Letters

Acute pancreatitis

BMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7149.1982b (Published 27 June 1998) Cite this as: BMJ 1998;316:1982

Normal serum amylase does not exclude severe acute pancreatitis

  1. James K Torrens, Specialist registrar,
  2. P H M McWhinney, Senior registrar
  1. Department of Infectious Diseases, Seacroft Hospital, Leeds LS14 6UH
  2. Intensive Care Unit, Chelsea and Westminster Hospital, London SW10 9NH
  3. 24 Manor Park, Richmond, Surrey TW9 lXZ

    EDITOR—Mergener and Baillie highlight the problem of diagnosing acute pancreatitis if too much reliance is placed on the serum amylase level, drawing attention to the relatively low specificity of the test.1 They also state that amylase is rapidly cleared from the kidneys, and this, along with other factors, may lead to a normal serum amylase level even in the presence of necrotising pancreatitis.2

    We have recently seen two patients with severe necrotising pancreatitis and normal serum amylase levels (one of whom also had a normal result on abdominal ultrasonography), which led to a delay in establishing the correct diagnosis. Computed tomography showed pancreatic necrosis in both cases, and both patients required management in intensive care; one died subsequently from sepsis and multiorgan failure.

    Clinicians need to be aware not only of alternative causes of raised serum amylase but also of the fact that a normal serum amylase does not exclude severe forms of acute pancreatitis, which are associated with a high morbidity and mortality.

    References

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    Major haemorrhage may be a late complication

    1. Ganesh Suntharalingam, Senior registrar,
    2. Richard Keays, Consultant,
    3. Neil Soni, Director
    1. Department of Infectious Diseases, Seacroft Hospital, Leeds LS14 6UH
    2. Intensive Care Unit, Chelsea and Westminster Hospital, London SW10 9NH
    3. 24 Manor Park, Richmond, Surrey TW9 lXZ

      EDITOR—In their clinical review of acute pancreatitis Mergener and Baillie point out that patients often get worse before they get better and so outcome may depend on careful monitoring for complications.1 Such a review should also raise awareness of potential life threatening complications even if they are rare. One such is delayed major haemorrhage due to large vessel erosion associated with pancreatitis, which we believe is an underrated phenomenon because of its perceived infrequency.

      Major haemorrhage complicating both acute and chronic pancreatitis is well described and of formidable severity. Flati et al reported eight cases and reviewed a further 389 cases in the literature, finding a mortality of 60.4% in haemorrhage associated with acute pancreatitis.2 The condition is potentially treatable: embolisation under radiological guidance is an established technique, 3 4 while surgical treatment by pancreatic resection or vessel ligation has been reported in 15 patients with pancreatic disease, six with acute pancreatitis.5 A comprehensive search of the computerised patient database at our own intensive care unit has shown that of the 36 patients admitted to the unit with acute pancreatitis during 1990-8, five developed acute major haemorrhage. Two had pseudoaneurysms of the splenic artery embolised by angiography and survived the haemorrhagic episode (one died later), two died of uncontrollable bleeding from lumbar vessels despite laparotomy, and one died suddenly of haemorrhage after discharge from the unit. In four of these five cases the haemorrhage occurred as a late event in patients who were recovering from the most severe stage of their pancreatitis. This is an important incidence in a clearly defined group of patients and suggests that haemorrhage in patients with acute pancreatitis that requires support in an intensive care unit is underreported.

      Thus we found that although major vessel haemorrhage complicating acute pancreatitis is uncommon, it has a significant rate of occurrence, particularly after severe disease requiring support in an intensive care unit. Its onset may be rapid and catastrophic, and it is potentially treatable by radiological and surgical measures once identified. We believe that this makes it worthy of listing in even the most generalised discussion of acute pancreatitis, as awareness is essential for rapid recognition and intervention.

      References

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      Alexander the Great may have died of acute pancreatitis

      1. Lars H Breimer, Clinical research physician
      1. Department of Infectious Diseases, Seacroft Hospital, Leeds LS14 6UH
      2. Intensive Care Unit, Chelsea and Westminster Hospital, London SW10 9NH
      3. 24 Manor Park, Richmond, Surrey TW9 lXZ

        EDITOR—Mergener and Baillie's clinical review of acute pancreatitis prompted me to remember the circumstances surrounding the death of Alexander the Great.1 Alexander was 32 when he died on 10 June 323 BC in Babylon after an illness lasting 12 days. The exact cause of his death has never been established, but the descriptions are consistent with acute pancreatitis as a consequence of an extended period of excessive alcohol intake.2

        Sources agree that Alexander became ill unexpectedly on 29 May, when he attended a party dining and drinking into the night, but the descriptions vary about what followed. One account claims that Alexander suddenly felt ill while drinking; another that he shouted with pain as if struck through the liver with an arrow; and a further source indicates that he did not sicken until just after leaving the party.

        All accounts agree that Alexander gradually declined after the party but remained rational, discussing the next campaign. After a day he was moved to another palace, which was cooler. By 7 June, however, he was very ill and returned to the main palace. Two days later various commanders and officers visited him. The next day he died. There is a story that, realising that he was about to die, he crawled out of his room (he was too weak to walk) to commit suicide by throwing himself into the river, but he was intercepted.

        Thus Alexander seems to have had a sudden onset of severe, probably upper, abdominal pain which may have radiated to his back. He then declined over almost two weeks but remained lucid. He spent this time lying down. The likely diagnosis is acute pancreatitis, with a perforated ulcer as the main differential diagnosis. A dissecting aneurysm or malaria is unlikely, as is poisoning, although this last is possible. Finally, he could have suffered a spontaneous pneumothorax at the banquet. He had received a chest wound at the fort of Multan on the return from the Indus.

        Alexander had settled in Babylon after his disastrous return from India, when he had lost his army. He was planning new campaigns, initially against Arabia, but he probably considered that he would have difficulty mustering new forces. Also, because he had had India in his hand and lost it, everything else would have seemed trivial. Thus accounts of Alexander holding recurrent drinking parties, sitting up all night, and then sleeping it off the next day are plausible.

        References

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