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Causes of obvious jaundice in South West Wales
  1. E H Forrest1,
  2. J A H Forrest1
  1. 1Department of Gastroenterology, Victoria Infirmary, Langside Rd, Glasgow G42 9TY, UK
  1. Correspondence to:
    E H Forrest;
  1. J G C Kingham2,
  2. M W Whitehead2,
  3. I Hainsworth3
  1. 2Department of Gastroenterology, Singleton Hospital, Sketty, Swansea SA2 8QA, UK
  2. 3Department of Pathology, Morriston Hospital, Swansea SA6 6NL, UK

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We read with interest the article describing the causes of obvious jaundice (serum bilirubin >120 μmol/l) in South West Wales (Gut 2001;48:409–13). The authors make the point that contrary to the perception of many doctors, viral hepatitis is an unusual cause of jaundice (two of 121 cases) while sepsis/shock is a relatively common cause (27 of 121 cases).

We have performed a retrospective assessment of 100 cases of jaundice identified on biochemical testing who had presented to the Accident and Emergency Department or had been admitted to the acute medical or surgical admission wards at Stobhill Hospital, Glasgow. Our survey therefore looked at acute admissions with jaundice while that of Whitehead et al also included established inpatients who developed jaundice (22 of 117 inpatient cases). We drew a lower cut off levelof serum bilirubin (>60 μmol/l) as above this level jaundice should be clinically detectable.

The causes of jaundice we identified differed significantly from those of Whitehead et al (fig 1). The predominant cause in our series was alcoholic liver disease (ALD) which may reflect the catchment area of our hospital. Only two patients presenting with jaundice had a diagnosis of “shock/sepsis”. It should be noted that 20 of the 27 patients with “shock/sepsis” in the South West Wales series developed jaundice as inpatients. Rather than suggest “shock/sepsis” as a common reason for jaundice which is often overlooked, it might have been more accurate to note that jaundice due to shock/sepsis often occurs in a particular clinical setting such as an intensive care unit, postoperatively, or in patients with multiple medical problems. In this context we doubt the aetiology of the jaundice is “overlooked”. Our own study clearly indicates that shock/sepsis is indeed an unusual reason for patients to present to medical care with jaundice.

The authors also noted that 16 of 61 patients with common bile duct (CBD) stones had a bilirubin level greater than 120 μmol/l, and comment that such high levels of bilirubin are more likely to be related to malignant obstruction. In contrast with this, our own series demonstrated that 10 of 29 patients with CBD stones had bilirubin values greater than 120 μmol/l. There was no difference in mean bilirubin values between patients with CBD stones and those with malignant disease (120 (±15) v 168 (±28) μmol/l), nor indeed with those with ALD (142 (±18)).

We also have a concern about the accuracy of diagnosis on a retrospective review of the causes of liver disease, particularly as gastroenterologists managed only one third of patients in the Welsh study. In our series we noted that few patients had a “complete” serological screen for liver disease. It is therefore possible that patients might have been inadequately investigated and so were placed in an inappropriate diagnostic group.

The authors also highlight the value of the aspartate aminotransferase:bilirubin ratio in the assessment of jaundice. A further analysis of our own data does not substantiate the use of this value in diagnosis. Mean values for ALD, gall stone related jaundice, and malignancy were 3.5, 3.8, and 2.7, respectively (NS).

In conclusion, we believe that the perception of most clinicians that shock/sepsis is an unusual cause for patients to present with jaundice to medical care is an accurate one. Shock/sepsis related jaundice is much more likely to develop among inpatients with complex disease. We do agree that viral hepatitis is an unusual cause for jaundice, although investigation of viral disease is still an important aspect of the assessment of such patients. We also agree that jaundice is associated with a significant inpatient death rate (32% in Whitehead's series and 19% in our own).

Figure 1

Causes of jaundice. ALD, alcoholic liver disease.

Authors' reply

We thank Drs E and J Forrest for the interest they have shown in our article on jaundice and we were pleased to learn of their retrospective assessment of 100 cases of jaundice presenting to acute services in a large Glasgow hospital. Although they emphasised the differences between their experience and ours, this is the nature of medical correspondence and we were more struck by the similarities which we found gratifying. The series cannot be compared too closely because of differences in methodology and case ascertainment. In particular, our study was prospective, community and hospital based, and included all patients with bilirubin values greater than 120 μmol/l. Forrest and Forrest's observations are retrospective, relate specifically to patients presenting to hospital because of jaundice, and use a cut off bilirubin level of >60 μmol/l.

We will respond to their comments seriatim.

  1. The commonest cause of presentation with jaundice to Stobhill Hospital was alcoholic liver disease. In Swansea, if analysis is restricted to those 95 patient presenting to hospital with jaundice, then alcoholic cirrhosis ran a very close second to malignancy as the commonest cause.

  2. As Forrest and Forrest point out, sepsis/shock is not a common cause of jaundice requiring admission to hospital either in Glasgow or Swansea, but in our experience was the predominant cause of jaundice developing while in hospital for other reasons. As to whether it is overlooked, our results speak for themselves—in over one third of our sepsis/shock cases jaundice had been erroneously attributed to some other cause by the clinical team managing the case.

  3. Ten of 29 (34%) Glasgow cases and 16 of 61 (26%) Swansea cases with common bile duct (CBD) stones had bilirubin levels >120 μmol/l. Given the relatively small sample sizes we consider these to be similar rather than dissimilar proportions. The absolute values of bilirubin from the two centres cannot be compared without knowledge of the timing of samples. Clearly, samples taken on admission might show lower bilirubin levels than samples taken later on, particularly with malignant biliary obstruction awaiting mechanical relief. Our experience is that gall stone biliary obstruction was often transient and not profound whereas malignant obstruction led to ever increasing levels of bilirubin unless there was mechanical intervention.

  4. We share Forrest and Forrest's concern about the accuracy of diagnosis on retrospective case note review but respectfully point out that our study was prospective while theirs was retrospective. We accept that not every patient in the Swansea series had every investigation but we cannot consider it good practice to perform tests unless clinically indicated. Thus most patients with proven obstructive jaundice did not have serological tests whereas most patients with intrinsic hepatocyte dysfunction did.

  5. Our observations on aspartate aminotransferase (AST):bilirubin ratios were for interest alone. We did not propose that this should be used as a test but simply commented that the ratio had some diagnostic value. Our only comment on the Glasgow figures relates to their patients with alcoholic liver disease where the ratio was reported to be 3.5. Mean bilirubin level for this group was 142 μmol/l which translates to a mean AST value of approximately 500 IU/l. This is an exceptionally high figure for AST in alcoholic liver disease where AST is characteristically much lower, usually <200 IU/l.

  6. Causes of jaundice and causes of jaundice requiring hospital admission are not the same and clinicians should guard against using the experience of one clinical setting when assessing another.

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