Home > Publications > Selected CasesHealth > Selected Investigations Completed AprilJuly 2002 > Part II, Case no. E.1072/00-01
Complaint against: Southend Hospital NHS Trust
Complaint as put by Mr and Mrs T
1. The account of the complaint provided by Mr and Mrs T was that on 12 August 1999 Mrs T, who had a history of pre-eclampsia (raised blood pressure) in a previous pregnancy, and who was then 34 weeks pregnant, was admitted to Southend Hospital (the Hospital) with raised blood pressure, itching, sickness and high levels of protein in her urine; she had an ultrasound scan and was discharged the next day. The Hospital is managed by Southend Hospital NHS Trust (the Trust). Mrs T was admitted again on 19 August with raised blood pressure and protein in her urine and discharged the following day. On 13 September Mrs T was admitted with raised blood pressure, headache, visual disturbance and protein in her urine. Blood tests and a CTG (Cardiotocographa recording of the baby’s heartbeat) were taken, but no ultrasound scan. The following day at 8.00am, Mrs T was given medication for high blood pressure. Her blood pressure was checked at 1.00pm and 8.00pm, but no other monitoring of her or her baby was carried out. Mrs T went into labour at 9.00pm and gave birth to her son, Baby Y. Sadly, staff were unable to resuscitate him, and he died shortly after birth. In December, a senior registrar (the Senior Registrar) at another Trust (the second Trust) reviewed Mrs T’s records and suggested that she had been suffering from obstetric cholestasis (a reversible liver disease specific to pregnancy). (Note: staff at the second Trust were not subject to this complaint.) Mrs T complained to the Trust but was dissatisfied with the responses she received. She requested an Independent Review, but that was refused by the Trust’s Convener.
2. The matter investigated was that Mrs T’s care and treatment was unsatisfactory in that staff at the Trust:
(a) failed to diagnose that Mrs T was suffering from obstetric cholestasis; and
(b) did not monitor Mrs T and her baby adequately.
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Investigation
3. The statement of complaint for the investigation was issued on 14 September 2000. Comments were received from the Trust and relevant papers, including Mrs T’s clinical records, were examined. Two professional Assessors, both Consultant Obstetricians and Gynaecologists, were appointed to advise on the clinical aspects of the case. Their report is reproduced in full at paragraph 19 of this report.
Mr and Mrs T’s evidence
4. In a letter to the Ombudsman, dated 19 August 2000, Mr and Mrs T wrote:
‘… you will see … that [at the time of the initial complaint in November 1999] … I believed my baby [Baby Y] had died through lack of attention to my pre-eclampsia. This was especially upsetting as I had similar problems with my previous baby and was delivered at 38 weeks. He [my previous baby] was perfectly fit and healthy and I believe that if this procedure had been followed, [Baby Y] would be with us now.
‘Because I needed to know why my baby had died and because I was so appalled at the care I had received at [the Hospital] I personally contacted [a consultant physician at the second Trust (the Consultant Physician)]. My intention was to find out more about pre-eclampsia and why my baby died. … I was seen by [the Senior Registrar]. … From the information that I supplied about my symptoms during pregnancy a probable diagnosis of obstetric cholestasis was made. …
‘… [on 13/14 September 1999] I was in hospital feeling pretty awful and pleading with [the consultant in charge of [Mrs T’s] obstetric care at the Trust (the Consultant)] to deliver me. I was given medication for my high blood pressure at 8.00am and my blood pressure was only taken at 1.00pm and 8.00pm. No one came to monitor my baby at all until I went into labour and called for help at 9.00pm – that is 13 hours without any one checking my baby. I believe that had I received appropriate care and treatment my baby need not have suffered and died. Why were we not monitored?
‘… With respect to [the Consultant], if a holistic picture had been sought, alarm bells would have rung. Here I presented, a woman who had made herself bleed with scratching, had protein urea [sic], high blood pressure and feeling awful. I was also 39 weeks pregnant.
‘… I can assure you that all staff involved in my care were very aware of the severity of my itching; this definitely is supported by the medical records … In all I can find about eight references to my itching. … On 19.08.99 I sat up all night with the midwife … because I couldn’t sleep with the itching. I’d ripped my legs to pieces but couldn’t stop – blood and scars were very apparent, and the scars are still apparent to this day. The notes said that they would monitor the itching, but they didn’t. [The Consultant] was also aware … I even said to him my blood pressure isn’t going to get any better when I’m in such a state.
‘I was prescribed: Diprobase, Calamine Lotion and Piriton. None of the medications prescribed had any effect at all. Why wasn’t any further action taken to investigate my symptoms? Especially as these medications are known not to be effective in the case of obstetric cholestasis.
‘… I am really worried that professionals who were treating me were unable to make the diagnosis [of obstetric cholestasis] when they were aware that I had many of the symptoms … I also had dark urine (which is another symptom of cholestasis). I was just told that I should drink more but I drank copious amounts during pregnancy and the dark urine and itching persisted. Once again a simple test could have avoided the tragic outcome. …
‘I went to [the second Trust] expecting to find out more about pre-eclampsia and how I could avoid losing another baby, but since learning from them the symptoms of cholestasis … I fail to see how the classic signs that I had were overlooked by professionals at [the Trust].
‘I had watched my baby’s heartbeat disappear and had to scream for someone to do something … After an emergency Caesarean my baby died …
‘[The Consultant] has stated that he should have done a bile acid test but didn’t. Why not? … He should have acted, and if he was unsure of the blood results he should have asked for a second opinion. …
‘… I fail to see how … no one looked at the symptoms as a whole and made the correct diagnosis. …
‘… The symptoms were there and medically recorded – both for cholestasis and high blood pressure – the appropriate action could and should have been taken at the time …’
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5. On 3 December 1999, Mrs T was seen by the Senior Registrar, who then wrote to Mrs T’s GP on 6 December saying:
‘… I had the opportunity to review [Mrs T’s] hospital notes and on further questioning it became clear that she has suffered severe pruritis in both [her 1997 and 1999] pregnancies. She reports using a hairbrush to scratch herself and inducing marked scars from scratching. These bled and she continues to have residual scarring as a consequence. She was unable to sleep and when asked if she noticed any change in the colour of her urine or faeces, she told me that her urine was noted to be dark, and that she was often advised to drink more, as she may be dehydrated. She has no history of pruritis outside pregnancy. On review of her hospital notes, one bilirubin reading was slightly raised [to 21] on 19th August, although this reduced to 14 by 13th September, one day prior to delivery. Her ALT [alanine transaminase – a liver enzyme] was normal in August but the reading one day prior to delivery was 40 and the AST [aspartate transaminase – another liver enzyme] was 36.
‘I have explained to her that she gives a good history for a diagnosis of obstetric cholestasis. However, her liver function tests were not markedly raised and it would be very useful to try to confirm the diagnosis. … it would be possible to check the bile acid level [from blood samples taken at the time of delivery] … and if this is raised it would be additional confirmation of the diagnosis …’
6. On 20 December 1999, the Consultant Physician wrote to the Consultant. His letter included:
‘… [Mrs T] … was seen by [the Senior Registrar] [who] is particularly expert in obstetric cholestasis and I [have] discussed [Mrs T] [with her] ... Not surprisingly her conclusions were similar to mine.
‘… we have the results of our own investigations and they only complicate matters further … [the] persistence of abnormal liver function in a patient with features otherwise of obstetric cholestasis would suggest a rather more profound abnormality of bile transport such as BRIC (benign recurrent intrahepatic cholestasis)’ [see paragraph 17]
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Trust response to the statement of complaint
7. In his formal response of 4 October 2000 to the statement of complaint the Trust’s Chief Executive (the Chief Executive) wrote:
‘… I believe the Trust has, over the months, made a full attempt to address [Mr and Mrs T’s] concerns and has offered every support to [Mrs T] since the tragic loss of their baby, [Baby Y]. I very much regret that the Trust has not been able to resolve this matter to [Mr and Mrs T’s] satisfaction.
‘… It is true to say that obstetric cholestasis was not diagnosed during [Mrs T’s] pregnancy. I understand that this is an extremely rare condition in the white population and although in retrospect [Mrs T] was thought to have cholestasis, at the time her liver function tests were normal, which would have been the significant clinical marker. The subsequent investigations suggested obstetric cholestasis as a possible diagnosis but did not confirm that she had that condition during her pregnancy ...
‘At the meeting held on the 26th January 2000 [Mr and Mrs T] acknowledged that [Mrs T’s] care had been appropriate for a patient with pre-eclampsia and, in fact, the practice at [the Hospital] exceeds the monitoring guidelines recommended by the Royal College of Obstetrics and Gynaecology. [Mrs T’s] antenatal care was later endorsed by [the Consultant Physician] at [the second Trust] and in the report given by the [Clinical Adviser to the Trust’s Convener] ...
‘I accept that certain aspects of [Mrs T’s] general experiences were less than satisfactory. I also accept that her blood pressure was not monitored for seven hours on 14 September, the day of [Baby Y’s] delivery. The Trust has apologised for this. However, the [CTG] tracing taken that morning was satisfactory. With pre-eclampsia it is accepted practice for a tracing to be performed once daily. Subsequent to the internal enquiry following [Baby Y’s] death the Trust has adopted the practice that a CTG tracing should be performed twice daily, even if the first trace is normal. There is no indication to perform twice daily, even if the first trace is normal. There was no indication to perform an ultrasound or Doppler scan prior to delivery since these tests would not have contributed anything to the clinical picture of mild pre-eclampsia.
‘In summary, as I understand it, the clinical picture would appear to point to the cause of [Baby Y’s] death as being an undefined acute event, since the previous CTGs were all within normal limits. It is very unfortunate that the exact cause of the tragedy will never be known and I do understand how difficult this must be for the [family].
‘… I can confirm [that] all Labour Ward protocols have been reviewed …’
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Trust’s protocols and guidance
8. I have seen that the Trust’s labour ward protocols were updated in October 2000 and that they include guidance on the ‘Management of hypertension, severe hypertension and pre-eclampsia’ in obstetric practice. The guidance includes:
‘The obstetric registrar must be informed of any persistently elevated blood pressure (diastolic above 90 mm Hg, or a rise of 20 mm Hg above the booking blood pressure …)
‘For [a] decision on delivery, [CTG] and assessment of cervical status will also be necessary. The aims of management are:
- Reduce blood pressure.
- Sedate the mother.
- Prevent fits.
- Make plans for delivery. …’
9. The Trust also developed a new protocol in October 2000 for the management of ‘Intrahepatic cholestasis of pregnancy (obstetric cholestasis)’. Included in the list of clinical features are severe pruritis affecting the limbs and trunk (usually developing during the third trimester), abnormal liver function tests (possibly associated with dark urine), anorexia and malabsorption of fat with steatorrhoea (loss of fat in the stool). The protocol goes on to say that complete recovery is usually rapid, following delivery. Diagnosis is based on abnormal liver function tests. The protocol says that the third stage of labour should be managed actively, as there is an increased risk of postpartum haemorrhage; the foetus should also be monitored closely. However, prediction of foetal compromise is difficult and early delivery at 37-38 weeks may decrease perinatal mortality.
10. On 23 April 2001 the Trust provided this Office with the following information on bile acid testing at the hospital in 1999.
‘The first request for this test was in August 1998 and was prompted by the patient herself. It would seem from … [the] correspondence that this patient had a particular interest in obstetric cholestasis. … the next request … was dated 26th November 1999 … initiated by [a consultant obstetrician and gynaecologist]. There were a further 10 tests on blood from 8 patients, one of which was done retrospectively on a sample of [Mrs T’s] blood taken on the 17th September 1999. All these 11 samples were requested by medical staff. …’
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Clinical background information
11. In this next section of the report, I set out some background information on liver function, obstetric cholestasis and related clinical conditions. This information has been provided by one of the Ombudsman’s professional advisers, who is an expert in metabolic conditions of the liver.
12. Obstetric cholestasis is a condition which occurs in some women in the third trimester during pregnancy. The term describes the slowing of bile flow (cholestasis) in the intrahepatic bile ducts (within the liver). Bile acids are manufactured by the liver cells and secreted into the intrahepatic bile ducts, and accumulation of these bile acids may cause the clinical symptom of pruritis (itching of the skin). This symptom can be very distressing for the patient, but it is not in itself dangerous. In addition, this condition results in retention of more bile pigment in the circulation (bilirubin), which may give the patient a yellow tinge (jaundice) and darken the colour of the urine. More rarely, other features of liver dysfunction occur, such as steatorrhoea giving rise to pale stools, or reduction in function of the liver (manifested by a reduction in the production of one of the essential clotting factors, prothrombin). This means that the patient may be more likely to bruise or bleed. The condition resolves in the puerperium (childbirth) and this suggests that the foetus or placenta may produce a substance which causes the change in bile flow. The condition may be associated with an increased incidence of perinatal morbidity and mortality.
13. The outcome of obstetric cholestasis is usually benign, but there is an increased risk of foetal distress and unexplained stillbirth. The reason why there may be an increased incidence of mortality and morbidity to the foetus in this condition is not clear. However, early delivery is recommended following confirmation of the maturity of the foetal lung, particularly in a patient with a previous history of foetal distress or stillbirth. Spontaneous labour may occur.
14. There is a strong tendency for cholestasis to recur in subsequent pregnancies, or when taking the oral contraceptive pill. There is also a strong familial history, although the inheritance is unclear. Use of a synthetic bile acid (ursodeoxycholic acid, UDCA) may be helpful in reversing liver dysfunction and pruritis, but its protective effect on the foetus is uncertain.
15. The diagnosis of obstetric cholestasis is often made on clinical grounds when patients complain of the characteristic generalised itching (pruritis) described above, which may or may not be associated with jaundice. The skin irritation is due to an increase in circulating bile acids. This resolves in the puerperium in the absence of pruritogenic (causing itchiness) skin, medical or underlying liver disease. In order to establish the diagnosis of this condition, there must also be derangement of biochemical liver function tests, primarily elevated serum alkaline phosphatase, gamma glutamyl transferase (GGT), bile acids and occasionally transaminases.
16. Alkaline phosphatase is an enzyme which may be present in circulation and comes from the liver and from the placenta. The level of this enzyme in circulation increases during normal pregnancy. The Ombudsman’s professional adviser has commented that it is uncertain in Mrs T’s case whether some of the circulating alkaline phosphatase came from the biliary tract in relation to the cholestasis. She considers that it would have been helpful to have measured another of the biliary tract enzymes, GGT (paragraph 15), which, if found to be increased, would have been further evidence of cholestasis. She has said that it would be advisable for this to be done when seeking to diagnose obstetric cholestasis; the standard profile of most biochemical machines for blood-testing would be set up to do this.
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Benign recurrent intrahepatic cholestasis (BRIC)
17. This is a rare condition characterised by recurrent episodes of cholestasis in the absence of any mechanical or pharmaceutical cause of obstruction of bile, and where there is restoration of normal liver function between episodes. Pruritis usually precedes jaundice in the attacks. As with obstetric cholestasis, liver dysfunction may occur, e.g. this may be manifested by easy bruising or bleeding due to a reduction in the measured prothrombin time. UDCA is useful for treating both the pruritis and in reducing or reversing episodes of cholestasis, because this synthetic bile acid reduces the endogenous (normal liver production of) bile acids. UDCA itself does not cause skin irritation.
Liver dysfunction
18. The liver is composed of many cells which are arranged in cords of cells surrounded by blood and bile channels, and divided into separate sections (lobules) within the different liver lobes. Each group of liver cells (within a lobule) is supplied by a branch of the portal vein (bringing blood containing nutrition and substances absorbed from the bowel), and the hepatic artery (bringing oxygen). Each liver cell has many functions in clearing the blood of nutritious substances and waste products and secreting new substances to be circulated around the body. Liver cells have an enormous capacity to regenerate themselves. In the past, the liver structure and individual liver cells were visualised by microscopy after taking a sample of the liver (liver biopsy) but this is now usually unnecessary because there are various enzymes (protein substances) which can act as biochemical markers for the structure of the liver cells. For example, the enzyme alkaline phosphatase comes from the outer membrane of the liver cell and the bile ducts; GGT comes from the bile ducts; and alanine (ALT) and aspartate (AST) transaminases come from the inside of the liver cell (cytosol). In cholestasis, more alkaline phosphatase and GGT appear in circulation. Where there is severe damage to the liver cell, such as may occur with infective hepatitis, more ALT appears in the blood.
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The Assessors’ report
19. I set out next in its entirety, the report from the Ombudsman’s Assessors for this investigation.
Report by the Professional Assessors to the Health Service Ombudsman for England of the clinical judgments of staff involved in the complaint made by
Mr and Mrs T:
Professional Assessors: Mr A, MD FRCOG
Consultant Obstetrician and
Gynaecologist
Miss B, MD FRCS FRCOG
Consultant Obstetrician and
Gynaecologist
Matters considered and basis of report
i) We have considered the matters set out in paragraph two of the Ombudsman’s report. The following documents were made available to us: Mrs T’s medical and nursing records and all the correspondence relating to the complaint made to the Trust.
Mrs T’s obstetric history
ii) We note from the records that Mrs T previously conceived two ectopic pregnancies – one in the right fallopian tube in 1995 and one in the left fallopian tube in 1996. In 1997 she conceived again and went on to deliver a healthy male infant on 18 September 1997. In her fourth pregnancy she was delivered of a male infant by Caesarean section on 14 September 1999. However, the baby died shortly after delivery.
Clinical management of obstetric cholestasis
iii) In our own units, patients presenting with generalised pruritis and a possible diagnosis of obstetric cholestasis in the third trimester have their liver enzymes, and liver function tests and serum bile acids measured. If there is evidence of raised aspartate transaminase or raised bile acids then intensive monitoring of the foetus and delivery by 37-38 weeks is recommended.
Comments on the obstetric history of Mrs T’s pregnancy in 1997
iv) The care given during Mrs T’s 1997 pregnancy was not subject to this investigation. However, information about that pregnancy is given here to provide contextual information to the 1999 pregnancy. We note that, in her full term pregnancy in 1997, Mrs T suffered from generalised itching in the third trimester, for which she was prescribed Piriton and Calamine and written in the case notes dated 9 September 1997 were the words ‘pregnancy rash.’ Liver tests were performed which were all in the normal range for the Hospital’s laboratory, with the exception of an increase in the enzyme alkaline phosphatase. This may increase during normal pregnancy, as it is secreted from the placenta.
v) Mrs T was re-admitted on 14 September 1997 with recurrent headache and raised blood pressure which was treated with an anti-hypertensive agent, Methyl Dopa, for some weeks (at a dose of 500mg three times a day). The picture in this patient at that time might also have been complicated because Methyl Dopa may, in itself over that period of time, have made the pruritis worse. There appear to be no other references in the 1997 notes to itching and/or rash. Labour was induced solely because of high blood pressure on 17 September 1997 and Mrs T was delivered of a healthy boy by forceps under epidural on 18 September 1997. The baby’s weight was 3.57kg.
vi) During Mrs T’s 1997 pregnancy, the clinical feature of pruritis raises the possibility of pregnancy cholestasis. However, at the time, the bilirubin was normal. The alkaline phosphatase enzyme, which was also slightly raised, was probably increased as a direct result of the pregnancy. Whilst it is a distinct possibility that Mrs T did suffer from obstetric cholestasis during the 1997 pregnancy, equally, such minor abnormalities could also relate to her anti-hypertensive medication (Methyl Dopa).
Obstetric History of the Index (1999) Pregnancy
vii) Mrs T booked for confinement at the Hospital in her fourth pregnancy in February 1999. Using her last menstrual period and ultrasound scanning, her estimated date of delivery was 19 September 1999. Her pregnancy progressed normally until 34 weeks’ gestation, on 12 August 1999, when she developed signs of hypertension (blood pressure of 140/100) and proteinuria. She also complained of generalised itching: there are references in the notes to ‘itch’ on 12, 13, 15, 19 and 20 August. This was treated with Calamine and Piriton. Liver function tests were also measured on 19 August. The bilirubin was noted to be 14 (normal range <20 mmol/l), ALT 28 (normal range <65 iu/l), AST 29 (normal range 5-40 iu/l), alkaline phosphatase 400 (normal range <180 iu/l).
viii) On 13 September 1999, because of persistent hypertension (a blood pressure measurement of 140/100), Mrs T was admitted to Hospital. Repeat liver enzyme and liver function tests on 13 September 1999 showed the bilirubin was 14, ALT 40 and AST 36, alkaline phosphatase 381. Mrs T’s blood pressure settled on admission but was 140/100 again at 1.00pm on 14 September 1999 and she was prescribed Methyl Dopa (one dose of 500mg) as a treatment for this. A CTG taken at 8.22am on 14 September was normal. Mrs T subsequently went into spontaneous labour. The next CTG test was carried out at 8.55pm and was of some concern in that it was noted that there were no accelerations of the foetal heart. Further CTGs at 9.20pm and 9.29pm were abnormal and indicated foetal distress. Mrs T underwent an emergency Caesarean section, which resulted in delivery of a male baby who died shortly after delivery.
Comments on complaint (i) – the Trust failed to diagnose obstetric cholestasis
ix) There is evidence in the case notes that Mrs T suffered from pruritis in both her 1997 and her 1999 pregnancies. Her pruritis appeared to start in the third trimester and resolved in the puerperium. This suggests, on clinical criteria, that she may have suffered from obstetric/pregnancy cholestasis.
x) However, despite the clinical features suggesting cholestasis, the liver enzymes and bilirubin, which may become abnormal with this condition, were within the normal ranges for the Hospital’s laboratory. It is notable that bile acids were not requested at this time. Had they been measured and found to be increased, this would have confirmed the clinical diagnosis of obstetric cholestasis.
xi) The Consultant Physician at the second Trust suggested retrospectively in December 1999 that Mrs T possibly had obstetric cholestasis in her 1999 pregnancy. He commented on the ALT enzyme, which is usually reduced in pregnancy: in Mrs T, it was just at the upper limit of normal (readings 40 & 36 respectively). He and his Senior Registrar put weight on the further rise of ALT and fall of alkaline phosphatase after pregnancy and raised the question as to whether Mrs T might also have the condition of BRIC. Although that is a possibility, it cannot be confirmed without other tests, including bile acids, and exclusion of other causes of liver disease. In our view, Mrs T did not have BRIC.
xii) It was appropriate that Mrs T had liver enzyme tests performed in 1997 and in 1999. No bile acids were requested, as would now be usual medical practice. However, such tests would not have been routinely carried out in 1997. We note that the Clinical Assessor to the Convener said in his report dated 10 June 2000, ‘based on the liver function tests available to me in the notes I would not have referred this patient for bile salt analysis … and I do not think that the majority of district general hospital consultants would have done so either.’ We would agree with that. On the basis of the liver enzymes and bilirubin measurements, no abnormality was highlighted by the Hospital’s laboratory in either pregnancy. The increase in alkaline phosphatase was more likely to be predominantly due to normal pregnancy, probably deriving from the placenta, rather than due to slowing of bile flow in the bile ducts in the liver. We note that there has now been a change in the protocol at the Trust as regards bile salt analysis requests in that from early 2000 onwards there has been a forty-fold increase in requests for bile salt analysis from the previous year.
xiii) In view of the clinical evidence of cholestasis (i.e. pruritis), however, and, as noted by the Clinical Assessor to the Convener in his report, the question is not so much whether or not measurement of serum bile salts should have been carried out, but more whether induction of labour should have been recommended. There was some uncertainty about this at the time, which was influenced mainly by the state of the cervix (for comments on this, see complaint (ii) below) and possibly by not appreciating how marked the pruritis was. Mrs T believes that she should have been induced earlier because of obstetric cholestasis. However, we consider, on the basis of her minimal symptoms and essentially normal liver enzyme tests, apart from the alkaline phosphatase, that there was no indication to induce her. In other words, her clinical symptoms of obstetric cholestasis were not severe enough to warrant induction of labour. That said, there were other clinical features which did warrant early induction (see our comments on complaint (ii) below.) We would agree with the Clinical Assessor to the Convener who said that this whole area is a ‘gradually evolving scene’ and that currently no minimum standards have been set by the Royal College of Obstetricians and Gynaecologists for the delivery of the foetus in evolving cholestasis of pregnancy. One of us has recently co-written an editorial, published in the British Medical Journal, which states, ‘Obstetric cholestasis (or intrahepatic cholestasis of pregnancy) remains widely disregarded as an important clinical problem, with many obstetricians still considering its main symptom, pruritis, a natural association of pregnancy …’. *
xiv) As we note above, the liver enzymes and bilirubin tests measured in two of Mrs T’s pregnancies (1997 and 1999) were in the normal ranges for the biochemical laboratory at the Hospital. That is not unusual and the diagnosis may be made early on clinical grounds alone. Mrs T had symptoms of pruritis in both pregnancies without biochemical evidence of cholestasis. The Hospital’s medical staff therefore saw no reason to request a bile acid measurement at that time and it would appear, in any case, that this was not then common practice at the Hospital (paragraph 10). That was reasonable in the circumstances at the time. The medical staff also did not see any reason to induce labour on the basis of Mrs T’s liver function tests or her symptoms of itch. We consider that that too was reasonable at the time. As we note above, Mrs T’s minimal symptoms of cholestasis were not sufficient of themselves to warrant inducing her. Given the lack of understanding of that condition in 1999, we conclude that the care given to Mrs T with respect to the cholestasis was not unreasonable. We would conclude that, with such normal liver tests, if Mrs T did have cholestasis, it was of minor order.
Comments on complaint (ii)the Trust failed to monitor Mrs T and her baby
xv) We note that the Trust has accepted that Mrs T’s blood pressure should have been monitored on 14 September 1999; the Trust has apologised for that. The Trust has also said that the CTG taken on the morning of admission was adequate in the circumstances, given that staff believed that Mrs T was suffering from pre-eclampsia. (That was a reasonable diagnosis in the circumstances of high blood pressure and proteinuria.) We note that the Trust has also reviewed all labour ward protocols and has changed its policy on the taking of CTGs. We feel that this is now in line with current practice.
xvi) As has already been pointed out in the previous paragraph, however, Mrs T had symptoms of pre-eclampsia (significantly raised blood pressure and proteinuria) on 14 September 1999 and she was 39 weeks pregnant. In view of that, we believe that consideration should have been given to inducing labour, rather than just treating the raised blood pressure. Failure to do so put Mrs T at risk of fits and also put the foetus at risk. It is important to note that this was a second pregnancy in which Mrs T’s blood pressure had been raised. The Clinical Assessor to the Convener noted that there had been hesitation in the decision to induce Mrs T due to the state of the cervix. It is our view that the state of the cervix is not an issue in the induction of labour: prostaglandins can be used to ripen and soften the cervix for delivery. Thus Mrs T could have been induced and, if she had been, closer monitoring would have taken place and foetal distress may have been picked up earlier. That would also have allowed earlier recourse to Caesarean section. Sadly, we will never know whether this would have prevented the tragic outcome for Mrs T’s baby.
Conclusion
xvii) It is our opinion, based on the evidence we have seen, that the care that Mrs T received during the third trimester in 1999, in respect of the cholestasis, did not fall below that which she could reasonably have expected in the circumstances and that, despite the possibility of pregnancy cholestasis, this of itself was not a feature which would have decided early induction of labour. Nevertheless, given Mrs T’s general conditionraised blood pressure, proteinuria (and notwithstanding possible obstetric cholestasis)we consider that she should have been induced earlier. That course of action would have led to further monitoring of the foetus; foetal distress may therefore have been picked up sooner, and there would have been earlier recourse to Caesarean section. We consider, therefore, that the monitoring of Mrs T and her baby was inadequate. It is our view that there are many factors which may have contributed to the demise of the foetus. The Trust has already apologised for certain failings in this case but there is no evidence that they acted other than in a competent fashion, given the laboratory results that they had.
Recommendations
- We recommend that in any future pregnancies, Mrs T has careful monitoring of liver tests including bile acids and clotting studies as well as blood pressure.
- Although the Trust revised its labour ward protocols in October 2000, we recommend that the guidelines covering management of hypertension, severe hypertension and pre-eclampsia should be further reviewed in the light of our findings in paragraph xvi above.
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Findings (a)
20. Mrs T has complained that her care and treatment were inadequate. In considering the complaint that the Trust failed to diagnose obstetric cholestasis, I have taken into account the views of the Ombudsman’s Assessors as set out in paragraph 19. Mrs T complained that she had all the typical symptoms of obstetric cholestasis: her itching was so severe that she was using a hairbrush to scratch herself and making herself bleed; she had proteinuria, dark urine, high blood pressure and was ‘feeling awful.’ She said that staff ignored these symptoms. When she supplied a list of her symptoms to the staff at the second Trust in December 1999, a probable diagnosis of obstetric cholestasis was made. The Chief Executive has acknowledged that Trust staff did not diagnose obstetric cholestasis. He has pointed out, however, that it is an extremely rare condition in the white population and that Mrs T’s liver function tests were normal at the time. He added that, while subsequent investigations carried out by the second Trust suggested that obstetric cholestasis was a possible diagnosis, those tests did not confirm that Mrs T had the condition during her pregnancy. He also pointed out that the diagnosis was made only retrospectively by the second Trust, and that, in September 1999, staff had thought that Mrs T was suffering from pre-eclampsia. The Assessors consider that the diagnosis of pre-eclampsia was reasonable in the circumstances, given Mrs T’s presentation with high blood pressure and proteinuria.
21. The Assessors have commented that, had bile acids been measured and found to be increased, that would have confirmed the clinical diagnosis of obstetric cholestasis. They have said that such tests would now be usual medical practice and they note that the Trust has indeed changed its policy in this respect. That said, it is acknowledged that the results of Mrs T’s liver function tests were essentially normal, and the Assessors have commented that it was therefore not unreasonable in the circumstances at the time that Mrs T was not referred for further bile salt analysis. The liver function test results suggest that the cholestasis was of a minor order; and, given those results, the Assessors conclude that it was also reasonable in the circumstances at the time in 1999 that Trust staff did not decide to induce labour in so far as obstetric cholestasis is concerned. In other words, Mrs T’s presentation in terms of obstetric cholestasis was not one that would have indicated early induction of labour.
22. The Assessors conclude that Mrs T’s care during the third trimester of her 1999 pregnancy, in respect of cholestasis, did not fall below that which she could reasonably have expected in the circumstances. It is clear that staff did not realise that Mrs T might have obstetric cholestasis, especially given the normal liver enzyme test results and liver function tests. I note the advice of the Ombudsman’s professional adviser (paragraph 16) that it would be helpful in making a diagnosis of obstetric cholestasis to measure the level of GGT. I infer from the Assessors’ report, that the condition of obstetric cholestasis was not properly understood by obstetricians in 1999 and, indeed, I note that a recent editorial by one of the Assessors indicates that that seems to remain the case among many obstetricians today. It is in that context that I consider that it was not unreasonable that the clinicians in charge of Mrs T’s care in 1999 did not diagnose obstetric cholestasis. I do not uphold the complaint. I refer the Trust to the recommendation made by the Ombudsman’s Assessors in paragraph 19; I also recommend that the Trust considers the possibility of measuring the GGT levels of patients who are suspected of having obstetric cholestasis.
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Findings (b)
23. Mrs T complained that she and her baby had not been adequately monitored. She said that she had high blood pressure but this was only monitored at 1.00pm and 8.00pm on the day of her delivery; no other form of monitoring was carried out until she requested help at 9.00pm that evening. She believes that the lack of attention to her condition led to Baby Y’s death. The Chief Executive has acknowledged that the blood pressure monitoring was inadequate on 14 September 1999, in that Mrs T’s blood pressure was not taken for a period of seven hours. He has apologised for that. He has said, however, that the CTG tracing taken on the morning of 14 September was satisfactory and had been appropriate for a patient with pre-eclampsia, from which staff believed Mrs T was suffering at that time. The Trust has, nevertheless, now adopted the practice of taking a CTG tracing twice daily, even if the first trace is normal. The Assessors believe that that is more in line with current practice. They conclude that the monitoring of Mrs T and her baby was inadequate: I agree.
24. The Assessors have raised a further serious concern. They point out that Mrs T had pre-eclampsia (she had significantly raised blood pressure and proteinuria) and she was in her 39th week of pregnancy. They consider that those factors taken together were an indication for labour to be induced and that staff should not, therefore, simply have treated the raised blood pressure. It is their view that, if Mrs T had been induced earlier, closer monitoring would have taken place and foetal distress might have been picked up sooner. That would also have allowed earlier recourse to Caesarean section. Unfortunately, it is not possible to say whether that would have altered the tragic outcome, or to confirm confidently the cause of Baby Y’s demise. Nevertheless, Mrs T had a condition that warranted induction of labour; the proper management of which would have resulted in increased monitoring of both Mrs T and Baby Y. I, therefore, uphold the complaint that the monitoring of Mrs T and her baby was inadequate. I recommend that the Trust reviews its protocols on the management of patients with hypertension, severe hypertension and pre-eclampsia, as suggested in the Assessors’ report at paragraph 19.
Conclusions
25. This is a very sad case and I send my deepest sympathy to Mr and Mrs T for their tragic loss. I have set out my findings in paragraphs 20-24. The Trust has agreed to implement my recommendations in paragraphs 22 and 24 and have asked me to convey through my reportas I do – its apologies to Mr and Mrs T for the shortcomings I have identified.
* British Medical Journal, Volume 324, 19 January 2002.
Short report of this investigation
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