Last week, I received a call from my specialist about a man who was admitted 24 hours ago with diabetic ketoacidosis. His metabolic acidosis was severe, pH 6.9 and given bicarbonate therapy. His ketoacidosis improved with insulin therapy but his amylase level was increased. Because of possible acute pancreatitis, I admitted him to ICU for observation.
I reviewed him later in the ICU and noticed that his ABG on admission still showed AG metabolic acidosis (and require insulin for ketoacidosis) but in general he was improving. His Ranson score for initial 24 hours was only 1 and within 48 hours score was less than one. No significant finding on US abdomen/hepatobiliary, but CT scan was not done. He was discharged well the following day.
Comment:
The most common precipitating causes for DKA and HHS are infection and discontinuation of or inadequate insulin therapy. Others are acute illnesses such as CVA, MI and acute pancreatitis. Sometimes I used the pneumonic I GET SMASHED to go through the possible precipitating events.
Serum amylase and lipase are the standard tests to diagnose acute pancreatitis, but are often elevated in patients with DKA who do not have pancreatitis. As a result, the diagnosis of pancreatitis in patients with DKA should be based upon clinical findings and CT scan. The mechanisms for hyperamylasemia and hyperlipasemia in DKA are not well defined, but the following observations have been made:
1. In 100 consecutive cases of DKA, 11 had acute pancreatitis as confirmed by CT scan. The most common causes were hypertriglyceridemia and alcohol intake. 2 did not have abdominal pain. (Am J gastroenterol 2000)
2. In a review of 134 consecutive episodes of DKA in patients with no CT evidence of acute pancreatitis, elevations of serum amylase and lipase ( 3x or higher) were seen in 17 and 24% respectively. Abdominal pain was present in 19% of the series. (Am J of gastroenterol 2000)
3. The source of these nonspecific amylase elevations is most often salivary though may also be pancreatic. The source of nonspecific lipase elevations is not known.
4. The rise in amylase correlates with pH and plasma osmolality, while the rise in lipase correlates only with plasma osmolality. Peak values are seen within 24 hours of presentation.
I reviewed him later in the ICU and noticed that his ABG on admission still showed AG metabolic acidosis (and require insulin for ketoacidosis) but in general he was improving. His Ranson score for initial 24 hours was only 1 and within 48 hours score was less than one. No significant finding on US abdomen/hepatobiliary, but CT scan was not done. He was discharged well the following day.
Comment:
The most common precipitating causes for DKA and HHS are infection and discontinuation of or inadequate insulin therapy. Others are acute illnesses such as CVA, MI and acute pancreatitis. Sometimes I used the pneumonic I GET SMASHED to go through the possible precipitating events.
Serum amylase and lipase are the standard tests to diagnose acute pancreatitis, but are often elevated in patients with DKA who do not have pancreatitis. As a result, the diagnosis of pancreatitis in patients with DKA should be based upon clinical findings and CT scan. The mechanisms for hyperamylasemia and hyperlipasemia in DKA are not well defined, but the following observations have been made:
1. In 100 consecutive cases of DKA, 11 had acute pancreatitis as confirmed by CT scan. The most common causes were hypertriglyceridemia and alcohol intake. 2 did not have abdominal pain. (Am J gastroenterol 2000)
2. In a review of 134 consecutive episodes of DKA in patients with no CT evidence of acute pancreatitis, elevations of serum amylase and lipase ( 3x or higher) were seen in 17 and 24% respectively. Abdominal pain was present in 19% of the series. (Am J of gastroenterol 2000)
3. The source of these nonspecific amylase elevations is most often salivary though may also be pancreatic. The source of nonspecific lipase elevations is not known.
4. The rise in amylase correlates with pH and plasma osmolality, while the rise in lipase correlates only with plasma osmolality. Peak values are seen within 24 hours of presentation.
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