JRSM >
Volume 96, Number 5 >
Pp. 228-229
Department of Surgery, University Hospital of Wales, Heath Park, Cardiff CF14 4XN, UK
Correspondence to: Dr Rhianwen Stiff, 26 Canada Road, Heath, Cardiff CF14 3BW, UK E-mail: rhianwenstiff{at}hotmail.com
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The 31 consultants who returned our questionnaire (69% response rate; 317 consultant-years' experience) could recall only 5 cases of pancreatitis associated with hypothermia, in 2 of which other aetiological factors were judged primary. In case-notes for 100 months of emergency admissions at a single hospital we identified 310 patients with hypothermia and 1153 with acute pancreatitis; none had the dual diagnosis. Of the hypothermic patients, none had abdominal pain typical of acute pancreatitis. In 43 serum amylase was measured because the patient was unable to give a full history and in 2 of these the enzyme was slightly raised; both had experienced a cerebrovascular accident, which is a known cause of hyperamylasaemia.
Considered alongside the weak evidence from previous studies, these findings offer negligible support for the idea that hypothermia is a clinically relevant risk factor for acute pancreatitis.
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| METHODS |
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| RESULTS |
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Analysis of medical records
Between April 1990 and August 1998, 210 patients were admitted with a
diagnosis of hypothermia and 1153 with a diagnosis of acute pancreatitis; none
had both. Of those with hypothermia, the mean age was 62.5 years (range 1-97),
male to female ratio 3:2. None of the hypothermic patients complained of
abdominal pain at the time of admission. 43 had their serum amylase measured,
the reason in all cases being absence of a clinical history due to a reduced
level of consciousness at the time of admission. Amylase was above normal in
2, but in neither was it greater than 250IU/L; both these patients had had
cerebrovascular accidents and survived the hypothermic episode; neither, at
any stage, had evidence of abdominal pain.
| DISCUSSION |
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In 1969 Mant1 reported necropsies in 43 patients who had been hypothermic, and described pancreatic changes varying from occasional foci of fat necrosis to frank haemorrhage in 29 (67%). He suspected that the lesions were due to the hypothermia and seems to have dismissed the possible contribution of other factors: 3 had been sleeping in the open during cold weather in London; 7 had a history of mental illness; 3 had Alzheimer's disease; 3 had severe chronic debilitating natural disease (unspecified); and 3 had become hypothermic as a result of criminal activity (a neglected infant, a road-accident victim left at the roadside and an elderly woman left bound and gagged in her home). In 1982, Foulis2 tried to clarify the relation with a morphological analysis of 8 cases. From the patterns of pancreatic necrosis he proposed three possible mechanisms: (1) microcirculatory shock of hypothermia causing pancreatic necrosis; (2) both hypothermia and pancreatitis secondary to alcohol abuse, and (3) severe pancreatitis the primary disease with hypothermia developing especially in the socially deprived. Of Foulis' 8 patients, 2 had gallstones and 3 were chronic alcoholics; 5 had had unrecordable blood pressure on admission, prompting a hypothesis that hypotension rather than hypothermia might be a risk factor for pancreatitis. With so few patients it is difficult to draw conclusions.
The only other published evidence comes from two isolated cases. Mahood and Evans3 described hypothermia and pancreatitis in a man of 65: he was a known alcohol abuser; moreover, he developed disseminated intravascular coagulopathy before any clinical or biochemical evidence of pancreatitis. The second4 came from a series of 45 cases of fatal acute pancreatitis: the pancreatitis was said to have occurred ‘... possibly from hypothermia’ but this patient also had unexplained somnolence and the association was not straightforward
Both hypothermic patients with hyperamylasaemia in our study had suffered cerebrovascular accidents, and intracranial bleeding is a known cause of raised serum amylase. Bouwman and colleagues found hyperamylasaemia in 6 of 10 patients with isolated head trauma and CT evidence of intracranial bleeding, and concluded that serum amylase is not a reliable marker for pancreatic trauma in a patient with multiple injuries.5
Probably the most telling evidence against a direct role of hypothermia in causing pancreatitis comes from pancreatic transplantation where a procured organ is submerged in ice for up to 24 hours and on rewarming is expected to function normally. Although slight hyperamylasaemia is not uncommon after transplantation, moderate or severe acute pancreatitis is rare. In view of the lack of positive evidence, and indeed a tendency towards negative evidence, we conclude that hypothermia is unlikely to be an important risk factor for the development of acute pancreatitis.
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