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Third trimester itch: Obstetric Cholestasis a serious condition of pregnancy.

Introduction

Obstetric cholestasis, also known as intrahepatic cholestasis of pregnancy, is a relatively uncommon liver disorder that classically presents in the third trimester (Royal College of Obstetricians and Gynecologists [RCOG], 2006). The main concern with obstetric cholestasis is a risk of prematurity and sudden intrauterine fetal death in previously healthy fetuses (RCOG, 2006). In this article we have used a fictionalized case report, with changes made to protect confidentiality, based on a scenario from practice to provide an overview of obstetric cholestasis, the investigations, diagnosis, risks and management options for this condition.

Pathophysiology

Obstetric cholestasis is the most common liver disease which is unique to pregnancy (McDonald 1999). The incidence is estimated as 0.7% of pregnancies in a multiethnic population (Abedin, Weaver, & Egginton, 1999). Around 448 pregnant women per year in New Zealand would be expected to contract this disease. Ch'ng, Morgan, Hainsworth and Kingham (2002) consider that this figure may be an under-representation of the problem due to failure of diagnosis.

Nichols (2005) describes the pathogenesis of obstetric cholestasis as the slowing of the normal flow of bile in the maternal liver, causing an increase of bile acids in the blood. This leads to damage of the liver cell membrane and consequential rise in liver enzymes in the maternal blood. There is also an increased transfer of bile acids from the mother to her fetus. Its causes are not well understood, but generally agreed to be multifactorial, with genetic, environmental and hormonal components (Lammert, Marschall, & Matern, 2003). Risk factors include a family history of obstetric cholestasis, gallstones, previous obstetric cholestasis, multiple pregnancy, older maternal age and Chilean or Scandinavian ethnicity (Bruce & Watson, 2007).

Symptoms and Biochemistry

Diagnosis is suggested if a woman in the third trimester of pregnancy develops itching without a rash and at least one biochemical liver abnormality (Walker, Nelson-Piercy, & Williamson, 2002). Exclusion of other causes of itching and liver disorders is necessary for the diagnosis (RCOG, 2006). The itching is described as intense, beginning on the hands and feet, later spreading to the limbs and body in an ascending pattern, but without skin rashes (Nichols, 2005). Itching is prior to or in tandem with raised serum bile acids and accompanied or followed by other abnormal liver function tests (LFTs), most commonly raised alanine transferase (ALT) and aspartate aminotransferase (AST) (Walker et al., 2002).

Serum bile acids (SBA) are the most sensitive marker of biochemical liver abnormality, "the biochemical hallmark" (Nichols, 2005, p. 220) but it usually takes several days to get a result. However, according to Walker et al. (2002), most biochemical liver abnormalities are diagnostic in the presence of itching and with the exclusion of other liver disorders. ALT and AST are elevated in 60% of cases of obstetric cholestasis (Milkiewicz, Elias, Williamson & Weaver, 2002) and are usually two to three times normal levels (Walker et al., 2002). There may however, be up to a ten fold increase (Popli, Roberts, & Mills, 2006). Alkaline phosphatase (ALP) may be elevated up to four times normal levels (Popli et al., 2006). Milkiewicz et al (2002) also found gamma glutamyl transpeptidale (GGT) raised in 30% of their patients with obstetric cholestasis. Nichols (2005) describes diagnosis as complicated by lack of uniform criteria. The only consistency in the studies she reviewed was a steady increase in bilirubin, ALP, ALT, AST and SBAs.

Other associated symptoms, according to McDonald (1999), include jaundice, with a 20 to 25% incidence one to four weeks after the onset of itch. Urinary tract infection is also found in 50% of women diagnosed. McDonald (1999) also lists possible gastrointestinal symptoms, such as malaise, nausea, loss of appetite, mild upper right quadrant abdominal pain and pale bowel motions (steatorrhoea). The decreased absorption of fat soluble vitamins leads to abnormal prothrombin time and increased risk of postpartum haemorrhage (PPH). Some women have a history of cholesterol gallstones (Milkiewicz et al., 2002).

Diseases that can be easily excluded via blood tests and scanning, include Hepatitis A, B, C and E plus Cytomegalovirus, HIV, Epstein Barr, Herpes Simplex, Toxoplasmosis, Pre-eclampsia and HELLP, autoimmune liver diseases, gallstones, acute fatty liver, diabetes, primary biliary cirrhosis and sepsis (McDonald, 1999). Occasionally these conditions may co-exist with obstetric cholestasis and confuse the diagnosis.

While the condition of obstetric cholestasis is distressing for the mother, with intense itching and sleep deprivation, there are no serious short-term health risks. However women do suffer psychological, social and physical distress with the severe itching and sleep disturbances (Bruce & Watson, 2007). The main concern is for fetal risk of spontaneous and iatrogenic prematurity, fetal compromise and especially sudden intrauterine death (Milkiewicz et al., 2002). Despite many studies of fetal assessment and maternal medications, RCOG (2006), advise that "there is no evidence that any specific treatment improves maternal symptoms or fetal outcomes" (p5). Lack of possible advice about specific treatment is the reason why active management by induction of labour or/and caesarean section at 37 to 38 weeks is advised in order to avoid the risk of late stillbirth. This is common practice in most maternity units.

Case Report

Kelly (not her real name), was a 39 year old woman of European descent, with two children, and in her third pregnancy. She presented on a cold winter's day for her routine Lead Maternity Carer (LMC) midwifery assessment at 33 weeks gestation, with generalized itching which had developed over the last two weeks. The itching had started on the palms of her hands and soles of her feet, but had spread up her legs, down her arms and over her body. She reported that the itching was disrupting her sleep. On examination, there was no sign of a rash or any sign of jaundice. Her urinalysis was clear, fundal height equal to dates, good fetal movements were present and she was normotensive. Although she had no history of viral illnesses, abdominal discomfort, and gallbladder or liver diseases and was not on any medications apart from iron tablets, she reported some malaise, nausea, and loss of appetite. There was no history of steatorrhoea. Initial antenatal blood tests, high vaginal swab, midstream urine and 28 week full blood count, polycose screen and midstream urine had been normal.

Kelly had two normal births previously.

However the second birth was complicated by a large PPH requiring four units of blood.

She did have some itching near the end of her second pregnancy. Her family history did not include liver disease, but Kelly was born five weeks premature and her grandmother had an unexplained stillbirth at term. It was explained to Kelly that an uncommon liver problem called obstetric cholestasis causes itching in pregnancy and if untreated may be hazardous for unborn babies. It could be diagnosed with blood tests. LFTs, full blood count and midstream urine were requested.

Kelly's LFTs came back with raised ALP, ALT and AST, but with a normal full blood count. Her midstream urine showed an asymptomatic infection, which was treated with the suggested antibiotic. A discussion with the duty obstetric registrar concluded that Kelly may have obstetric cholestasis. Further blood tests including screening for viral infections, clotting studies, kidney function tests, full blood count and SBAs were requested. In addition, a pregnancy and maternal liver scan were booked.

Further tests showed that Kelly's SBAs were raised along with a steady rise in ALP, ALT and AST. Her liver scan showed no sign of liver or gallbladder disease. Her APPT and Prothrombin time were normal as was her full blood count. Viral tests for Hepatitis A, B, C and E plus Cytomegalovirus, HIV, Epstein Barr, Herpes Simplex and Toxoplasmosis were negative. The pregnancy scan showed a healthy fetus on 70th centile, with normal liquor, dopplers and biophysical profile (BPP). Exclusion of other possible causes of liver dysfunction combined with itching in the absence of a rash confirmed the diagnosis of obstetric cholestasis.

Kelly and her partner were given explanations and patient information pamphlets, which were downloaded from the internet from the RCOG (2006) website and British Liver Trust (2007), along with copies of her blood test results and scan reports. Ideas to manage the itching were discussed, including a low fat diet, good water intake, skin lotions and keeping cool. Kelly and her partner were advised of the importance of monitoring Kelly for symptoms of liver damage and of assessing her baby's wellbeing, because of the risk of sudden fetal demise after 37 weeks. An appointment was made for Kelly to see a duty obstetric specialist within the week.

The duty obstetric specialist appointment at 34 weeks was a disappointment. Kelly was seen by a junior registrar who advised that itching is common in pregnancy and her LFTs and SBAs were not really significant compared to the local laboratory non-pregnant level. This was surprising advice considering Kelly's LFTs and SBAs results (table 1). Kelly said she felt embarrassed during the consultation especially as her partner asked her if she was disappointed that she was fine! Meanwhile she was increasingly distressed by the itching, even resorting to the extent of using a hard bristled brush up and down her legs.

At Kelly's 35 weeks assessment, her pregnancy remained unremarkable, with clear urinalysis, her fundal height was equal to dates, she had good fetal movements and was normotensive. However, Kelly's itch had increased, so it was highly likely that her SBAs and other LFTs were becoming more abnormal. The tests were repeated and came back showing further rise in LFTs including SBAs. Another urgent duty obstetric specialist appointment was made for Kelly.

Kelly was under strict instructions to advise me if there was any reduction in fetal movements, or of other concerns. She was given a script for oral vitamin K 10mg daily as she was worried about PPH and had read the information pamphlets cautioning that obstetric cholestasis can reduce absorption of vitamin K, leading to PPH (RCOG, 2006). Her previous large PPH was still fresh in her mind. She has graphic memories of her haemorrhage and the drama of the situation as it unfolded, and also of a personal sense of helplessness.

At the appointment with the duty obstetric specialist at 36 weeks, Kelly refused to see the registrar and insisted on a consultation with the specialist. He listened to Kelly, checked her blood test results and perused the copy of RCOG (2006) obstetric cholestasis 'Green Top' guidelines that had been downloaded from the RCOG website and stapled to Kelly's LMC referral. He agreed that Kelly had a diagnosis of obstetric cholestasis and booked an induction of labour at 38 weeks. He recommended a low fat diet, liver cleansing herbal preparation and stress reduction. Sleeping medication, antihistamine phenergan and skin lotions were offered. A cardiotocograph (CTG) was performed on the day of the consultation, but the specialist did not order any other fetal surveillance because he explained to Kelly that there is no specific fetal monitoring that can reliably foretell fetal outcome in obstetric cholestasis.

Kelly was pleased to have a confirmed diagnosis. She explored the information on herbs via the obstetric cholestasis patient information websites and made an informed decision not to try them. Her diet was already low in fat. She had used a variety of skin lotions including calamine, hydrocortisone and aqueous cream. However she felt they only provided very short term relief and that ice packs, cold showers and scratching were more useful. She tried sleeping medication and the antihistamine phenergan, but did not enjoy the drowsiness associated with the medication, especially as it did not improve the itch. Being told to reduce her levels of stress was not helpful, in the presence of a persistent and untreatable itch, and news that the condition may be fatal for the baby. Kelly had conflicting feelings about the effects of her condition and her baby, alternating between resentment and guilt.

Despite being advised of the lack of evidence of any benefit from fetal monitoring, Kelly was keeping a kick chart and requested twice weekly CTGs and a further scan for her own reassurance. The scan confirmed good fetal growth and liquor volume with normal BPP. By the time Kelly's induction date arrived, she was scratching constantly. The blood tests taken on the day before the induction showed a further increase in LFTs. Kelly was induced with prostaglandin gel and went into labour a few hours after the second dose. Light meconium was noted in the liquor, but the fetal heart remained reassuring throughout. Kelly coped well, with entonox for pain relief, and a healthy baby girl was born normally. She had an Apgar score of 8 and 10 and weighed 3630 gms. To reduce the risk of haemorrhagic disease of the newborn, the baby was given an intramuscular injection of vitamin K. Mindful of her history of PPH, Kelly's third stage was actively managed with IV syntocinon and a postpartum syntocinon infusion. Her blood loss was within normal limits. Kelly successfully breastfed her baby.

The follow-up LFTs at two weeks postpartum were normal and Kelly reported resolution of itching within two days following birth. She was given copies of all her maternity information. Contraception was discussed and Kelly was cautioned about the chance of developing obstetric cholestasis symptoms with the oestrogen containing contraceptive pill, due to the hormonal effect on the liver. The 40 to 90% risk of obstetric cholestasis recurring in another pregnancy was also impressed upon Kelly. She was adamant that she would not be able to cope with the physical and emotional discomfort of such severe itching in another pregnancy, as it totally consumed her life and soul for the last weeks of her pregnancy. She consequently requested a tubal ligation.

Discussion

Kelly's case had many characteristic features of obstetric cholestasis, including the development of itching without a rash and at least one biochemical liver abnormality in the third trimester of pregnancy, as described by Walker et al (2002). Her itching was intense and distressing. It began on her hands and feet, later spreading to the limbs and body in an ascending pattern, without any skin rash. Her itching was in tandem with raised SBAs and accompanied by other abnormal LFTs of raised bilirubin, ALP, ALT and AST.

Kelly had some malaise, nausea, and loss of appetite. She also had a typical urinary tract infection at the time of diagnosis of obstetric cholestasis (McDonald, 1999). Her symptoms occurred in winter, and this fits with known seasonal variation which may have a relationship to diet, and in particular, inadequate selenium intake (Lammert, Marschall, Glantz, & Matern, 2000). She experienced itching near the end of her second pregnancy with an unexpected PPH requiring four units of blood. Unfortunately her LFTs were not examined at this time so a retrospective diagnosis of obstetric cholestasis, with possible associated clotting disorder, was not possible.

Kelly was vague about her family ethnic origins, but thought they may have come from somewhere in the UK. So it was unknown whether she shared a genetic predisposition, as described by Beuers and Pusl (2006), as coming from the 'hot spots' of Chile and Bolivia (with risks increased by 5 to 15%) or Scandinavia and the Baltic States (with risks increased by 1 to 2 %). However Kelly's unexplained pre-maturity, and her grandmother's stillbirth, could indicate a genetic link. It is considered that around 16% of obstetric cholestasis cases are familial and several recent studies show a genetic predisposition (Nichols, 2005). One theory being investigated by Beuers and Pusl (2006) is that 'leaky gut' may predispose some women to obstetric cholestasis, with the suggestion of a genetic factor affecting both intestinal and liver function.

[FIGURE 1 OMITTED]

According to RCOG (2006) the current stillbirth rate for women with obstetric cholestasis is comparable to the general population in the UK, falling from a high of 107 stillbirths per 1000 obstetric cholestasis affected pregnancies in the earliest reported study in 1976, to more recent studies post-1980 showing 9.1 stillbirths per 1000 pregnancies. Obstetric cholestasis was unknown until the 1950s (Lammert et al., 2000) and as Williamson et al., (2004) indicate, recent active management of the condition with fetal surveillance and timed early delivery before 38 weeks, is likely to be the reason for these improved outcomes. They advise that in singleton pregnancies affected by obstetric cholestasis, stillbirth is most likely to occur from 37 weeks gestation, although this may be earlier in multiple pregnancies. Equally, they caution about fetal risks from early delivery, and advise these risks need to be balanced with the risks of stillbirth.

It is uncertain how obstetric cholestasis causes the increased fetal risk of spontaneous and iatrogenic prematurity, fetal compromise and intrauterine death (Milkiewicz et al., 2002). However, it is thought to be related to SBA levels causing an increase in myometrial contractivity of the uterus, with stillborn infants showing signs of acute anoxia and meconium stained liquor. Meconium stained liquor is thought to be caused by the raised SBA levels in the fetus having a peristaltic effect on the fetal bowel, as described by Nichols (2005). Another theory is there may be a vasoconstrictive effect of high levels of SBA on placental veins added to a possible meconium induced vasoconstriction of the umbilical vein (Bruce & Watson, 2007).

It has been proposed that obstetric cholestasis may be divided into mild obstetric cholestasis and severe obstetric cholestasis. This is defined as SBAs being under or over 40 micromol/L and is related to the probability of fetal complications which increase by 1-2% per additional micromole/L (Glantz, Marschall, & Mattsson, 2004). Kelly's SBA levels rose from 11 micromol/L at 33 weeks to 22 micromol/L at 35 weeks, which would put her in the mild obstetric cholestasis category. However Kelly did not have her bile acid levels repeated at 38 weeks, although there is little doubt these would have been increased, as in the previous two weeks her AST, ALT, bilirubin and ALP had all increased significantly.

In the New Zealand 'Guidelines for Consultation with Obstetric and Related Specialist Medical Services (Referral Guidelines),' obstetric cholestasis is coded as a Level 3. Level 3 code states "The Lead Maternity Carer must recommend to the woman that the responsibility for her care be transferred to a specialist, given that her pregnancy, labour, birth or puerperium (or the baby) is or may be affected by the condition" (Ministry of Health, 2007). However the contrast between Kelly's two obstetric specialist consultations highlights the difficulty in diagnosis of obstetric cholestasis. Popli et al., (2006) suggest this may be due to lack of consensus of the criteria for diagnosis. They caution that while it is generally agreed that abnormal liver function tests are indicative of obstetric cholestasis, there is no uniform agreement, and diagnosis is only made by exclusion of other causes of hepato-biliary dysfunction.

Knowing that Kelly's baby was at risk of acute lethal anoxia (Nichols, 2005), which could not be predicted or prevented by fetal monitoring (RCOG, 2006), caused high stress for Kelly until she was admitted for induction of labour at 38 weeks. Kelly was counselled about of the lack of evidence of any benefit from fetal monitoring. However, after reading obstetric cholestasis patient information, she made her own decision to keep a kick chart and requested twice weekly CTGs and a further scan. She explained that "I can't sit back and do nothing and I need the reassurance that my baby is still alive and well, at least during the time on the CTG."

Management and Treatment Options

General comfort measures suggested by Nichols (2005) and conveyed to Kelly, included a low fat diet, good water intake, 'liver strengthening' herbal remedies such as milk thistle and dandelion, skin lotions, keeping cool with ice packs, cotton clothing, cool baths and a reduction in stress. Topical emollients are known to be safe (RCOG, 2006), but as Kelly found, they only provide temporary relief of itching. Kelly did not like the effect of night sedation medications, such as antihistamines, suggested by RCOG (2006). Burrows, Clavisi and Burrows (2001) report that antihistamines, while providing night sedation are not effective at alleviating itching. However she was happy to take oral vitamin K 10mg daily orally to reduce risk of PPH and fetal haemorrhage (RCOG, 2006)

Medications that may have reduced Kelly's symptoms include ursodoexycholic acid (UDCA). This is an oral medication and the dosage is 600 mg up to 1 gm/daily (Bruce & Watson, 2007). Kelly's obstetric specialists declined to prescribe UDCA for her, as she came under the mild cholestasis category, and UDCA only has provisional consent under section 23 of the New Zealand Medicines Act. Some studies showed improved fetal outcome with UDCA, although others are inconclusive (Saleh & Abdo, 2007). However, it is the most widely used medication in the United Kingdom to treat obstetric cholestasis (RCOG, 2006). Saleh and Abdo (2007) consider UDCA to be the best available therapy to alleviate pruritis and to lower maternal and fetal SBAs. Furthermore it has no adverse side effects reported, except occasional mild diarrhoea (Milkiewicz et al., 2002).

Burrows et al. (2001) describe further medications to treat obstetric cholestasis, alone or in combination with ursodoexycholic acid, such as S adenosyl methionine (SAMe). However since SAMe is usually given twice daily as an intravenous infusion, and does not appear to be any more effective than ursodoexycholic acid, it has fallen out of favour. Other treatments that have fallen out of favour include Cholestyramine, which may improve symptoms of itching in some women but is unpleasant to ingest and may exacerbate vitamin K deficiency. Activated charcoal and guar gum have unpleasant gastrointestinal side effects, are ineffective and no longer in use.

Recent research has suggested that dexamethasone may be useful when obstetric cholestasis is unresponsive to UDCA, especially in women of Asian and South American origin (Diac et al., 2006). However according to Saleh and Abdo (2007), dexamethasone is less effective than UDCA at reducing SBAs and not effective in alleviation of pruritis or reduction of ALT. RCOG (2006) warns that repeated courses of dexamethasone used for fetal lung maturation have potential fetal and neonatal neurological effects, and should not be used as the initial treatment of choice for obstetric cholestasis.

To have a diagnosis of obstetric cholestasis, postnatal testing for LFTs should be deferred for at least ten days postpartum, as levels may increase in this time (David, Kotecha & Girling, 2000). However, all symptoms usually disappear within one to two days after delivery (Milkiewicz et al., 2002) and biochemistry must have returned to normal within a few weeks after birth, for the definitive diagnosis of obstetric cholestasis to be made (Walker et al., 2002). This was the case with Kelly.

Kelly successfully breastfed her baby girl and was reassured that there were no contraindications to breastfeeding with obstetric cholestasis (RCOG, 2006). Kelly was informed that the risk of obstetric cholestasis manifesting in another pregnancy were as high as 40 to 60 % (Nichols, 2005) and up to 90% (Williamson et al., 2004). Her choice of a tubal ligation for permanent contraception resolved the potential of developing obstetric cholestasis symptoms with the oestrogen containing contraceptive pill (RCOG, 2006). Kelly was cautioned that women who have had obstetric cholestasis were more likely to be later diagnosed with hepatitis C, non-alcoholic cirrhosis, gallstones, cholecystitis and non-alcoholic pancreatitis (Ropponen, Sund, Riikonen, Ylikorkala, & Aittomaki, 2006) and regular health checks with her general practitioner were suggested.

Implications for midwifery practice

The aim of discussing this case is to increase midwives awareness of obstetric cholestasis. Knowledge of symptoms and tests will provide the information required to assist in accurate diagnosis. This will enable timely referrals to an obstetric specialist and will facilitate appropriate management of women with obstetric cholestasis in order to decrease the risk of adverse outcomes for mother and baby. To this end, we have developed a flow chart that will inform midwives assessment, investigation and decision-making about obstetric cholestasis (Figure 1). Midwives, especially those who provide continuity of care, have the huge advantage of an ongoing partnership relationship with the woman and the opportunity to provide her and her family with information, support and follow-through care.

Conclusion

Obstetric cholestasis is a serious condition of the third trimester of pregnancy, and carries a risk of prematurity and sudden intrauterine fetal death in previously healthy fetuses. Obstetric cholestasis affects the woman's psychological, social and physical well-being, through the distress of intense itching and associated sleep deprivation. Lammert et al., (2003) advise "Despite the potential for adverse maternal and fetal/neonatal outcomes, cholestasis of pregnancy is often neglected and treated expectantly" (p.123). Investigations for obstetric cholestasis should be considered if a woman in the third trimester of pregnancy, develops itching without a rash and has at least one biochemical liver abnormality. However, diagnosis can be difficult, and includes exclusion of other causes of itching and liver disorders.

It is important that midwives realize that they, in partnership with women, have the power to prevent adverse outcomes, even in situations when difficulties in diagnosis may affect management of obstetric cholestasis. The obstetric cholestasis flow chart (Figure 1) will support midwives' confidence in this area. Midwives are the main providers of primary maternity care in New Zealand and are the gatekeepers for access to diagnosis and referral for treatment for pregnant women who develop this condition. If midwives don't listen then who will?

Accepted for publication: Feb 2008 Cromin, R. Maude, R, (2008) Third Trimester Itch: Obstetric Cholestatis a serious condition of pregnancy. New Zealand College of Midwives Journal 38, 20-25

References

Abedin, P., Weaver, J., & Egginton, E. (1999). Intrahepatic cholestasis of pregnancy: Prevalence and ethnic distribution, Ethnicity and Health, 4(1/2), 35-37.

Beuers, U., & Pusl, T. (Eds.). (2006) Intrahepatic cholestasis of pregnancy as an indicator of biliary diseases: a population-based study. Hepatology, 43(4), 647-649.

British Liver Trust, (2007). Obstetric cholestasis. Retrieved Sept 1, 2007, from: http://www.britishlivertrust.org.uk

Bruce, K., & Watson, S. (2007). Management of intrahepatic cholestasis of pregnancy: A case report, Journal of Midwifery and Women's Health, 52(1), 67-72.

Burrows, R., Clavisi, O., & Burrows, E. (2001). Interventions for treating cholestasis in pregnancy. Cochrane Database for Systemic Reviews, 2. Retrieved June 1, 2007, from: http:// www.theCochraneLibrary.com.

Chambers, J. (2006). The Obstetric Cholestasis Support Website. Retrieved June 1, 2007, from http://www.ocsupport.org.uk.

Ch'ng, C., Morgan, M., Hainsworth, I., & Kingham, J. (2002). Prospective study of liver dysfunction on pregnancy in Southwest Wales, Gut, 51(6), 876-880.

David, A., Kotecha, M., & Girling, J. (2000). Factors influencing postnatal liver function tests. BGOG: An International Journal of Obstetrics and Gynecology, 107(11), 1421-1426.

Diac, M., Kenyon, A., Nelson-Piercy, D., Girling, J., Cheng, F., Tribe, R, Goodman, J., Shennan, A., & Williamson, C., (2006) Dexamethasone in the treatment of obstetric cholestasis: a case series. Journal of Obstetrics and Gynecology, 26(2), 110-114.

Glantz, A., Marschall. H., & Mattsson, L. (2004). Intrahepatic cholestasis of pregnancy: Relationships between bile acid levels and fetal complication rates, Hepatology, 40, 467-474.

Lammert, F., Marschall, H., Glantz, A., & Matern, S. (2000). Intrahepatic cholestasis of pregnancy: Molecular pathogenesis, diagnosis and management, Journal of Hepatology, 33,1012-1021.

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Nichols, A. (2005). Cholestasis of pregnancy: A review of the evidence, Journal of Perinatal and Neonatal Nursing, 19, 217-225.

Popli, K., Roberts, J., & Mills, P. (2006). Obstetric cholestasis presenting with unusually high levels of transaminases, Scottish Medical Journal, 51(1), 57.

Ropponen, A., Sund, R., Riikonen, S, Ylikorkala, O., & Aittomaki, K. (2006). Intrahepatic cholestasis of pregnancy as an indicator of biliary diseases: a population-based study. Hepatology, 43(4), 723-728.

Reyes, H., Zatpata, R., Hernandez, I., Gotteland, M., Sandoval, L., Jiron, M., Palma, J., Almuna, R., & Silva, J. (2006). Is a lecky gut involved in the pathogenesis of intrahepatic cholestasis of pregnancy? Hepatology, 43(4), 715-722.

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Authors:

Robin Cronin BA IBCLC RM RCompN

LMC Midwfe Tauranga

Correspondence to: robincronin@xtra.co.nz

Robyn Maude PhD candidate MA (Midwifery) RM RN

Lecturer Graduate School of Nursing,

Midwifery and Health

Victoria University Wellington

Correspondence to: Robyn.Maude@vuw.ac.nz
Table 1

                      Non Pregnant              Normal Pregnant

Itch Gestation
Onset

ALT (IU/L)            1 - 40 (i)                1 - 30 (i)
AST (IU/L)            1 - 30 (i)                1 - 21 (i)
ALP (U/L)             25 - 100 (i)              125-250 (i)
Bilirubin (umol/L)    2 - 20 (iii)              3-14 (iv)

Serum Bile Acids/     3.2+/-2.9 (ii)            6.7 +/-3.6 (ii)
Bile Salts (umol/L)
GGT (IU/L)            18 +/- 5 (ii)             15 +/-7 (ii)

                      Obstetric
                      Cholestatis               Kelly

Itch Gestation
Onset

ALT (IU/L)            100 +/- 127 (ii)          131
AST (IU/L)            85 +/-126 (ii)            66
ALP (U/L)             825 +/- 380 (ii)          167
Bilirubin (umol/L)    20-25%                    11
                      jaundiced (v)
Serum Bile Acids/     36 +/-32.8 (ii)           22 at 35 wks
Bile Salts (umol/L)                             NB: No test at 38 wks
GGT (IU/L)            47 +/-36 (ii)             20

                      Local Lab
                      Values

Itch Gestation
Onset

ALT (IU/L)            0 - 45
AST (IU/L)            0 - 40
ALP (U/L)             40 - 100
Bilirubin (umol/L)    20 - 20

Serum Bile Acids/     0 - 15
Bile Salts (umol/L)
GGT (IU/L)            0 - 50

Table 1: Laboratory values - Obstetric cholestasis

i Tran (2005) ii Reyes et al (2006) iii Local Laboratory Values (2007)
iv Popli, Roberts and Mills (2006) v Nichols (2005)

* Data shown as mean +/- SD (Reyes et al, 2006)

* Markers of liver function are reduced during pregnancy due to
expansion of extracellular fluid with exception of Alkaline
phosphatase (ALP) which is elevated from ALP of placental origin
(Tran, 2005).

* Serum bile acids (SBAs) are the "the biochemical hallmark" (Nichols,
2005, p.220) of obstetric cholestasis but take up to one week for test
results in New Zealand.

* Rises in Alanine transferase (ALT) and aspartate aminotransferase
(AST) increase in 60% of cases of obstetric cholestasis (Milkiewicz,
Elias, Williamson & Weaver, 2002) and are usually two to three times
normal levels (Walker, Nelson-Piercy & Williamson, 2002) but may be
up to ten fold increase (Popli, Roberts & Mills, 2006).

* ALP may be elevated up to four times normal levels (Popli, Roberts &
Mills, 2006).

* "Although a wide variety of cut-off points have been used for
defining abnormal LFTs and bile salts, pregnancy specific ranges
should be applied "(RCOG, 2006, p.2).
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Title Annotation:PRACTICE ISSUES
Author:Cronin, Robin; Maude, Robyn
Publication:New Zealand College of Midwives Journal
Article Type:Clinical report
Date:Apr 1, 2008
Words:5224
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