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Author's Response

Lowe, Mark E

Journal of Pediatric Gastroenterology and Nutrition: July 2011 - Volume 53 - Issue 1 - p 112
doi: 10.1097/MPG.0b013e31821c1164
Letters to the Editor

Division of Gastroenterology, Hepatology and Nutrition Children's Hospital of Pittsburgh of UPMC Pittsburgh, PA, USA

To the Editor: I would like to thank Dr Hauer for suggesting that hypothermia be included in the differential of acute pancreatitis. The literature on hypothermia as a cause of pancreatitis is sparse, particularly in pediatrics. Like many proposed etiologies for acute pancreatitis, the role of hypothermia is based on temporal associations rather than cause and effect. The few reports, such as the one cited in the letter, are retrospective and include small numbers (1,2). The patients had variable and usually incomplete investigations to exclude other possible causes of pancreatitis. In some, there were other comorbid conditions, such as gallstones, that could cause pancreatitis. Often it is impossible to determine whether the hypothermia preceded the symptoms of acute pancreatitis. Perhaps the hypothermia was a response to systemic inflammation secondary to pancreatitis, especially in children with autonomic dysfunction.

Other investigators have looked for a connection between hypothermia and pancreatitis in necropsies of patients who had been hypothermic. The results are inconclusive. A study from 1969 described foci of pancreatic fat necrosis or hemorrhage in 67% of 43 patients, suggesting that hypothermia could result in pancreatic injury (3). A more recent study of 143 necropsies failed to confirm the high incidence of pancreatic hemorrhage, raising doubt about a causal relationship between hypothermia and acute pancreatitis (4). Furthermore, in animal models of acute pancreatitis, hypothermia protects against pancreatic injury and systemic inflammation (5).

Underlying this discussion is a critical issue. We know little about the etiologies and treatment of acute pancreatitis; it is impossible to make concrete conclusions in many cases. Until we have better information, which can only come from a systematic study of acute pancreatitis in children, the approach suggested in the accompanying letter seems reasonable. If no other etiology for acute pancreatitis is found in a patient with a temporal association of hypothermia and acute pancreatitis, then simple measures to maintain body temperature should be used going forward.

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1. Hauer JM. Central hypothermia as a cause of acute pancreatitis in children with neurodevelopmental impairment. Dev Med Child Neurol 2008; 50:68–70.
2. Stiff RE, Morris-Stiff GJ, Torkington J. Hypothermia and acute pancreatitis: myth or reality? J R Soc Med 2003; 96:228–229.
3. Mant K. Autopsy diagnosis of accidental hypothermia. J Forensic Med 1969; 16:126–130.
4. Preuss J, Lignitz E, Dettmeyer R, et al. Pancreatic changes in cases of death due to hypothermia. Forensic Sci Int 2007; 166:194–198.
5. Fujimoto K, Fujita M, Tsuruta R, et al. Early induction of moderate hypothermia suppresses systemic inflammatory cytokines and intracellular adhesion molecule-1 in rats with caerulein-induced pancreatitis and endotoxemia. Pancreas 2008; 37:176–181.
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