; birth weight 2500 g) by caesarean section at week 36 of gestation. Both mother and child are in good health to date.

et

SiR-The

772

1 2

Berman EJ, Waite P, Gerig L, Bakemier RE. Omentocavopexy, further analysis. Arch Surg 1963; 86: 1008. Britton RC. Pregnancy and esophageal varices. Am J Surg 1982; 145: 421-25.

3

Whelton JM, Sherlock S. Pregnancy in patients with management and outcome. Lancet 1968; ii: 995-98.

hepatic cirrhosis:

Ascitic fluid protein concentration SIR-There is a common misconception, repeated by Freers al (Jan 20, p 197),’ that ascitic fluid in patients with congestive heart failure is a transudate. More often than not, the protein content of ascites in such patients is indicative of an exudate (more than 25 g/L).2 Similarly high protein concentration is found in ascitic fluid in patients with constrictive pericarditis and with Budd-Chiari syndrome. Freers et al suggest ascites in patients with endomyocardial fibrosis may be due to peritoneal inflammation. Their results, however, are not incompatible with a cardiac cause of ascites. Protein content of peritoneal fluid is determined by both portal pressure and the oncotic pressure exerted by serum proteins, opposing forces that must be in balance in the stable Serum patient.3 haemodynamically protein concentration is highly variable in patients with ascites, which limits the usefulness of measuring ascitic total protein concentration in isolation. The serum-ascites albumin

gradient (serum albumin concentration minus ascitic fluid albumin concentration) is influenced by only one variableportal pressure-and better categorises ascites than does ascitic total protein concentration.; A patient with a high gradient (more than 11g/L) has portal hypertension, usually due to cirrhosis or heart failure. The higher the gradient, the higher the portal pressure. A patient with a low gradient (less than 11 g/L) does not have portal hypertension and most often has peritoneal carcinomatosis or tuberculosis. Most of the patients reported by Freers et al had right ventricular a involvement and presumably degree of portal if in part caused by Even the ascites was hypertension. inflammation mixed a high serum(ie, ascites), peritoneal ascites albumin gradient would be expected. A more pertinent question is why some patients with heart failure, particularly those with tricuspid regurgitation and with constrictive pericarditis, often have prominent ascites with little peripheral oedema. We suggest the pronounced right heart pulsations in these patients are preferentially transmitted to the hepatic vein, which enters the inferior vena cava below the right atrium, resulting in liver and ascites. congestion *Cornelius C Cronin, Miriam

training, a tiered system of referral is also important. Many health facilities need renovation, equipment, and supplies if they are to function as effective referral points. Maternal care activities should be monitored continuously by audit. For this purpose it is recommended that maternal and perinatal mortality committees be with basic

established at the district level motherhood.

*Gijs Walraven, Jos

van

as

a

step towards safer

Roosmalen

*Medical Research Council Laboratories, Banjul, Gambia; and Leiden Hospital, Department of Obstetrics, 2300 RC Leiden, Netherlands

1 2

3 4

5

University

Panter KR, Hannah ME. Umbilical cord prolapse: so far so good? Lancet 1996; 347: 74. Walraven GEL, Mkanje RJB, van Roosmalen J, Van Dongen PWJ, Dolmans WMV. Perinatal mortality in home births in rural Tanzania. Eur J Obstet Reprod Biol 1995; 58: 131-34. Van Roosmalen J, van der Does CD. Caesarean birth rates worldwide. Assessments of determinants. Trop Geogr Med 1995; 47: 19-22. Barret JM. Funic reduction for the management of umbilical cord prolapse. Am J Obstet Gynecol 1991: 654-57. World Health Organization. New estimates of maternal mortality. Wkly Epidemiol Rec 1991; 66: 345-48.

Duggan

Department of Medicine, Cork University Hospital, Wilton, Cork, Ireland

Male 1 Freers J,

2

Mayanja-Kizzo H, Rutakingirwa M, Gerwing E. Endomyocardial fibrosis: why is there striking ascites with little or no peripheral oedema? Lancet 1996; 347: 197. Runyon BA. Cardiac ascites: a characterization. J Clin Gastroenterol 1988, 10: 410-12.

3 Hoefs JC. Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients with chronic liver disease. J Lab Clin Med 1983; 102: 260-73.

Umbilical cord

prolapse in rural Africa

SiR-Panter and Hannah (Jan 13, p 74)’ assert that no new have evolved since the 1950s for umbilical cord prolapse. We agree. However, the increased use in industrialised countries of elective and intrapartum caesarean section for the non-cephalic or unengaged is not and feasible, may also be inappropriate, presentations in many parts of rural Africa. In this region, most women still deliver at home; the numbers with high-risk pregnancies who deliver in hospital are low, and transfer facilities from home to hospital are often inadequate when they are most needed.Furthermore, maternal mortality after caesarean section in African hospitals has been reported to be 1-8% (range 0’65-5%);3 this compares unfavourably with the estimated rate of less than 0-1% in the industrialised countries. For these reasons we advocate consideration of alternatives to caesarean section. When there is full dilation of the cervical os, forceps or breech extraction can be considered. When cervical dilation in a multiparous woman has reached 6 cm or more, emergency vacuum extraction can save the life of the baby without endangering the mother. Funic reduction for the management of a proplapsed umbilical cord has been successful in some cases.4 We mention that elevation of the presenting part can be achieved by filling the bladder, and this allows more time to initiate proper treatment. This technique can be used outside hospital before referral. The present crisis in safe motherhood in rural Africa, where maternal mortality is not decreasing,’ shows that there is a need to address several priorities: improvement in the quality of institutional care in combination with appropriate basic training, continuing education, and supervision of selected traditional birth attendants and village health workers. Besides a motivated village midwife treatments

reproductive hazards and occupation

SiR-Thonneau and colleagues (Jan 20, p 204)’ note that pregnancy is significantly delayed when the man is a driver or is occupationally exposed to heat. I have noted that reproductive hazards associated with male occupations may be usefully indexed by low sex ratios (proportions male)2 in their children. Significantly low offspring sex ratios have been reported for men who are drivers3 and men occupationally exposed to heat (eg, carbon setters4 and divers5). Perhaps the delayed conceptions and low sex ratios are hormonally mediated (eg, by low testosterone or high gonadotropin levels). Either way, a low offspring sex ratio may prove to be a useful alternative to sperm counts, conception waits, or homone assays as an indicator of male reproductive hazards. William H James Galton Laboratory, University College London, London NW1 2HE, UK

1 2 3 4 5

Thonneau P, Ducot B, Bujan L, Mieusset R, Spira A. Heat exposure as a hazard to male fertility. Lancet 1996; 347: 204-05. James WH. Occupations associated with low offspring sex ratios. Am J Ind Med 1994; 25: 607-08. Dickinson H, Parker L. Do alcohol and lead change the sex ratio? J Theor Biol 1994; 169: 313. Milham S. Unusual sex ratio of births to carbon setter fathers. Am J Ind Med 1993; 23: 829-31. Lyster WR. Altered sex ratio in children of divers. Lancet 1982; ii: 152.

Controlling tuberculosis SiR-Reichman is indignant about inadequate WHO attention to tuberculosis (Jan 20, p 171),’ but the following points are worthy of consideration. In 1995, WHO had a deficit of US$177 million in membership dues and the USA was$104 million in arrears.2 Second, despite annual expenditure of more than$3000 per person on health care in the USA (ten times greater than the total per capita income of half the world’s population) about 40 million US citizens have no, or inadequate, health insurance. Further, health statistics for the USA reveal that it lags well behind many industrial nations of similar or lesser wealth,3 which raises questions about the US commitment to the "ethical imperative to cure disease and 773