The HELLP syndrome

British Journal of Obstetrics and Gynaecology August 1997, Vol. 104, pp. 887-891

The HELLP syndrome Introduction Haemolysis, elevated liver enzymes and low platelets (HELLP syndrome) have been well described as complications of pre-eclampsia and eclampsia for many years'-5. However, there is much debate about the incidence, nature, clinical significance and management of HELLP syndrome in severe pre-eclampsia and eclampsia. The syndrome was originally described as EPH (oedema, proteinuria, hypertension) gestosis type B by Goodlin et d4, who stated that it had been reported in the obstetric literature for about 100 years. Weinstein first considered this condition to be a unique variant of severe pre-eclampsia and called it 'the HELLP syndrome' in reference to the laboratory abnormalities6. Interestingly, McKenna et aL7 considered HELLP syndrome as misdiagnosed pre-eclampsia, while Greer et al. considered it as mild disseminated intravascular coagulation that was missed because of 'technical inadequacy'. The majority of women will have moderate or severe hypertension but the spectrum of the syndrome has been widened to include women with the 'HELLP' features but with normal or only mild elevation in blood pressure and no significant proteinuria9J0. The incidence of the HELLP syndrome has been suggested at approximately 20% of severe pre-eclampsia"J2 but the exact incidence may well be different to this as the diagnosis is often missed because the varying presentation causes confusion. There appears to be no difference in severity and occurrence of the HELLP syndrome between twin pregnancy and singleton ge~tation'~. Regardless of whether the HELLP syndrome exists as a distinct entity or as part of a spectrum of pregnancy complications, it generally presents before term and is associated with significant adverse maternal and perinatal outcome5.

A systematic review of all papers pertaining to the HELLP syndrome was carried out using the CD-ROM MEDLINE system (1 966-1 996) and also by secondary hand search of relevant papers. English language journals only were used for this review. In all, 390 papers were identified, 204 of which were printed in the English language. Of these, 18 1 contained relevant

, information for the purposes of this review article.

Diagnosis and classification The terminology and diagnostic criteria used to describe the syndrome have been confusing and inconsistent in the past. A number of previous studies have included women who had no evidence of haemolysis. When

haemolysis has been mentioned, the diagnosis was based largely on the presence of an abnormal peripheral smear (burr cells or ~chistocytes'~ are suggestive of a micro-haemangiopathic haemolytic anaemia) or a raised reticulocyte count. A low haptoglobin level is also a useful marker of haem01ysis'~J~. Other haemolysis markers include lactate dehydrogenase, bilirubin (serum, urine), urobilinogen (urine), fragmentocytes and free haemoglobinI6 In the most severe cases, disseminated intravascular coagulation (DIC) will co-exist with the haemolytic anaemia. The syndrome of ELLP has been described where there has been no haemolysis5.

There is no consensus regarding exactly which liver function test abnormalities should be used to diagnose the syndrome but the majority of papers refer to elevated transaminases. There is not even consensus about normal range of liver function tests for pregnancy, and the limited data available are from relatively small num- bers of However very recently, reference ranges for levels of alanine and aspartate transaminase, bilirubin, alkaline phosphatase and gamma glutamyl transferase, by gestational age in pregnancy, have been proposed20. These are cross-sectional data from over 400 women with a normal pregnancy. It has been shown that liver function test abnormalities generally do not agree well with the degree of liver injury2'. However in cases manifesting extreme elevation of aspartate aminotransferase and lactate dehydrogenase levels, there is a high risk of maternal mortality22.

The traditionally accepted definition of thrombocytopenia is a platelet count of less than 150,000 per microlitre. More recently, however, this has been broadly divided by the Mississippi triple class system23 with class I HELLP syndrome referring to a maternal platelet count of < 50,OOO/pL, class I1 to a platelet count > 50,000 to < lOO,OOO/pL and class I11 to a platelet count > 100,000 to < 150,OOO/pL, with haemolysis and raised liver enzyme levels. Whilst the exact value of this classification remains unclear in terms of management, currently its usefulness is restricted to categorisation and audit. Apart from HELLP syndrome, the differential diagnosis of thrombocytopenia in pregnancy includes immune thrombocytopenic purpura, 'gestational' thrombocytopenia, pre-eclampsia-associated thrombocytopenia, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura and the haemolytic uraemic syndrome.

The pathogenesis of the HELLP syndrome remains an enigma. It has been proposed that disorders including the HELLP syndrome, thrombotic thrombocytopenic

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purpura, the haemolytic uraemic syndrome, acute fatty liver of pregnancy and acute renal failure may all be part of a spectrum of the same disease process24. Although the pathogenesis may be similar, these are not the same disease. The common link appears to be endothelial cell injury with subsequent vasospasm, platelet activation, an abnormal platelet prostacyclin- thromboxane ratio, and decreased release of endothe- lium-derived relaxing factor, all of which play a central role in the pathogenesis of these disorders. Activated protein C resistance resulting from a mutation in coagulation factor V has now emerged as the leading cause of thrombosis in pregnancy and recent data links the HELLP syndrome with factor V R506 Q mutation25. Other theories on the aetiology and pathogenesis of the HELLP syndrome include complement activation with anaphylatoxin release26, nitric ~ x i d e ~ ~ , ~ ~ , genetic29 and hydralazine-induced hepatocellular damage30.

Clinical presentation

The classical presentation of the HELLP syndrome is a white, multiparous woman with a past history of a poor pregnancy outcome and who is more than 25 years old. The woman is mostly seen before 37 weeks of gestation and her clinical features are often vague. In nine out of ten cases there is epigastric or right upper quadrant pain such that other conditions may be considered first- gallstone colic, cholecystitis, hepatitis, pancreatitis, hia- tus hernia, and perforated peptic ulcer. Rarer conditions such as acute fatty liver of pregnancy with or without profound hyp~glycaemia~' and the Budd-Chiari syndrome may also be considered. Nausea or vomiting will be present in about half the women and others will have non specific viral, flu-like symptoms; most women will have felt unwell for only a few days. Hypertension and proteinuria may be absent or only slight. It has been suggested that all pregnant women having any of the above symptoms should have a full blood count with platelet and liver enzyme determinations irrespective of the blood pressure32. Feeling generally unwell or having a flu-like illness has been highlighted by Tomsed3 as being under-appreciated in the HELLP syndrome. Women may develop some of these symptoms during conservative management for pre-eclampsia and it is sensible to measure platelet counts and liver enzyme levels at frequent intervals. The HELLP syndrome may also present with convulsions, jaundice, gastrointestinal bleeding, haematuria, bleeding from the gums and pain in the renal angle, chest or shoulder. Sibai et ale5 showed that because of the tendency to present with vague symptoms, the average delay in making the correct diagnosis of HELLP was eight days (range 3-22). General physicians and surgeons thus need to be

aware of the possibility of the HELLP syndrome in all pregnant women under their care.

In nearly one third of cases the HELLP syndrome presents after delivery. The onset was a few hours to six days after birth, the majority being within 48 hours32. In this series 15% of women developed the HELLP syndrome during the second trimester.

Treatment When the HELLP syndrome is diagnosed the main priority is to assess and stabilise the woman's condition, especially coagulation dysfunction. There- after, fetal wellbeing should be evaluated by ultrasound biophysical profile, umbilical artery Doppler and cardiotocography. Third, a decision needs to be made as to whether immediate delivery is indicated.

The consensus of opinion for severe cases (eg. class I HELLP) is that control of hypertension and immediate delivery, invariably by caesarean section, is the treatment of choice. A woman with moderate HELLP syndrome at a gestational age greater than 34 weeks should also be delivered immediately. Those who are remote from term should be transferred to a tertiary referral centre once the maternal condition is stable34. Before 34 weeks, the woman should be delivered if her condition cannot be controlled rapidly. Where delivery is not indicated immediately, antenatal corticosteroids should be administered for 48 hours to promote fetal lung maturity. When a course of steroids has been com- pleted in the setting of the HELLP syndrome, neonatal outcome is significantly improved in cases compared with controls35. The woman and her baby must be assessed continually during this period and she should be delivered if her condition worsens.

In milder cases of the HELLP syndrome occurring near term induction of labour is appropriate; however at very early gestational ages where the cervix is very unfavourable, elective caesarean section is preferred36. Milder cases such as class I11 may even be allowed to proceed to term and to undergo a spontaneous vaginal delivery, and in certain cases temporising management may improve fetal and neonatal as well as maternal out- come37. However, the woman's condition must be mon- itored very closely during this time, and the condition of her baby assessed regularly, as intrauterine growth retardation is common9.

Standard pain relief in labour with opioid drugs and nitrous oxide is appropriate. Local infiltration of the perineal skin can be used for vaginal delivery. The use of epidural analgesia and/or anaesthesia in the presence of thrombocytopenia is controversial. A platelet count of greater than lOO,OOO/pL is regarded as a safe cutoff point for insertion of a Tuohy needle, but where the platelet count is less than lOO,OOO/pL most anaesthetists

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are against epidural block. When other elements in the coagulation screen are abnormal, epidural block is con- tra-indicated. Anaesthesia and the HELLP syndrome has been extensively reviewed e l ~ e w h w e r e ~ ~ . ~ ~ .

Although bleeding in the gravid patient is related to more factors than platelet count alone, women with the HELLP syndrome in whom an intrapartum platelet count above 40,00O/pL is maintained are unlikely to have clinically significant postpartum bleedinp. In cases of severe thrombocytopenia with platelet counts of less than 20,00O/pL, correction by platelet transfusion is indicated. Before caesarean section correction of thrombocytopenia is particularly important. Platelet consumption occurs rapidly and the effect of platelet transfusion is transient. Repeated platelet transfusions are not advocated in the absence of haemorrhage as delivery itself will usually lead to a reversal of the thrombocytopenia. In cases of coagulation dysfunction, the defective plasma components may be replaced by administration of fresh frozen plasma, packed red cells and anti-thrombin 111.

Women with the HELLP syndrome should be moni- tored very carefully, for at least 48 hours after delivery, ideally in an intensive care facility. The use of a central venous pressure catheter may prove invaluable for fluid balance. The syndrome will resolve within 48 hours of delivery in most women, and an upward trend in platelet count and a downward trend in lactate dehydrogenase concentrations should be apparent in women without complications by the fourth postpartum daf'. A more protracted postpartum recovery period should be expected for progressively severe expressions of the HELLP syndrome4*. Regular assessment of liver, renal and coagulation function is essential during this critical period. Those women who develop disseminated intravascular coagulation may show delayed resolution or even deterioration. In resistant cases or when clinical deterioration occurs, plasma exchange should be considered as a therapeutic option as it has been shown to be successful43.

New developments in management Case reports and case series have suggested that when corticosteroids are used to accelerate fetal lung maturity, a temporary significant improvement in the severity of the HELLP syndrome may Heyborne et ~ l . ~ ~ , in a series of five cases, showed a temporary reversal of the HELLP syndrome using low- dose aspirin and corticosteroids; the average prolongation of pregnancy was four weeks with no reported long term maternal morbidity. More recently, a randomised trial by Magann et uL4* has shown that the administration of high doses of steroids (10 mg of dexamethasone intravenously every 12 hours until delivery) between 24

and 37 weeks of gestation resulted in stabilisation and significant improvement in the laboratory and clinical manifestations of the HELLP syndrome, compared with a control group. The average prolongation of pregnancy was 41 hours with steroids, compared with 15 hours in the controls. This treatment may be particularly helpful in facilitating a safer transfer of a sick mother to a tertiary referral centre. Magann has also shown that high dose corticosteroid administration after birth leads to a more rapid recovery from the disease than controls49.

Maternal and fetal outcome

Pregnancies complicated by severe pre-eclampsia and eclampsia and the HELLP syndrome are associated with a poor outcome for the mother and her infant, the reported perinatal mortality being 77 to 370 per 10004*5,7. Maternal morbidity and mortality are also significant. Maternal complications are common and potentially life-threatening. Disseminated intravascular coagulation, placental abruption and acute renal failure are Other complications include eclampsia, cerebral haemorrhage, adult respiratory distress syndrome (ARDS) and hypovolaemic shock. HaematomaS1, infarction52 and rupture53 of the liver have also been described. Eclampsia is more likely to be associated with the HELLP syndrome at earlier gestational ages. The outlook for a woman with eclampsia and the HELLP syndrome is much worse than with eclampsia alone54. Six studies have specifically looked at maternal mortality associated with the HELLP syndrome, with a quoted range of 1 * I% to 24.2%5.6,",50,55,56. Overall, 29 cases of maternal death were reported among 746 cases reviewed in these studies (3.9%). It is hoped that the outcome for mother and baby will improve with better understanding of the disease process, consequent earlier diagnosis, and continued improvements in maternal and neonatal intensive care standards.

Counselling after birth Accurate prediction of the risk of recurrence of the HELLP syndrome has been difficult because of the rarity of the disease. However, Sullivan et al.57 have recently performed an extensive retrospective analysis over a twelve year period of 481 women with the HELLP syndrome, in which the risk of recurrence was approximately 20%. The recent CLASP study58 has shown that low dose aspirin prophylaxis may be of benefit where severe pre-eclampsia has developed at very early gestational ages, and so it would seem logical to prescribe aspirin to women whose previous HELLP syndrome had occurred early in pregnancy.

Sibai32 has shown that the use of oral contraceptives is safe in women who have had the HELLP syndrome:


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none of 86 women showed evidence of the syndrome while using the combined oral contraceptive pill.

Conclusions The HELLP syndrome is rare. Its presentation is vari- able, resulting in delayed diagnosis, and inappropriate medical and surgical treatments. Treatment depends on a number of factors, mainly the severity of the condition and the gestational age of the fetus. The outlook for the woman and her baby is poor. High dose corticosteroids may be beneficial. Improved understanding of the disease process with earlier diagnosis should improve outlook in the future. The risk of recurrence of the HELLP syndrome is approximately 20%.

Acknowledgements I would like to thank Dr M. De Swiet and Professor C. Rodeck for their help and advice in the preparation of this paper. The editorial advice is also greatly appreciated.

Michael Geary, Clinical Research Fellow University College London Medical School, Department of Obstetrics and Gynaecology, London

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The HELLP syndrome

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