Lesson of the Week: Upper abdominal pain in pregnancy may indicate pre-eclampsia

Case reports Case 1

A 28 year old primigravida attended her general practitioner's surgery at 34 weeks' gestation with pain in the right upper quadrant, nausea, and vomiting. An antacid was prescribed for presumed reflux oesophagitis. Her blood pressure was not measured and her urine was not tested for protein. The symptoms persisted, and five days later she presented to the hospital antenatal clinic. On examination her blood pressure was 140/80 mm Hg and urine analysis showed proteinuria (2+). She had appreciable tenderness of the right hypochondrium. Further investigation disclosed a moderate thrombocytopenia (56x10⁹/l) and raised serum concentrations of aspartate aminotransferase (225 U/l) and uric acid (0.37 mmol/l). Concentrations of haemoglobin, urea, alkaline phosphatase, and albumin all lay within the normal ranges for pregnancy. There was no evidence of haemolysis, and the standard clotting times were not prolonged. A midstream urine sample was clear of white and red cells at microscopy. Pre-eclampsia with raised liver enzyme concentrations and a low platelet count was diagnosed. As the cervix was unfavourable caesarean section was performed to deliver the baby, a girl weighing 2100 g; she required minimal resuscitation. With intensive monitoring and supportive care, the woman made a complete recovery over 72 hours, her blood pressure, aspartate aminotransferase concentration, and platelet count all returning to within normal limits.

Case 2

A 26 year old woman complained of epigastric pain at 36 weeks in her first pregnancy. Her general practitioner diagnosed dyspepsia and prescribed an antacid mixture. Her blood pressure and urine were not checked. The pain continued, and at a routine antenatal visit two days later she was found to be hypertensive (135/105 mm Hg) and to have proteinuria (2+). On investigation in hospital that day she had moderate thrombocytopenia (78x10⁹/l) and raised serum concentrations of aspartate aminotransferase (142 U/l) and uric acid (0.41 mmol/l). Standard clotting times were normal and there was no evidence of haemolysis. The fetus was normally grown and had a reactive heart rate pattern. An attempt was made to induce labour with dinoprostone gel (2 mg, two doses, six hours apart; Prostin E2 gel, Upjohn). Twelve hours later labour had not progressed and her platelet count had fallen further to 39x10⁹/l. A caesarean section was performed under general anaesthetic, with a platelet transfusion being given during surgery. A girl weighing 2300 g was delivered in excellent condition. The woman's platelet count rose steadily to 120x10⁹/l and her liver enzyme abnormality reversed within 48 hours of delivery. Her hypertension settled by the fifth day.

Case 3

A 27 year old woman complained of epigastric pain at 22 weeks' gestation in her second pregnancy; her first pregnancy had ended as a spontaneous abortion at 18 weeks. Analysis of urine showed proteinuria (1+), but her blood pressure was not measured. Her general practitioner diagnosed a urinary tract infection and prescribed an antibiotic. Four days later she had a moderate antepartum haemorrhage (<500 ml) and was transferred to hospital. By the time of admission the bleeding had stopped. The uterus was soft and not tender, but she was tender in the right hypochondrium. Her blood pressure was 160/110 mm Hg, and a urine sample tested positive for protein (3+). Detailed investigation showed a mildly raised serum concentration of aspartate transaminase (84 U/l) and thrombocytopenia (91x10⁹/l). Her serum albumin concentration was low (28 g/l), but there was no evidence of haemolysis or disseminated intravascular coagulation. A urine sample was clear at microscopy. The fetal heart pattern was reactive, but an ultrasound scan showed the fetus to have symmetrical growth retardation with oligohydramnios. Doppler umbilical artery blood flow analysis showed reversed flow in diastole. An attempt was made to control the hypertension with methyldopa (500 mg thrice daily) and nifedipine (10 mg thrice daily; Bayer), but without success. Repeat blood sampling confirmed the initial results. Delivery was considered necessary to prevent severe maternal complications, and, in view of the fetus's extreme prematurity, labour was induced using a prostaglandin E2 pessary (2.5 mg; inhouse preparation). The fetus died shortly after uterine contractions started. A normally formed male fetus weighing 450 g was delivered spontaneously 12 hours later. Thereafter, the woman recovered rapidly, and she was discharged home three days later.

Discussion

Pre-eclampsia is a progressive disorder of endothelial function that is unique to pregnancy and probably results from various microvascular diseases.1 It arises in the placenta but may affect all major organ systems, including the brain, kidney, liver, and lung. Although most cases of pre-eclampsia are first detected at routine screening of symptom free women attending routine antenatal clinics, the mode of presentation is highly variable and a small proportion of women present with the symptoms of systemic complications such as headache, visual disturbance, and eclampsia. Pre-eclampsia complicated by raised liver enzyme concentrations and a low platelet count with or without haemolysis is at least as common as eclampsia and often more difficult to manage,1 but it is less well recognised.3 Several authors have reported high rates of serious maternal and perinatal problems such as hepatic rupture, renal failure, pulmonary oedema, placental abruption, and perinatal asphyxia.*RF 2,4-6* Early diagnosis and prompt action are essential, therefore, to help avert life threatening complications. Although the clinical progression of pre-eclampsia is usually slow, occurring over days and sometimes weeks, rapid deterioration may occur and occasionally result in multisystem failure within the course of a few hours.7 Detailed monitoring and supportive care may reduce the risk of complications, but ultimately the only means of controlling the condition is delivery of the fetus (and placenta). Early recognition of fulminant cases allows maximum time for assessment and stabilisation before delivery, including enhancement of fetal lung maturity with exogenous corticosteroids,8 and transfer to a unit adequately equipped for maternal and neonatal intensive care.

Our three case reports confirm that epigastric pain is often a grave symptom in pregnant women. They also emphasise that blood pressure must be measured and urine tested for protein in all women troubled by upper abdominal pain after 20 weeks of pregnancy. Women with pre- eclampsia complicated by raised liver enzyme concentrations and thrombocytopenia with or without haemolysis may be normotensive and aproteinuric at initial presentation.^9,10 Therefore blood pressure measurement and urine analysis cannot be relied on to exclude the diagnosis of pre-eclampsia. Given that clinical deterioration may be rapid, women with upper abdominal pain and tenderness must be admitted to hospital immediately to test for hepatic dysfunction, haemolysis, and thrombocytopenia.